Cardiac, the reference

The algorithm checks urgency first because, when life or limb is threatened, delay is itself the danger. Tests and consults only hold up an operation that has to happen anyway. The team accepts that the risk of major cardiac events is higher and treats the patient medically while moving to theatre. The time threshold has changed. The 2014 guidance, which Miller and Barash reproduce, counted surgery as an emergency within 6 hours. The newer AHA/ACC guideline narrows emergency to under 2 hours. Under either definition, cardiac assessment is skipped.

Delaying surgery for cardiac results. Deep T waves, ST depression and a small troponin rise look like an acute coronary syndrome, so serial enzymes and a cardiology opinion seem prudent. But a bleeding cerebral aneurysm is an emergency. Waiting for results delays securing it, and the algorithm sends emergencies straight to theatre.

The AHA/ACC guideline defines emergency surgery as an immediate threat to life or limb with little or no time for clinical evaluation, typically under 2 hours. Miller and Barash give the superseded 6-hour cut-off. Either way, patients go straight to surgery without further cardiac assessment.

Sources: Miller 10eAHA/ACC 2024 · §1.5Barash 9e

A test is worth doing only if it alters a decision: revascularising coronary disease before the planned operation, which delays it, refining medical therapy, or choosing a palliative path. Coronary treatment stands on its own indication, not as a ticket through surgery, so a result that would trigger treatment anyway justifies testing. Stress testing is kept for poor or unknown capacity, below 4 METs. Those at or above it proceed. If a patient cannot exercise, dobutamine is used to raise myocardial oxygen demand instead.

Testing based on risk alone. Elevated risk feels like a reason to investigate, but risk alone never triggers testing. A patient achieving 4 METs goes ahead without a stress test. Even with poor capacity, the test is justified only if a positive result would change the plan.

Guidelines treat coronary intervention independently of surgery. Extra tests are reasonable when results alter decisions, such as revascularisation before surgery, medical optimisation or palliation. Stress testing suits capacity under 4 METs. Echocardiography answers focused questions, like unexplained dyspnoea or very low exercise capacity.

Sources: Stoelting 8eBarash 9eMiller 10e

Urgency is the first question in the ACC/AHA pathway. Cardiac testing before surgery is only worth doing if its benefit outweighs the harm of putting off the operation. In a true emergency, the delay itself is the bigger danger. No test result would let the operation be cancelled or safely postponed. So the cardiac risk is accepted once the decision to operate is made. It is then managed with haemodynamic monitoring, serial ECGs and cardiac enzymes, and early treatment of any cardiovascular complication after surgery.

Catheterisation delays emergency operation. Recent infarction plus overt heart failure feels like an active cardiac condition demanding angiography first. But catheterisation, and any revascularisation it prompts, delays an operation that cannot wait; in an emergency, the surgery takes priority and cardiac risk is handled through perioperative monitoring and treatment.

Guideline algorithms grade urgency first: emergency surgery proceeds to theatre without further cardiac assessment. Effort shifts to postoperative surveillance (serial enzymes, ECGs, haemodynamic monitoring) and early treatment of cardiovascular complications. For time-sensitive, non-emergency surgery, testing is weighed against the cost of delay.

Sources: Stoelting 8eMiller 10e

Before surgical risk or functional capacity is scored, the guideline pathway first asks whether an unstable cardiac problem is present. Angina at rest that nitrates relieve is unstable angina. ST elevation means an acute coronary syndrome is under way. Both are active conditions, so the heart comes first. Cardiology assesses and treats the patient, and only after that is the planned operation weighed again on its risks and benefits. Ordering more tests or going ahead with surgery skips this step.

Stress testing for rest angina. Stress testing sounds like the logical cardiac work-up, and one text even links active conditions with noninvasive testing. But testing is for risk-stratifying stable patients when the result would change management. A patient with rest angina already has an active condition that needs cardiology treatment, not more tests.

Before non-emergency surgery, the guideline pathway first rules out active cardiac conditions, including unstable angina. These need guideline-directed treatment and cardiology evaluation, with elective surgery delayed and reconsidered afterwards. A suspected acute coronary syndrome warrants urgent cardiology consultation.

Sources: Stoelting 8eFaustMiller 10e

A preoperative test is only worth doing if its result would change management. Before a low-risk procedure, the chance of finding coronary anatomy bad enough to change the surgical outcome is small. Testing therefore adds cost and delay without improving outcomes. Known coronary disease or risk factors do not change this. Functional capacity only matters once the patient is in the elevated-risk group. Stress testing comes after that, when capacity is poor or unknown.

Stress testing in low-risk surgery. In a known cardiac patient, a stress test feels like the careful choice, and stress testing is part of the algorithm. But it is kept for elevated-risk patients with poor or unknown functional capacity, and only when the result would change management. Low-risk surgery never gets to that step.

The guideline advises against testing stable patients before low-risk non-cardiac surgery: it is costly, delays surgery and has not improved outcomes. The chance of finding coronary anatomy that would change the outcome is small, with or without coronary disease or risk factors.

Sources: AHA/ACC 2024 · §4.3AHA/ACC 2024 · §4.5Stoelting 8e

Assessment runs in order: clinical risk first; functional capacity matters only for elevated-risk patients. The risk index scores established heart, cerebrovascular or renal disease and high-risk surgery. Hypertension, smoking, lipids and non-insulin diabetes do not score, and knee replacement is not high-risk. This patient leaves the pathway early, and stair climbing limited by joint pain is irrelevant. Stress testing only adds cost and delay. If a test must be chosen, brain natriuretic peptide is the screen advised for anyone with risk factors or aged 65 or over.

Stress testing despite low-risk status. Poor or unknown functional capacity does send patients to pharmacological stress testing, so joint pain seems to fit. But that branch applies only after a patient is judged elevated-risk. With a risk index of zero the patient never reaches it.

Low-risk patients (RCRI 0) need no further cardiac work-up or stress testing. For elevated risk with poor or unknown capacity, Stoelting refers for pharmacological stress testing; Miller advises natriuretic peptides in patients with cardiovascular disease, symptoms or risk factors.

Sources: AHA/ACC 2024 · §4.3Stoelting 8eMiller 10eFaustOutside our books: Preoperative functional workup for patients with advanced lung cancer (2016)AHA/ACC 2024 · §4.2.1

Perioperative MI and cardiac death happen because of ischaemia in heart muscle supplied by diseased coronary arteries. Diabetes, smoking, hypertension and ageing mostly raise risk by building up atherosclerosis, or by signalling that it is there. Once coronary disease is established, the lesion that surgical stress acts on is already present. The other conditions still add some independent risk, but their main effect has already happened. That is why the excess MI and cardiac mortality in arteriopaths is explained by how often they have coronary disease.

Risk factors over documented disease. Diabetes appears in every cardiac risk index and table of clinical predictors, so it looks like the strongest factor. But it mostly raises risk by speeding up coronary atherosclerosis. Once coronary disease is documented, that disease is the direct cause of perioperative infarction and cardiac death.

Coronary disease is probably the leading cardiac comorbidity. In vascular patients, excess perioperative MI and cardiac death reflect its high prevalence; postoperative deaths are mostly infarcts in known ischaemic patients. Age, smoking and insulin-treated diabetes independently predict adverse events.

Sources: Stoelting 8eMiller 10eBarash 9e

Extra cardiac tests are only worth doing if the result would change the plan. Clinical risk factors such as diabetes, hypertension or age only mean that capacity must be checked. A patient who manages 4 METs or more without symptoms is unlikely to produce a test result that changes management, so they go ahead. Low-risk operations carry under 1% cardiac risk, so these patients skip the capacity step. Only poor or unknown capacity leads to further work-up, and these texts handle that through older ACC/AHA guidance.

Stress testing with adequate capacity. Insulin-treated diabetes, older age and hypertension are cardiac risk factors, so a stress test feels thorough. But risk factors only prompt the capacity check. Once the patient manages 4 METs or more without symptoms, a stress test cannot change management, so it is not indicated.

Barash, Stoelting, Faust and an endocrine review agree: elevated-risk patients with 4 METs or more proceed untested, and low-risk surgery (under 1% risk) needs no tests. For poor or unknown capacity, following older ACC/AHA guidance, stress testing is allowed only if it would alter management.

Sources: Barash 9eOutside our books: Pituitary Surgery (2026)FaustStoelting 8e

METs express effort as multiples of resting oxygen uptake; 4 METs marks adequate pre-operative reserve. Walking depends on pace: Barash puts a slow stroll of a block or two in its lowest band, level 4 mph walking at 4; Miller scores a short level walk at 3. If pace is unstated, use 4 METs. Swimming is strenuous: Miller (fast) 10, Barash above 10. Singles tennis: Miller 7, Barash above 10, so the tennis statement fails by Miller. Gardening (4) is true in both; choose it.

Swimming rated at ten METs. Eight is a real figure in Miller's table, so it looks familiar. But it belongs to slow jogging and rapid stair-climbing. Brisk running or jogging sits two steps higher, at 10, alongside fast swimming. Slow rope-jumping is also off by one: Miller scores it 9, not 8 or 10.

Miller gives single figures: a short level walk 3, gardening 4, singles tennis 7, slow jogging 8, slow rope-jumping 9, quick swimming or brisk running 10. Barash groups by band: level walking at 4 mph reaches 4 METs; swimming and singles tennis exceed 10.

Sources: Miller 10eBarash 9e

Brugada syndrome is an inherited sodium-channel disorder. It produces an ECG that mimics right bundle branch block, with coved ST elevation across the right chest leads, in a heart without significant structural disease. The danger is ventricular tachycardia or fibrillation, which kills young, apparently well people suddenly. So a bundle branch block in a healthy young adult is not reassuring when a relative died suddenly: the pattern may be the marker of the disease. Echo looks for structural disease, which is typically absent; only cardiology assessment addresses the arrhythmia risk.

Echocardiography before cardiology evaluation. Echocardiography feels like the thorough, proactive step for an abnormal ECG and a worrying family history. But the likely culprit is an electrical, not structural, disorder, so the heart usually looks normal on echo and a clear scan falsely reassures. The arrhythmia risk needs specialist cardiology assessment first.

Brugada is a genetic sodium-channel disease causing right precordial coved ST elevation with a pseudo-RBBB, and sudden arrhythmic death in the young. An abnormal ECG, or a family history of sudden death alongside an ECG abnormality, warrants cardiology review; this is not a benign variant.

Sources: Miller 10eStoelting 8e

Enlargement is itself an indication for repair, so the operation is the treatment and medical therapy beforehand adds little. A beta-blocker meant to lower perioperative cardiac risk has to start well before the operation. Faust warns against starting it on the day of surgery. Barash's goal of easing aortic wall strain by lowering contractility and arterial pressure is still valid, but the anaesthetist pursues it during the anaesthetic. Pre-emptive anti-impulse therapy before theatre belongs to aortic dissection, not to an aneurysm awaiting repair.

Preoperative beta-blocker delays repair. Lowering heart rate and pressure to cut aortic wall stress is standard for dissection, so a beta-blocker feels protective here too. For an aneurysm already heading to repair, a beta-blocker started on the day of surgery is advised against and delays the real cure, which is the operation.

A rapidly enlarging aneurysm warrants surgical repair. Urgent aortic cases go to theatre promptly with whatever optimisation the time allows. Beta-blockers given to reduce perioperative risk must not be started on the operative day. During the anaesthetic, lowering contractility and pressure limits aortic strain.

Sources: FaustBarash 9eStoelting 8eAHA/ACC 2024 · §7.7

Basal crackles show the heart failure is decompensated, not a stable baseline. Guidelines class this, like severe valve disease, as an active or unstable cardiac condition. Heart failure is the strongest single predictor of cardiac complications and death around surgery. Monitoring can only show deterioration as it happens; it does not reverse the congestion. So the safe course is to find and treat the causes first. The elective operation is reconsidered only when the patient is compensated and the balance of risk and benefit is acceptable.

Monitoring decompensated heart failure. An arterial line and closer haemodynamic control feel like a responsible answer, especially when the patient reports no symptoms. But the crackles mean the failure is already decompensated. Monitoring leaves that risk in place. For a non-emergency case, the guidance is to delay and optimise, not to monitor through it.

Decompensated heart failure carries very high risk, and surgery should wait unless it is lifesaving. Unstable conditions, including severe valve disease, may call for delay, a cardiology review and optimisation. Active conditions should be treated before the planned operation is reconsidered.

Sources: Miller 10eStoelting 8e

Suitability for day surgery depends on both patient and procedure. Day units are for operations with few postoperative complications that need little intensive medical or nursing input. A stable patient with severe systemic disease can go home the same day only after minimal-risk surgery, such as cataract surgery under topical anaesthesia. Many patients fit for that would not be fit for anything slightly riskier as a day case. The answer is to move the case to an inpatient setting. Planned admission for safer care is not a failure.

Cancelling procedure over admission. Severe heart failure makes you want to stop everything. But nothing says this patient is decompensated. What's wrong is the day-case setting, not the operation. The sources say the fix is to change where he is managed and to admit him, not to deny him the procedure.

Day surgery suits low-complication procedures needing no intensive postoperative care. Stable ASA IV patients should have only low-risk surgery, such as cataract, in ambulatory centres; this suitability does not extend to riskier procedures, where unplanned admission may improve care.

Sources: Barash 9eOutside our books: Association Between Heart Failure and Postoperative Mortality Among Patients Undergoing Ambulatory Noncardiac Surgery (2019)Outside our books: Day-case surgery guideline 2022 (2022)Stoelting 8e

Early definitive fixation of a hip fracture improves outcome, hence the 48-hour North American target in Miller. Joint replacement loads the heart: Miller lists cardiac events first after hip and knee arthroplasty, though unranked; after hip fracture, delirium affects a quarter of patients per BJA Education, outside the textbooks. Two knees in one sitting concentrates the physiological insult into one anaesthetic, so the HSS guideline by Urban, also outside the textbooks, stages the operation for ASA class III, age ≥75 or LVEF below 40%.

Staging bilaterals with this EF. Single-knee staging feels prudent when the ejection fraction is 50%, but that value is not below Memtsoudis's consensus cut-off of under 50% and sits well above Urban's 40%. At ASA 2 and age 50 she meets no exclusion in either outside source, so bilateral surgery proceeds.

Miller holds that early fracture care improves outcomes and cites US and Canadian advice to operate on hip fractures within 48 hours; it lists cardiac events first after arthroplasty. Urban's HSS guideline excludes age ≥75, ASA class III and LVEF under 40% from bilateral surgery.

Sources: Miller 10eOutside our books: Are postoperative complications more common with single-stage bilateral (SBTKR) than with unilateral knee arthroplasty: guidelines for patients scheduled for SBTKR (2006)Outside our books: Anaesthesia for hip fracture repair (2020)

Brugada syndrome is inherited. It is caused by a faulty cardiac sodium channel, and the heart muscle itself is normal. The channel defect produces coved ST elevation across the right chest leads, with a QRS resembling right bundle branch block. Echo and other imaging are usually normal, so the patient seems fit before surgery. The arrest comes from electrical instability, not pump failure. VT or VF may therefore be the first sign in a young, apparently well patient, and the typical ECG is often only noticed afterwards.

Cardiomyopathy diagnosis in healthy patient. Cardiomyopathy is a well-known cause of arrhythmic arrest with an abnormal ECG, so it looks like a reasonable diagnosis. But it is a disease of the heart muscle, and this patient was healthy. Brugada syndrome causes ECG changes and VT or VF even though the heart's structure is normal.

Brugada syndrome is a genetic sodium-channel disorder. It produces a pseudo-RBBB with coved ST segment elevation over the right-sided precordial leads. The heart has no significant structural disease and cardiac imaging is usually normal. VT or VF can cause sudden arrest or death in young patients.

Sources: Miller 10eMayo review

Order the test only when the result could change perioperative management. A reduced ejection fraction predicts major adverse cardiac events, and the lowest fractions carry the most risk. Breathlessness with no diagnosis may hide undetected ventricular dysfunction. In a known heart-failure patient, a change in status means the old measurement no longer shows current function. In a well patient, or one whose stable disease is already characterised, repeating the scan rarely changes the plan. It adds cost and delay without benefit.

Prior diagnosis alone justifies testing. Previous heart failure sounds high-risk, and a low ejection fraction does predict cardiac events. But a past diagnosis alone does not justify testing. The guideline trigger is worsening dyspnoea or another change in clinical status.

Guidelines support pre-operative LV function assessment for breathlessness of unknown cause, and for current or prior heart failure with changed symptoms or clinical status. Routine testing is not advised. Stable known dysfunction may be selectively rechecked if not assessed within the previous year.

Sources: Barash 9eMiller 10e

A test earns its place only when its result could change risk estimation or management, so an ECG is aimed at intermediate- or high-risk surgery, orthopaedic included, in patients likely to have coronary disease. The guidelines differ on age. European guidance counts age 65 or over as a risk factor. The 2024 American guideline sets no age cut-off: an ECG is reasonable with known cardiovascular disease before elevated-risk surgery, optional in asymptomatic patients, and of no benefit before low-risk surgery. Routine chest films add no prognostic information.

Renal failure always warrants an ECG. Renal failure is a genuine cardiac risk marker, so this looks like a clear indication. But the indication pairs the disease with the operation: renal failure earns an ECG only before intermediate-risk surgery, and a mastectomy is low risk, where neither European nor American guidance supports routine ECGs.

European guidance suggests an ECG before intermediate- or high-risk surgery with known ischaemic disease, risk factors including age 65 or over, or symptoms. Chest films only selectively, e.g. advanced COPD or a suspected mediastinal mass. A resting ECG may be normal in angina.

Sources: Miller 10eBarash 9eStoelting 8e

Most perioperative infarcts are non-ST-elevation events and are often silent, so the ECG can miss them. The diagnosis therefore rests on release of cardiac-specific biomarkers. The cardiac troponin isoforms, I and T, rise within 3 hours of injury and stay raised for 7 to 10 days. They are more specific than CK-MB. Perioperative myocardial injury is itself defined by an absolute or relative rise in troponin, so troponin is the test to send.

Troponin C confirms myocardial injury. It is a troponin, and the 'c' looks like it stands for cardiac, so it seems the obvious pick. But the cardiac-specific troponin assays measure the I or T isoforms. Troponin C is not the marker used to confirm myocardial injury, so it cannot confirm acute coronary syndrome.

Cardiac troponins T or I rise within 3 hours of injury, persist for 7 to 10 days and are more specific than CK-MB. Most postoperative infarcts are NSTEMIs, diagnosed by ECG change and/or biomarker release. Perioperative injury is defined by a rise in troponin.

Sources: Stoelting 8eMiller 10e

Nitrate relieves ischaemia by cutting preload and dilating coronaries, and aspirin stops the platelet thrombus growing, so both act at the bedside. Troponin is sent at once because it confirms injury and sorts risk. In a stable patient without ST elevation, the thrombus is usually not fully occlusive, so angiography can wait while monitoring and serial markers continue. With ST elevation, a vessel is occluded and delay costs muscle, so reperfusion becomes the time-critical step, weighed against surgical bleeding from the antiplatelet and anticoagulant load PCI requires.

Deferring troponin in ischaemia. Troponin looks like a test that can wait behind treatment, so it is picked as least urgent. But guidance calls for troponin in every patient with postoperative ischaemic ECG changes or typical chest pain; it is part of the immediate work-up, whereas catheterisation in a stable non-ST-elevation picture is not.

After confirmed postoperative ischaemia, nitroglycerin, aspirin, a beta blocker and a statin are given unless contraindicated; troponin is recommended for ischaemic ECG changes or chest pain; stable, minimally symptomatic patients do not need urgent angiography; for reperfusion people, time to revascularisation is crucial.

Sources: Miller 10eFaustStoelting 8e

Central venous pressure poorly reflects right ventricular filling, and wedge pressure can mislead when the left side is failing or stiff. A pulmonary artery catheter directly measures stroke volume, cardiac output and both vascular resistances. It also permits mixed venous sampling, showing tissue oxygen extraction. It is most useful when large fluid shifts meet a heart that cannot cope, or when distinguishing cardiogenic from distributive shock. Its outcome benefit is contested, so reserve it for these patients.

Pulmonary artery wedge in stenosis. Valve disease is one of the reasons a catheter gets placed, so a tight mitral valve looks like an obvious indication. But the obstruction breaks the link between left atrial pressure and left ventricular end-diastolic pressure. The wedge then stops reflecting left ventricular filling and can mislead fluid management.

The sources list catheter monitoring in major surgery with big fluid shifts or blood loss when patients have right heart failure or pulmonary hypertension, left failure resistant to therapy, shock or multi-organ failure, inotrope or balloon pump dependence, suprarenal aortic clamping, or liver transplantation.

Sources: Miller 10eBarash 9e

Breathlessness on trivial effort signals poor functional capacity. It may reflect ventricular dysfunction, heart failure or ischaemia, and its cause here is unknown, so it cannot be written off as deconditioning. Insulin-treated diabetes adds cardiac risk. Combining two or more risk-index factors with capacity below 4 METs mandates further cardiopulmonary work-up. The targeted, non-invasive way to explain the symptom is to assess ventricular function directly. That finding then shapes risk counselling and anaesthetic planning.

Stress testing for breathlessness. Poor exercise tolerance in a diabetic seems to fit the stress-testing branch of the algorithm, so this feels like the textbook move. But the presenting problem is breathlessness with no known cause. For that, the sources endorse evaluating ventricular function, not provoking ischaemia.

Echocardiography to assess ventricular function is considered reasonable when dyspnoea has no identified cause. A risk-index score of 2 or more with capacity under 4 METs should prompt further cardiopulmonary work-up. Dyspnoea on minimal effort signals likely extensive coronary disease and greater perioperative risk.

Sources: Barash 9eStoelting 8e

Hypotension, tachycardia or anaemia can leave the heart muscle with less oxygen than it needs. The result is a supply-demand (type 2) injury, and injured heart cells release troponin into the blood. Most of these patients have no chest pain, and the injury peaks after surgery, not during it. That makes troponin the only practical way to find the injury. A rise means real heart muscle damage, not general inflammation, so it marks a patient at much higher risk of dying soon.

Non-troponin biomarker predicts mortality. It sounds like a cardiac risk biomarker, so it seems a reasonable pick for a patient who has diabetes, hypertension and high cholesterol. But the perioperative sources link only troponin to 30-day mortality. Troponin detects acute heart muscle injury, which is what causes the short-term risk after surgery.

A multinational trial found that an abnormal troponin independently predicted death at 30 days, whether or not the patient had ischaemic symptoms. Mortality was 9.8% with myocardial injury and 1.1% without. Guidelines list hypotension as a cause of supply-demand mismatch that should be corrected.

Sources: FaustAHA/ACC 2024 · §9.2Miller 10e

The index weights predictors equally, so risk reflects factor count, not severity. Surrogate markers count: nitrate therapy indicates ischaemic heart disease even with stable angina. Thresholds apply: diabetes scores only if insulin-treated; renal impairment only above 2.0 mg/dL. The surgical item is defined by the body cavity entered, so a laparoscopic abdominal operation still scores. Lee derived the rates in one cohort and validated them in a second, giving two sets of figures, each named after its cohort.

Laparoscopic cholecystectomy is minor surgery. People miss the surgical criterion, assuming low-risk laparoscopic cholecystectomy, then stop at two factors. The index defines the item by cavity entered, not access route, so laparoscopy still scores. Adding nitrate-treated angina and insulin gives three factors: the high-risk class.

Lee's criteria: insulin treatment, creatinine >2.0 mg/dL, and nitrate-treated ischaemic heart disease. Complications by factor count (0–3+): derivation cohort 0.5%, 1.3%, 4%, 9%; validation cohort 0.4%, 0.9%, 6.6%, 11%.

Sources: FaustOutside our books: Derivation and prospective validation of a simple index for prediction of cardiac risk of major noncardiac surgery (1999)

Lee's index kept only bedside variables that independently predicted major cardiac complications. Its diabetes item is defined by insulin therapy, not by the diagnosis, so a patient controlled on oral agents adds nothing for diabetes. Each factor adds one point, and risk rises with the total. Current ischaemic chest pain or nitrate use counts as ischaemic heart disease. So stable angina plus tablet-treated diabetes totals one point, about 0.9% risk in Lee's validation cohort. An intraperitoneal operation, open cholecystectomy included, also scores one point.

Any diabetes scores in RCRI. Diabetes is a real cardiac risk factor. Older guideline lists name it without qualification, so any diabetic seems to score. The RCRI item specifically requires preoperative insulin therapy. Diabetes managed on oral hypoglycaemics adds no point, whereas renal impairment with a raised creatinine does.

RCRI factors score one point each: diabetes means preoperative insulin use; renal disease means creatinine over 2 mg/dL; ischaemic heart disease includes current ischaemic chest pain or nitrate use. One factor carried 0.9% risk in Lee's validation cohort.

Sources: Barash 9eFaustMiller 10e

In atrial fibrillation the atria do not contract effectively. Blood pools in the left atrium, clot forms there and fragments can embolise to the brain. How likely this is depends on the patient's other diseases. The score therefore gives weighted points for heart failure, hypertension, age above 75, diabetes and any previous embolism. The total sets how much stroke prophylaxis the patient needs. The scores are meant for atrial fibrillation that is not caused by mitral stenosis or a prosthetic valve.

CHA2DS2 in valvular fibrillation. It is tempting because rheumatic mitral disease causes atrial fibrillation and left atrial clot. But these scores were built for nonvalvular atrial fibrillation, which excludes mitral stenosis and prosthetic valves. What the score is applied to is the arrhythmia, not the valve disease.

Stoelting's CHA2DS2-VASc gives 2 points each for age 75 or over and previous stroke or TIA, 1 each for heart failure, hypertension, diabetes, vascular disease, age 65–74 and female sex. Miller: anticoagulate men scoring 2 or more and women 3 or more.

Sources: Stoelting 8eMiller 10e

Most chronic cardiac drugs protect the heart through the stress of surgery. Continuing them is the default. The exceptions are drugs whose action clashes with anaesthesia or fasting. ACE inhibitors and ARBs taken close to surgery predispose to hypotension. SGLT2 inhibitors provoke metabolic acidosis, classically ketoacidosis with near-normal glucose, and their effect outlasts one missed dose. Oral hypoglycaemics simply wait until the fast. A newly started beta-blocker needs gradual titration before surgery. Never give a beta-blocker with severe bradycardia, high-grade block, overt systolic failure or active bronchospasm.

Holding SGLT2 day-of surgery. Holding every oral diabetic drug on the morning of surgery feels uniform and safe. SGLT2 inhibitors are the exception. Their acidosis risk, often with near-normal glucose, persists beyond a single missed dose, so they must be stopped days, not hours, beforehand.

Most long-term cardiovascular drugs, beta-blockers and statins included, are continued. ACEI/ARB within 24 hours raise hypotension risk. New beta-blockers begin at least 1 week ahead, titrated slowly. Metformin and sulfonylureas skip the surgical morning. SGLT2 inhibitors are withheld 3 to 4 days.

Sources: Miller 10eStoelting 8eAHA/ACC 2024 · §6.3Faust

Official drug-name endings (US and WHO naming lists), separate from anaesthesia texts, encode a drug's target. Heparin and LMWHs work via antithrombin, bridging it to thrombin. -xaban drugs directly inhibit factor Xa; -gatran and hirudin-derived -irudin drugs directly inhibit thrombin. Warfarin, a vitamin K antagonist, has no class ending. Not every drug carries one: argatroban, a direct thrombin inhibitor, has neither ending.

Dabigatran inhibits factor Xa. Dabigatran is taken by mouth and grouped with rivaroxaban and apixaban as a direct oral anticoagulant, so people assume it shares their target. Its -gatran ending marks a thrombin inhibitor. Only the -xaban drugs block factor Xa.

The texts list bivalirudin, argatroban and oral dabigatran as direct thrombin inhibitors, and apixaban, rivaroxaban and edoxaban as anti-Xa agents. Heparin binds antithrombin and thrombin at once. Warfarin is an oral vitamin K antagonist, and the naming lists assign it no class ending.

Sources: Stoelting 8eMiller 10eOutside our books: USAN stem list (cumulative) and WHO INN Stem Book 2018: drug-name stems (2018)

A fresh stent depends on dual antiplatelet therapy until it heals, and a drug-eluting stent needs that cover longer than a bare-metal one. Surgery usually forces clopidogrel to stop; doing so early invites in-stent thrombosis. So if clopidogrel was stopped too soon before elective surgery, cancel, restart it and rebook at 6 months from placement. Surgery that cannot wait after a STEMI favours a bare-metal stent, then at least 30 days, which replaces the older 4 to 6 weeks, or balloon angioplasty alone, then at least 2 weeks.

Twelve-month delay for stable stent. One year was the older blanket rule for drug-eluting stents and some texts still print it, but it exceeds the current minimum. For stable disease the minimum is 6 months; the 12-month delay applies only to stents placed for an acute coronary syndrome.

Surgery waits at least 30 days after a bare-metal stent and at least 6 months after a drug-eluting one, or 12 months if placed after ACS. Older advice gave 4 to 6 weeks and up to 12 months. Balloon angioplasty alone allows 2 weeks.

Sources: Stoelting 8eMayo reviewMiller 10e

A drug-eluting stent needs uninterrupted dual antiplatelet therapy during its early months. Surgery forces a choice: stop the second antiplatelet drug and risk in-stent thrombosis, or continue it and accept surgical bleeding. Waiting until the stent is 6 months old lowers the thrombotic risk enough for elective surgery to be reasonably safe. Stenting for an acute coronary syndrome carries more early risk, so the wait extends to 12 months. A disc prolapse causing only numbness is not an emergency, so the surgery is elective and must wait.

Year delay for stable stent. A year is tempting because older guidance and review books gave 12 months of clopidogrel after any drug-eluting stent, and ACS-placed stents still need 12 months. For a stent placed for stable disease, current guidance sets the minimum at six months, so waiting a year delays surgery for no benefit.

Textbooks advise deferring elective noncardiac surgery until a drug-eluting stent is at least 6 months old, or 12 months if placed for ACS, since early antiplatelet cessation risks stent thrombosis. Surgery at three to six months is reserved for cases where delay is riskier.

Sources: Stoelting 8eMiller 10e

A recent infarct leaves the myocardium at risk, so even without intervention surgery should wait more than 60 days. Catheterisation after an infarct usually means a stent. A new stent can clot, and dual antiplatelet therapy is still needed; for a drug-eluting stent this risk has settled enough by 6 months. Surgery makes the blood more likely to clot and may force antiplatelet therapy to stop, so operating early risks stent thrombosis. Aspirin carries on through surgery; only the P2Y12 agent may be paused.

Year applies to all stents. A year is the 2024 guideline's preferred wait after stenting for an acute coronary syndrome, so it looks safest. The textbook interval after a drug-eluting stent is six months, and that is the answer taught here; know both figures and which source gives each.

Without coronary intervention, wait at least 60 days after infarction. After a drug-eluting stent, ideally delay elective surgery 6 months. After PCI for acute coronary syndrome, the 2024 guideline prefers 1 year; 6 months applies to stents for chronic coronary disease. Continue aspirin when possible.

Sources: Barash 9eAHA/ACC 2024 · §7.5

A stent is most likely to clot soon after it is placed. The stress of surgery also makes blood clot more easily. Stopping antiplatelet drugs early therefore risks the stent blocking and causing a myocardial infarction. Waiting lets this risk fall, and surgery becomes reasonable once its benefit outweighs the remaining cardiac risk. If surgery truly cannot be delayed, the patient keeps antiplatelet cover to protect the stent. Aspirin especially should continue. If a P2Y12 inhibitor was stopped, restart it as early as bleeding allows. Heparin cannot replace platelet inhibition.

Heparin replaces stopped antiplatelets. Stopping antiplatelets and giving heparin looks like a sensible balance between bleeding and clotting. But heparin does not replace platelet inhibition and should not be used as a bridge. Stopping antiplatelets leaves a recent stent unprotected while surgery is already making the blood more likely to clot.

US guidance allows time-sensitive surgery from 3 months when benefit outweighs cardiac risk. If surgery cannot be postponed, proceed on dual therapy or aspirin alone. Continue aspirin, restart the P2Y12 inhibitor promptly, and avoid heparin bridging.

Sources: AHA/ACC 2024 · §7.5FaustMiller 10eStoelting 8eBarash 9e

Stoelting's year is the length of the dual antiplatelet course and the older wait before elective surgery. Miller's, like the current AHA/ACC guideline, treats a drug-eluting stent beyond 6 months as low risk. A stent over a year old meets both standards. If dual therapy has to stop, aspirin is the drug to keep. It continues to protect the stent, and in arthroplasty it also helps with chemical thromboprophylaxis. LMWH or a DOAC is the usual VTE prophylaxis alongside it.

Stopping aspirin after stent window. Fear of bleeding with a spinal makes stopping every antiplatelet drug feel safe. But once the stent is past the high-risk window, aspirin is the drug to keep through arthroplasty. It protects the stent and adds chemical thromboprophylaxis. Only the additional antiplatelet agents are stopped.

Stoelting advises at least a year of dual antiplatelet therapy and of waiting after a drug-eluting stent. Miller's rates stents beyond 6 months as low risk: aspirin continues in arthroplasty, doubling as VTE prophylaxis, and other antiplatelets stop per pharmacology and renal function.

Sources: Miller 10eStoelting 8e

When the mitral valve is narrowed, the pressure difference across it depends on how much blood flows through and how long diastole lasts. Labour raises cardiac output, which increases flow. Pain causes tachycardia, which shortens diastole. Both make the gradient steeper and can turn a stable woman symptomatic. Early neuraxial analgesia blunts the sympathetic surge. Topping up the block before the second stage keeps heart rate controlled when stress peaks.

Avoiding labour with stenosis. It is tempting because labour clearly stresses a narrowed valve, so avoiding labour seems safest. But the sources prefer vaginal delivery for mild and moderate risk. The danger of labour is pain-driven tachycardia and extra flow, and early, well-titrated neuraxial analgesia controls both.

A three-band table grades valve area mild over 1.5 cm², moderate 1–1.5, severe under 1.0. Another text calls under 1.5 severe, with pulmonary systolic pressure over 50 and mean gradient 10 or more. For moderate risk: vaginal delivery, early neuraxial analgesia, second-stage epidural top-up.

Sources: Barash 9eMiller 10eStoelting 8e

Guidelines now give endocarditis prophylaxis to far fewer patients. They no longer target people with a high lifetime chance of catching endocarditis. They target people who would have the worst outcome if infection took hold. Prosthetic valves are in that group, and so is prosthetic material used in a valve repair, such as an annuloplasty ring or artificial chords. A mitral repair therefore counts as high risk only when prosthetic material was implanted.

Heart rate control over prophylaxis. You may reach for heart rate goals, which dominate the haemodynamic plan for unrepaired valve lesions. A history of repair shifts the question. The implanted ring is what puts the patient in the high-risk group, so the specific issue here is endocarditis prophylaxis.

The high-risk list includes prosthetic material used to repair a valve, such as annuloplasty rings and chords. One guideline names repair with a prosthetic ring explicitly. The indications for prophylaxis have been sharply narrowed to patients most likely to do badly if endocarditis develops.

Sources: Outside our books: 2023 ESC Guidelines for the management of endocarditis (2023)Miller 10eStoelting 8e

Prophylaxis is kept for patients in whom endocarditis is both more likely and more lethal, because dental work that breaches gum or mucosa causes transient bacteraemia. Prosthetic valves, homografts included, and valve-repair material stay foreign surfaces for life, so they qualify with no time limit. Prosthetic material in a fully repaired defect counts only during the first six months, unless a residual leak sits at or beside it. Unrepaired cyanotic lesions, including shunts and conduits, qualify throughout.

Clindamycin without penicillin allergy. Clindamycin is tempting because it was long the standard dental alternative. This child has no allergy, so a first-line agent is indicated, and for IV use that means weight-based cefazolin. Clindamycin no longer appears even among the listed alternatives for penicillin allergy.

Guidance limits prophylaxis to patients at high risk of endocarditis and bad outcomes: prosthetic valves including homografts, repair material, unrepaired cyanotic disease, and repaired defects with material within six months or residual leaks. Non-allergic children may receive cefazolin 50 mg/kg IV, maximum 1 g.

Sources: Miller 10eOutside our books: 2023 ESC Guidelines for the management of endocarditis (2023)

Unrepaired cyanotic congenital heart disease is one of the specific high-risk conditions, so this child needs prophylaxis. A child's dose goes up with weight until it reaches the adult ceiling, so a small child gets a weight-based fraction of the adult gram. Cephalosporins are fine without a penicillin allergy. You only avoid them after anaphylaxis, angioedema or urticaria with penicillin or ampicillin. Clindamycin has been removed from current prophylaxis recommendations, so it is no longer an option for anyone.

Clindamycin without weight scaling. Clindamycin is tempting because it was the old standby when penicillin couldn't be used, and an IV dose sounds right for theatre. It fails because this child has no allergy, current guidance has dropped clindamycin for prophylaxis, and a fixed dose isn't scaled to weight.

Both guidelines give cefazolin or ceftriaxone at 50 mg/kg IV or IM for children, up to the 1 g adult dose. They list unrepaired cyanotic congenital heart disease as high risk. They bar cephalosporins only after serious penicillin reactions and no longer recommend clindamycin.

Sources: Outside our books: 2023 ESC Guidelines for the management of endocarditis (2023)Outside our books: Prevention of Viridans Group Streptococcal Infective Endocarditis: A Scientific Statement From the American Heart Association (2021)

Doppler echo measures the stenosis directly. It shows where the obstruction lies, how tight it is, whether other valve lesions coexist and how well the left ventricle is coping. These findings set the perioperative risk and the haemodynamic plan. An ECG or chest film shows only indirect effects, such as hypertrophy or a dilated ascending aorta. Neither can grade how severe the valve lesion is.

ECG determines stenosis severity. ECG is cheap and quick, and the work-up usually starts with it. It may show left ventricular hypertrophy with strain. But these changes are indirect and non-specific. An ECG cannot measure the obstruction, so it cannot tell you how severe the stenosis is or whether surgery is safe.

Transthoracic Doppler echo is the preferred test for aortic stenosis, confirming the diagnosis and showing lesion site, severity, associated lesions and ventricular function. Perioperative guidelines advise echo whenever significant valve stenosis or regurgitation is clinically suspected, including from a murmur.

Sources: Stoelting 8eMiller 10e

A narrowed aortic valve fixes stroke volume, so the heart cannot raise its output when the vessels dilate. A sudden sympathetic block lowers systemic vascular resistance and diastolic pressure. Coronary flow to the thickened left ventricle then drops, which causes ischaemia and a further fall in output, so the problem feeds itself. The danger is a fast, deep fall in resistance, not the block itself. A catheter lets you build the block in steps, so you can see each small fall and correct it early.

Contraindicate neuraxial block outright. A tight valve and older teaching push people to refuse. But the texts list aortic stenosis only as a relative contraindication and recommend a slowly titrated catheter technique to manage the risk. Refusing outright goes against the texts and withholds analgesia that can be given safely under control.

The texts call aortic stenosis a relative contraindication to spinal or epidural block, because lower vascular resistance reduces coronary perfusion. Each patient should be judged on severity, ventricular function and urgency. A catheter given in small repeated doses offers more haemodynamic control.

Sources: FaustMiller 10e

Revascularisation should be decided by the heart's condition, not the planned operation. In stable coronary disease, a randomised trial found bypass or stenting before vascular surgery safe, but it neither prevented postoperative infarction nor improved long-term survival. Benefit occurs only with intrinsically dangerous lesions: acute coronary syndrome or left main stenosis. Trials excluded left main disease and severe multivessel disease with poor ventricular function. The latter may justify revascularisation in its own right, but no trial shows it prevents perioperative events.

Routine revascularisation prevents infarction. Fixing a tight lesion before stressing the heart feels protective. In stable disease outside the left main, the key trial found that bypass or stenting before vascular surgery prevented neither postoperative infarction nor late death, and it delays the operation.

Preoperative revascularisation for perioperative cardiac benefit is supported only in STEMI, high-risk NSTEMI and left main disease; otherwise not, even before high-risk surgery, unless independently indicated. Key trial: no reduction in postoperative infarction or mortality; left main excluded.

Sources: AHA/ACC 2024 · §6.1.1Barash 9eMiller 10eAHA/ACC 2024 · §4.3

Torsades grows out of delayed ventricular repolarisation, which the ECG shows as a long QT interval. Deficits that slow repolarisation are the ones that set it up. Low calcium lengthens the ST part of the QT, and high calcium shortens it. Low magnesium makes the ventricles more irritable and specifically predisposes to torsades. That is why giving magnesium is first-line treatment even when the serum level is not yet known. Standard antiarrhythmics can make torsades worse.

High potassium lengthens QT interval. Low potassium, not high, lengthens the QT; high potassium causes peaked T waves and a widening QRS. Hypocalcaemia also lengthens the QT.

Low calcium lengthens QT; high calcium shortens it. Low magnesium raises ventricular tachycardia risk, including torsades, which is linked with long QT, low potassium, low calcium, low magnesium and bradycardia. Treat with 1–2 g IV magnesium over 5 minutes, repeated if needed.

Sources: Mayo reviewFaustMiller 10eBarash 9e

When the left bundle is blocked, the septum is activated from the right side, not from left to right. The small septal q wave in the lateral leads therefore disappears. The left ventricle is then activated late and slowly through muscle, so the QRS widens. Its large leftward force comes last and is unopposed, so the lateral leads show a broad, notched R and V1 is mainly negative. In right bundle block the late unopposed force is right-sided instead, which gives the terminal R′ in V1.

Deep S indicates RBBB only. A deep S wave suggests right bundle branch block, so people choose it as the odd one out. In RBBB, however, the deep S appears in leads I and V6. In LBBB, V1 is mainly negative, because the delayed left ventricle directs forces away from the right chest leads.

Complete LBBB needs a QRS longer than 120 ms, no Q waves in I, V5 and V6, and a broad, notched or slurred R in the lateral leads. V1 shows a negative RS complex. The rSR′ pattern in V1–V2 belongs to right bundle block.

Sources: Stoelting 8eBarash 9e

The epsilon wave is a small, reproducible deflection seen in the right chest leads. It sits after the QRS complex and before the T wave. It comes from late activation of diseased right ventricular muscle. For that reason, the diagnostic criteria for arrhythmogenic cardiomyopathy class it as a depolarisation and conduction abnormality. Because the signal is low-voltage, ECG filtering and sampling can hide it or mimic it. This is why its diagnostic weight was later reduced. Its link to this cardiomyopathy still stands.

Long QT syndrome is tempting because the epsilon wave lies between the QRS and the T wave, which is where people look for repolarisation problems. But the epsilon wave is a late depolarisation signal from the right ventricle. It is not a lengthened QT interval.

Padua criteria define the epsilon wave as a repeatable low-voltage signal between QRS end and T-wave onset in right chest leads. Task Force Criteria counted it major; Padua 2020 made it minor, because sampling rate, filtering and observer disagreement affect it.

Sources: Outside our books: The 2020 Padua Criteria for diagnosis and phenotype characterization of arrhythmogenic cardiomyopathy in clinical practice (2022)Outside our books: Diagnosis of Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia (ARVC/D): Proposed Modification of the Task Force Criteria (2010)

Pericarditis is a clinical diagnosis. It needs two of four features: pleuritic chest pain, a friction rub, the typical ECG pattern and a new or growing effusion. The ECG sign is ST elevation spread across the leads, or PR depression. The pain also sets it apart from ischaemia. It is sharp and pleuritic, it gets worse when the patient breathes in or lies flat, and a change of posture can ease it.

Myocardial infarction. ST elevation makes people think of infarction first. That fits when the chest pain is ischaemic. When the elevation is diffuse and the pain is pleuritic and changes with posture, pericarditis is the answer. Pericarditis can also follow an infarct, where it is easily mistaken for recurrent angina.

The textbook lists widespread ST elevation or PR depression as one of four diagnostic criteria for pericarditis, and two criteria are needed. The pericarditic pain is pleuritic and positional, unlike myocardial ischaemia.

Sources: Stoelting 8e

Most ischaemia around surgery comes from high oxygen demand. It shows as ST depression, and the leads over the anterolateral wall pick this up best, although they cannot tell you which artery is responsible. V5 on its own is the best single lead, with V4 next. Two leads over the anterolateral wall therefore catch more episodes than one of them paired with lead II. Lead II looks at the inferior wall and is useful for rhythm, but adds less for ischaemia. A precordial lead needs the five-electrode system.

II and V5 most sensitive pair. II and V5 is shown on almost every theatre monitor and is taught for monitoring rhythm and ischaemia together, so it feels right. It is the usual display, not the most sensitive pair. Two anterolateral precordial leads detect more ischaemia than one inferior lead plus one precordial lead.

In high-risk noncardiac surgical patients, V5 was the most sensitive single lead (75%) and V4 came next (61%). Together, V4 and V5 reached 90%, against 80% for the usual II and V5 pairing. Five-lead systems put the precordial electrode at V5.

Sources: Miller 10e

The left main artery divides into two branches. The left anterior descending artery runs down the interventricular groove and supplies the anterior wall, the septum and the apex. The circumflex runs along the left atrioventricular groove around the side of the heart. Its obtuse marginal branches feed the lateral free wall. A critical stenosis or sudden occlusion of the circumflex therefore causes a regional wall motion abnormality in the lateral segments. On the ECG, it shows up in the high lateral leads.

Circumflex supplies sinoatrial node. The circumflex does give off a sinoatrial nodal branch, but this is present in fewer than half of people, so the SA node is not reliable circumflex territory. The lateral wall is consistently supplied by the circumflex, and that is what the question tests.

Textbooks assign the lateral wall to the circumflex (obtuse marginal branches), anterior wall to the left anterior descending artery, and inferior wall to the right coronary artery. Leads I and aVL ischaemia indicates circumflex; it supplies the SA node in only 40–50%.

Sources: Barash 9eMiller 10eStoelting 8eFaust

Rheumatoid arthritis is a systemic inflammatory disease, and the pericardium is its most frequent cardiac target. When the pericardium is inflamed, the roughened layers grate against each other and cause a rub. The pain is pleuritic, and fever reflects the inflammation. Inflammation of the epicardial surface affects the whole heart, not a single coronary territory. The ECG therefore shows ST elevation, and often PR depression, across many leads instead of one territorial pattern.

Myocardial infarction. Chest pain with ST elevation makes you think of infarction first, and ischaemia must be excluded. Infarction, however, raises ST in the lead group matching one coronary territory. It does not explain a friction rub, fever, or ST elevation spread across every lead in a patient with rheumatoid arthritis.

Pericarditis, the commonest cardiovascular manifestation of rheumatoid arthritis, presents with typical chest pain, friction rub, fever and diffuse ST elevation. Diagnosis needs two of four: pleuritic pain, rub, diffuse ST elevation or PR depression, new or worsening effusion. Ischaemic ST changes are territorial.

Sources: Stoelting 8eFaust

A fixed valvular obstruction lowers stroke volume and slows ejection, so the trace is low, climbs slowly and peaks late. In regurgitation, pulse pressure widens and the pulse shows two systolic peaks. Mid-systolic outflow obstruction gives an early spike followed by a dome. A failing ventricle alternates strong and weak beats. In tamponade the tense pericardium caps total heart volume. Inspiratory right ventricular filling therefore takes away left ventricular preload, and systolic pressure drops.

Pulsus paradoxus is pulsus alternans. Paradoxus and alternans both vary from beat to beat, so people mix them up for a failing ventricle. Paradoxus follows spontaneous inspiration and points to tamponade. Severe systolic failure instead switches amplitude every other beat, whatever the breathing phase: that is pulsus alternans.

The source pairs each lesion with a waveform. Stenosis gives a small, slow-rising pulse. Regurgitation gives a double peak with wide pulse pressure. Hypertrophic cardiomyopathy gives spike-and-dome. Systolic failure gives alternating amplitude. Tamponade gives an inspiratory systolic fall of more than 10 mm Hg.

Sources: Miller 10eMayo review

The atria still depolarise, so P waves keep their rhythm. The impulse then fails to cross the atrioventricular node or the conducting tissue below it. Without ventricular depolarisation there is no QRS and no ventricular contraction. Nothing is ejected, so the arterial waveform loses a beat at exactly that point. Loss of coordinated atrioventricular timing also reduces left ventricular filling and stroke volume. A loose ECG lead would remove the P waves too, and could not alter arterial pressure, which is transduced separately.

Bradycardia. Bradycardia is tempting because a dropped beat briefly lengthens the gap between pulses. But it describes the rate, not the cause. The visible sign is P waves that fail to conduct to the ventricles, and that defines atrioventricular block. Apart from the dropped beat, the rate may be normal.

Second-degree block is recognised by a P wave with no QRS after it. In Mobitz type II the PR interval stays constant and a beat is dropped without warning. Losing atrioventricular synchrony sharply lowers stroke volume and blood pressure.

Sources: Stoelting 8eBarash 9eMiller 10e

The left ventricle ejects a large stroke volume quickly. This gives a steep upstroke and the first systolic peak. The pressure wave then reflects back from the peripheral circulation and adds a second systolic peak. In diastole, blood runs off in two directions: forwards to the tissues and backwards through the incompetent valve into the ventricle. Diastolic pressure therefore falls and the pulse pressure widens.

Aortic stenosis. Aortic stenosis also changes the arterial trace, so it seems a natural answer for any abnormal waveform. However, stenosis gives a small, slow-rising, late-peaking single hump. It does not give two systolic peaks with a wide pulse pressure.

Two systolic peaks point to significant aortic regurgitation: forward ejection makes the first, a reflected wave the second. The trace rises sharply, with wide pulse pressure and low diastolic value. Aortic stenosis instead gives a small pulse with delayed upstroke.

Sources: Mayo reviewMiller 10e

Fluid in the pericardium squeezes the heart all the way through the cardiac cycle. When the tricuspid valve opens in early diastole, blood cannot pass freely from the right atrium into the right ventricle, so the normal fall in atrial pressure is lost. That fall is the y descent. The systolic x descent is still present and now dominates, so the trace looks single-peaked. Venous pressure rises steeply, but diastolic ventricular volume, stroke volume and cardiac output all fall.

Tricuspid regurgitation. Tricuspid regurgitation also raises right-sided pressure and distorts the venous trace, so it mimics tamponade after penetrating cardiac injury. However, systolic backflow into the atrium causes a tall c–v wave and abolishes the x descent. Tamponade does the opposite: it preserves the x descent and loses the y descent.

Tamponade markedly raises venous pressure and reduces diastolic volume, stroke volume and cardiac output. The venous trace becomes monophasic, led by the systolic x descent. The y descent is reduced or absent because the right atrium cannot empty in early diastole.

Sources: Miller 10e

Each part of the trace reflects right atrial mechanics. Atrial contraction just before the ventricle produces the a wave at end-diastole. At the start of isovolumic ventricular contraction, the closed tricuspid valve bulges towards the atrium, producing the c wave in early systole. Pressure then falls in the x descent, still systolic. During ejection, venous return raises pressure to the v wave in late systole. When the tricuspid valve opens, pressure falls in the y descent, a diastolic event.

C wave is end-diastolic pressure. The c wave follows the a wave and sits beside the R wave, so it is easily mistaken for the end-diastolic wave. This is wrong: the c wave arises in early systole from isovolumic ventricular contraction bulging the tricuspid valve towards the atrium. The a wave is end-diastolic.

The c wave, x descent and v wave are systolic; the a wave and y descent are diastolic. The a wave is end-diastolic atrial contraction, c is early-systolic isovolumic contraction, v is late-systolic atrial filling, and y is atrial emptying through the open tricuspid valve.

Sources: Miller 10e

The a wave comes from the right atrium contracting at the end of diastole. When the atria fibrillate there is no coordinated atrial contraction, so this peak disappears. The c wave then becomes the prominent early peak, and the v wave and y descent are still there. Irregular R–R intervals on the ECG back up the diagnosis. Other atrial problems make the a wave bigger rather than removing it. A narrowed tricuspid valve slows atrial emptying. In atrioventricular dissociation the atrium contracts against a closed valve.

Third-degree AV block. Complete heart block tempts because the atria and ventricles no longer work together, so the atrial wave seems likely to vanish. But the atria still contract. When an atrial contraction meets a closed tricuspid valve it makes a giant cannon wave, which is the opposite of an absent a wave.

Atrial fibrillation loses the a wave; the c wave stands out, the v wave and y descent remain, and the ECG R–R interval varies. Tricuspid stenosis enlarges the a wave, atrioventricular dissociation gives a cannon wave, and tamponade shows a dominant x descent.

Sources: Miller 10eBarash 9e

Arterial CO2 and CO2 in perfused alveoli are nearly equal. But exhaled gas also carries gas from alveoli that are ventilated yet unperfused, which holds no CO2 and dilutes the end-tidal sample. Anything that stops blood reaching ventilated alveoli widens the gap: a clot in the pulmonary arteries, a falling cardiac output or overdistended lung all enlarge that unperfused fraction. When flow is restored, more alveoli are perfused and end-tidal CO2 climbs back toward arterial. In arrest, how much CO2 reaches the lung depends on blood flow, not ventilation.

Faster ventilation. Low end-tidal CO2 usually points to a ventilation problem, so bagging harder feels logical. During arrest, though, the CO2 reaching the lung is limited by blood flow, not by ventilation. Faster breaths do not fix the number. Better compression technique does, because it perfuses more alveoli.

In healthy lungs, end-tidal CO2 sits 2–5 mmHg below arterial. Dead space, pulmonary vascular disease, low cardiac output, overdistension and embolism widen the gap. In CPR, readings below 10 mmHg reflect low flow, predict failed resuscitation and should guide compression technique.

Sources: Miller 10eStoelting 8eBarash 9e

During diastole the tricuspid valve is open, so the right ventricle fills from the atrium. Its pressure climbs until it equals atrial pressure at end-diastole. The pulmonary valve is shut, so pulmonary artery diastolic pressure sits above ventricular diastolic pressure. It still decays steadily as blood drains into the lung circulation. Numbers alone can mislead, so use the diastolic slope to tell the chambers apart. Valves can be damaged as the catheter crosses them. A catheter left in place also keeps rubbing the endocardium and the leaflets.

Rising PA pressure means improvement. It is tempting because the pulmonary artery has the higher numbers, so a climbing trace looks like progress. But a pressure that rises through diastole is the ventricle filling through an open tricuspid valve. Pulmonary artery diastolic pressure steps up and then falls.

The source says right atrial and ventricular end-diastolic pressures are equal. Entering the pulmonary artery shows as a diastolic step-up. Ventricular pressure climbs with filling while arterial pressure falls with lung runoff. Valve injury is listed under catheterisation and under catheter residence.

Sources: Miller 10e

Wedge pressure mirrors LVEDP only while an uninterrupted fluid column joins catheter tip, pulmonary veins, left atrium and ventricle at end-diastole. Anything adding pressure upstream of the ventricle makes the wedge read high: alveolar pressure from PEEP squashing vessels into zone 1 or 2 conditions, obstruction at the mitral orifice, or regurgitant systolic v waves lifting mean atrial pressure. It reads low when ventricular pressure climbs after the column is cut: in aortic regurgitation the backflow shuts the mitral valve early, so the late diastolic rise never reaches the atrium.

Mitral prolapse. Mitral prolapse is tempting because the mitral valve sits between atrium and ventricle, so any mitral lesion feels as though it could hide ventricular pressure. But the resulting regurgitation adds systolic v waves that lift mean atrial pressure, so the wedge overestimates rather than underestimates.

The listed causes of a wedge reading above LVEDP are positive-pressure ventilation, PEEP, a catheter tip outside zone III, raised pulmonary vascular resistance, left atrial myxoma and mitral stenosis or regurgitation. A stiff ventricle and aortic regurgitation, through early mitral closure, make it read below.

Sources: Miller 10e

True mixed venous blood exists only in the pulmonary artery, where upper and lower body venous returns have combined and coronary sinus blood has joined in the right ventricle. A superior vena cava sample captures upper-body return alone, omitting those streams. In health, central saturation is slightly below pulmonary artery saturation (70% versus 75%). In critical illness, central saturation runs higher than mixed venous. Global extraction is summarised by the arteriovenous oxygen content difference, normally 3–5 mL/dL; values outside this range are abnormal.

SVC saturation replaces mixed venous. Both are drawn from central catheters and move together with haemodynamic change, so an SVC sample seems equivalent. It misses lower-body and coronary venous blood, and the gap between the two varies and changes direction in critical illness, so one cannot stand in for the other.

Central saturation is sampled in the superior vena cava and normally reads 70% against 75% in the pulmonary artery. In critically ill patients it runs higher than mixed venous but still tracks it during haemodynamic change. Normal arteriovenous oxygen difference is 3–5 mL/dL.

Sources: Barash 9eMiller 10e

A valve opens or shuts only when the pressure difference across it reverses. At end diastole the mitral valve shuts. Pressure then rises while volume stays fixed, until it passes aortic pressure and the aortic valve opens. Volume falls during ejection. When ventricular pressure drops below aortic pressure, the aortic valve shuts at the end-systolic corner. Pressure falls again at constant volume until the mitral valve opens. That point ends isovolumic relaxation and starts filling, which carries volume back to end diastole.

Aortic opening occurs at point C. It is tempting because it is the next event after isovolumic contraction, and diagrams that start their letters at a different corner move it onto C. In the standard scheme, starting at end diastole, aortic opening is B. C is the end-systolic corner, where the aortic valve shuts.

The loop runs anticlockwise. Its corners are end diastole with mitral closure, aortic opening, end systole with aortic closure, and mitral opening. The sides between them are isovolumic contraction, ejection, isovolumic relaxation and filling. The aortic valve shuts once ventricular pressure falls below aortic pressure.

Sources: Barash 9e

Pulse contour software must locate the boundary between systole and diastole on the arterial trace, and the dicrotic notch provides it; over- or underdamping, arrhythmias or aortic regurgitation blur that landmark and corrupt the estimate. The oesophageal probe lies alongside the descending aorta, continuously measures blood velocity from the Doppler shift, and converts it to stroke volume using an estimated aortic cross-sectional area. Aortic valve disease or thoracic aortic pathology alters flow or aortic dimensions, breaking these assumptions.

Valve lesions irrelevant to contour. Because the probe samples the descending aorta rather than the valve itself, people assume valve lesions do not matter. Yet aortic stenosis, regurgitation and thoracic aortic disease all make the velocity-to-volume conversion unreliable; regurgitation also degrades pulse contour readings.

Pulse contour needs an optimal trace with a discernible notch; damping errors, arrhythmias and aortic regurgitation cause error. Oesophageal Doppler continuously measures descending aortic Doppler shift, pairs velocity with estimated aortic area, and is likely inaccurate with aortic valve or thoracic aortic disease.

Sources: Miller 10e

Ischaemia shows up as abnormal regional wall motion, and each wall segment belongs to a particular coronary artery. At mid-papillary level, one short-axis slice cuts through the whole ring of mid-ventricular wall. Between them, those segments are supplied by the LAD, the circumflex and the right coronary artery, so one picture covers all three territories. Each mid-oesophageal view shows only two opposite walls, so it misses some territories. One exception: during off-pump grafting, when the heart is lifted, mid-oesophageal views may give better images.

Mid-oesophageal long-axis view detects ischaemia. It is easy to confuse with the mid-oesophageal long-axis view, which does show left ventricular walls. The aortic long-axis view, however, is centred on the outflow tract, aortic valve and root. It shows very little ventricular muscle, so it cannot survey the coronary territories.

At mid-papillary level, the transgastric short-axis slice includes wall segments fed by each of the three main coronary arteries, so it suits ischaemia detection. A mid-oesophageal four-chamber image shows just two walls. During beating-heart distal grafting, mid-oesophageal imaging may be preferable.

Sources: Mayo reviewMiller 10e

A sudden large clot loads the right ventricle, which dilates and fails. Both ventricles share a fixed pericardial space, so the swollen RV pushes the septum towards the left. The septum flattens into a D shape and squeezes the LV, so LV filling and output fall, which leads to shock. The four-chamber view shows both ventricles side by side, so you can compare their sizes and see the septum shift. With McConnell's sign, the RV free wall stops moving while the apex still contracts.

Apical four-chamber view shows RV size. It is tempting because it shows the right atrium and the venae cavae, where a clot in transit might be seen. But it does not show the LV next to the RV, so you cannot compare their sizes or see the septum flatten.

Massive PE means sustained hypotension or shock with no other cause. Echo signs: McConnell's sign, RV diameter over 30 mm (parasternal long-axis), RV area over 90% of LV area (apical four-chamber), D-shaped septum. A dilated RV can compress the LV through interdependence.

Sources: Miller 10eBarash 9e

Venous ECMO cannulae enter from the femoral vein and travel up the inferior vena cava into the right atrium. Some are advanced on into the superior vena cava. The bicaval plane shows both cavae entering the right atrium, with the atrial septum in the same image, so the tip's route and final position can be seen. Take care not to mistake the coronary sinus for the IVC. Advancing the probe confirms the true IVC, which continues below the diaphragm beside the liver.

Bicaval view adequate for cannulation. It shows the right atrium and septum, so it looks adequate for a right-heart procedure. It fails because it does not display the caval inflow along its length. A cannula rising from the IVC or passing into the SVC cannot be tracked, and its tip cannot be positioned reliably.

The mid-oesophageal bicaval view is recommended for guiding placement of bypass and ECMO cannulae. A multi-stage femoral venous cannula can be advanced into the SVC under TEE guidance. The IVC is confirmed by showing its continuation below the diaphragm next to the liver.

Sources: Barash 9e

Air drawn into an open vein rides venous return through the superior or inferior vena cava into the right atrium. The bicaval view displays both caval inflows and the atrium in a single image, so bubbles appear as bright echoes at their point of arrival, before they disperse into the right ventricle and pulmonary circulation. The four-chamber view shows the right heart but not the caval inflow. TOE is the most sensitive air monitor, so even very small volumes are seen.

Four-chamber image of the right heart. The four-chamber view is the most familiar TOE image and does show the right atrium and ventricle, so it feels adequate. It omits both caval inflows, where entrained air first arrives, and the sources use it only occasionally as a backup to bicaval.

Sources show bubbles in the right atrium on the mid-oesophageal bicaval image, name bicaval the preferred monitoring view, and use four-chamber only occasionally. TOE is the most sensitive monitor, detecting about 0.02 mL/kg; precordial Doppler about 0.05 mL/kg, or 0.25 mL in the heart.

Sources: Outside our books: Anesthesiology Considerations and Management of Venous Air Embolism in Patients in the Semisitting Position: A Single-Center Review (2025)Miller 10eBarash 9e

The circumflex runs in the left atrioventricular groove. Its obtuse marginal branches spread over the free lateral wall of the left ventricle. The LAD runs down the front of the heart and perfuses the anterior wall. The RCA's distal branches perfuse the inferior wall. At mid-papillary level, one short-axis slice cuts across all three territories. This makes it the standard view for monitoring ischaemia: a new regional wall motion abnormality points to the culprit vessel. The borders overlap, so the anterolateral and inferolateral edges vary between patients.

LAD supplies lateral ventricular wall. The LAD's diagonal branches can reach the anterolateral region, so people link it with the lateral side. On the short-axis ring, though, the lateral free wall is circumflex territory. The LAD's own territory is the anterior wall.

The circumflex usually perfuses the lateral segments through its obtuse marginal branches, the LAD the anterior wall and the RCA the inferior wall. The LAD sometimes contributes anterolaterally and the RCA inferolaterally. The mid-papillary short-axis view shows all three territories.

Sources: Miller 10eBarash 9eMayo review

When pericardial pressure rises above the pressure inside a chamber, that chamber is squeezed while it relaxes, because that is when its own pressure is lowest. The thin, low-pressure chambers give way first. The right atrium buckles during ventricular systole, then the right ventricle folds in during diastole as pericardial pressure keeps rising. The atrium can buckle briefly without true tamponade, so its collapse is sensitive but nonspecific. Right ventricular diastolic collapse needs a higher pericardial pressure, so it separates tamponade from a simple effusion better.

Right atrial collapse is specific. Right atrial collapse is usually the earliest chamber sign, so it looks like the best answer. But brief atrial inversion also happens without tamponade, so it is nonspecific. It also occurs in ventricular systole, not diastole. Right ventricular diastolic collapse is the more specific sign.

The texts say chamber collapse during relaxation is what separates tamponade from a simple effusion. Transient right atrial collapse can occur without tamponade. Right ventricular diastolic collapse is highly sensitive and specific, and more specific than right atrial collapse.

Sources: Stoelting 8eMiller 10eBarash 9e

The probe is stiff and is passed partly blind. If the wall is already torn, narrowed, distorted or actively bleeding, pushing the probe can tear right through it or make the bleeding worse. Probe perforation and major haemorrhage are rare but often fatal. Healed old surgery, a past bleed, varices, inflamed mucosa and poor clotting only raise the risk. In those cases you weigh the benefit against the risk rather than refusing outright. An existing oesophageal injury is the clearest case where you should never insert the probe.

Previous upper GI bleeding history. It looks like the milder choice because a history of upper GI bleeding is only a relative contraindication. But continued bleeding is active haemorrhage, which is absolute. Of these oesophageal problems, only surgery done long ago is relative.

Absolute contraindications: perforation, strictures, masses, diverticula, tracheo-oesophageal fistula, recent upper GI surgery, active bleeding, oesophageal injury. Relative: earlier oesophageal or gastric surgery, past bleeding, varices, oesophagitis, ulceration, neck irradiation, coagulopathy. Probe-related perforation or haemorrhage is often fatal.

Sources: Barash 9e

Valve area measures the fixed anatomical orifice, so it anchors the grade. The transmitral gradient climbs as the orifice narrows only when flow is held steady. A high cardiac output exaggerates it, and general anaesthesia can make it understate the lesion. Read the area first, then confirm with the other markers. In moderate disease the mean gradient is 5–10 mmHg and pulmonary systolic pressure is 30–50 mmHg.

Area under 1.5 cm² is severe. "Severe" tempts because Miller and the current valve guideline call any area under 1.5 cm2 severe. The three-band grading keeps severe for an area under 1.0 cm2 with a mean gradient above 10 mmHg. When area, gradient and pulmonary pressure all fall in the middle band, grade it moderate.

Barash's three-band table: mild over 1.5, moderate 1–1.5, severe under 1.0 cm2, with parallel gradient and pulmonary pressure bands. Miller calls any area under 1.5 cm2 severe, with pulmonary systolic pressure over 50 mmHg and mean gradient 10 or more.

Sources: Barash 9eMiller 10e

A healthy aortic valve opens to 3 to 4 cm2. As the cusps stiffen and the opening narrows, the left ventricle must generate a higher systolic pressure to eject the same stroke volume, so the pressure drop across the valve rises. Area shows how tight the orifice is; gradient shows the pressure the ventricle pays to push blood through it. Gradient also depends on flow, so a failing ventricle can show a smaller gradient despite a tighter valve. Never downgrade a critically small orifice because the gradient looks modest.

Borderline stenosis is moderate grade. A borderline opening just below the cut-off makes a middle grade seem cautious. But moderate disease requires an area of at least 1 cm2 and a gradient of no more than 40 mmHg. Both values here exceed those limits, and it also names the wrong valve.

Standard tables grade mild disease by a gradient under 20 mmHg and moderate by 20–40 mmHg. Severe disease means an orifice under 1 cm2 or a mean gradient above 40 mmHg. The gradient can fall as left ventricular function declines.

Sources: Stoelting 8eBarash 9eMiller 10e

Outcome in dilated cardiomyopathy depends on how far the pump failure has progressed. A raised CVP shows that the right ventricle is failing as well as the left, so the disease is biventricular, and that worsens the outlook. A very low ejection fraction, high left-sided filling pressure, low cardiac index and hypotension all show that forward output is failing. Pulmonary hypertension shows that back-pressure is reaching the right heart. Low blood pressure, not high blood pressure, marks advanced disease.

Ejection fraction below thirty per cent. A low ejection fraction does indicate poor prognosis, and a cut-off of thirty per cent is a familiar general one in heart failure. However, the dilated cardiomyopathy prognostic list sets a lower threshold. Raised CVP is listed without any threshold, so it matches exactly.

The source lists haemodynamic predictors of a poor outcome in dilated cardiomyopathy: ejection fraction below 25%, wedge pressure over 20 mm Hg, cardiac index under 2.5, systemic hypotension, pulmonary hypertension and a raised CVP. Involvement of both ventricles makes the outlook worse.

Sources: Stoelting 8e

Ejection fraction is the share of end-diastolic volume that the ventricle ejects with each beat. When contractility fails, as in systolic dysfunction, less of that volume is ejected, so the fraction falls. The ventricle then dilates and thins, a pattern typical of dilated cardiomyopathy. In preserved-fraction failure the main problem is diastolic: the ventricle is stiff and fills poorly, but it still ejects a normal share of what it holds. A third heart sound, which reflects a dilated, poorly contracting ventricle, is heard more often when the fraction is reduced.

Diastolic dysfunction. Crackles, pulmonary hypertension and enlarged atria point to raised filling pressures, which suggest a stiff, diastolic ventricle. But the classification depends only on the ejection fraction number. A value below the reduced cut-off, together with dilated ventricles and a third heart sound, means reduced-fraction failure.

The universal classification defines reduced fraction as 40% or below, mildly reduced as 41–49% and preserved as 50% or above. Systolic dysfunction underlies reduced-fraction failure. Dilated cardiomyopathy usually leads to it, and a third heart sound is commoner in it.

Sources: Miller 10eBarash 9eStoelting 8e

The papillary muscles tether the mitral leaflets through the chordae. Infarction or ischaemia of a papillary muscle, usually the posterior one after inferior infarction, stops the leaflets closing. Blood then leaks from the left ventricle back into the left atrium throughout systole, which gives a holosystolic murmur loudest at the apex. Septal rupture can also cause a pansystolic murmur, but it comes with a parasternal thrill and a left-to-right shunt. Cardiogenic shock is a result of these lesions, not a murmur.

Tricuspid regurgitation. Tricuspid regurgitation also gives a pansystolic murmur, so it looks like an equally good fit. But infarction usually damages the left ventricle and its papillary muscles. The valve that fails is therefore the mitral, and the sources tie the post-infarction murmur to mitral incompetence heard at the apex.

Mitral regurgitation produces a holosystolic murmur best heard at the apex. Acute mitral regurgitation after infarction is linked to posterior papillary muscle ischaemia or infarction, usually with inferior MI. Septal rupture also gives a pansystolic murmur, together with a parasternal thrill.

Sources: Miller 10eStoelting 8e

The tricuspid leaflets are malformed and sit lower than normal, towards the apex. The inflow part of the right ventricle therefore lies above the valve and acts as part of the atrium. The misshapen anterior leaflet, often full of holes, also fails to close, so blood flows back into the right atrium with every systole. The extra atrialised chamber and the volume load from regurgitation both enlarge the right atrium. The main defect is not in the left heart.

Enlarged left atrium. Left atrial dilation is tempting because in congenital heart disease any atrial enlargement sounds plausible. But the defect is in the tricuspid valve, which is on the right side. Both the regurgitant jet and the atrialised ventricle enlarge the right atrium, not the left.

Ebstein anomaly is a malformed, downward-displaced tricuspid valve that atrialises the right ventricle; a large holed anterior leaflet leaks, enlarging the right atrium, which may fibrillate. It is listed among right-to-left shunt lesions in which intravenous air can embolise to the arteries.

Sources: Stoelting 8eFaustMayo review

Rheumatoid arthritis is a systemic inflammatory disease, and its main cardiac feature is inflammation of the pericardium, which can progress to an effusion. The pain comes from the inflamed serous lining, so it behaves like pleuritic pain. Anything that moves or stretches the inflamed layers makes it worse, such as lying flat or taking a breath. Leaning forward eases it. Ischaemic pain is different: it is a constant pressure that does not change with posture or breathing.

Myocarditis. Myocarditis is tempting because it is also an inflammatory heart condition that can occur in systemic disease. However, the textbooks name pericarditis as the heart condition seen in rheumatoid arthritis. Pain that changes with posture and breathing points to the pericardium, not the heart muscle.

Pericarditis is one of several cardiovascular conditions listed, and it can involve pericardial fluid with tamponade physiology. Its pain is retrosternal, sharp or stabbing and pleuritic. It is worse on inspiration or lying down, and posture changes such as leaning forward may relieve it.

Sources: Miller 10eStoelting 8e

Blood leaves the thick-walled left ventricle through a fixed narrowing, so stroke volume cannot rise to compensate. The hypertrophied muscle is perfused mainly in diastole and has high oxygen demand. A fast rate cuts diastolic time, reducing filling and coronary supply, so ischaemia follows; a very slow rate cuts output. The stiff ventricle depends on filling volume, and vascular tone sustains the pressure driving coronary flow, so reducing preload or afterload brings hypotension, ischaemia and a downward spiral.

Tachycardia. A faster rate looks like a way to raise output when stroke volume cannot increase. But tachycardia shortens diastole, starving the thick ventricle of filling time and coronary flow while raising its oxygen demand, so ischaemia follows. The target is a normal to low rate, avoiding frank bradycardia.

Stenotic, pressure-overloaded valves do best at a slow-normal rate, since a longer diastole aids filling and coronary flow; too slow a rate lowers output. Preload and afterload should be kept or raised, sinus rhythm preserved, and hypotension avoided.

Sources: Mayo reviewStoelting 8eBarash 9e

If a valve area is smaller than the cut-off and the gradient is higher than the cut-off, the disease is severe, because both values are beyond the thresholds. Narrowing the opening further only makes the obstruction worse. It never helps. The gradient depends on how hard the ventricle pushes blood through the narrowing. If systolic function fails, the gradient can fall even though the valve is still tight. When area and gradient disagree, check ventricular function, stroke volume and flow reserve. In older adults the usual cause is age-related degeneration.

Afterload reduction relieves obstruction. Lowering afterload helps failing ventricles and leaking valves, so it sounds right here too. In aortic stenosis, though, the main obstruction is the fixed narrowing at the valve. Lowering systemic resistance mostly drops pressure beyond the valve and does not relieve the obstruction. The statement is false.

Severe disease usually, though not always, shows an area under 1.0 cm2 and a mean gradient over 40 mm Hg. The gradient may fall as systolic function declines. When area and gradient disagree, flow needs further assessment. Age-related degeneration is the commonest cause in adults.

Sources: Miller 10eStoelting 8e

When the membrane reaches threshold, fast sodium channels open. Sodium flows into the cell down its concentration and electrical gradient, so the membrane depolarises almost instantly and briefly overshoots zero. Calcium comes in later and more slowly, through L-type channels. Its inward current, balanced by potassium leaving, holds the membrane depolarised during the plateau. Outward potassium currents then return the cell to its resting potential.

Calcium initiates depolarisation. Calcium is tempting because it is the ion most linked to heart muscle and contraction. In a ventricular cell, though, calcium enters through slow L-type channels during the plateau, after the upstroke has finished. It sustains depolarisation but does not start it.

The textbooks say a rapid inward sodium current produces the ventricular upstroke and overshoot. Slow calcium entry through L-type channels produces the plateau, and outward potassium currents bring about repolarisation.

Sources: Miller 10e

After the sodium-driven upstroke, a potassium channel opens quickly and then closes. The brief loss of potassium gives a short, partial fall in voltage before calcium entry sustains the plateau. At rest in working myocytes, the inward rectifier keeps the membrane polarised and stable, and increasing it hyperpolarises the cell. Almost no net ion movement occurs during diastole in fast-response cells. The sodium–potassium pump maintains the ion gradients that this resting potential depends on.

Potassium current causes phase 1. It is tempting because it is a repolarising potassium current. However, it carries potassium outflow during the plateau and drives phase 3 repolarisation. The brief, limited early notch is attributed mainly to the transient outward current, whose rapid activation and short life match that phase.

Phase 1 is described as a short, limited repolarisation due largely to the transient outward potassium current. Phase 4 rest is maintained by the potassium inward rectifier. One source also credits the sodium–potassium ATPase and notes minimal ionic flux in fast-response diastole.

Sources: Miller 10eStoelting 8e

After the fast sodium upstroke, L-type calcium channels open slowly and stay open. Positive charge flowing in through these channels roughly cancels the positive charge leaving as potassium, so the membrane voltage stays nearly flat. Ventricular membranes also become less permeable to potassium, which slows its exit. When the calcium channels inactivate, outward potassium current exceeds calcium entry and the cell repolarises. Calcium is removed from the cell later, mainly by sodium–calcium exchange, so calcium leaving the cell plays no part in holding the plateau.

Potassium maintains plateau phase. Potassium does leave the cell throughout the plateau, and it dominates the phases on either side, so it seems like a reasonable choice. But potassium loss on its own would repolarise the cell. The plateau exists only because inward calcium balances that outward current.

The sources credit the plateau to a slow inward calcium current through L-type channels, balancing potassium outflow. Sodium entry causes the rapid depolarisation, and repolarisation happens once outward potassium current exceeds calcium entry. Calcium is pumped out mainly by the sodium–calcium exchanger.

Sources: Miller 10eStoelting 8e

During the plateau, calcium enters through L-type channels while potassium leaves, and the two roughly balance. As calcium entry fades, the outward potassium currents become larger than it. Positive charge then leaves the cell overall, so the membrane potential falls back to rest. Sodium entry causes the upstroke, not recovery. Sodium leaves the cell through the Na–K ATPase at rest, which restores ion gradients but does not repolarise the membrane.

Calcium drives repolarisation. Calcium influx sets the long plateau just before repolarisation, so people link it to the downslope. But calcium entry holds the membrane depolarised. Repolarisation starts only when outward potassium current becomes larger than calcium entry, so the correct ion movement is potassium outflow.

Miller links phase 0 and the overshoot to fast sodium entry, and the plateau to slow calcium entry through L-type channels. It links phase 3 to outward potassium currents that exceed calcium entry. The Na–K ATPase maintains the resting phase 4.

Sources: Miller 10e

Protamine is a polycationic protein from salmon sperm that directly neutralises heparin. Its dose follows the amount of heparin given, either by a fixed ratio or by a titration assay. It is given only after separation from bypass, once the patient is stable, because protamine can cause severe hypotension, pulmonary hypertension and right ventricular failure. If that failure becomes intractable, the bypass circuit is the rescue. Heparin must be restored first so the patient can safely go back on bypass.

Fresh frozen plasma reverses heparin. FFP is tempting because bleeding after bypass is often treated with clotting products. Here, though, the problem is heparin still circulating, and only its specific antagonist, protamine, neutralises it. Plasma supplies clotting factors but does not reverse heparin.

Heparin is neutralised with protamine, a polycationic protein from salmon sperm, dosed by a fixed 1 mg per 100 U ratio or a titration assay once haemodynamics are stable. Severe reactions cause hypotension, pulmonary hypertension and right ventricular failure, sometimes requiring bypass to restart.

Sources: Barash 9eMiller 10e

Protamine can release thromboxane and complement C5a, which cause a sudden rise in pulmonary artery pressure. The right ventricle distends and fails against this load. Too little blood reaches the left heart, so systemic pressure collapses. Once the failure is intractable, only the bypass circuit can take over the circulation and offload the right heart. The circuit cannot be used while anticoagulation is reversed, so heparin must be given first. Heparin also makes the heparin–protamine complexes smaller. For the same reason, protamine is started while the aorta is still cannulated.

Amrinone restores perfusion. Amrinone is an inodilator, so it seems to fit a failing, pressure-loaded right ventricle. But with no measurable systemic pressure, more vasodilation and inotropy cannot restore flow through a distended ventricle. Only mechanical takeover by resuming bypass, with heparin given first, rescues the patient.

Severe protamine reactions cause hypotension and raised pulmonary pressures, progressing to intractable RV failure and collapse, requiring return to bypass. First reheparinise so bypass can resume; this also makes the complexes smaller. Protamine is therefore given before aortic decannulation.

Sources: Miller 10eBarash 9e

The arterial line feeds straight into the aorta and the cerebral vessels. Every further revolution of the pump drives more air into the patient, so ending forward flow and clamping lines and shunts is the only step that stops more air getting in. After that the team removes air from the patient: head-down tilt, carotid compression and retrograde cerebral perfusion if the surgeon agrees. The circuit is cleared of air before bypass is restarted.

Head-up positioning. Positioning feels like a quick, useful first move. But head-up tilt puts the brain uppermost, where buoyant bubbles will head. The recommended tilt is the opposite, steep head-down, and it only follows halting the pump. Raising flow simply pumps in more air.

Perfusion guidelines say the pump must stop immediately, all lines and shunts are clamped, and the team is told. Deep head-down positioning, carotid compression and retrograde cerebral perfusion follow. A reported case used exactly this sequence.

Sources: Outside our books: National Heart Center Perfusion Guidelines (2026)Outside our books: Effective handling of substantial arterial air embolization during extracorporeal perfusion (2019)

When the pump takes over, the patient's blood mixes with the circuit's priming fluid straight away. Diluted blood has lower viscosity, so systemic vascular resistance falls. Pressure depends on flow and resistance, so mean pressure drops unless pump flow rises. The drop is predictable and short-lived. It usually recovers when cooling begins, when a vasoconstrictor raises resistance, or when volume is added.

Anaphylaxis. Anaphylaxis seems likely because pressure falls sharply and many drugs and blood products are given around bypass. But this fall happens at the moment bypass starts and follows a known mechanism: dilution lowers resistance. It is an expected physiological change, not an allergic reaction.

Starting bypass dilutes the blood almost immediately and reduces systemic vascular resistance. Low blood pressure is common afterwards unless flow is increased. It persists until cooling starts, resistance is raised with drugs or volume is restored.

Sources: Faust

Inflation just after aortic valve closure pushes blood aside and lifts aortic diastolic pressure. That pressure drives flow into the relaxed coronary bed. Sudden deflation just before ejection leaves a low-pressure space in the aorta, so the ventricle ejects against less impedance. Better ejection leaves less blood behind, so the chamber shrinks. By Laplace's law, a smaller chamber under lower pressure has less wall tension, so oxygen demand falls while supply rises. A ventricle that grows larger would mean unloading has failed.

Ventricular cavity enlarges during pumping. The first two effects are right, and the word 'augmentation' suggests that the ventricle fills more. But lower afterload lets the ventricle empty more completely, so it gets smaller. A bigger ventricle would raise wall tension and oxygen demand, which is the opposite of what the device is for.

Deflating the balloon just before ventricular contraction lowers aortic pressure and afterload, easing left ventricular emptying and reducing wall stress and oxygen demand. Inflating just after aortic valve closure raises diastolic pressure, increasing coronary perfusion, improving myocardial supply and cardiac output.

Sources: Mayo reviewMiller 10e

Cardiac output depends on preload, contractility and afterload, and catheter numbers separate them. Pump failure gives low output with high filling pressures; an underfilled heart gives low output with filling pressures that are not raised. So a mid-range wedge with a low index points away from failure and towards inadequate volume. The high resistance is reflex vasoconstriction propping up a falling pressure: vasodilating removes that prop and deepens hypotension, while driving an empty ventricle harder raises oxygen demand without adding stroke volume. Fill first, then reassess.

Vasodilation to reduce afterload. The raised resistance and published advice to reduce afterload after cardiac surgery make vasodilation tempting. But that advice sits alongside optimising preload, and here the blood pressure is already low. The high resistance is compensation for underfilling; dilating the vessels before filling them drops pressure further.

Catheter data classify shock: low output with low filling pressures is hypovolaemic, low output with high filling pressures is cardiogenic. Postoperative hypotension from reduced preload responds well to intravenous fluid, and after heart surgery managing low output starts with optimising preload.

Sources: Miller 10e

Blocking angiotensin removes one of the body's main vasoconstrictor responses to a falling pressure. Bypass sets off a systemic inflammatory response, and nitric oxide relaxes vascular smooth muscle. Together they cause a low-resistance state in which the heart may pump well but the vessels have little tone. Catecholamine receptors can be overwhelmed, so drugs that act by other routes help. Vasopressin works through its own vascular receptors, and methylene blue or hydroxocobalamin counter the nitric oxide pathway.

Transfusion reaction from blood product. Pump blood was given just before the collapse, so it is tempting to blame a transfusion reaction or the blood product. The drop fits a known vasodilatory pattern instead: long-term renin–angiotensin blockade plus the inflammatory insult of bypass. Together these cause a severe, sustained loss of vascular tone.

Chronic ACE inhibitor or ARB therapy, long bypass times and the inflammatory response predispose to vasoplegia. Continuing ACE inhibitors around surgery was linked to more vasoplegia. Vasopressin treats cases unresponsive to catecholamines, and nitric oxide involvement supports methylene blue and hydroxocobalamin.

Sources: Miller 10eBarash 9e

Bypass and aortic handling can release particles into the circulation, and these can lodge in the retinal arteries. The retina supplied by the blocked vessel loses its blood flow straight away. The patient notices painless loss of vision, the pupil reacts abnormally, the retina looks pale and the arterioles look narrow. In surgery outside the heart, retinal artery occlusion usually comes from pressure on the eye. In cardiac surgery, emboli are the extra cause. Cortical blindness is different: the optic disc and pupil responses stay normal.

Occipital lobe infarction. Tempting, as occipital lesions do occur after CABG, but the scenario describes an uneventful operation with no hypotension. Occipital infarction usually follows posterior circulation or watershed events and is often bilateral. Normal fundus and pupils do not fit an embolic retinal picture.

Perioperative retinal artery occlusion is usually caused by eye pressure, though emboli can cause it in cardiac surgery. It causes painless vision loss, a pale ischaemic retina and abnormal pupils. Cortical blindness is often bilateral, with a normal disc and pupils.

Sources: Miller 10eBarash 9e

Cerebral oxygen consumption follows neuronal electrical activity. It falls by roughly 6–7% for each degree of cooling. As the brain cools, cortical firing slows step by step until, in deep hypothermia, the cortex becomes electrically silent. So when surgery needs deep hypothermic circulatory arrest, the team keeps cooling until the EEG is silent before the arrest starts. They do not rely on extra barbiturate or propofol to produce the silence.

27 degrees produces EEG silence. 27 °C is the well-known cut-off for profound hypothermia, below which the brain can survive long periods without blood flow. That makes it feel like the temperature at which the brain switches off. But the EEG is not yet silent at 27 °C. Full suppression needs much deeper cooling.

Cerebral oxygen consumption drops about 6–7% per degree of cooling, and the EEG can be fully suppressed at a core temperature of about 18–20 °C. Before circulatory arrest, cooling should be used to make the EEG silent rather than extra drugs.

Sources: Mayo reviewMiller 10e

The clamp suddenly raises resistance to left ventricular ejection. Pressure and flow proximal to it therefore climb. Higher systolic wall tension makes the ventricle work harder and consume more oxygen. If supply cannot keep up, subendocardial demand ischaemia shows as ST depression. Below the clamp, venous beds collapse and constrict, which shifts blood centrally, so preload and filling pressures rise. The heavier afterload usually lowers cardiac output, while heart rate changes little.

Reduced coronary perfusion from clamping. It is tempting because ST depression usually signals reduced supply, and ischaemia feels like a flow problem. But pressure proximal to the clamp rises, so coronary perfusion pressure is kept up. The ischaemia comes from the extra work of ejecting against the clamp, which raises oxygen demand.

Pressure above the clamp rises because of sudden impedance to aortic outflow and higher systolic wall tension. Flow and vascular resistance above the clamp increase, heart rate barely changes and cardiac output usually falls. Venous redistribution raises preload and filling pressures.

Sources: Miller 10eStoelting 8e

Spinal cord perfusion pressure is the arterial pressure reaching the cord minus the pressure inside the spinal canal. A cross-clamp cuts flow to the aorta below it, where the intercostal feeders arise. At the same time, clamping sets off a reflex rise in CSF pressure. Distal bypass restores flow beyond the clamp, and draining CSF removes the opposing pressure. Both widen the perfusion gradient. Lowering blood pressure would narrow it, so proximal hypertension is kept up during clamping rather than induced hypotension.

Proximal perfusion protects spinal cord. It sounds like the bypass circuit used in these repairs. However, that circuit perfuses the aorta beyond the clamp, because the cord's blood supply arises downstream. Supporting the circulation above the clamp does nothing for the cord. Distal perfusion combined with CSF drainage is what protects it.

Protective adjuncts include left atrium-to-femoral bypass for distal perfusion, CSF drainage, reimplanting key intercostal arteries and keeping proximal pressure high while clamped. Clamping raises CSF pressure, and drainage counters this. In a randomised trial, drainage cut the relative risk of a postoperative deficit by 80%.

Sources: Stoelting 8eBarash 9eMiller 10e

Removing the clamp suddenly makes systemic vascular resistance collapse as the ischaemic lower body reperfuses. Blood pools in the dilated distal bed, which causes central hypovolaemia. Vasoactive and cardiodepressant mediators also wash into the circulation. Closing the aorta again, with the clamp or finger pressure, restores afterload and proximal pressure. This gives time to replace volume, and a slower second release lets the mediators return in smaller amounts. Fluid loading is therefore the preventive step before release, not the first response to collapse.

Fluid administration for unclamping collapse. Fluid is a natural choice because central hypovolaemia drives unclamping hypotension. But volume loading is the preventive step taken just before release. Once pressure has collapsed with the distal bed wide open, the immediate move is to reocclude the aorta and then release it again gradually.

Unclamping causes marked falls in blood pressure and systemic vascular resistance, chiefly from central hypovolaemia. Give 10–20 mL/kg crystalloid immediately before release. Release slowly to allow volume replacement and slow mediator washout from ischaemic tissue.

Sources: Stoelting 8eMiller 10e

A ruptured aneurysm causes haemorrhagic shock before any clamp is applied, so the patient arrives hypovolaemic and unstable, then suffers clamp-related ischaemia. Poor blood pressure control and existing kidney disease drive kidney injury, making renal failure much more common after emergency than elective repair. Spinal cord risk depends on clamp site: infrarenal repair seldom cuts off the cord's supply, unlike thoracic repair. These complications lead to one dominant outcome, perioperative death, which has barely improved in decades.

Acute renal failure is outcome. Acute renal failure is tempting, being the classic complication after ruptured aneurysm repair and far more frequent than after elective surgery. But it is only one route to the final outcome, not the worst outcome itself. Perioperative death affects about half of patients, outranking any single organ failure.

Perioperative mortality for ruptured AAA has stayed at nearly 50% for four decades. After emergency repair for rupture, 26% developed AKI, against 4% renal failure after elective surgery, and this was linked to unstable haemodynamics. Spinal cord injury after elective infrarenal repair is only 0.2%.

Sources: Miller 10eBarash 9eStoelting 8e

At very fast rates, diastole is too short for the ventricles to fill, and AF also loses the atrial contribution to filling. Cardiac output and blood pressure fall. Low pressure cuts coronary perfusion while tachycardia raises oxygen demand, so ischaemia sets in and worsens further. A synchronised shock restores an organised rhythm at once and does not rely on circulation that is already failing. Negatively inotropic or vasodilating drugs act more slowly and can deepen the hypotension, so they are for patients who are stable.

Amiodarone for unstable atrial fibrillation. Amiodarone seems a safe, familiar antiarrhythmic for AF and poor ventricles, but it is a slower, drug-based strategy that can lower blood pressure. It is used for stable patients or when shocks fail, not first line in shock.

The sources say unstable patients with AF or other supraventricular tachycardias should be cardioverted with a synchronised shock straight away, especially when hypotension and ischaemia accompany the arrhythmia. Drugs to control the ventricular rate are the approach only when haemodynamics are stable.

Sources: Miller 10eMayo review

When blood pressure holds, the danger of a fast irregular rhythm is the rate itself, not failing perfusion. A beta blocker, or a calcium channel blocker, slows conduction through the AV node. This lengthens diastole, which improves ventricular filling and myocardial oxygen balance. An immediate shock is kept for patients whose rate is already causing heart failure, angina or haemodynamic collapse. AV nodal blockers are avoided when an accessory pathway or preexcitation is suspected.

Amiodarone for atrial fibrillation rhythm. Amiodarone is the familiar antiarrhythmic for atrial fibrillation and can restore sinus rhythm, so it looks definitive. In a stable patient, though, rate control comes first, and a beta blocker is the first-line choice. Amiodarone's thyroid side effects also make it unattractive in someone with thyroid disease.

Electrical cardioversion converts atrial fibrillation most effectively but is indicated for heart failure symptoms, angina or haemodynamic instability. With stable vital signs, rate control using a beta blocker or calcium channel blocker is the primary goal, unless accessory pathways or preexcitation are suspected.

Sources: Stoelting 8e

The sinus node fires faster when sympathetic drive rises or vagal tone falls. A ruptured, inflamed viscus causes fluid loss and septic vasodilatation, which lower preload and vascular tone. The sympathetic system then raises the heart rate to keep cardiac output and blood pressure up. So the fast rate is compensation, not the disease. Forcing it down with a beta-blocker or antiarrhythmic removes that support and can make hypotension worse. Drugs or shocks aimed at the rhythm itself miss the cause. The rate settles once volume and infection are corrected.

Beta-blocker for compensatory tachycardia. A beta-blocker seems sensible because it slows a fast heart and improves myocardial oxygen balance. But this rate is a sympathetic response to fluid loss and sepsis. Beta-blockade is meant for sinus tachycardia that is not due to hypovolaemia. Here it would remove compensation and worsen hypotension.

Hypovolaemia is a common cause of tachycardia in recovery, and haemorrhage and septic shock are serious ones. Sinus tachycardia comes from sympathetic stimulation or vagal withdrawal. Treatment targets the likely cause, and beta-blockers are kept for sinus tachycardia not caused by hypovolaemia or light anaesthesia.

Sources: Miller 10eBarash 9eStoelting 8e

Assume a wide-QRS tachycardia of uncertain origin is ventricular until proven otherwise. When it causes hypotension or shock, the fast rate is the cause, so it must be ended at once. An electrical shock does this whether the focus is ventricular or supraventricular with aberrant conduction. Drugs act more slowly and suit stable patients. If a pulse is present, the shock is synchronised. Only pulseless VT gets unsynchronised defibrillation.

Procainamide before cardioversion. Procainamide is tempting because it is an accepted drug for wide-complex tachycardia and treats both VT and aberrant SVT, so it looks careful and complete. But drugs are for stable patients or for when a shock fails. In a hypotensive patient, waiting for a drug to work risks collapse.

The sources agree that an unstable wide-complex rhythm is presumed to be VT and needs urgent synchronised cardioversion. Procainamide or amiodarone are alternatives only for stable patients. Electrical treatment is indicated for instability or failed drugs. Pulseless VT is defibrillated instead.

Sources: Mayo reviewBarash 9eFaustMiller 10e

Adenosine transiently blocks AV nodal conduction, terminating node-dependent re-entry circuits. It is cleared within seconds, so give it as a rapid push immediately followed by a saline flush. If the first dose fails, double it before abandoning the drug. Central line injection or dipyridamole potentiates its effect; with dipyridamole, asystole risk means using a smaller first dose. Reserve electrical cardioversion for haemodynamic compromise: hypotension, shock, ischaemic chest pain, heart failure or acute confusion.

Cardioversion for patient agitation. Agitation suggests altered mental state, tempting shock. But instability means rate-related compromise: hypotension, shock, ischaemic chest pain or heart failure. A hypertensive patient is still perfusing. Since the drug hasn't been given at full dose, escalate the dose before cardioverting.

Adults: 6 mg rapid IV push with saline flush, then 12 mg if needed. Mayo review lowers initial dose to 3 mg with central line or dipyridamole. Rate-related compromise (shock, acute mental status change) requires synchronised cardioversion.

Sources: Stoelting 8eMayo reviewMiller 10e

Paediatric SVT is usually a reentrant loop, and a synchronised shock interrupts that circuit. A child who is unstable cannot wait for slower options. Vagal manoeuvres and adenosine are for the stable child. Adenosine only blocks AV nodal conduction for a short time, so it is used when there is time to spare. Shock energy depends on body weight. Start in the low range. Move to the higher dose only if the first shock does not restore sinus rhythm.

20 joules initial dose. Twenty joules sounds familiar from older children and adults, and people tend to think a bigger shock works better. In a small infant, though, it is more than even the escalation dose. The first dose is calculated per kilogram, which gives a single-figure number of joules.

Children with unstable reentrant SVT get synchronised cardioversion starting at 0.5–1 J/kg. If that fails, increase to 2 J/kg. Stable children have time for other treatments, such as adenosine, which briefly blocks AV nodal conduction.

Sources: Miller 10e

In synchronised mode the device waits to detect an R wave and times the shock to it. VF has no organised rhythm and no R wave, so a synchronised shock has nothing to trigger on. An unsynchronised shock at defibrillation energy depolarises the whole myocardium at the same moment. That gives a normal pacemaker the chance to take over and restore a working rhythm. VF needs prompt electrical treatment, and the pads are already on the patient.

Chest compressions for ventricular fibrillation. VF is a cardiac arrest rhythm, so starting compressions feels like the natural reflex. But here the VF is witnessed and monitored, and the defibrillator is already attached and charged. The definitive step is a prompt unsynchronised shock, which the sources name as the treatment for VF.

Cardioversion only works when there is an R wave to synchronise to. Without an organised rhythm, an unsynchronised defibrillating shock is required. VF should be defibrillated promptly. Amiodarone is kept for haemodynamically stable VT or an uncertain rhythm.

Sources: Stoelting 8eMiller 10e

Atropine works by removing vagal muscarinic tone, so it helps only when the slowing starts at the sinus or AV node. When the block is below the node, as in Mobitz II or complete block with a wide QRS, vagal tone is not the cause and atropine fails. Dopamine's beta effects raise heart rate and contractility directly, without depending on vagal tone. At higher doses it also constricts vessels, which supports blood pressure. It treats both the slow rate and the low pressure while definitive pacing is set up.

Transvenous pacemaker for bradycardia. A pacing wire looks like the definitive fix for severe bradycardia after coronary instrumentation. But a transvenous pacemaker takes time to prepare. The sources give a beta-agonist infusion, or transcutaneous pacing, first as a bridge. The pacemaker comes once the patient is stable, not as the first step.

Atropine is first-line for symptomatic bradycardia: 1 mg IV every 3–5 minutes, up to 3 mg total. Block below the AV node rarely responds. Use transcutaneous pacing or beta-agonists until transvenous pacing is ready. Dopamine is advised when atropine fails or while awaiting a pacemaker.

Sources: FaustMiller 10e

The monitor shows electrical activity, not perfusion. A wide complex may be ventricular tachycardia with a pulse, pulseless ventricular tachycardia, or pulseless electrical activity, each treated differently. Without a pulse it is cardiac arrest: compressions start at once, and a shock is given only for ventricular fibrillation or pulseless ventricular tachycardia; pulseless electrical activity is not shocked but gets compressions and a search for reversible causes. With a pulse, an unstable patient gets synchronised cardioversion, which needs an organised rhythm to lock onto; stable patients may have an antiarrhythmic infusion.

Immediate synchronised cardioversion before assessing pulse. Cardioversion seems decisive for wide-complex tachycardia, but synchronised shock requires an organised rhythm with a pulse. If pulseless, start compressions; defibrillate only for ventricular fibrillation or pulseless ventricular tachycardia, not pulseless electrical activity. If stable, drugs may suffice. Shocking first skips assessment.

Recognising arrest comes first. A pulse check should last at most 10 seconds, with compressions if no pulse is definitely felt. Pulseless electrical activity is organised activity without a pulse; synchronised cardioversion suits monomorphic ventricular tachycardia with a pulse; antiarrhythmic infusions suit stable wide-complex tachycardia.

Sources: Miller 10eStoelting 8e

The narrow valve fixes stroke volume, so the heart cannot raise its output to make up for a fall in pressure. The thickened ventricle needs a good aortic pressure to perfuse its coronaries. When pressure falls, coronary flow falls, and ischaemia weakens the ventricle. Output then drops further and pressure falls again, so it becomes a downward spiral. The ischaemia here is caused by the low pressure. Raise the pressure first, keep the ventricle filled, and keep the rate normal, neither fast nor slow.

Nitrate for ischaemia relief. New ischaemic changes on the ECG make a nitrate the reflex choice. But here the ischaemia comes from low pressure in a thickened ventricle. Venodilation cuts filling in a preload-dependent heart and lowers pressure further, so coronary perfusion gets worse.

Hypotension in aortic stenosis must be recognised and treated immediately to protect coronary perfusion. These patients are preload-dependent. Low pressure and tachycardia impair coronary flow. Avoid sudden changes in vascular resistance, and recognise and treat ischaemia promptly.

Sources: Barash 9eStoelting 8eMiller 10eFaust

Coronary and organ perfusion depend on arterial pressure, so hypotension in heart failure must be treated first. Noradrenaline raises mean arterial pressure mainly by vasoconstriction, restoring perfusion pressure more effectively than dopamine. A failing ventricle tolerates increased resistance poorly, so vasodilating inotropes, such as dobutamine or milrinone, are favoured only when blood pressure is normal. If tissue perfusion remains poor after pressure is corrected, add inotropic drugs or counterpulsation.

Adrenaline for cardiogenic hypotension. Adrenaline is tempting because it both increases contractility and constricts vessels, and it is used for low-output states after cardiac surgery. In this setting, though, the texts treat it as an inotrope and name noradrenaline as the vasopressor for hypotensive cardiogenic shock.

The texts rank noradrenaline above dopamine for hypotension in cardiogenic shock. They start inotropes or a balloon pump only when perfusion stays poor at an adequate pressure. Vasodilating inotropes are first-line only when the patient is not hypotensive. Noradrenaline restores pressure in refractory systolic failure.

Sources: Stoelting 8eFaust

A failing ventricle tolerates increased afterload poorly, so a drug that strengthens contraction and widens vessels can raise cardiac output while keeping blood pressure stable. In cardiogenic shock, however, output is already too low to supply the brain, kidneys and other essential organs. With blood pressure already low, dobutamine's vasodilatation lowers perfusion pressure further, including coronary flow to the ischaemic ventricle. Noradrenaline reliably increases systemic vascular resistance and arterial pressure, with a modest boost to contractility, restoring the pressure the organs need.

Dobutamine in cardiogenic shock. Dobutamine is tempting because it is the familiar heart-failure inotrope. It strengthens contraction and unloads an afterload-sensitive ventricle. It fails here because its vasodilation lowers an already low pressure. Once organs are hypoperfused, the books switch to an inoconstrictor to rebuild perfusion pressure.

Inodilators are first-line for the afterload-sensitive failing ventricle only while systemic hypotension is absent. Dobutamine suits early shock without organ hypoperfusion. When hypoperfusion is present, an inoconstrictor should replace it. Noradrenaline gives strong vasoconstriction and a dependable rise in vascular resistance and arterial pressure.

Sources: FaustStoelting 8e

Local anaesthetics block cardiac sodium and potassium channels, so cardiac toxicity appears as conduction failure: bradycardia, atrioventricular block and other arrhythmias. Lipid emulsion is run alongside a modified resuscitation. Lidocaine is itself a local anaesthetic, so using it as the antiarrhythmic adds more of the offending drug; amiodarone is preferred, especially for bupivacaine toxicity. Vasopressin is linked to worse outcomes. Calcium channel blockers and β-blockers are also on the avoid list. Adrenaline is kept to small initial doses. A heart that still fails to respond is supported with cardiopulmonary bypass.

Lidocaine for local anaesthetic toxicity. Lidocaine is the familiar antiarrhythmic for ventricular arrhythmias in standard resuscitation, so it is tempting. In local anaesthetic toxicity it is another local anaesthetic and adds to the channel blockade. Guidance substitutes amiodarone and says to avoid any further local anaesthetic.

Adjust standard resuscitation: start adrenaline below 1 µg/kg. For ventricular arrhythmias, prefer amiodarone to lidocaine. Avoid vasopressin, calcium channel blockers, beta blockers and further local anaesthetic. If lipid emulsion and vasopressor therapy fail, start cardiopulmonary bypass.

Sources: Barash 9eFaustMiller 10e

Raised pericardial pressure squeezes the chambers, so each beat can eject only a small, fixed amount. Filling depends on venous pressure staying above pericardial pressure. Output then depends on heart rate and on keeping that filling gradient. Vasodilation, a myocardial depressant, bradycardia or blood loss all reduce venous return, remove the gradient and let blood pressure collapse. Extra intravascular volume raises the effective filling pressure and restores flow between the chambers.

Cardiopulmonary bypass for hypotension. When blood pressure collapses during cannulation, rushing onto bypass feels decisive. But hypotension at this stage usually comes from blood loss or lost venous return. The source treats bleeding and hypovolaemia with small fluid boluses through the checked arterial cannula. It lists bypass as one option for dysrhythmias.

The goals are to avoid hypovolaemia, vasodilation, bradycardia and a depressed myocardium. Give fluid before induction and keep the heart rate high-normal. Once the arterial cannula is confirmed free of air, treat hypotension from blood loss with 100-mL volume increments.

Sources: Miller 10eStoelting 8e

Removing the plaque exposes the carotid sinus, which temporarily over-reads arterial pressure and triggers a vagal, cardioinhibitory reflex. Hypotension from this cause comes with a slowed heart, and the circulation still looks well filled: cardiac output is preserved or high and vascular resistance is low. A baroreflex cannot make the heart race. Hypotension with a rising heart rate therefore indicates compensation for lost volume, and early after this operation the likely source is a wound haematoma. Postoperative hypertension has the opposite cause: sinus denervation removes the baroreceptor brake.

Carotid sinus syndrome. This is the standard textbook explanation for hypotension soon after endarterectomy, so it jumps out. It works through a reflex that slows the heart, though, so it cannot explain a fast pulse. Tachycardia means an underfilled circulation is compensating, and here that points to bleeding.

The sources link early post-endarterectomy hypotension to a newly exposed, overactive carotid sinus. It causes hypotension or bradycardia, and cardiac output is preserved. Wound haematomas are common, seen in 5.5% of patients in NASCET.

Sources: Outside our books: Carotid Stenosis (2023)FaustMiller 10eStoelting 8e

Deformity correction needs wide exposure, dissection along the paravertebral muscles and forceful distraction of vertebrae. This opens large venous beds, so bleeding can be massive. The same open veins can also let air in. Either can cause sudden cardiovascular collapse, so keeping the patient normovolaemic is the core haemodynamic task. Scoliosis and mitral valve prolapse probably share an embryonic or connective-tissue origin, so the valve lesion is an expected companion of the spinal deformity. The sources do not present it as the defining hazard of the operation.

Mitral valve prolapse limits pressure. A known valve lesion tempts people to see a clash: pressure high enough to protect the spinal cord, yet low enough for the valve. The sources mention prolapse only as a known association of scoliosis. They highlight haemorrhage, and blood pressure instability here usually follows the bleeding.

Scoliosis correction brings risks of heavy bleeding, venous air embolism and cord ischaemia. Extensive exposure and distraction can cause massive haemorrhage and circulatory collapse. That makes maintaining normovolaemia, cell salvage and antifibrinolytics core goals. Mitral valve prolapse is a recognised cardiac association of scoliosis.

Sources: Miller 10eBarash 9e

Head-down tilt shifts blood from the legs to the right heart, raising preload. Healthy hearts keep output steady; a failing ventricle with mitral regurgitation has little reserve, so filling pressures may rise, causing congestion. The stress comes from the position and pneumoperitoneum, not the robot, so first limit the tilt and introduce it in steps, watching the response. Reviews advise avoiding steep tilt in high-risk patients and considering an extraperitoneal route; if the heart is decompensated or the trial fails, open surgery is safer and conversion is no failure.

Convert to open surgery by default. Converting to open feels safest for a failing heart facing steep tilt and pneumoperitoneum. But the danger lies mostly in the tilt, which can be limited and trialled, so a compensated patient keeps the minimally invasive benefit. Open surgery is the fallback when decompensated or tilt is not tolerated.

Steep head-down tilt moves blood from the legs into the right atrium, raising preload; fit patients adapt with unchanged output. Patients who would otherwise need open surgery may still benefit robotically, and tilt can be introduced gradually to test tolerance first.

Sources: Miller 10e

Both drugs stop the nerve terminal from clearing noradrenaline and related transmitters from the synapse. Catecholamines build up and sympathetic stimulation grows. The result is raised blood pressure and heart rate, higher myocardial oxygen demand, arrhythmias, cerebrovascular events and more seizures. The fault is blocked uptake. Faster reuptake would do the opposite. Long-term abuse uses up catecholamine stores, so a chronic user may not behave like an acutely intoxicated patient.

Increased catecholamine reuptake. People confuse the direction. Reuptake is the right step to think about, so 'increased reuptake' sounds like a mechanism. But faster reuptake would clear catecholamines sooner and reduce sympathetic tone. That is the opposite of the hypertension, tachycardia and ischaemia these drugs cause.

The texts state cocaine and amphetamines impair uptake of sympathomimetic transmitters, raising risk of hypertension, tachycardia, seizures and ischaemia, with stroke and arrhythmias in addicts. Acutely intoxicated amphetamine users presenting for emergency surgery may be hypertensive, tachycardic and hyperthermic; chronic use depletes catecholamine stores.

Sources: Miller 10eBarash 9eStoelting 8e

Pacemakers exist to treat bradycardia that produces symptoms. Three questions decide the need. Does the rhythm cause symptoms? Where does conduction fail? Is there a reversible cause? Disease below the AV node, in the His–Purkinje system, is unstable and tends to progress, so it favours pacing. A slow rate without symptoms does not reach the threshold for pacing. Nor does syncope that has not been tied to a slow rhythm or pauses.

Syncope alone without documented bradycardia. It is tempting because it pairs sinus node disease with syncope, which sounds severe. Syncope counts only when bradycardia or pauses are documented or provoked at electrophysiological study. 'Unexplained' means that link is missing. Documented symptomatic bradycardia is an indication on its own.

The texts require pacing for bradycardia or conduction delay causing syncope or presyncope. Sinus node indications include documented symptomatic bradycardia, syncope with bradycardia or pauses induced at electrophysiological study, and symptoms with a rate below 40 bpm. Disease below the node favours permanent pacing.

Sources: Miller 10eBarash 9e

A demand pacemaker inhibits its output when it senses activity. Diathermy noise can be mistaken for intrinsic conduction, so pacing stops and a pacemaker-dependent patient loses their rhythm. A magnet closes the reed switch, disabling sensing and the demand function, so the generator paces at a fixed rate regardless of underlying rhythm. This is temporary, not reprogramming. In an ICD, a magnet only blocks tachyarrhythmia detection and cannot force asynchronous pacing. Metabolic upset such as hyperkalaemia can separately cause failure to capture.

Asynchronous mode for ICD diathermy. It takes the pacemaker rule and applies it to every ICD. The risk from diathermy with an ICD is inappropriate anti-tachycardia therapy, so that function is suspended for cautery above the umbilicus. Asynchronous pacing matters only if the patient is pacing-dependent, and it needs reprogramming, not a magnet.

A magnet closes the reed switch, stopping sensing and demand function and giving fixed-rate asynchronous pacing, so diathermy is not read as native conduction. ICDs must be inactivated for cautery above the umbilicus; magnets cannot make them pace asynchronously. Hyperkalaemia can cause failure to capture.

Sources: FaustMiller 10e

A pacemaker or ICD reacts to any electrical signal its leads pick up. Fasciculating skeletal muscle produces myopotentials. The pacemaker can take these for the heart's own ventricular beats and hold back pacing, which is dangerous in a patient who depends on it. An ICD may also read the same muscle noise as an abnormal rhythm. Bipolar leads have their two poles close together, so stray signals rarely get into the circuit. Bipolar diathermy passes current only between two adjacent tips. Rocuronium causes no fasciculation.

Bipolar diathermy causes interference. Diathermy is the textbook source of electromagnetic interference, so any cautery sounds dangerous. But bipolar current passes only between two tips next to each other, with no return pad. It causes little interference, and operating below the umbilicus keeps the current well away from the generator and leads.

Suxamethonium fasciculation can inhibit a normally functioning pacemaker, which mistakes muscle potentials for intrinsic ventricular beats. An ICD may read muscle movement as abnormal rhythm. Unipolar leads pick up more interference than bipolar leads; bipolar diathermy causes little interference.

Sources: Stoelting 8eFaustBarash 9e

Diathermy produces electromagnetic interference, and the pacemaker's generator can sense it. A patient who relies on the device for every beat is at risk if pacing is disturbed, so diathermy use should be kept as low as possible. A magnet held over the generator closes an internal reed switch. This turns off sensing and demand function, so the device paces at a fixed rate whatever interference arrives. Reprogramming can do the same job, but only if a programmer and someone who can use it are available.

Device reprogramming for surgery. Reprogramming is the ideal, controlled way to make a device asynchronous, so it looks like the most expert answer. But it needs a programmer and someone trained to use it. In an emergency with neither available, a magnet over the generator gives protective asynchronous pacing.

Texts advise precautions limiting electromagnetic interference from diathermy. Magnets protect pacemaker-dependent patients in theatre: placed over the generator, a magnet trips a reed switch, stopping sensing and demand function and giving fixed-rate asynchronous pacing. Reprogramming versus magnet use depends partly on programmer availability.

Sources: FaustMiller 10e

An ICD contains both a shock circuit and a pacemaker. Diathermy interference can be read as a fast rhythm, provoking an unwanted shock; a magnet blinds the tachyarrhythmia sensing so no therapy is delivered, yet the bradycardia pacing carries on as programmed and cannot be made asynchronous by a magnet. A standalone pacemaker's magnet response is model-specific: most, but not every, device paces at a fixed rate. Magnet use does not preclude external pads; pacing or defibrillation pads belong on the chest whenever device functions are suspended.

Magnet reliably produces asynchronous pacing. Asynchronous pacing is the classic magnet response, so this feels right. The word 'always' sinks it: the response varies by make and model, holding only for most pacemakers, and never applies to the pacing function inside an ICD, which needs reprogramming.

A magnet over an ICD suppresses arrhythmia detection and therapy but cannot force its pacemaker into asynchronous mode. Most, not all, pacemakers go asynchronous with a magnet. ICDs misread interference as tachyarrhythmia, and pads should be applied when device functions are disabled.

Sources: Miller 10eAHA/ACC 2024 · §6.6

The code follows how the device works. It first says where it delivers current. Next it says where it listens for the heart's own electrical activity. Third, it says what it does when it detects a beat: it holds back output (inhibition), fires (triggering), both, or nothing. Rate response is an extra feature. A separate sensor, driven by things like physical activity, adjusts the rate whatever the heart's own rhythm is doing. So it sits after the basic pace–sense–respond sequence.

Rate modulation in core pacemaker code. The R in modes like DDDR or VVIR is well known, so people often think it belongs to the core letters. It fails because the third place is always the response to a sensed event (O, I, T or D). Rate modulation is the fourth letter.

The generic pacemaker code has five positions: chamber paced, chamber sensed, response to sensing, programmability or rate modulation, and multisite pacing. The third letter is none, inhibited, triggered or dual. An R in the fourth place means a sensor adjusts the rate.

Sources: Mayo reviewFaust

An implanted device cannot distinguish genuine cardiac signals from electrical noise. Fasciculating or jerking skeletal muscle produces myopotentials that the leads may detect. The device may then withhold pacing, or detect a false tachyarrhythmia and deliver a shock. The wider the spacing between a lead's two poles, the more stray signal enters the circuit, so unipolar leads act as bigger aerials than bipolar leads. Interference fades with distance, so diathermy well below the generator and leads rarely matters. Choice of anaesthetic drug does not change device thresholds.

Bipolar leads increase interference risk. Lead type does affect how easily a device picks up interference, and the word 'bipolar' sounds like a hazard. However, the risk runs the other way. Bipolar poles sit very close together, so little stray signal gets in. The unipolar configuration is the more vulnerable one.

The sources list succinylcholine fasciculation, myoclonus, direct muscle stimulation and electroconvulsive therapy as causes of wrongly inhibited or triggered device output. Unipolar leads are more vulnerable to interference than bipolar leads. Diathermy below the umbilicus seldom disturbs transvenous devices. Anaesthetic agent choice is unaffected.

Sources: FaustStoelting 8eAHA/ACC 2024 · §6.6

The outflow obstruction is dynamic: it tightens when the ventricle contracts harder or its cavity becomes smaller. Dopamine adds contractility and rate. Nitroglycerin cuts preload; nitroprusside cuts afterload so the ventricle empties further. Each shrinks the cavity, raises the gradient and reduces forward flow. A beta-blocker slows the rate, lengthening filling, and softens contraction, so the cavity stays larger, the gradient and mitral regurgitation fall, and forward output rises. Hypotension is therefore treated with fluid and alpha-agonists, not inotropes.

Dopamine for reduced cardiac output. Dopamine raises output in most low-output states, so it looks like the obvious answer. In obstructive HCM its extra contractility and rate make the ventricle squeeze into a narrowing outflow tract; the gradient climbs and forward output falls rather than rises.

Beta-blockade slows the heart and depresses contractility, markedly lowering the dynamic outflow gradient and linked mitral regurgitation and easing symptoms. Inotropes, beta-agonists, nitroglycerin and reduced afterload all worsen obstruction; the stated goals are raised afterload, reduced contractility and beta-blockers.

Sources: Barash 9eMayo review

HOCM obstruction is dynamic. The outflow tract narrows when the ventricle is underfilled, afterload falls, the heart rate rises or contractility increases. Induction lowers preload and systemic resistance, and the resulting tachycardia shortens filling time, so the obstruction worsens and pressure falls further. Fluid restores ventricular volume and holds the tract open. Phenylephrine raises afterload without beta stimulation. Atropine speeds the heart and worsens the obstruction. Beta-agonists add inotropy and heart rate, both of which tighten the obstruction.

Adrenaline for hypotension in HOCM. Adrenaline is the reflex choice for severe hypotension, and it is paired with fluid, so it looks complete. In HOCM its beta effects increase contractility and heart rate. Both narrow the outflow tract, so cardiac output and blood pressure can fall further.

The guideline puts intravenous fluid first for perioperative hypotension, then alpha-agonists such as phenylephrine or vasopressin in place of beta-agonists. The textbook calls beta-agonists contraindicated because higher contractility and heart rate aggravate outflow obstruction.

Sources: AHA/ACC 2024 · §6.3.1Stoelting 8e

Reduced dystrophin makes skeletal and cardiac muscle membranes fragile. Cardiomyopathy and arrhythmia follow their own course, so mild limb weakness does not reassure about the heart. Complications occur even in lightly affected patients. Suxamethonium depolarises the unstable sarcolemma, causing rhabdomyolysis and hyperkalaemia. Miller and Barash put true MH risk at general-population level, calling these reactions MH-like. Stoelting still lists Becker among myopathies strongly associated with MH. Either way, avoid suxamethonium and volatiles.

Mild weakness excludes cardiac involvement. Becker patients are often only mildly weak and still walking, so people assume the heart is spared and skip cardiology. But heart involvement does not follow limb strength, and perioperative complications occur even in patients with mild disease.

Most Becker patients have cardiac abnormality (50–70%), but only 10% are clinically significant; mild disease is not protective. Suxamethonium is contraindicated (rhabdomyolysis, hyperkalaemia). One text gives MH mutation risk at population level; another lists Becker as highly associated with MH.

Sources: Miller 10eStoelting 8e

High levels of circulating catecholamines keep the heart under constant sympathetic drive. Beta-receptor stimulation raises contractility and makes arrhythmias more likely. Alpha-mediated vasoconstriction raises afterload and myocardial oxygen demand. Long exposure damages the myocardium, causing a cardiomyopathy that can present as pump failure and electrical instability. A true paroxysm adds a sudden pressure surge on top, which risks stroke, infarction, acute failure and dysrhythmias. Between attacks, examination may be normal unless long-standing hypertension has already left its effects.

Paroxysmal hypertension is typical. The textbook attack of headache, sweating and palpitations is so vivid that people assume episodic hypertension is the norm. The sources describe the hypertension as usually sustained, with true paroxysms only occasional. Paroxysms matter because of their acute cardiovascular complications, not because they are common.

Hypertension is usually sustained and only occasionally paroxysmal. A true paroxysm can push pressure dangerously high, risking cerebral bleeding, heart failure, dysrhythmias or infarction. Catecholamine-induced cardiomyopathy may present with heart failure, and raised sympathetic tone can trigger malignant arrhythmias.

Sources: Barash 9e

Collapsed lung causes hypoxaemia by shunting blood through alveoli that are not ventilated. Cardiac output is untouched, so blood pressure holds. Ischaemia in a ventricle that is already dilated and weak reduces forward flow, which causes hypotension, tachycardia and poor perfusion. At the same time, left-sided filling pressure rises and backs up into the pulmonary circulation. Fluid then fills the alveoli, which causes breathlessness and desaturation. One cardiac process therefore explains both the low pressure and the low saturation.

Pulmonary embolism in obese patient. Embolism does produce hypoxaemia with hypotension, and chest pain, tachycardia and an obese ICU patient make a clot feel likely. But these features only overlap with the other diagnosis. Active ischaemia on a known dilated, failing ventricle already explains both findings, and nothing points specifically to a clot.

Cardiogenic shock shows low systolic pressure, sometimes with pulmonary oedema and hypoxaemia. Acute cardiac injury presents with dyspnoea, pulmonary oedema and shock. Decompensated failure causes pulmonary congestion. Unlike embolism or tension pneumothorax, atelectasis usually lowers oxygenation without hypotension.

Sources: Stoelting 8eFaustBarash 9e

Pulling on the extraocular muscles sets off a reflex that ends in vagal output to the heart. The usual result is sinus bradycardia, but other arrhythmias can occur, including asystole. Hypercarbia and hypoxaemia lower the threshold for the reflex, so the same pull causes a bigger vagal response that happens more often. A light plane of anaesthesia also leaves the reflex free to fire, while a deeper plane helps block it. Opioids are the exception: fentanyl, sufentanil and remifentanil augment the reflex.

Opioids augment oculocardiac reflex. Anaesthetic depth does change the reflex, and opioids used to deepen anaesthesia actually augment it, so it sounds right. But the texts link the stronger reflex to shallow depth. Deepening general anaesthesia is listed as a way to block the reflex, not to worsen it.

Hypercarbia and hypoxaemia increase the reflex's frequency and severity by lowering its threshold. Shallow anaesthesia may do likewise, whereas deeper general anaesthesia may block it. Opioids, however, augment the reflex during strabismus surgery.

Sources: Barash 9eMayo reviewMiller 10e

The medulla receives input from stretch receptors in the aortic arch and the carotid sinus. More stretch, from rising pressure or a surgeon pressing on the sinus, suppresses sympathetic outflow, so vagal tone dominates: the heart slows and vessels dilate. Haemorrhage unloads them, so rate and contractility rise. The carotid and aortic bodies are separate chemosensors: hypoxia or acidosis drives ventilation and also triggers parasympathetic slowing of rate and force; only persistent hypoxia switches on central sympathetic stimulation. A bleeding patient with bradycardia and activated receptors is showing the chemoreflex.

Baroreceptor reflex from haemorrhage. In a bleeding trauma patient, the baroreceptor story comes to mind first: unloaded pressure sensors raise sympathetic drive, rate and contractility. But carotid and aortic bodies are chemosensors. When hypoxia or acidosis activates them, they act through the vagus to lower heart rate and contractility.

Manipulating the carotid sinus activates the baroreflex, abruptly slowing the heart and dropping pressure; stopping the manipulation promptly restores haemodynamics. Raised baroreceptor input inhibits sympathetic output, favouring vagal slowing and vasodilation. Chemoreceptor activation boosts ventilatory drive while parasympathetic activity cuts heart rate and myocardial contractility.

Sources: Miller 10eBarash 9e

Noxious stimuli in the left ventricular wall, such as ischaemia, excite ventricular receptors whose unmyelinated vagal afferents raise parasympathetic tone, so rate and pressure fall while coronary vessels dilate: a protective triad. At the carotid sinus, surgical handling activates baroreceptors, which reflexly slow the heart and drop pressure; removing the stimulus reverses it. Chemoreceptors in the carotid and aortic bodies are different: severe hypoxaemia or acidosis, as in profound haemorrhage, makes them drive breathing up and, via the vagus, reduce heart rate and myocardial contractility.

Baroreceptor unloading in shock. Haemorrhage unloads baroreceptors, which would raise rate and contractility, so people reflexly pick this. But this patient is bradycardic in deep shock: that is the chemoreceptor reflex responding to hypoxaemia and acidosis, and its vagal output lowers contractility, not raises it.

The Bezold–Jarisch reflex follows noxious left ventricular stimulation and yields hypotension, bradycardia and coronary dilatation. Chemoreceptors fire when PaO2 falls under 50 mm Hg or with acidosis; parasympathetic activity slows the heart and depresses the myocardium. Carotid-sinus bradycardia and hypotension resolve once surgical manipulation stops.

Sources: Miller 10e

Left ventricular wall chemoreceptors and mechanoreceptors detect a noxious ventricular insult, for example ischaemia or an underfilled chamber. Their signal travels in unmyelinated vagal C-fibre afferents. The response is a surge of parasympathetic tone with sympathetic withdrawal. Vagal efferents slow the heart, cardiac output falls and pressure drops further, while the coronary bed dilates. Slowing the heart cuts myocardial work, so the reflex is considered protective. Serotonin 5HT-3 receptors help mediate it.

Carotid sinus reflex causes bradycardia. The carotid sinus reflex is tempting, as pressing on the sinus slows the heart and lowers blood pressure. But carotid baroreceptors sense arterial pressure; when it falls they unload and drive tachycardia. A slow heart despite low pressure in ischaemic chest pain suggests a reflex arising in the ventricle itself.

Harmful stimulation of left ventricular receptors causes hypotension, bradycardia and coronary dilatation via vagal C-fibre afferents. Serotonin receptors mediate this reflex, raising parasympathetic tone and vagal output, slowing the heart, reducing cardiac output and deepening hypotension.

Sources: Miller 10eBarash 9e

When the left ventricle contracts, its pressure rises to about aortic pressure or higher. This squeezes the vessels running through its wall, especially those in the subendocardium, so almost no blood enters them until the muscle relaxes. The right ventricle has less muscle and develops much lower pressure inside its cavity. Aortic pressure therefore stays above the compressive force for the whole cardiac cycle, and its coronary flow continues during systole. Anything that shortens diastole or lowers aortic diastolic pressure threatens supply to the left ventricle most.

Left ventricle perfused during systole. People remember that one ventricle gets coronary flow in both phases and assign it to the larger, more important left ventricle. But the left ventricle's own systolic pressure squeezes its wall vessels shut, so its flow is almost entirely diastolic. Only the low-pressure right ventricle keeps being perfused through systole.

Coronary flow to the left ventricle is almost entirely diastolic. Contraction compresses the subendocardial vessels, and ventricular pressure can reach systemic pressure. Right ventricular perfusion normally continues through both systole and diastole because the right ventricle has less muscle and a low systolic cavity pressure.

Sources: FaustBarash 9eMayo reviewStoelting 8e

The donor heart has lost its autonomic nerve supply, so reflex and vagal control of rate and contractility are gone. Atropine and glycopyrrolate only work by removing vagal tone. That tone no longer exists, so the rate does not rise. Indirect sympathomimetics such as ephedrine rely partly on nerve-mediated release, so their effect is weakened. The myocardial beta-receptors are still intact. Drugs that bind them directly therefore raise rate and contractility much as they would in a normal heart.

Atropine treats transplanted heart bradycardia. Atropine is the reflex first-line drug for bradycardia in resuscitation algorithms, so it looks like the obvious choice. A transplanted heart has no vagal input to block, so an anticholinergic leaves the rate unchanged. The child stays hypotensive while time is wasted.

The sources agree that denervation removes normal control of rate and contractility. Anticholinergics fail to speed the graft and ephedrine-type indirect agents act weakly. Adrenaline and isoprenaline act as they would in a normal heart and remain effective for bradycardia.

Sources: Stoelting 8eMayo reviewBarash 9e

The graft has no sympathetic or vagal nerve supply, but its adrenergic receptors remain. Drugs that bind those receptors directly, such as adrenaline or isoprenaline, work normally. Effects that depend on the nerves fail. Atropine has no vagal tone to block. Ephedrine's indirect component has no nerve terminals to act on, so its effect is blunted. Digoxin cannot slow AV conduction through the vagus. Vasodilators lower the pressure with no reflex rise in heart rate, so hypotension can be severe.

Hydralazine causes reflex tachycardia post-transplant. In a normal heart, hydralazine reliably causes reflex tachycardia, so this looks like a safe, true statement. After transplantation the reflex pathway to the heart is cut. Vasodilators then cause hypotension, sometimes marked, with no rise in rate to compensate. Even a mild reflex tachycardia should not be expected.

Sources agree that directly acting catecholamines behave as they do in a normal heart. Ephedrine's effect is blunted and atropine fails to raise the rate. Vasodilators such as hydralazine can cause marked hypotension without reflex tachycardia. Digoxin no longer slows AV conduction.

Sources: Stoelting 8eOutside our books: Orthotopic Heart Transplantation (2024)Outside our books: Perioperative Care of Heart Transplant Recipients Undergoing Non-Cardiac Surgery (2021)Outside our books: Anaesthesia for heart transplantation (2021)

Portal hypertension drives local nitric oxide and prostaglandin release, dilating the splanchnic bed and lowering systemic resistance. Arteriovenous shunts let oxygenated blood bypass the tissues, so mixed venous saturation is high, around 90%, and cardiac output rises. Hypotension therefore comes from lost vascular tone, not pump failure. Milrinone adds inotropy the heart does not need and more vasodilation, which lowers resistance further. An alpha agonist restores tone directly.

Milrinone improves cirrhotic hypotension. Low blood pressure prompts a reflex to support the heart, and milrinone sounds like a sensible inotrope. But output is already raised. Milrinone's vasodilating action cuts the already low resistance further, so hypotension worsens rather than improves.

Cirrhotic patients are hyperdynamic, with mixed venous saturation near 90%, raised output, low peripheral resistance, expanded volume and arteriovenous shunts. Milrinone's inotropic and vasodilating effects are unneeded. Drugs with alpha-agonist action can help if hypotension needs treatment.

Sources: Mayo reviewMiller 10e

Cardiac output is heart rate multiplied by stroke volume. Factors are grouped by origin. Rate and contractility belong to the heart muscle itself. Rate comes from pacemaker firing, set mainly by autonomic tone. Contractility is myocardial performance regardless of load. Preload (stretch from filling before systole) and afterload (resistance to ejection) are set outside the heart, by venous return and the arterial tree. A faster rate raises output only while diastolic filling stays adequate.

Preload is intrinsic cardiac determinant. Preload is often listed next to heart rate as a main determinant, and a fluid challenge raises output through the Starling mechanism. That makes it feel intrinsic. It is actually a loading condition, set by venous return filling the ventricle. It couples heart to circulation, so it is extrinsic.

Cardiac output has four determinants. Intrinsic to the heart: heart rate, governed mainly by the autonomic nervous system, and contractility, defined as performance independent of loading. Extrinsic, coupling heart to vasculature: preload and afterload.

Sources: Miller 10e

The heart's preganglionic accelerator neurones leave the upper thoracic cord. A high neuraxial block or a cervical cord injury therefore removes sympathetic drive and allows bradycardia. Vagal acetylcholine acts through M2 receptors. These link to the inhibitory Gi/o protein and switch off adenylyl cyclase, which slows the heart rather than exciting it. Sympathetic fibres reach the ventricles most densely, while vagal supply is concentrated above them.

M1 muscarinic receptor innervates heart. People reach for M1 because it is the first-numbered subtype. M1, like M3 and M5, couples to Gq and activates phospholipase C. The main cardiac receptor is M2, which couples to inhibitory Gi/o, and that fits vagal slowing.

The sources say the preganglionic cardiac accelerator fibres come from T1–T4. The atria have a sparser sympathetic supply than the ventricles. M2 is the main muscarinic subtype in the heart, and it couples to Gi/o to inhibit adenylyl cyclase.

Sources: Miller 10e

Stretch receptors sit in the right atrial wall and at the junction where the venae cavae enter. When right-sided filling rises, they send signals up vagal afferents to the medullary cardiovascular centre, which reduces parasympathetic tone, so the rate climbs. Stretching the atrium also excites the sinoatrial node directly, which adds to the speeding. Heart rate therefore follows venous inflow. The size of the rate change depends on the baseline rate before the stimulus.

Arterial baroreceptors mediate Bainbridge reflex. Arterial baroreceptors are also stretch receptors, so they seem a natural answer when pressure or volume rises. But venous and arterial pressure receptors act in opposite directions on heart rate. The venous-side reflex that speeds the heart as the right side fills is Bainbridge's.

Bainbridge receptors lie at the cavoatrial junction and in the wall of the right atrium. Raised right-sided filling pressure signals via the vagus to the medulla, reducing parasympathetic activity and raising heart rate. Direct atrial stretch of the sinoatrial node contributes. Venous and arterial stretch receptors have opposing effects.

Sources: Miller 10eBarash 9e

The electrical stimulus first drives parasympathetic outflow, which slows the heart and lowers pressure. The seizure then triggers sympathetic activation, which raises heart rate and blood pressure for several minutes. This surge sharply increases myocardial oxygen demand. Patients with coronary disease are therefore exposed to ischaemia and rhythm disturbances. That makes the cardiovascular system the organ system most affected by ECT, and the reason cardiac events dominate its serious complications.

ECT directly causes tachycardia. Tachycardia and hypertension is the most visible and longest-lasting part of the response, so people remember it best. But it is the second phase. Brief vagal slowing with a drop in pressure comes before the sympathetic surge.

Response has two phases: parasympathetic, with slowing heart rate and falling pressure, then sympathetic, with tachycardia and hypertension lasting minutes. Most ECT deaths, roughly 1 in 5000 treatments, are from myocardial infarction and dysrhythmias. Transient ischaemia is fairly common.

Sources: Stoelting 8e

Straining against a shut glottis pressurises the chest; this pressure is transmitted to the great veins, so the CVP reading goes up, yet the gradient driving blood back to the right heart shrinks. Less filling means lower output and falling arterial pressure; baroreceptors respond with sympathetic vasoconstriction and tachycardia. When the glottis opens, pooled venous blood floods in and is ejected into a constricted arterial tree, so pressure overshoots and a vagal reflex slows the heart. The sequence needs an intact autonomic arc.

High CVP reflects increased venous return. It is tempting to assume a raised CVP means more blood is returning, or to remember the surge of venous return after release. During the strain, the high CVP only reflects transmitted chest pressure; the return gradient falls, so venous return drops.

Forced expiration against a closed glottis raises intrathoracic and central venous pressure but lowers venous return, output and blood pressure, prompting reflex tachycardia and vasoconstriction; on release, pressure briefly overshoots and heart rate slows.

Sources: Miller 10eBarash 9e

Ion channels control how quickly each ventricular action potential repolarises. An inherited mutation in one of these channels slows repolarisation. The action potential lasts longer, and the corrected QT lengthens with it. The cardiac sodium channel NaV 1.5 is one recognised culprit. During the long repolarisation, afterdepolarisations can fire premature ventricular beats. These can turn into torsades de pointes, a pulseless polymorphic ventricular tachycardia. The fault lies in repolarisation, not in heart structure or conduction pathways. Its danger is sudden cardiac death.

Structural cardiomyopathy ECG indicates channelopathy. Inherited heart diseases that cause sudden death are easy to confuse. Long QT, Brugada and short QT syndromes are ion channelopathies. Hypertrophic and dysrhythmogenic right ventricular cardiomyopathies are structural diseases. An ECG sign of a structural cardiomyopathy says nothing about the channel defect behind long QT syndrome.

Textbooks describe congenital long QT syndrome as a myocardial repolarisation disorder that lengthens the corrected QT, risking polymorphic ventricular tachycardia and sudden cardiac death. It is grouped with Brugada and short QT syndromes as channelopathies and linked to the cardiac sodium channel NaV 1.5.

Sources: Miller 10eBarash 9eStoelting 8e

5-HT3 antagonists and droperidol delay ventricular repolarisation, so on an already long QT they add torsades risk. Repeating the failed prophylactic class within 6 hours adds little, so rescue needs a new class. Metoclopramide, a dopamine antagonist, is that switch and sits outside Miller's recovery-room QT list; its efficacy is uncertain, so it is the safer, not the stronger, choice. Registers grade it a conditional torsades risk and list it among drugs to avoid in congenital long QT where possible, so monitor the ECG and prefer cyclizine when available.

Repeat ondansetron as reflex rescue. Ondansetron is the reflex recovery rescue, and a small dose looks harmless. But setrons are among the commonest recovery QT-prolongers, and granisetron already failed as prophylaxis, so a same-class repeat adds little. Conversely, metoclopramide is not risk-free; it is the least bad of these drugs.

Recovery guidance names 5-HT3 antagonists and droperidol among its commonest QT-prolonging drugs. Rescue needs a class not used prophylactically; setrons help only after 6 hours. Metoclopramide is a listed rescue, though 10 mg efficacy is uncertain. Known long QT needs monitoring.

Sources: Miller 10eBarash 9eOutside our books: Fourth Consensus Guidelines for the Management of Postoperative Nausea and Vomiting (2020)

Acetylcholine acts on muscarinic M3 receptors in both the coronary endothelium and the vascular smooth muscle. In a healthy artery the endothelial response wins: nitric oxide raises cGMP and relaxes the muscle, so the net effect is dilation. That dilation is indirect because it depends on the endothelium. When the endothelium is damaged, only the smooth-muscle response is left, and the artery constricts. Adenosine dilates coronaries, mainly in hypoxic tissue. Histamine can either constrict or dilate, depending on receptor subtype. With hyperoxia, coronary flow falls along with myocardial oxygen use.

Histamine is coronary vasoconstrictor. Histamine does constrict coronary arteries through H1 receptors, so it looks correct. But it also dilates them through H2 receptors, so its net effect is mixed. Acetylcholine is the classic direct constrictor: its dilation relies on the endothelium, and it constricts once the endothelium fails.

Acetylcholine dilates healthy coronaries by an endothelium-dependent nitric oxide pathway but constricts them when the endothelium is dysfunctional. Histamine constricts via H1 and dilates via H2. Adenosine dilates mainly during hypoxia. Hyperoxia lowered coronary flow together with myocardial oxygen consumption.

Sources: Barash 9eFaustMiller 10e

The right arm gets its blood from the arch before the narrowing, so it shows the pressure reaching the heart and brain. The repair is done through a left thoracotomy with the aorta cross-clamped. Any artery at or beyond the clamp can lose its trace or give a falsely low reading just when you need it most. The same idea explains why the right radial is chosen elsewhere: of the peripheral sites, it tracks the flow closest to the heart and brain.

Left radial artery line safe. The left radial is familiar and handy for a right-handed operator, and it is still an upper-limb site. But the left subclavian leaves the arch close to the narrowing and may be caught in the aortic clamp. Its reading can then vanish or understate pressure during the crucial phase.

For coarctation repair via left thoracotomy with aortic cross-clamping, the textbook recommends a peripheral cannula and indwelling arterial catheter in the right arm, used intra- and postoperatively. Separately, the right radial is preferred because it reflects flow nearest the heart and brain.

Sources: Miller 10e

Current entering through the skin spreads through ion-rich tissue, and only a small share crosses the heart. Fibrillation therefore requires far more external current than current applied directly to the myocardium. Above the let-go level, muscles stay contracted and the victim cannot release the source. At very large currents the heart is held in sustained contraction rather than fibrillating. Normal rhythm then returns, but breathing stops for a time, and burns form where current density is high.

High current causes ventricular fibrillation. People expect a bigger current to do more harm to the heart, so they read a very large shock as certain ventricular fibrillation. The table says otherwise. Fibrillation belongs to the 100–300 mA band. At 6,000 mA the myocardium stays contracted and normal rhythm comes back afterwards.

For a one-second mains-frequency contact: 1 mA is perceived; up to 5 mA is harmless; 10–20 mA exceeds let-go threshold; 100–300 mA causes fibrillation with respiratory centre intact; 6,000 mA causes sustained myocardial contraction, then normal rhythm, temporary respiratory paralysis and possible burns.

Sources: Barash 9e

The ventricular septal defect lets desaturated blood bypass the lungs whenever resistance to right ventricular ejection exceeds systemic resistance. Anything that lowers systemic resistance, such as hypotension from dehydration or afterload-reducing drugs, or that tightens the infundibulum, such as catecholamine surges or β-stimulation, pushes more blood right-to-left and deepens cyanosis. Raising systemic resistance pulls flow back to the lungs. β-blockade relaxes the spastic infundibulum and reduces spells, whereas β-stimulating inotropes such as isoprenaline or dopamine do the opposite.

Beta-blockers worsen tetralogy spells. A negative inotrope looks dangerous in a hypoxic, struggling child, so people call it inappropriate. But β-blockade relaxes the spastic infundibulum and is a recognised escalation step for spells. The harmful choice is the β-stimulating inotrope, which worsens spasm and shunting.

Keep fasting short so hydration prevents hypotension that favours right-to-left flow. For spells, a systemic vasoconstrictor raises SVR and reduces shunting, then a short-acting β-blocker or sedative eases outflow spasm. β-blockers cut spell frequency and severity; isoprenaline lowers afterload and worsens shunting and spasm.

Sources: Stoelting 8eMayo reviewFaust

Children with limited cardiac reserve depend on their own catecholamine drive. Agents that depress the myocardium or blunt sympathetic tone can precipitate collapse. That includes thiopental and even small opioid doses. A volume-depleted child has no reserve to absorb the resulting fall in pressure. Ketamine works the opposite way: its sympathetic stimulation sustains heart rate and right-sided filling pressure. This is why it suits patients prone to right-to-left shunting. Slow titration matters more than which drug is chosen.

Ketamine contraindicated in congenital heart disease. Ketamine is a sympathomimetic, so people assume it is risky in a fragile circulation. The sources say the opposite. It can be given in congenital heart disease, particularly where right-to-left shunting is likely, because its sympathetic drive supports heart rate and filling.

Ketamine can be used in congenital heart disease, especially with a tendency to right-to-left shunting. Thiopental drops blood pressure in volume-depleted neonates and should be avoided in those with heart disease. Opioids can cause marked haemodynamic deterioration by reducing catecholamine release.

Sources: Miller 10eBarash 9e

A volatile agent reaches the brain only in blood that has passed through ventilated alveoli. In a right-to-left shunt, part of the cardiac output skips the lungs. This adds agent-free venous blood to arterial blood, so arterial and brain partial pressures rise more slowly. In a left-to-right shunt, the extra flow just goes round the lungs again. If systemic output is maintained, the brain still receives agent at the usual rate. Even very high pulmonary flow does not dilute or delay intravenous drugs to any meaningful degree.

Left-to-right shunt delays inhalational induction. Delayed inhalational induction looks right because the extra pulmonary blood flow seems to dilute agent or draw it away from the alveoli. However, the shunted blood simply goes back through the lungs, and with normal systemic flow the brain gets agent as usual. Slowing belongs to right-to-left shunts.

When blood bypasses the lungs in a right-to-left shunt, induction slows, and tetralogy is named as an example. A left-to-right shunt makes no significant difference if systemic flow is normal. Even markedly raised pulmonary flow has little clinical effect on intravenous induction speed.

Sources: FaustBarash 9eStoelting 8e

After birth, pulmonary vascular resistance falls over the first weeks to months. As it falls, a ventricular septal defect sends more and more blood from left to right, so the lungs are overfilled and the heart is volume-loaded. Heart failure follows. In an infant it shows at feeds, which are their hardest exertion, as laboured fast breathing, tiredness and poor growth. Already-oxygenated blood goes round the lungs again, so no deoxygenated blood reaches the systemic circulation and the child is not cyanosed.

Atrial septal defect causes infant heart failure. An atrial septal defect is also an acyanotic left-to-right shunt with a murmur, so it looks like a close match. But the textbook list of newborn lesions that present as heart failure names the ventricular defect. In an infant, heart failure showing at feeds points to a ventricular shunt.

Newborn heart lesions are cyanotic (tetralogy, transposition) or present as heart failure (ventricular septal defect). Infant heart failure shows as feeding difficulty, tiredness, laboured breathing and failure to thrive, becoming more obvious as pulmonary resistance falls and shunting increases.

Sources: Miller 10eBarash 9e

Oxygenated left-heart blood crossing a defect raises saturation in the right-sided chamber it enters. Blood mixes as it moves on, so chambers downstream keep that higher saturation, and chambers upstream see only systemic venous blood. The superior vena cava is the reference because its saturation is predictable and, with no shunt, close to pulmonary artery saturation. Right-heart saturation varies a little normally, so only a rise above the level-specific threshold counts. A lower value further downstream does not move the shunt further along.

Ventricular septal defect shows atrial step-up. A ventricular septal defect, the commonest shunt in an infant who sweats while feeding, is the reflex answer. However, its shunt enters the right ventricle, raising ventricular saturation above atrial. Here the atrium is highest, so there is no ventricular step-up.

Oximetry runs sample the caval veins and right heart chambers to find where saturation first steps up. An atrial shunt shows a rise of 10% or more from the SVC, staying high downstream. Ventricular and great-vessel shunts need smaller mean rises of 5%.

Sources: Outside our books: Right Heart Catheterization: Best Practices and Specific Considerations (2026)Outside our books: Hemodynamic assessment of atrial septal defects (2018)Outside our books: The uses of right heart catheterization in cardio-pulmonary disease: State-of-the-art (2025)

Without a subpulmonary ventricle, blood reaches the lungs passively, against pulmonary vascular resistance. Positive intrathoracic pressure opposes this flow, cutting ventricular filling and causing hypotension. Negative-pressure spontaneous breaths aid venous return, improving output. Yet ventilation must stay adequate, because hypoventilation raises PVR and equally starves the lungs of flow. Preload is vital, so avoid dehydration, but these patients tolerate fluid overload poorly, so give fluid in small titrated boluses.

Controlled ventilation optimal for Fontan physiology. Controlled ventilation feels safer, securing the airway and CO2 control, and suits standard GA. In Fontan physiology, however, positive intrathoracic pressure impedes passive lung blood flow and lowers preload, risking severe hypotension; it is the fallback, used with low inspiratory pressures, only when spontaneous breathing proves inadequate.

Sources state positive pressure ventilation harms pulmonary blood flow and can cause life-threatening hypotension by reducing preload, while pain-free spontaneous breathing improves haemodynamics. If ventilating, optimise preload and limit inspiratory pressures; fluid overload is poorly tolerated, so give cautious titrated boluses.

Sources: Barash 9eStoelting 8e

A narrowed valve limits how much the heart can raise its output. Pregnancy increases cardiac output, heart rate and circulating volume. A tight left-sided valve cannot pass the extra flow, so pressure builds up behind it. This leads to pulmonary oedema, heart failure, arrhythmias and sometimes death. Regurgitant lesions handle the same load much better, so they rarely kill.

Aortic stenosis highest maternal cardiac risk. Aortic stenosis is also a highest-risk left-sided stenosis, but only when symptomatic, and some women with severe disease tolerate pregnancy well. Severe mitral stenosis is highest risk regardless of symptoms and causes the most maternal cardiac deaths.

Severe mitral stenosis and symptomatic severe aortic stenosis are both lesions for which pregnancy is contraindicated. Mitral stenosis is the leading cardiac cause of maternal death worldwide. Stenotic valves cannot raise output as pregnancy demands.

Sources: Outside our books: Pregnancy Complicated by Valvular Heart Disease: An Update (2014)Outside our books: Valvular Heart Disease in Pregnancy (2024)Outside our books: 2025 ESC Guidelines for the management of cardiovascular disease and pregnancy (2025)Barash 9e

The right ventricle has a thin wall and copes badly when its afterload rises. Hypoxaemia, a raised carbon dioxide tension and acidaemia each constrict the pulmonary vessels. This pushes pulmonary artery pressure up and puts more load on a right ventricle that is already struggling. So care is built around three things: keep pulmonary resistance low, support right ventricular contractility, and keep fluid balance steady. The ventricle is harmed by too little fluid and by too much.

Aggressive fluid therapy pulmonary hypertension goal. It is tempting because these patients depend on preload, and hypovolaemia must be corrected quickly. But the right ventricle also fails when it is overfilled, so fluid is given slowly in small amounts. Deliberately raising preload is not the primary goal. Preventing rises in pulmonary resistance is.

The main anaesthetic aim is avoiding hypoxia, hypercarbia, acidosis and hypovolaemia, which raise pulmonary pressure. Lower pulmonary resistance, support right ventricular inotropy and reduce its afterload. Give fluids cautiously, as the ventricle tolerates neither depletion nor excess.

Sources: Stoelting 8eFaust

A ventricular assist device takes the blood returning to the failing side of the heart and pumps it past the failed ventricle, which restores forward flow. Durable left-sided pumps are built for long-term support. They can become the final treatment when transplant is not an option, and they let the patient live outside intensive care. Short-term support devices are for acute cardiogenic shock and for bridging to recovery, not permanent care. Simply observing leaves a symptomatic patient on drugs that have already failed.

Right-sided device provides destination therapy. It is tempting because it is also an implanted assist device. But destination therapy uses durable left-sided devices that drain the failing left ventricle. A right-sided device alone does not unload the left ventricle or restore systemic output.

The texts list destination therapy as a use for assist devices in advanced heart failure patients who are not transplant candidates and whose medical treatment has failed. Durable LVADs provide long-term support in this role. Short-term devices are used mainly for acute cardiogenic shock.

Sources: Stoelting 8eMayo reviewBarash 9e