Respiratory & Thoracic, the reference

Postoperative FEV1 is estimated by scaling the preoperative FEV1 to the share of functioning lung that will remain after resection. Expressing it as a percentage of the predicted value corrects for age, sex and height. The result estimates the ventilatory reserve left after surgery. Miller and GOLD both describe the cut-off as a band rather than one number. Risk starts to climb once the value falls below 40%, although not every such patient develops complications. Below 30% the patient is in the high-risk group.

Stair climbing predicts post-resection complications. Stair climbing is a practical whole-patient fitness test. It measures exercise and cardiopulmonary reserve, a separate assessment best quantified by maximal oxygen consumption, but not post-resection lung mechanics. Predicted postoperative FEV1 is the most valid single predictor of respiratory complications.

Miller names the predicted postoperative FEV1 percentage as the best single predictor of respiratory complications after thoracotomy. Risk rises below 40% and is high below 30%. Barash derives the value by multiplying preoperative FEV1 by the fraction of lung expected to remain.

Sources: Miller 10eBarash 9e

Predicted postoperative lung function is estimated from the share of functioning subsegments that are resected. Taking the middle and lower lobes from an already reduced FEV1 leaves a predicted value close to 30%. Risk is graded on this figure: low above 40%, raised below 40% and high below 30%. Above 30%, extubation in theatre is acceptable if other function and comorbidities allow. In the 20% to 30% band, good cardiopulmonary function plus effective epidural analgesia still allows extubation in theatre. Staged weaning is kept for patients who fail cardiopulmonary criteria.

Plan intensive care for FEV1 45%. A predicted value under 40%, near the high-risk line, makes planned ventilation in intensive care feel safe. But staged weaning is meant for patients who fail cardiopulmonary and parenchymal criteria. Near this boundary, a working thoracic epidural makes early extubation in theatre reasonable.

Predicted postoperative FEV1 is calculated by counting removed lung subsegments. Risk is raised below 40% and high below 30%. Above 30%, with adequate other function, extubation in theatre is acceptable. Patients failing minimal cardiopulmonary criteria need staged weaning; the 20–30% band is assessed separately.

Sources: Miller 10e

Vital capacity shows how much respiratory reserve the patient has. In the long term, spinal fusion stops lung function getting worse. In the short term, surgery makes pulmonary function worse for about 7 to 10 days. A patient who already has very little reserve may not cope with that early drop while breathing alone. So the lower the vital capacity before surgery, the more likely the patient will need mechanical support afterwards.

Use FEV1 for scoliosis risk assessment. Forced expiratory volume is the spirometry figure most people know from lung-resection risk scoring, so it seems the natural predictor. For scoliosis, though, the books use vital capacity as the measure of reserve. Only a severely reduced vital capacity predicts ventilation after surgery, and a moderate reduction does not.

Barash describes preoperative vital capacity as a reliable sign of respiratory reserve. It says ventilator support after surgery is likely when vital capacity is below 40% of predicted, because lung function gets worse for 7 to 10 days after the operation.

Sources: Barash 9e

Lung separation is essential for two reasons. First, contamination: blood or pus from a diseased lung can drown the healthy lung and destroy gas exchange. Lavage fluid is a deliberate contaminant and must also be confined. Second, loss of control over ventilation: a fistula, disrupted airway or giant bulla takes or leaks positive-pressure breaths, so ventilation must be directed to one side. Deflating a lung for pneumonectomy, aortic or oesophageal surgery only improves the surgeon's view. These operations can proceed without isolation, so those indications are relative.

Lung isolation mandatory for pneumonectomy. Pneumonectomy is the largest lung resection and the classic double-lumen tube case, so isolation feels mandatory. However, isolation there only improves surgical exposure. The healthy lung faces no soiling and no ventilation leak, so the textbooks list it as a high-priority relative indication, not an absolute one.

Barash and Faust agree on the absolute indications: protective isolation for infection or massive haemorrhage, controlling ventilation for bronchopleural fistula, a unilateral cyst or bulla, or major airway disruption, and unilateral lavage. Pneumonectomy, thoracic aortic surgery and oesophageal surgery appear only as relative, exposure-driven indications.

Sources: Barash 9e

A right-sided tube has to ventilate the right upper lobe through a slot. It shifts easily during surgery, and that lobe's ventilation is then compromised, so left tubes are preferred. The bronchial limb goes into the lung that is not being operated on. A left tube is harmful or impossible when the left bronchus is the operative site, as in transplant, sleeve resection or disruption. The same applies when tumour or a descending thoracic aortic aneurysm narrows the left bronchus. In those cases a right tube is chosen.

Tube side matches operative side. It feels natural to match the tube's side to the side of the operation. But the bronchial limb sits in the lung that is not being operated on. A right lung transplant therefore takes a left-sided tube. It is a left lung transplant that calls for a right-sided tube.

Right-sided tubes are used for: a distorted left bronchial entrance, tumour compression, descending thoracic aortic aneurysm, surgery on the left mainstem bronchus, left lung transplant and left tracheobronchial disruption. Otherwise a left tube is preferred, unless carinal or proximal left bronchial lesions forbid it.

Sources: Miller 10eFaustBarash 9e

A blocker has to be steered into the target bronchus with a bronchoscope, so it takes longer to seat. Barash quotes about 3 minutes for an Arndt blocker against 2 for a left double-lumen tube. A meta-analysis agrees that double-lumen tubes go in faster and more reliably. Once in place, surgical handling dislodges a blocker more easily, so it needs repositioning more often. It also allows only minimal suction of the isolated lung. What it gains is airway safety: blockers cause less airway injury.

Bronchial blocker faster insertion than DLT. It is tempting because a blocker slides through an ordinary single-lumen tube, and that feels quicker. It is wrong because the blocker must be guided into place with a bronchoscope. Both the textbook table and the trial timings show it takes longer than a double-lumen tube.

Miller's comparison table lists slower positioning, more frequent repositioning and only minimal suction to the isolated lung as blocker drawbacks. A Barash trial and a meta-analysis agree that placement is slower, so expect a blocker to take longer. Airway injury is less common with blockers.

Sources: Miller 10eBarash 9e

Surgeons once chose the largest tube that would pass. Faust says airway injury rises with tube size, so it now favours smaller tubes: 35 Fr suits most women and 37 Fr suits men. Miller's table builds on that default by adding height. A woman taller than 160 cm moves up to 37 Fr, and men split at 170 cm into 39 or 41 Fr. Faust's sex-only figure is the starting point. Once height is known, the table decides.

35 Fr appropriate for all women. 35 Fr is tempting because one textbook calls it right for most women, and smaller tubes cause less airway trauma. That figure ignores height. Once a woman is taller than 160 cm, the height-based table moves her up to 37 Fr.

Miller's table gives women 35 Fr under 160 cm and 37 Fr above; men 39 Fr under 170 cm and 41 Fr above. Faust links tube size to airway trauma, recommending 35 Fr for most women and 37 Fr for men.

Sources: Miller 10eFaust

Shunt through the collapsed lung causes the fall. A decline over minutes, even to low saturations, is gradual: give full oxygen and check the tube bronchoscopically before anything else; interrupting surgery to re-expand both lungs is reserved for a sudden plunge. Miller then adds ventilated-lung PEEP, except in emphysema, before low CPAP; Barash gives non-dependent CPAP first, except during VATS, then PEEP. Either order is safe if PEEP stays 5–10 and the lungs are never swapped. If re-expansion is impossible, non-dependent CPAP beats excessive PEEP, especially in emphysema.

Apply PEEP to ventilated lung. It puts PEEP on the correct lung, the ventilated dependent one, so it looks right. But the books keep ventilated-lung PEEP at or below 10, because higher pressure worsens shunt, and Miller avoids PEEP in emphysema. The safer choice is to give the non-dependent lung CPAP.

Miller separates a severe or sudden fall, treated by re-expanding both lungs, from a gradual one. For a gradual fall: full oxygen and a bronchoscopic tube check, then ventilated-lung PEEP before low CPAP. Barash gives non-dependent CPAP first, then PEEP 5–10.

Sources: Miller 10eBarash 9e

Hypoxic pulmonary vasoconstriction moves blood away from the collapsed, unventilated lung, which limits shunt. Volatile agents blunt this reflex, and the effect grows with dose. At or below 1 MAC, modern agents such as sevoflurane are only weak inhibitors, so their effect at usual depths is modest. Going above that removes more of the reflex and widens the shunt. Systemic vasodilators work directly: they relax the constricted pulmonary arterioles, so blood flows back into the hypoxic lung and venous admixture rises.

Deeper sevoflurane preserves HPV adequately. Modern volatiles are described as weak HPV inhibitors, so deepening sevoflurane looks harmless, and deeper anaesthesia feels like a fix. But the weakness only applies up to 1 MAC. The inhibition is dose-dependent, so going higher removes more of the reflex and makes desaturation worse.

For gradual desaturation during one-lung ventilation, an early step is to cut volatile agents below 1 MAC. Volatile inhibition of HPV rises with dose but stays weak at or below 1 MAC. Nitroglycerin and nitroprusside both reduce HPV.

Sources: Miller 10e

Wheeze on the day shows the airways are inflamed and irritable, so handling the airway risks severe bronchospasm. GINA finds no extra perioperative risk across asthma as a whole, but Barash calls acute wheeze an emergency and postpones elective surgery. These fit together: well-controlled asthma is safe to anaesthetise, active wheeze is not. Miller adds a short oral steroid course before surgery for poorly controlled patients, and that takes days. No book gives a fixed number of days. Surgery waits until treatment has restored control.

Bronchodilator addresses untreated asthma adequately. Salbutamol before induction is real prophylaxis, and a short-acting beta-agonist is first-line for wheeze, so going ahead looks reasonable. But a bronchodilator only relaxes the muscle for a short time. It does nothing about a month of untreated inflammation, so the airway stays primed to spasm under anaesthesia.

Barash treats acute wheezing as an emergency and postpones elective surgery. Miller advises a short preoperative oral steroid course for newly diagnosed or poorly controlled asthma. GINA finds no added perioperative risk across the general asthma population.

Sources: Barash 9eMiller 10eOutside our books: Global Strategy for Asthma Management and Prevention (2024)

Miller says mild asthma that is well controlled carries no more perioperative risk than having no asthma. A little residual wheeze therefore reflects reversible bronchial smooth-muscle tone. It is not on its own a reason to stop. A β-agonist relaxes that muscle and blunts the reflex bronchospasm set off by induction and airway instrumentation. This is why Miller recommends it as prophylaxis and Faust suggests it immediately before induction. Barash's call to postpone covers a different situation: acute wheezing from an active exacerbation, which is a medical emergency.

Cancel surgery for mild wheeze. Cancelling feels safe because wheeze sounds like active disease, and textbooks say wheezing postpones surgery. That warning is about the acute wheezing of an exacerbation. In controlled asthma, a mild wheeze is managed with a bronchodilator before induction, and cancelling without need has its own practical and economic costs.

Mild, well-controlled asthma adds no perioperative risk. β-agonists given beforehand reduce the chance of bronchospasm at induction, and an inhaled bronchodilator just before induction is advised for higher-risk patients. Acute wheezing is treated as a medical emergency.

Sources: FaustMiller 10eBarash 9e

Untreated apnoea causes repeated airway obstruction, night-time arousals and daytime sleepiness. It also marks the patient as a likely difficult airway with postoperative risk. Positive airway pressure keeps the upper airway open, so it treats the disorder itself. Barash reports that in obese apnoea patients, CPAP combined with weight loss improved blood pressure and glucose and lipid handling. This means part of the metabolic upset follows from the untreated apnoea. Many patients tolerate CPAP poorly and alternatives exist, but CPAP is still the first step to take before surgery.

Treat fasting glucose not sleep apnoea. The raised fasting glucose catches the eye, and controlling it is good practice. But it does nothing for the airway obstruction or the respiratory risk around surgery. CPAP treats the apnoea that drives the risk, and it may also help bring the glucose down.

Barash says to consider starting CPAP before surgery, above all in severe apnoea. In obese patients, CPAP plus weight loss improved blood pressure and glucose and lipid metabolism. Anyone with confirmed or suspected apnoea should be treated as high risk for a difficult airway.

Sources: Barash 9e

An overnight sleep study records breathing across the whole night. It detects obstructive events and also separates them from central apnoea, hypoventilation and sleep-related hypoxaemia. History and examination cannot reliably tell simple snoring from true apnoea. Home sleep apnoea testing is less accurate where non-obstructive breathing disorders are likely, especially in significant cardiorespiratory disease. In those patients a home study may miss or misclassify the problem, so full polysomnography remains the definitive test.

Home testing gold standard for OSA. Home sleep apnoea testing is tempting because it is convenient, widely used and can be enough to start treatment. It is not the best investigation because it is the less complete test. In patients with significant cardiorespiratory disease it may miss central apnoea, hypoventilation or hypoxaemia.

The guidelines and textbooks agree that overnight polysomnography is the gold standard for diagnosing obstructive sleep apnoea and other sleep-disordered breathing. Clinicians should weigh the chance of non-obstructive disorders before using home testing in cardiorespiratory disease. Clinical assessment alone separates snoring from apnoea poorly.

Sources: FaustOutside our books: Clinical Practice Guideline for Diagnostic Testing for Adult Obstructive Sleep Apnea: An AASM Clinical Practice Guideline (2017)Stoelting 8e

Barash says helical CT pulmonary angiography has replaced radionuclide ventilation–perfusion scanning as the first-line test for confirming embolism. V/Q scanning or formal pulmonary angiography is kept for patients with poor renal function, where contrast may harm the kidneys, or for an equivocal CT. D-dimer rises in many critical illnesses, so a high value cannot establish embolism. In pregnancy, the RCOG also prefers CTPA to V/Q scanning when the chest film is abnormal.

D-dimer confirms pulmonary embolism diagnosis. D-dimer is a quick blood test linked to clot, so it can feel like a confirming test. It is often raised and nonspecific, especially in critically ill patients, so a high result cannot prove embolism. Only imaging confirms the diagnosis.

Barash: helical CT has replaced V/Q scanning as the main test for embolism; V/Q or angiography is reserved for renal impairment or equivocal CT. D-dimer is unhelpful in intensive care, being often raised. RCOG: choose CTPA over V/Q when the chest X-ray is abnormal.

Sources: Barash 9eOutside our books: Thromboembolic Disease in Pregnancy and the Puerperium: Acute Management (2015)

Pulmonary hypertension is a disease of the pulmonary vessels, not the airways. The arteriolar walls thicken and clots form in the small vessels. This removes capillary surface where alveolar gas meets blood, so carbon monoxide transfer falls. Airflow and lung volumes can stay near normal. Spirometry therefore often misses it, while gas transfer drops early. Even so, gas transfer is only an indirect sign. Echocardiography, which estimates right-sided pressures, tracks catheter-measured pressures more reliably than any lung function test.

FEV/FVC predicts pulmonary hypertension. Lung disease like COPD causes pulmonary hypertension, so spirometry seems the natural predictor. Yet first-second FEV/FVC measures airway obstruction, not the vessels. It can be normal in pulmonary hypertension, and in lung disease it tracks the vascular problem less closely than gas transfer.

In pulmonary hypertension, lung function testing can be unremarkable apart from a reduced carbon monoxide transfer. A sarcoidosis guideline noted that impaired gas transfer correlated with pulmonary hypertension, possibly more than reduced FVC, but echocardiography matched catheter pressures most reliably and is the screening test.

Sources: FaustOutside our books: Diagnosis and Detection of Sarcoidosis: An Official American Thoracic Society Clinical Practice Guideline (2020)

Systemic sclerosis damages small vessels as well as lung tissue, so the lungs can fail in two ways. Fibrotic interstitial disease is commoner; pulmonary arterial hypertension is less common. Together they cause most deaths. Both cause exertional breathlessness, so symptoms cannot separate them. Lung function testing is poor at spotting the vascular disease: apart from a fall in gas transfer it may be normal. Echocardiography estimates right ventricular systolic pressure and shows associated cardiac disease, so it is the first-line screen.

Attribute breathlessness to restrictive disease. It feels logical to blame the change on the known restrictive lung disease and simply repeat lung function tests. But pulmonary arterial hypertension can coexist, and those tests may look unchanged apart from reduced gas transfer. The vascular cause is then missed until the right ventricle fails.

Lung disease in systemic sclerosis is mainly interstitial and less often pulmonary arterial hypertension, and it accounts for most deaths. Pulmonary arterial hypertension presents with nonspecific exertional breathlessness. Lung function may be normal except for gas transfer. Transthoracic echocardiography is the initial screening test.

Sources: FaustBarash 9eStoelting 8e

Parenchymal sarcoidosis inflames and scars the interstitium, producing restrictive physiology: lung volumes shrink and alveolar–capillary bed is lost, so diffusing capacity falls. Full pulmonary function tests capture both changes and can be repeated to track progression; Barash ranks spirometry the most useful test and links low DLCO to sarcoid fibrosis. Echocardiography answers a different question: the ATS guideline reserves it for suspected pulmonary hypertension, such as breathlessness persisting despite treatment. Chest radiography stages disease but is insensitive to change.

DLCO alone indicates sarcoid progression. Diffusing capacity is the textbook marker of sarcoid fibrosis, so DLCO looks like the precise answer. But it is one measurement within the PFT set; alone it cannot separate parenchymal progression from pulmonary hypertension, which also lowers it. Full PFTs, with spirometric volumes, give the complete picture.

Barash notes diffusing capacity falls with the alveolar fibrosis of sarcoidosis and ranks spirometry as the most useful pulmonary function test. The ATS sarcoidosis guideline suggests echocardiography as the first test only when pulmonary hypertension is suspected, defined as dyspnoea persisting despite treatment.

Sources: Barash 9eOutside our books: Diagnosis and Detection of Sarcoidosis: An Official American Thoracic Society Clinical Practice Guideline (2020)

Transthoracic echo does not measure pulmonary artery pressure directly. It estimates right ventricular systolic pressure from the speed of the tricuspid regurgitant jet, so it is a screening test, not a diagnosis. An echo estimate cannot confirm that the pressure is high, and it cannot measure pulmonary vascular resistance. Catheterisation gives the true pressures and the resistance. With those figures the pulmonary hypertension can be classified correctly and treated before an elective moderate- or high-risk operation goes ahead.

Optimize lungs without confirming vascular pressure. Scoliosis causes restrictive lung disease, which drives pulmonary hypertension, so a pulmonology referral to optimise the lungs feels logical. But it targets the presumed cause without confirming or quantifying the pressure problem; a moderate echo estimate before major surgery first needs invasive confirmation by right heart catheterisation.

Stoelting advises right heart catheterisation before moderate- or high-risk surgery when history or echo suggests moderate or severe pulmonary hypertension. Barash describes echo as estimating right ventricular pressure from the tricuspid jet. Catheterisation is still required to confirm raised pressures and measure resistance.

Sources: Stoelting 8eBarash 9e

In OSA the upper airway collapses easily. Sedatives, opioids and inhaled agents depress breathing and airway patency, so general anaesthesia with systemic opioids adds respiratory risk that continues after surgery. A knee replacement is a peripheral limb operation, so the ASA guideline advises considering neuraxial block. Both the ASA and anaesthesia texts favour regional, opioid-sparing techniques with only light sedation. One branch matters: if the case would need deep sedation, the ASA prefers general anaesthesia with a secured airway to a deeply sedated, unprotected airway.

General anaesthesia with intubation for OSA. GA with ETT is tempting because OSA predicts a difficult airway and the ASA prefers a secured airway to deep unprotected sedation. But that preference applies only when deep sedation is needed. For a peripheral limb operation, neuraxial block avoids airway instrumentation, volatile agents and systemic opioid load.

The ASA guideline advises considering spinal or epidural block for peripheral procedures, and regional techniques to cut systemic opioid needs. It notes that OSA patients are especially sensitive to sedatives, opioids and inhaled agents. Perioperative texts list opioid-sparing methods, regional anaesthesia and light sedation.

Sources: FaustOutside our books: Practice Guidelines for the Perioperative Management of Patients with Obstructive Sleep Apnea: An Updated Report (2014)Barash 9e

There are two separate decisions here. The overall plan for an ambulatory OSA patient is a drug choice. These patients obstruct and stop breathing with respiratory depressants, so Barash advises short-acting agents such as remifentanil and avoiding opioids whose active metabolites linger. That lets them wake and breathe safely for same-day discharge. The induction step is about oxygen. Obesity shrinks functional residual capacity, and induction shrinks it further, so desaturation comes fast. Faust shows that positive pressure during mask preoxygenation limits that loss and buys apnoea time.

Pre-induction recruitment manoeuvre. Recruitment looks like a natural partner to PEEP. Miller, though, describes it as a sustained inflation followed by PEEP to prevent atelectasis in a patient already anaesthetised and ventilated. It is not the protective step before the airway is secured, and it is not a plan for safe same-day recovery.

Faust reports that CPAP plus PEEP, each 10 cm H2O, during mask ventilation limits the early fall in FRC at induction. Barash advises short-acting agents such as remifentanil for OSA patients and avoiding opioids with active metabolites. Miller uses recruitment, then PEEP, against atelectasis.

Sources: Barash 9eFaustMiller 10e

Volatile agents and nitrous oxide slow mucus transport. They lower ciliary beat frequency, break up the coordinated ciliary wave and alter the mucus itself. In vitro, intravenous agents do not depress cilia this way. In animal tracheal tissue, fentanyl actually stimulated ciliary activity. Ketamine is intravenous, but it drives salivary and tracheobronchial gland output, adding mucus unless an anticholinergic is given. Propofol also relaxes bronchial smooth muscle and lowers airway resistance in COPD. Retained secretions lead to plugging, atelectasis and hypoxaemia.

Sevoflurane equivalent to TIVA technique. Sevoflurane dilates the bronchi and is the least cilioinhibitory volatile, so it looks lung-friendly in COPD. But like every volatile it still reduces ciliary beat frequency and mucus clearance. Pairing it with remifentanil therefore cannot match a fully intravenous technique.

Halogenated volatiles reduce ciliary movement and beat frequency, but intravenous anaesthetics do not, and fentanyl stimulated cilia. Ketamine increases mucus secretion from salivary and tracheobronchial glands. Propofol lowers airway resistance in COPD by relaxing airway smooth muscle.

Sources: Miller 10eFaust

A fistula is a low-resistance leak: positive pressure applied before the healthy lung is sealed off escapes through it, wasting ventilation, building pleural tension and driving pus into the good lung. Keeping the patient breathing spontaneously until the double-lumen tube isolates the healthy side avoids this, which is why both current texts rank awake or spontaneous-breathing placement first. Barash warns that a relaxant-based rapid sequence risks soiling and tension pneumothorax; Miller accepts a modified rapid sequence only for a normal airway with bronchoscopic tube guidance.

Mask ventilation before lung isolation. Tempting because it includes a double-lumen tube and looks like Miller's modified rapid sequence. It fails because mask ventilation applies positive pressure before the healthy lung is isolated, pushing gas through the fistula with risk of tension pneumothorax and soiling; the books prefer spontaneous breathing until isolation.

Barash calls awake double-lumen intubation with spontaneous breathing ideal, offers spontaneous-breathing general anaesthesia as the alternative to avoid tension pneumothorax, and flags relaxant rapid sequence as risking contamination and tension pneumothorax. Miller permits a modified rapid sequence for normal airways with bronchoscope-guided tube placement.

Sources: Barash 9eMiller 10e

Positive pressure delivered to an open bronchial stump escapes into the pleural space. This wastes tidal volume and keeps the leak open. The fistula therefore absolutely indicates one-lung ventilation, which confines gas to the healthy lung. A double-lumen tube placed in the uninvolved bronchus does this, and isolation is confirmed before ventilating or moving the patient. Jet ventilation is the alternative because it ventilates at lower peak airway pressures, so less gas is driven through the defect. It can sometimes be difficult to use.

Pressure support for fistula ventilation. Pressure support sounds gentle because the patient breathes spontaneously. It still pushes positive pressure through an unisolated airway into the fistula, so it does nothing to stop the leak. The texts' answer is lung isolation or jet ventilation, not choosing a conventional mode.

Barash recommends a bronchial tube in the contralateral main bronchus, or jet ventilation, which gives lower peak airway pressures. Miller advises confirming lung isolation before applying positive pressure or repositioning the tube. One-lung ventilation is absolutely indicated in fistula.

Sources: Barash 9eMiller 10e

Positive pressure given to both lungs escapes through the fistula, so tidal volume is lost. Pus from the empyema can also spill into the good lung, especially when the patient is turned lateral. Placing the bronchial limb in the contralateral main bronchus separates the two sides. The healthy lung then gets full ventilation and is shielded from infected material.

Right-sided tube for right-sided fistula. A right-sided tube seems logical because the disease is on the right. But it puts the bronchial limb and cuff into the diseased, leaking bronchus instead of protecting the good lung. Right-sided tubes are also harder to seat around the upper lobe orifice.

Thoracic texts recommend a double-lumen tube for positive-pressure ventilation. It ventilates the normal lung without leak and protects it from contamination when turned lateral. The bronchial lumen goes on the side away from the fistula; left-sided tubes are easier to position.

Sources: Barash 9eMiller 10e

Pressure inside a bulla follows mean airway pressure. During spontaneous breathing it stays below the surrounding lung pressure, so the bulla does not overfill. Positive pressure reverses this: bulla pressure rises above that of the surrounding lung, risking overdistension and rupture. Rupture can cause tension pneumothorax with circulatory collapse, or a bronchopleural fistula that diverts the delivered breath. Nitrous oxide worsens this by diffusing into closed gas spaces and enlarging them. If positive pressure is unavoidable, give small, low-pressure breaths until the lung is isolated.

Nitrous oxide during spontaneous breathing induction. Nitrous oxide is a familiar part of paediatric gas induction because it speeds uptake and smooths the mask phase, and pairing it with the correct spontaneous breathing makes the option look complete. It fails because it moves into the bulla and enlarges it, bringing back the rupture risk.

Under positive pressure, bullae can hyperinflate and burst, causing tension pneumothorax or a bronchopleural fistula. Spontaneous breathing at induction is preferred until lung isolation; if that is impossible, use gentle low-pressure breaths. Nitrous oxide is avoided because it expands air-containing spaces, bullae included.

Sources: Miller 10eBarash 9e

Obstructed airways empty slowly, so if the next breath arrives before expiration finishes, gas is stacked in the alveoli: intrinsic PEEP. Its size rises with tidal volume and falls as expiratory time lengthens. Stacked gas raises intrathoracic pressure, cuts venous return and can drop blood pressure. A faster rate or longer inspiration steals expiratory time and worsens this. Stoelting advises watching minute ventilation for hypercapnia; Barash adds that the CO2 rise this strategy causes seems harmless and is outweighed by less trapping, so monitor it but accept it.

Increase ventilation rate for COPD hypercarbia. Raising the rate looks like the natural fix for a high CO2 because it boosts minute ventilation. In obstructed lungs it shortens each expiration, so more gas is trapped and intrinsic PEEP and intrathoracic pressure climb. Blood pressure can then fall.

Stoelting: cutting the rate or the I:E ratio buys exhalation time and lessens air trapping, which can destabilise the circulation. Miller: auto-PEEP rises with tidal volume and falls with longer expiration. Barash: the resulting hypercapnic acidosis appears harmless and is outweighed by less trapping.

Sources: Stoelting 8eMiller 10eBarash 9e

Barash finds no ventilator mode changes major outcomes, so the choice comes down to physiology, and Miller's approach supplies it. Bag the patient slowly at first to limit overdistension and pneumothorax. Then let the patient trigger assisted breaths rather than imposing every breath. Of the offered choices, SIMV is the mode that allows patient-initiated, pressure-supported breaths; PEEP is a setting, not a mode. Extrinsic PEEP raised only up to the patient's own intrinsic PEEP makes triggering easier and lowers the work of breathing.

Pressure control for severe asthma. PCV is a true ventilator mode, so it looks like the natural rival to SIMV. But asthmatic airway resistance keeps changing, so a fixed set pressure can deliver an inadequate tidal volume. PEEP, the other option, is a setting matched to intrinsic PEEP, not a mode.

Barash: no ventilator mode clearly changes major outcomes; choice is largely preference. Miller: hand-ventilate slowly after intubation to avoid overdistension and pneumothorax; pressure control is criticised as changing airway resistance alters delivered volume; extrinsic PEEP up to intrinsic PEEP improves triggering, reducing work of breathing.

Sources: Barash 9eMiller 10e

Delivering positive pressure through a nasal or face mask, without a tracheal tube, is the guideline standard of care because it lowers morbidity and mortality in hospitalised COPD patients in respiratory failure. As experience grew, many patients who were once intubated are now managed on mask ventilation, so invasive ventilation has lost its first-line place. The catch: the patient must be awake and cooperative, and the airway stays unprotected. A patient who cannot cooperate is a poor candidate, and a failed trial moves you to intubation.

Intubate for severe hypercapnic respiratory failure. Severe acidosis with a very high carbon dioxide looks like an obvious reason for a tube. But guidelines put mask ventilation first even in established hypercapnic failure. Intubation is the rescue when the non-invasive trial fails, or when the patient cannot cooperate or protect the airway.

The international COPD guideline calls non-invasive positive-pressure ventilation the standard of care for COPD exacerbations in respiratory failure and the first ventilatory mode unless absolutely contraindicated; an anaesthesia text agrees, reserving intubation for NIV failure, and a review notes it needs a conscious, cooperative patient.

Sources: Outside our books: Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease, 2025 Report (2025)FaustMayo review

Mask CPAP or NIV pushes gas into the pharynx. If the airway is not protected, some of that gas goes into the stomach, which raises the risk of vomiting and aspiration. Miller lists altered mental status only as a relative contraindication, so a mildly confused patient can still be considered. The stroke consensus says that deeply depressed consciousness, with GCS below 8, needs a secured airway. The two fit as a branch: mild confusion is weighed case by case, but deep coma means intubation, not a mask.

Recent bypass contraindicates NIV use. It feels forbidden because gas forced into the stomach might strain a fresh gastrojejunal anastomosis. Barash says this risk is theoretical. Non-invasive positive pressure after gastric bypass does not appear to increase major anastomotic leakage, so recent bypass is not a contraindication.

Miller lists haemodynamic instability, altered mentation, high aspiration risk, being unable to wear a mask, and refractory hypoxaemia as relative contraindications. Stroke guidance secures the airway when GCS is below 8. Barash finds no rise in anastomotic leak after gastric bypass.

Sources: Outside our books: Perioperative Care of Patients at High Risk for Stroke during or after Non-Cardiac, Non-Neurologic Surgery: Consensus Statement from SNACC (Mashour GA et al.) - 2014 predecessor of the 2020 guideline (2014)Miller 10eBarash 9eStoelting 8eMayo review

FEV1 falls whenever the lungs are small, so a low FEV1 on its own cannot tell narrowed airways from stiff, shrunken lungs. Dividing FEV1 by FVC corrects for the patient's own lung size. In restrictive disease FEV1 and FVC fall together in proportion, so the ratio is preserved. In obstruction, raised airway resistance slows expiratory flow. Less of the vital capacity leaves in the first second, so the ratio drops. Once obstruction is established, FEV1 as a percentage of predicted is used to grade its severity.

FEV1 alone defines airway obstruction. FEV1 is tempting because it does fall in obstruction and is used to stage COPD. It is not specific, though. It also falls in restrictive disease simply because lung volume is small, so only the ratio directly shows that the airways are obstructed.

The textbooks call a reduced FEV1/FVC the defining feature of obstruction, and a value below 70% indicates obstructive disease. In restrictive defects all lung volumes fall proportionally and the ratio stays normal. A low FEV1 there reflects small lungs, not obstruction.

Sources: FaustBarash 9eMiller 10e

Stiff lung tissue or chest wall limits expansion, so all volumes and capacities shrink together, including inspiratory capacity and the tidal breath. The airways are normal, so FEV1 falls only in step with FVC and the ratio does not drop. Barash describes the ratio as normal; Miller's and Faust say normal or increased, and that applies: a normal or high ratio both fit restriction. A healthy lung also has a normal ratio, so the ratio only excludes obstruction. A reduced volume, above all TLC, shows restriction.

Tidal volume increases in restrictive disease. Half of this option is correct, because inspiratory capacity does fall, and the fast breathing seen in fibrosis can be mistaken for bigger breaths. But restriction shrinks every volume. These patients take quick, shallow breaths, so tidal volume falls. It does not rise.

Barash says restriction lowers all lung volumes in proportion and leaves the ratio normal. Miller's and Faust say the ratio is normal or increased and treat a reduced TLC as the defining finding. A review lists reduced TLC and FRC in restriction.

Sources: Barash 9eMiller 10eMayo reviewFaust

The curved, rotated spine stiffens and shrinks the thoracic cage, which squeezes the lungs, so every static volume is smaller. Resting FRC drops because the chest wall cannot spring outward as far. The airways are not narrowed, so airflow is not obstructed. Barash calls FEV1 relatively normal; Mayo says it falls. Both fit: any fall in FEV1 only tracks the smaller vital capacity. The ratio is therefore preserved, and FEV1 is never the defining loss.

FEV1 most sensitive in scoliosis. FEV1 tempts because any abnormal spirometry feels like a fall in FEV1, and some texts say it can drop. But scoliosis restricts volume, not airflow. FEV1 is relatively preserved and shrinks only in step with vital capacity. FRC falls directly from chest-wall restriction.

Faust lists kyphoscoliosis among causes of reduced FRC through a restricted thoracic wall. Barash places scoliosis among restrictive diseases with lower FVC and TLC, a relatively normal FEV1 and a normal ratio. Mayo explains that the ratio holds because FEV1 and FVC drop together.

Sources: FaustBarash 9eMayo reviewStoelting 8e

Fat on the chest wall and abdomen pushes the diaphragm upward and stiffens the chest. This squeezes the volume between resting end-expiration and residual volume. Residual volume is largely preserved, so ERV shrinks first and proportionally most. FRC falls only because ERV is one of its parts. Airway calibre is usually unaffected, so the timed spirometric values stay near normal. That is why reduced ERV, rather than an abnormal FEV1 or FVC, is the early marker of obesity's effect on the lungs.

FRC most sensitive volume in obesity. FRC is the volume anaesthetists associate with obesity because its fall drives rapid desaturation at induction. However, FRC comprises ERV plus residual volume, and only ERV shrinks. FRC therefore changes later and proportionally less, making it the less sensitive indicator.

Barash names ERV as the most sensitive marker of obesity's effect on pulmonary function. It notes that forced expiratory volume in one second and forced vital capacity usually remain within normal limits.

Sources: Barash 9e

Breathing out from total lung capacity can go past the normal resting end-expiratory point, but the lungs never empty completely. A relaxed exhalation stops at functional residual capacity. Forcing out the expiratory reserve volume as well leaves only the residual volume, so FRC equals expiratory reserve plus residual volume. Residual volume is the gas that stays even with maximal effort. It rises sharply in obstructive disease, where airways do not empty fully and gas is trapped behind them.

Residual volume equals functional residual capacity. It is tempting because both describe gas left after breathing out, and FRC's full name contains the word 'residual'. But a normal expiration stops at functional residual capacity, which still holds the expiratory reserve volume. Residual volume is only what remains once that reserve has also been forced out.

Textbooks define residual volume as the air left after a maximal expiration, normally about 500 mL. Air left after a normal expiration is FRC, which is expiratory reserve volume plus residual volume. Obstructive disease with air trapping can raise residual volume markedly.

Sources: Outside our books: Pulmonary Function Tests (2011)Mayo review

After a full inspiration, a maximal expiration empties the lungs only partly. Some gas always stays in the lungs. This is the residual volume, and because it never reaches the mouthpiece a spirometer cannot record it. Vital capacity is the part that can be breathed out and measured, so it equals total lung capacity minus residual volume. Spirometry reads it directly, so the value depends on the patient cooperating and on the strength of both inspiratory and expiratory muscles.

Vital capacity equals total lung capacity. 'Total lung volume' sounds like 'the maximum', so it feels right. But it counts all the gas in the lungs at full inspiration, including the residual volume, which cannot be breathed out however hard the patient tries. Vital capacity is only the part that can be exhaled.

Anaesthesia texts define the forced form as the largest volume a person can breathe out after a maximal inspiration. They also say gas still remains in the lungs after maximal forced expiration, and that spirometry measures vital capacity directly.

Sources: Barash 9eFaust

A capacity is a sum of lung volumes. Total lung capacity adds together all four basic volumes: tidal volume, inspiratory reserve, expiratory reserve and residual volume. A maximal breath in fills the lungs to this ceiling. Breathing out forcefully from there gives the forced vital capacity. But expiration stops at residual volume, so some gas always stays in the lungs. The volume breathed out after a maximal inspiration is therefore smaller than total lung capacity by the residual volume.

Looks like TLC but actually VC. This option begins at the correct point, full inspiration, and so appears to describe total lung capacity. In fact it describes vital capacity, since it includes only the gas that can be breathed out. The residual volume, which remains in the lungs following maximal expiration, is not counted.

Faust defines total lung capacity as the largest volume of air the lungs contain. Miller describes spirometry as inspiration to total lung capacity, then forced exhalation measuring vital capacity. Stoelting shows expiration running from total lung capacity to residual volume.

Sources: FaustMiller 10eBarash 9eStoelting 8e

A rigid narrowing, such as a scarred tracheal segment, keeps the same calibre throughout the breathing cycle. It therefore caps peak flow equally on breathing in and breathing out, whether it lies inside or outside the chest. Both limbs plateau, and the loop looks like a box. In asthma and other obstructive lung disease, many small airways are narrowed, and that resistance matters more as lung volume falls during forced exhalation. Expiratory flow sags progressively, which carves a downward, concave scoop into the expiratory limb.

Tracheomalacia shows fixed obstruction pattern. Tracheomalacia also causes stridor from a central airway lesion, so it seems interchangeable with stenosis. But a floppy trachea collapses dynamically, so its calibre changes with the breathing phase. That variable obstruction flattens only one limb. A box with both limbs flat needs a rigid, fixed narrowing.

With tracheal narrowing, stridor is typical and both the inspiratory and expiratory curves flatten. This is the signature of fixed obstruction, which may be intra- or extrathoracic. In asthma, and in obstructive lung disease generally, the expiratory limb is scooped downward.

Sources: Stoelting 8eMiller 10e

Compliance is the volume gained for each unit of pressure applied, so it is the gradient of the curve. In emphysema the alveolar walls and elastic tissue are destroyed. Recoil falls and the lung inflates easily, so the gradient is steep. In fibrosis the stiff interstitium raises elastance, so the gradient is flat and breathing takes much more work. Asthma and bronchitis trap gas and raise lung volume, but the tissue's elasticity is unchanged. Their curve therefore moves up while staying parallel to normal.

Any elevated curve indicates emphysema. Asthma also puts the curve above the normal one, at higher lung volumes, so any high curve can look like obstructive disease in general. But asthma only moves the curve upward without changing its gradient. The curve that rises most steeply, with very large volumes at low pressure, is emphysema.

Miller describes a flatter slope with more work in fibrosis, a parallel upward shift with unchanged compliance in asthma or bronchitis, and a steeper slope from tissue loss in emphysema. The review text identifies the steep, high-volume curve labelled A as emphysema.

Sources: Mayo reviewMiller 10e

AHI is the number of apnoeas plus hypopnoeas per hour of sleep, measuring how often the upper airway narrows or closes overnight. Healthy adults have under 5 events per hour. Severity bands are arbitrary conventions. Some texts write them loosely as 5–15 and 15–30, but formal tables use half-open bands, so exactly 15 counts as moderate. A value well inside the lowest band is mild under either wording. At this level, diagnosis also needs symptoms such as daytime sleepiness, or comorbidity such as hypertension or atrial fibrillation.

AHI 5-15 classified as normal. Some sleep centres put their normal cut-off above 5 events per hour. Mild-range counts also need symptoms before the syndrome is diagnosed, so 'normal' can feel defensible. But the question asks for a severity grade, and any AHI from 5 to under 15 is graded as mild.

AHI is total apnoeas and hypopnoeas divided by total sleep time. Under 5 events/hour is physiological; mild is 5 to under 15, moderate 15 to under 30, severe 30 or more. At mild counts, the syndrome is diagnosed only with symptoms or comorbidities.

Sources: FaustMiller 10e

Relaxed, alert wakefulness shows alpha. Miller's marks sleep onset as the shift from alpha to slower theta. Stage 1 is that lower-amplitude theta; stage 2 keeps the theta background and adds spindles and K-complexes. The books draw the theta edges slightly differently: Miller's scoring table gives 4–7 Hz, its text 4.5–7.5 Hz, and Faust 4–8 Hz. These are different conventions, not a dispute. Every source names light sleep as theta, so anchor on the band name and accept any of these edges.

4-7 Hz marks sleep onset. It pairs the right number with the wrong band. 4–7 Hz really is the stage 1 range, so it looks correct at a glance. But that range is theta. Alpha is faster and marks relaxed wakefulness, and losing it is what signals sleep onset.

Miller's table defines stage 1 as lower-amplitude 4–7 Hz activity and stage 2 as that same background plus spindles and K-complexes, and its text calls stage 2 theta. Miller's puts theta at 4.5–7.5 Hz; Faust lists theta 4–8 Hz for drowsiness and first-stage sleep.

Sources: Miller 10eFaust

Cigarette smoke destroys bronchioles and alveoli. The lung loses the elastic recoil that holds small airways open, so they collapse during expiration. Chronic bronchitis adds a cough and sputum. An exacerbation is a short-lived worsening of these symptoms, usually when infection or another insult heightens airway inflammation. If obstruction worsens until carbon dioxide cannot be cleared, PaCO2 climbs above the patient's baseline. A PaCO2 beyond 60 mmHg, or a pH of 7.25 or lower, marks life-threatening respiratory failure.

Pneumonia as primary diagnosis. A productive cough with hypoxaemia looks like chest infection. But hypercapnic acidosis in a long-term smoker points to ventilatory failure from airflow obstruction. Pneumonia is a differential to exclude, and infection is a common trigger of an exacerbation, not a separate diagnosis.

GOLD defines an exacerbation as breathlessness, cough or sputum worsening over under 14 days. It grades PaCO2 above 60 mmHg or pH 7.25 or less as life-threatening, and advises excluding pneumonia, heart failure and embolism. Stoelting links COPD to smoking-related loss of recoil.

Sources: Outside our books: Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease, 2025 Report (2025)Stoelting 8e

The type reflects which process has failed. In type 1, gas exchange fails yet breathing still clears carbon dioxide, so PaCO2 stays normal or low. In type 2, the ventilatory pump fails, so carbon dioxide accumulates as oxygen falls. Anaesthesia textbooks define failure only as hypoxaemia or hypercapnia and never number the types. Hypercapnia means PaCO2 above 45 mmHg (6.0 kPa); some respiratory sources draw the type 2 line higher, at 6.5 kPa or 50 mmHg. Exactly 45 mmHg is not hypercapnic under any of these.

Calling upper-normal PaCO2 hypercapnia, so type 2. Type 2 tempts: a breathless patient after lung resection seems to hypoventilate, and 45 mmHg looks high. But hypercapnia means PaCO2 above 45 mmHg, so 45 is the upper limit of normal; the stricter 6.5 kPa or 50 mmHg lines sit further away. Carbon dioxide is cleared: type 1.

Respiratory sources define type 1 failure as PaO2 under 8 kPa with a normal PaCO2, and type 2 as hypoxia with PaCO2 over 6.5 kPa. An anaesthesia text defines failure after lung resection as PaO2 under 60 or PaCO2 over 45 mmHg.

Sources: Outside our books: Pulmonary Function Tests (2011)Miller 10eOutside our books: Consensus document for the selection of lung transplant candidates: An update from the International Society for Heart and Lung Transplantation (2021)Barash 9e

Emphysema damages airways, alveoli and pulmonary vessels, so ventilation no longer matches blood flow. In COPD this mismatch is the main gas-exchange defect. It lowers PaO2 and widens the alveolar–arterial gradient, while PaCO2 stays normal or falls. Pure hypoventilation raises PaCO2 and leaves the gradient normal. In COPD, CO2 retention tends to appear only late, once FEV1 falls below 25% of predicted, and fatigue of the breathing muscles can contribute.

Diffusion impairment. Emphysema destroys alveolar walls and lowers diffusing capacity, so a diffusion defect seems the obvious cause. But the guideline names the disturbed ventilation–perfusion distribution as the main cause of hypoxaemia in COPD. Reduced diffusing capacity is only an added finding.

GOLD names altered ventilation–perfusion distribution as the main cause of hypoxaemia in COPD, with or without hypercapnia, and lists reduced diffusing capacity as an extra effect. Stoelting's table gives mismatch as low PaO2, normal-to-low PaCO2 and a widened gradient, and hypoventilation as raised PaCO2.

Sources: Outside our books: Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease, 2025 Report (2025)Stoelting 8e

Alveolar gas is shared between oxygen and carbon dioxide. When ventilation falls, retained CO2 takes up more of the alveolus, so alveolar oxygen falls by about PaCO2 divided by the respiratory quotient. Healthy lungs still pass that lower alveolar oxygen into the blood, so arterial oxygen falls in step and the A–a gradient stays normal. V/Q mismatch, shunt and diffusion defects widen the gradient instead. After surgery, leftover anaesthetic agents and opioids blunt the ventilatory response to CO2, so hypoventilation is common. A modest amount of extra oxygen corrects it.

V/Q mismatch ventilation. V/Q mismatch is the commonest cause of hypoxaemia, and lungs after surgery often have some, so it feels like the safe answer. But it widens the A–a gradient while PaCO2 stays normal or low. A high PaCO2 with an oxygen fall that the gas equation fully predicts means hypoventilation.

Miller shows that with no A–a gradient on room air, raising PaCO2 from 40 to 80 mm Hg alone lowers PaO2 to 50 mm Hg. Stoelting describes hypoventilation as raised PaCO2 with a normal gradient; V/Q mismatching increases the gradient.

Sources: Miller 10eStoelting 8e

Blood flowing past alveoli receiving no gas never takes up oxygen, however rich the inspired mixture. This deoxygenated blood mixes with blood from healthy lung units, lowering arterial oxygen tension and widening the alveolar–arterial gradient. ARDS creates many such units through alveolar collapse and atelectasis, so hypoxaemia barely improves when the inspired oxygen fraction is increased. A normal arterial carbon dioxide level rules out hypoventilation, which always raises it.

V/Q mismatch main cause. Hypoxaemia is most often caused by V/Q mismatch, and shunt sits at one extreme of the V/Q range, so it looks like a safe choice. However, poorly ventilated units still receive some gas, so supplemental oxygen corrects them. Hypoxaemia that resists high FiO2 is the signature of true shunt.

ARDS is listed with atelectasis and congenital heart disease as causes of shunt. Adding inspired oxygen does not correct shunt hypoxaemia. In ARDS, blood gases show severe hypoxaemia with a raised alveolar–arterial gradient, which fits right-to-left shunt.

Sources: FaustMiller 10e

A clot stops blood flow to alveoli that are still ventilated, so those breaths carry away no CO2: alveolar dead space. Chemoreceptor and reflex drive then raise minute ventilation, so arterial CO2 is often kept from rising. Oxygenation is a separate branch. Barash pairs the dead space with ventilation–perfusion mismatch, which improves with extra oxygen; Miller lists emboli among causes of true shunt, where blood bypasses ventilated alveoli and added oxygen never reaches it. Hypoxaemia that stays despite high oxygen therefore means shunt.

Diffusion impairment barrier. Emboli feel like a barrier to gas transfer, and diffusion impairment is a recognised cause of hypoxaemia, so it sounds plausible. But no book names it for embolism: the clot removes perfusion, not alveolar–capillary transfer, and hypoxaemia resisting high oxygen marks shunt.

Barash says emboli enlarge physiological dead space and widen the arterial–end-tidal CO2 gap, with the CO2 effect often offset by faster breathing, alongside V/Q mismatch. Miller lists emboli among causes of true shunt, which, unlike mismatch, does not respond to supplemental oxygen.

Sources: Barash 9eMiller 10e

If the tube is not passed far enough, the bronchial tip opens above the carina, so gas from the bronchial lumen reaches both lungs. The inflated bronchial cuff then sits in the trachea and blocks the tracheal lumen, so ventilating that lumen gives no breath sounds. Only advancing places the tip in the left main bronchus; the cuff is deflated first, then the tube moved forward. Pulling back fixes the opposite fault, a tube sitting too deep with unequal sounds.

Deflate bronchial cuff only. Deflating the bronchial cuff is the first move the textbook describes, so it looks like the answer. But deflating alone leaves the tip above the carina. The tube is only in the right place once it has been advanced into the left main bronchus.

Bronchial opening lies above the carina; the bronchial lumen gives bilateral breath sounds, while the tracheal lumen is silent because the bronchial cuff blocks it. Correct by deflating the cuff, then rotating and advancing into the intended bronchus.

Sources: Barash 9e

When one lumen is clamped, gas can only leave through the other lumen's opening. With the tracheal lumen clamped, the lung you hear is the one the bronchial tip has entered. If that lung is the right, the tube has entered the wrong bronchus and blocks the right upper lobe takeoff, so only lower zones are heard. Clamping the bronchial lumen instead, the cuff seals the right bronchus, so tracheal-lumen gas reaches only the left lung, proving the tracheal opening sits above the carina.

Left lung sounds indicate placement. A left tube is meant to sit in the left bronchus, and the left lung is heard in full, so this looks like correct placement. But correctly placed, the bronchial lumen ventilates the left lung; here it gives right-sided sounds, so the tip is on the wrong side.

A left tube entering the right main bronchus is a recognised malposition. The opposite lung, whose connector is clamped, collapses and the right upper lobe is blocked, so prompt recognition and correction are essential. For a left tube, clamp the right-side connector.

Sources: Barash 9e

End-tidal gas blends CO2-rich gas from perfused alveoli with CO2-free gas from ventilated, unperfused ones, so it reads below arterial. Falling pulmonary flow from haemorrhage, hypotension or embolism leaves more alveoli unperfused: end-tidal CO2 drops while arterial CO2 holds, and the gap widens. Higher flow perfuses those units and the gap shrinks. Hypoventilation lifts both values together, so the gap stays normal. Shunt branches: the Mayo review finds intrapulmonary shunt, such as atelectasis, barely moves the gap because CO2 diffuses readily; Faust lists right-to-left intracardiac shunt as widening it.

Hypoventilation widens gradient. Hypoventilation raises arterial CO2, so it seems bound to open the gap. But the extra CO2 reaches perfused alveoli as well, so end-tidal climbs in step with arterial and the gradient stays normal. Only changes in perfusion or dead space, or a right-to-left shunt, pull the two apart.

Faust's capnography table shows hypoventilation leaves the gradient normal, while COPD, hypovolaemia, low output, embolism and right-to-left intracardiac shunt widen it and raised cardiac output narrows it. Stoelting attributes widening to alveolar dead space; the Mayo review finds pulmonary shunt changes it little.

Sources: FaustStoelting 8eBarash 9eMayo review

In volume-controlled ventilation with an end-inspiratory pause, peak pressure carries two loads: the pressure needed to drive flow through the airways, and the elastic pressure needed to stretch lungs and chest wall. Plateau is measured at zero flow, so it reflects only the elastic load. The peak-to-plateau gap, divided by flow, gives airway resistance. Narrowed airways widen that gap and leave plateau alone. Mainstem intubation, atelectasis and pneumoperitoneum stiffen the respiratory system, so they raise plateau and peak together.

Airway resistance only factor. It is the classic cause of a sudden pressure rise during laparoscopy, because insufflation pushes the carina upward. It fails because ventilating one lung lowers compliance. That raises plateau as well as peak, so the peak-to-plateau gap stays the same.

Resistance is estimated from the peak-minus-plateau difference divided by inspiratory flow. A change in that gap reflects altered airway calibre, as in intraoperative asthma. Mainstem intubation lowers compliance. Insufflation shows up as higher airway pressure through a compliance change.

Sources: Miller 10eBarash 9e

Bronchospasm under anaesthesia is usually reflex cholinergic constriction from airway stimulation, especially when anaesthesia is too light. Faust treats it as a crisis in which oxygen and deepening start at the same moment, since falling saturation is the immediate danger and depth abolishes the reflex. Stoelting names deepening, with volatile or propofol, plus a rapid inhaled beta-agonist as common first steps; sevoflurane and isoflurane bronchodilate in their own right. Reconciled: oxygen and depth together first, the beta-agonist immediately after.

Beta-agonist as first step. The beta-agonist is the specific bronchodilator, and Stoelting lists it among the common first steps, so it looks like the answer. But it treats the spasm, not the hypoxaemia. Faust puts oxygen and deepening first, and the bronchodilator follows.

Faust: once bronchospasm causes desaturation or poor ventilation, 100% oxygen and deeper anaesthesia must begin almost together. Stoelting: deepening with volatile or propofol, plus a rapid-acting inhaled beta-agonist down the tube, are common first steps; isoflurane and sevoflurane bronchodilate.

Sources: FaustStoelting 8e

Inhaled bronchodilators only reach airways that still carry gas. In severe obstruction, more puffs deliver little drug. Intravenous adrenaline reaches bronchial smooth muscle through the blood, and its beta-2 action gives strong bronchodilation. Steroids act too slowly for the crisis. Give a bolus first. If the spasm persists, titrate an infusion from 0.05–0.1 mcg/kg/min. One text prints a much higher per-minute infusion rate, which is probably a misprint. The texts agree on the bolus, and the lower infusion range is the safe one.

Increase salbutamol dose. Salbutamol is the familiar first-line bronchodilator, so giving more feels safe. Here it has already failed, and with severe obstruction little inhaled drug reaches the narrowed airways. The situation needs escalation, not more of the same: intravenous adrenaline.

Severe bronchospasm that does not respond to first-line measures is treated with IV adrenaline, starting with a bolus of about 1 mcg/kg. Life-threatening bronchospasm responds to it with marked bronchodilation. If bronchospasm persists, an infusion is started at 0.05–0.1 mcg/kg/min and titrated.

Sources: FaustBarash 9e

Hyperventilation during labour can trigger bronchoconstriction. This is a spasm of airway smooth muscle, and a beta2 agonist relaxes it quickly. Inhaling the drug puts it straight onto the bronchi. Repeated puffs therefore reverse airflow limitation fast in mild to moderate attacks while keeping the systemic dose low. The drawback of large doses near delivery falls on the baby. Maternal beta-agonist can leave the newborn hypoglycaemic, especially a preterm baby. After heavy use, the neonate's glucose is watched through the first day.

Steroids before reliever. Steroids are tempting because people link any asthma exacerbation with steroids. But they act on airway inflammation and work slowly. They do not give the rapid bronchodilation needed for bronchospasm triggered by labour, so the inhaled reliever comes first.

The asthma guideline advises treating labour bronchoconstriction with a SABA; salbutamol is the standard reliever. For mild to moderate attacks, give 4–10 puffs every 20 minutes in the first hour. After high-dose SABA in labour, monitor the neonate's glucose for 24 hours.

Sources: Outside our books: Global Strategy for Asthma Management and Prevention (2024)

In flow-limited lungs, breathing in meets no extra resistance but breathing out is badly obstructed. If the next positive-pressure breath arrives before the lung has emptied, gas builds up breath by breath (dynamic hyperinflation). The rising intrathoracic pressure squeezes the great veins, so less blood returns to the heart. The pressure also reaches the pulmonary artery, which raises right ventricular afterload. Cardiac output and blood pressure fall, even with the modest pressures of bag-mask ventilation at induction. Blood pressure can drop before any change in blood gases.

Anaphylaxis as cause. Anaphylaxis is the textbook cause of sudden hypotension around induction, so it comes to mind first. But it rarely causes low blood pressure alone: skin signs, bronchospasm or poor oxygenation usually come with it. An isolated fall in pressure once ventilation starts in a gas-trapping lung points to auto-PEEP.

Miller warns severe COPD risks hypotension on induction from auto-PEEP. Stoelting explains trapped gas accumulates when expiratory time is too short, raising intrathoracic pressure, reducing venous return and loading the pulmonary circulation. Differentials: tension pneumothorax, bronchopleural fistula.

Sources: Miller 10eStoelting 8e

As the scope advances it can press on the innominate artery. This cuts flow into the right subclavian, right vertebral and right common carotid arteries. The right radial pulse and right-hand oximeter signal disappear, but the heart is still beating normally, so it looks like a cardiac arrest. A left-sided reading stays normal. If nobody notices, reduced flow in the right carotid can starve the brain. A right-sided monitor gives early warning so the surgeon can move the scope. The pulse should come back once the pressure is off.

Great vessel compression. Compressing a great vessel during a mediastinal procedure sounds plausible, and it sits close to the airway. But pulmonary artery obstruction would cut cardiac output and oxygenation for the whole body. It would not cause a one-sided loss of pulse with normal heart rate, pressure and ECG.

Scope pressure on the innominate artery reduces flow to the right subclavian, vertebral and carotid arteries. The right radial pulse and right-hand oximetry vanish despite a normal ECG, mimicking a false arrest. Right-arm pulse monitoring is mandatory and helps prevent cerebral underperfusion.

Sources: Barash 9eMiller 10e

The texts advise keeping bullous patients breathing spontaneously, or on small low-pressure breaths, until the diseased lung is isolated; a large opioid dose then causes hypoventilation in patients who already retain CO2. Raised CO2 triggers sympathetic discharge, so heart rate and blood pressure climb together. A compliant bulla adds dead space, widening the arterial–end-tidal gap, so a normal-looking capnograph reading can hide a high arterial CO2. Positive pressure is different: it can inflate and burst a communicating bulla, behaving like a tension pneumothorax.

Bullae rupture likely. A history of recurrent pneumothorax makes rupture feel inevitable, and positive pressure can indeed burst a bulla. But this patient was breathing spontaneously after an opioid-only induction. The raised blood pressure also argues against tension physiology, which brings haemodynamic collapse and rising airway pressure.

The books do not settle this exact pattern of vital signs. Barash links severe hypercarbia to sympathetic tachycardia and raised arterial pressure, notes that compliant bullae waste tidal volume as dead space, and lists pneumothorax signs under positive pressure. Miller favours spontaneous breathing until isolation.

Sources: Barash 9eMiller 10e

Moving the patient often moves the tube. When the head and neck extend during or after turning, the endobronchial cuff can slip out of place. A tube in the wrong position can block part of the lung that should be ventilated, or trap gas behind the blockage. The full tidal volume then goes into less lung, so peak pressure rises. A fibreoptic scope shows exactly where the lumen and cuff now sit, and lets you reposition the tube while you watch.

Secretion blockage first. Secretions are a familiar cause of high airway pressure, and suctioning feels quick and harmless. But the pressure rose just after turning the patient, which points to a moved tube. Suctioning cannot find or fix a displaced bronchial cuff, so it delays the step that does.

The sources advise checking tube position again once the patient is in the lateral decubitus position. If peak pressure goes above 40 cmH2O during one-lung ventilation, malposition must be ruled out. Fibreoptic bronchoscopy is the recommended way to diagnose and correct a misplaced tube.

Sources: Miller 10eBarash 9e

During one-lung ventilation the whole tidal volume goes to the dependent lung, often at high pressure, so a bulla or tear there can leak air into its pleura under tension. Rising intrathoracic pressure collapses that lung and impedes venous return: obstructive shock, so hypoxaemia, hypotension and a falling end-tidal CO2 join the high pressure. Barash: a pressure above 40 cmH2O by itself means exclude tube malposition; Miller adds dependent-lung tension pneumothorax. Resuming two-lung ventilation supports oxygenation but does not relieve tension; decompression does.

Switch to two-lung ventilation. Both thoracic texts tell you to return to two-lung ventilation for an unstable or severely desaturating patient, so it looks safe. Here the problem sits in the ventilated lung itself: tension persists whatever you do with the other lung, and the shock only reverses after decompression.

Miller lists tension pneumothorax of the dependent, ventilated lung as an OLV hazard; intraoperative pneumothorax with raised peak pressure, hypotension and cyanosis needs immediate chest drain decompression. Barash: pressure above 40 cmH2O means excluding tube malposition, and instability means resuming two-lung ventilation meanwhile.

Sources: Miller 10eBarash 9e

Removing a lung shrinks the pulmonary vascular bed. Fluid that the remaining lung would once have handled now floods it, and oedema develops that can progress to acute lung injury. Right pneumonectomy carries more risk, probably because pulmonary artery pressures end up higher afterwards. High airway pressures during ventilation and alcohol misuse add to the risk. There is no specific cure. Management is supportive: restrict fluids, give diuretics and encourage a diuresis.

Myocardial infarction cause. Infarction can cause cardiogenic oedema with bilateral shadows, and tachycardia with desaturation fits, so it looks plausible. But nothing in the picture points to ischaemia. After pneumonectomy, the recognised cause of new bilateral infiltrates with refractory hypoxaemia is lung injury driven by fluid excess and the reduced vascular bed.

Independent risk factors for lung injury after resection are pneumonectomy, intraoperative fluid excess, high ventilatory pressures and alcohol misuse; more than 3 L of fluid in the first 24 hours is independently linked. Right-sided pneumonectomy carries greater risk, possibly from higher pulmonary artery pressures.

Sources: Miller 10eBarash 9e

This is acute lung injury affecting the one lung that remains, and its cause appears to be multifactorial. Large tidal volumes and high airway pressures during one-lung ventilation increase the inflammatory injury, so protective settings are advised: 5–6 mL/kg ideal body weight, peak pressure below 35 cmH2O and plateau pressure below 25 cmH2O. The key point is that the risk of getting it and the risk of dying from it are different numbers. Few patients develop it, but a large share of those who do will die.

30% mortality is accurate. A range topping out at 30% touches the bottom of the true range but is too low: quoted mortality is 30% to 50%. The low figures are traps: 4% is the incidence and 4.9% the overall 30-day mortality after pneumonectomy; neither is mortality once oedema develops.

Lung injury after pneumonectomy occurs in only 4% of patients. Its mortality is 30% to 50%, and its cause appears multifactorial. Lower tidal volumes and limited airway pressures are advised during one-lung ventilation. The overall 30-day mortality after pneumonectomy is much lower, at 4.9%.

Sources: Miller 10eOutside our books: Preoperative functional workup for patients with advanced lung cancer (2016)

In alveolar proteinosis the alveoli are filled with material, not collapsed. Extra PEEP has little to recruit, and shunt continues through the flooded units. Gas exchange recovers only once the material is physically washed out, and lavage also restores macrophage function. Lavage requires a double-lumen tube to isolate each lung, and oxygenation can fall further during the procedure. So it is planned as its own anaesthetic straight after surgery, not done as a rescue in the middle of an operation.

Increase PEEP recruitment. Raising PEEP is the usual reflex for desaturation during surgery, and it works for atelectasis or ARDS. In proteinosis the hypoxaemia comes from alveoli packed with material, not collapsed ones. Extra PEEP recruits little, and only clearing the material by lavage fixes oxygenation.

Stoelting says severe disease needs whole-lung lavage under general anaesthesia to clear the alveolar material and restore macrophage function. It warns that oxygenation may dip further during lavage and recommends a double-lumen tube. Miller calls lavage the most effective treatment for symptomatic disease.

Sources: Stoelting 8eMiller 10e

Proteinosis floods the alveoli with lipid-rich protein, so breathlessness, arterial hypoxaemia and batwing alveolar shadowing are the disease's own picture; severe cases are treated by whole-lung lavage. ARDS is judged by the Berlin definition, not the transfusion lung injury criteria: it needs an acute trigger within a week, and infiltrates nothing else explains, with fluid overload and cardiac oedema excluded. Known proteinosis already explains the shadowing, so a very low oxygen ratio alone does not make it ARDS. Fever is uncommon in proteinosis; when present it signals secondary infection.

ARDS better diagnosis. ARDS tempts because both lungs are shadowed and arterial oxygen stays very low on pure oxygen. But Berlin requires infiltrates that nothing else explains, and known proteinosis already explains both shadowing and hypoxaemia. Without fever, pneumonia is no better; the answer is severe proteinosis.

Proteinosis presents with breathlessness and arterial hypoxaemia and batwing alveolar opacities; severe cases need whole-lung lavage. Berlin ARDS needs onset within a week of a trigger, otherwise unexplained bilateral infiltrates, and exclusion of fluid overload or cardiac oedema. Fever in proteinosis indicates secondary infection.

Sources: Stoelting 8eMiller 10eOutside our books: Whole lung lavage for pulmonary alveolar proteinosis (2010)

A scarce donor lung is justified only if it gains the patient life, so the native disease must be more likely to kill them than the operation and its aftermath. Someone therefore needs a high (>50%) risk of death within 2 years without a graft and a >80% chance of surviving 5 years with one. Indicators include hypoxaemia, repeated exacerbations in CF, and pulmonary hypertension still at NYHA class III or IV after 3 months of combined treatment. A mildly limited patient gains nothing and still carries the risk.

NYHA class II suffices. Pulmonary hypertension is a valid indication, but NYHA class II patients are only mildly limited and not at high short-term mortality risk. Pulmonary arterial hypertension reaches listing only if the patient remains NYHA class III or IV after several months of combined therapy, including prostanoids.

People need over 50% risk of lung-disease death within 2 years without transplant and over 80% five-year post-transplant survival. In CF, high-risk markers are hypoxaemia, pulmonary hypertension and two or more exacerbations yearly needing IV antibiotics. In PAH, listing is at NYHA III–IV.

Sources: Outside our books: Consensus document for the selection of lung transplant candidates: An update from the International Society for Heart and Lung Transplantation (2021)Barash 9e

Older classic descriptions of the ideal donor were strict: Neizer lists age 20 to 45, a PaO2/FiO2 ratio above 350, no smoking history and clean imaging and bronchoscopy. Because donor organs are scarce, centres now accept extended-criteria donors who miss parts of that profile; Barash cites registry data showing donors under 64 do as well as those under 55. Oxygenation remains the floor: Miller's donor-management goal is PaO2 of 300 or more, so gas exchange is the requirement while age and smoking merely grade quality.

Age over 55 excludes. Classic ideal-donor profiles cap age, so an older donor looks like the weakest candidate or a disqualifier. But age beyond that profile only moves a donor into the extended-criteria group, with similar outcomes into the mid-sixties. It is not a bar that every donor must clear.

Miller's donor target is PaO2 300 or more. Neizer's ideal donor is aged 20 to 45, has a ratio above 350 and has never smoked. Barash: shortages drive extended criteria, donors under 64 fare like those under 55, and purulent secretions exclude a donor.

Sources: Miller 10eOutside our books: Addressing donor-organ shortages using extended criteria in lung transplantation (2020)Barash 9e

Harvesting the donor lung cuts its nerve supply, as well as its lymphatics and bronchial circulation. Secretions or collapse in the lower airways of the graft therefore do not trigger the normal cough reflex. Mucociliary clearance is also reduced early after surgery, so retained secretions build up. Telling the patient to cough is the one measure that depends on the missing reflex. Other approaches to hypoxaemia do not rely on the patient sensing secretions.

Encourage patient coughing. Specialist referral for chronic rejection looks too slow or irrelevant for acute desaturation in recovery, so people choose it as the exception. But rejection and infection are real concerns in these patients, so referral is a reasonable step. Encouraging coughing is the measure that cannot work.

Taking the donor lung severs its innervation, and the main result is loss of the cough reflex in the lower airways. Together with early impairment of mucociliary clearance, this predisposes recipients to aspiration and pneumonia.

Sources: Stoelting 8e

Clot blocks pulmonary arteries, adding dead space and disturbing gas exchange, so breathlessness and rapid breathing are usual features. However, PIOPED II found tachypnoea in just over half of proven cases and tachycardia in about a quarter. These features are common in ill patients without embolism, and pleuritic pain or haemoptysis was even commoner once embolism was excluded. Frequency in proven cases measures sensitivity, not predictive value. So no single finding confirms embolism; each only raises suspicion.

Tachypnoea consistently present. Tachypnoea is the commonest sign, but the figure overstates the finding, which was just over half. It measures how often the sign occurs in proven embolism, not how well it predicts embolism. No source gives a predictive value for any single finding.

Outside the textbooks, PIOPED II found tachypnoea in just over half and tachycardia in about a quarter of proven cases. Most patients who collapsed had dyspnoea. Pleuritic pain or haemoptysis was commoner without embolism. A critical-care text calls such findings nonspecific.

Sources: Outside our books: Clinical Characteristics of Patients with Acute Pulmonary Embolism: Data from PIOPED II (2007)Barash 9e

At the end of expiration, alveoli with too little surfactant tend to close. In neonatal respiratory distress syndrome, prematurity causes a surfactant deficit, so the lung loses its resting volume. The result is collapse, stiff lungs, hypoxia and a higher work of breathing. Positive pressure held through expiration props these units open mechanically. This restores end-expiratory lung volume and keeps the recruited alveoli open. Oxygenation and compliance improve as a consequence. The pressure does a job surfactant normally does, but it does not repair the surfactant deficit.

Stimulates the lung to make more surfactant. Respiratory distress syndrome is a surfactant-deficiency disease, so an answer about surfactant feels like it targets the cause. But positive pressure is purely mechanical. It holds collapsing alveoli open in place of the missing surfactant and does nothing to how much surfactant the lung makes or releases.

Steady positive pressure at end-expiration raises functional residual capacity and stops alveoli collapsing, which improves oxygenation. Surfactant normally keeps alveoli distensible and maintains resting lung volume. When it is lacking, alveoli collapse and hypoxia follows. Positive pressure works well when lung volume is reduced.

Sources: Miller 10eBarash 9e

PEEP keeps airway and pleural pressures high through every breath. That pressure is passed to the great veins and right atrium, so less systemic blood is pushed back into the chest. With less blood returning, the ventricles fill less and stroke volume falls, and cardiac output and arterial pressure fall with it. A patient with a low circulating volume has little reserve, so the drop is larger. PEEP may also change pulmonary vascular resistance, but this matters little for cardiac output.

Improves cardiac filling. PEEP raises intrathoracic pressure, which tempts one to expect better cardiac filling. In fact, higher pleural pressure impedes venous return, reducing filling and output, particularly in volume-depleted patients.

The texts agree that the higher airway and pleural pressures from PEEP reduce venous return, cardiac filling and cardiac output, which lowers arterial pressure. Hypovolaemia makes this worse. Any change in pulmonary vascular resistance has little effect on output.

Sources: Miller 10eMayo review

During anaesthesia the dependent parts of both lungs lose air. This makes the lungs smaller and stiffer. The cause is the anaesthetised state itself, not any particular drug or technique, so the incidence does not change with the type of anaesthesia. Barash calls it universal and Miller gives a figure of about 90%. Both mean almost every patient. A plain chest film usually misses these collapsed areas, but CT shows them appearing quickly in the dependent lung.

Rare on radiography. Collapse is rarely seen on routine postoperative chest films, so a low figure feels clinically right. It is wrong because plain radiography cannot show this atelectasis. CT reveals that it affects almost every anaesthetised patient.

CT shows densities forming quickly in the dependent zones of both lungs during anaesthesia, not visible on conventional radiography. Miller puts the incidence at about 90% whatever the anaesthetic; Barash calls it universal with any anaesthetic, attributing lung shrinkage to deaeration.

Sources: Miller 10eBarash 9e

Small airways lack intrinsic rigidity and rely on outward pull from surrounding lung tissue. As ageing lungs lose elastic recoil, more inflation is needed for the same tethering, so closing capacity rises with age, faster than FRC. Once it exceeds resting volume, dependent airways close during normal breathing and those units collapse and shunt. Miller puts the crossover at 45 supine and 65 upright; Faust places the upright point later, but both agree the supine crossover comes first.

Increased FRC prevents closure. FRC does genuinely rise with age, so 'increased FRC' looks like the age-related lung change being tested. But a larger resting volume would hold airways open, not close them; atelectasis arises because closing capacity climbs faster and overtakes FRC.

Closing capacity and FRC both rise with age, but closing capacity rises far more steeply, so airway closure occurs above FRC first when supine and later when upright; below closing capacity dependent small airways collapse, worse in the elderly, causing shunt.

Sources: Miller 10eFaustBarash 9e

Each breath first fills the conducting airways. These carry gas but have no alveolar–capillary interface, so that gas is breathed out unchanged; this is anatomical dead space. Adding alveoli that are ventilated but not perfused gives physiological dead space. In a healthy adult breathing spontaneously, dead space is a third of each tidal volume, so the larger remainder reaches exchanging units. Positive-pressure ventilation enlarges the dead fraction towards a half. Per minute, alveolar ventilation is minute ventilation minus dead-space ventilation.

Whole tidal volume participates. Tidal volume is the whole inhaled breath, so it feels like the gas that exchanges. But the first part of every breath only fills the conducting airways and is exhaled unchanged. Only the portion beyond dead space reaches surfaces where exchange happens.

Alveolar ventilation is the share of ventilation reaching alveoli and respiratory bronchioles that exchanges gas. Physiological dead space is normally one third of tidal volume in spontaneous breathing and up to 0.5 under positive pressure. Anatomical dead space ventilates only conducting airways.

Sources: Miller 10eBarash 9eFaust

Arterial content is oxygen bound to haemoglobin plus a small dissolved fraction. When saturation and PaO2 do not change, the dissolved part stays fixed. Any fall in content therefore means haemoglobin was lost. Remove the dissolved part and divide by constant × saturation to get the haemoglobin now. The fall is the starting value minus that. Books quote different constants: Faust 1.39 mL/g, Barash 1.36 and Miller 1.34. Use the one that reproduces the given starting content (Faust's). The others give nearly the same rounded haemoglobin.

Haemoglobin decreased by five. It is tempting because haemoglobin fell by exactly five. This question asks for the current level: (14.6 minus three quarters) ÷ 1.39 gives about ten g/dL, as do 1.36 and 1.34. Only a question about the drop has five g/dL as its answer.

Faust calculates content as haemoglobin × 1.39 × saturation plus PaO2 × 0.003. The dissolved term matters only with very low bound oxygen or very high PaO2. Barash uses the same equation with 1.36, and Miller uses 1.34.

Sources: FaustBarash 9eMiller 10e

The alveolar gas equation gives alveolar oxygen tension as barometric pressure minus water vapour pressure (47 mmHg), multiplied by FiO2, minus alveolar CO2. On room air this gives about 110 mmHg. Switching to FiO2 1.0 multiplies the first term several times over, lifting alveolar tension into the high hundreds. Healthy lungs keep the alveolar–arterial gap narrow, so arterial tension rises almost as far. The expected arterial value is therefore well above 400 mmHg and higher than the ranges usually offered.

Supplemental oxygen unnecessary. Haemoglobin is almost fully saturated on air, so extra oxygen seems pointless, but this confuses content with tension. Saturation plateaus, while dissolved oxygen and partial pressure keep rising with alveolar tension. A value this low on pure oxygen indicates impaired gas exchange.

Alveolar oxygen tension is (barometric pressure − water vapour) × FiO2 − alveolar CO2. On air, the alveolar–arterial gap is under 10 mmHg. Thoracic teaching treats arterial tension above 400 mmHg on FiO2 1.0 as safe reserve. Above saturation, extra carriage is dissolved oxygen.

Sources: Barash 9eMiller 10eFaust

Oxygen gets from inspired air to the cell only by diffusion, so each step down the cascade must have a lower partial pressure than the step before it. The mitochondrion is the final sink. It keeps using up oxygen for aerobic metabolism, which holds its own tension low. That low tension keeps the gradient that draws oxygen out of capillary blood into the cell. So mitochondrial tension is a small fraction of the arterial value, but in health it stays well above zero.

Lowest value most accurate. People who know mitochondrial tension is very low may choose the smallest number, assuming it is nearest the true floor. However, the source gives the normal range as four to twenty-two mm Hg in a healthy person breathing room air, so a value of one to two is below it.

Miller gives normal arterial oxygen tension as about 100 mm Hg. Inside the mitochondria, where the oxygen is used, it falls to between 4 and 22 mm Hg.

Sources: Miller 10e

When ventilation stops, the body keeps producing CO2 but cannot clear it, so it accumulates. This is pure alveolar hypoventilation, one way anaesthesia disturbs CO2. Barash's respiratory chapter gives about 10 mmHg in the first minute, then 3.5 mmHg per minute; its bronchoscopy section on apnoeic oxygenation gives about 6 mmHg, then 3 mmHg per minute. Both show a rapid first-minute rise followed by a slower, steady climb, so treat the figures as a range. Insufflated oxygen can maintain oxygenation but does not prevent CO2 rising.

Dead space ventilation wasted. People reach for dead space whenever CO2 values change, and it does widen the gap between arterial and end-tidal CO2. But once ventilation has stopped, no breath is being delivered at all, so none can be wasted. CO2 rises because nothing removes it, not because gas is reaching unperfused alveoli.

Barash gives two estimates for the rise during apnoea. One is about 10 mmHg in the first minute, then 3.5 mmHg per minute. The other applies after paralysis and stopping positive-pressure ventilation: about 6 mmHg, then 3 mmHg per minute.

Sources: Barash 9e

Underventilation lets carbon dioxide build up. Once arterial carbon dioxide rises above normal, intraocular pressure rises. Low arterial oxygen also raises it. During intraocular surgery the anaesthetist sets the ventilation, so these two blood gases are levers they control directly. If pressure in the eye climbs, increase ventilation to bring carbon dioxide back down and correct the hypoxaemia. Do not raise carbon dioxide or accept a falling oxygen level, because both push intraocular pressure higher.

Oxygen actively lowers pressure. Hypoxaemia raises intraocular pressure, so it is easy to assume that adding oxygen will actively lower it. The source only says that low oxygen and high carbon dioxide raise the pressure. The lever it names, and the one that moves pressure, is carbon dioxide: high carbon dioxide raises intraocular pressure.

Departures from the physiological range, such as occur with hypoventilation and with arterial hypoxaemia, raise intraocular pressure.

Sources: Mayo review

Low barometric pressure lowers alveolar and then arterial oxygen tension. Peripheral chemoreceptors sense the hypoxaemia and raise minute ventilation within seconds to minutes. The extra breathing washes out carbon dioxide and makes the blood alkaline, which would tend to slow breathing again. Over hours to weeks the kidneys excrete more bicarbonate. This lowers pH again, so ventilation can keep rising. Climbers who acclimatise well show a stronger hypoxic ventilatory response.

Ventilation normalises with acclimatisation. The early alkalosis from hyperventilation looks as if it should switch breathing back off. That makes 'ventilation stays at baseline' sound plausible. It is wrong because the kidneys lose bicarbonate and correct the pH, so ventilation keeps climbing. A persistently raised ventilation is the core of acclimatisation.

Miller calls the hypoxic ventilatory response the most important part of adapting to altitude. Peripheral chemoreceptors quickly increase minute ventilation. The kidneys then excrete more bicarbonate over hours to weeks. This lowers blood pH and probably helps ventilation keep increasing.

Sources: Miller 10e

CO occupies haemoglobin binding sites, reducing oxygen content, and shifts the dissociation curve leftwards, so the remaining bound oxygen is released less readily to tissues. Dissolved oxygen is unaffected, so arterial PaO2 is usually normal. Blood remains bright red, so the patient is not cyanosed. Carotid bodies sense PaO2, not oxygen content or saturation, so provide no respiratory drive. Ventilation rises only when tissue oxygen delivery falls enough to cause anaerobic metabolism, and the resulting lactic acid stimulates breathing.

Oxygen-haemoglobin curve leftshift. The left shift is a real CO effect and appears in every textbook, so it feels like the answer. However, it only reduces tissue oxygen release and stimulates no chemoreceptor. Ventilation rises only once that reduced release causes lactic acidosis, the actual trigger.

CO lowers oxygen content and impairs tissue oxygen release, yet PaO2 is often normal and the patient looks bright red. Carotid bodies sense PaO2, so ventilation rises only when tissue hypoxia causes lactic acidosis, a recognised feature of CO poisoning.

Sources: Mayo reviewMiller 10eBarash 9e

The curve plots minute ventilation against PaCO2. A rightward shift means the respiratory centre waits for a higher PaCO2 before it increases drive; a leftward shift is the reverse. Hydrogen ions from a metabolic acid excite the carotid bodies directly. As the cerebrospinal fluid becomes acidic, they also excite the medullary chemoreceptors. This extra drive raises ventilation at every PaCO2, so the patient hyperventilates down to a lower PaCO2. Opioids and sedatives depress the medulla, which pushes the curve the other way.

Opioids cause leftward shift. Opioids are the classic example of a drug that moves the CO2 response curve. Someone who remembers the shift but not its direction may pick them. In fact they depress medullary drive, so the curve moves right and flattens, causing hypoventilation rather than hyperventilation.

Metabolic acidosis raises ventilation via chemoreceptors: blood acid acts on the carotid bodies, and cerebrospinal fluid acid on the medullary chemoreceptors. A rightward shift means drive rises only at a higher PaCO2. Opioids flatten the curve and shift it rightwards.

Sources: FaustMayo reviewMiller 10e

In zone 2 the alveolar pressure is higher than the pulmonary venous pressure. The capillaries are compressed at their downstream end, so the alveolar pressure becomes the effective back-pressure. This is the 'waterfall' zone. Venous pressure is hidden behind that narrowing, so arterial minus alveolar pressure sets the flow. Arterial pressure still matters. The gap widens lower in the zone, so flow increases. Further down, venous pressure rises above alveolar pressure. That region is zone 3, where arterial minus venous pressure drives flow.

Venous pressure exceeds alveolar. It is easy to remember that venous pressure is involved and get the order backwards. Venous pressure above alveolar pressure defines zone 3, not zone 2. In zone 2 the alveolar pressure is higher than the venous pressure. That is why the vessels narrow and venous pressure stops controlling flow.

Standard anaesthesia texts describe zone 2 as arterial above alveolar above venous pressure. The driving pressure there is the arterial–alveolar difference, which increases down the zone. In zone 3 both arterial and venous pressures exceed alveolar pressure, and flow follows the arterial–venous difference.

Sources: Barash 9eMiller 10eFaust

Alveolar pressure is roughly the same throughout the lung. Vascular pressures rise with depth because of gravity. In the dependent regions, arterial and venous pressures both climb above alveolar pressure, so the vessels stay open along their whole length and alveolar pressure cannot narrow the outflow end. Flow is then set by arterial minus venous pressure. Both rise equally with depth, so this gradient stays the same down the zone. In zone 2, alveolar pressure still sits between arterial and venous pressures, so that zone behaves like a waterfall.

Alveolar pressure between arteries. This is the zone 2 order. It is tempting because arterial pressure does exceed alveolar pressure here. It fails because in zone 3 venous pressure has also risen above alveolar pressure. Alveolar pressure is therefore last, not in the middle, and flow depends on the arterial–venous difference.

Miller and Barash agree that in zone 3, alveolar pressure is lower than both pulmonary arterial and venous pressures. Flow is driven by the arterial–venous difference, which stays constant down the zone. In zone 2, alveolar pressure lies between arterial and venous pressures.

Sources: Barash 9eMiller 10eFaust

Two groups of vessels respond to lung volume in opposite ways. Extra-alveolar vessels stay open because the surrounding lung tissue pulls on their walls. As the lung deflates, that pull is lost, so the vessels' own elastic recoil narrows and kinks them, and resistance rises. Alveolar capillaries are squeezed by stretched alveoli, so they only matter at high volumes. Adding both together gives a U-shaped curve with its lowest point at functional residual capacity. This is why a collapsed lung pushes blood flow away from itself.

Reduced capillary compression lowers vascular resistance. It is tempting because alveolar capillaries are least squeezed when the alveoli are small. Someone thinking only about capillaries would expect resistance to fall. At low volumes, though, the large extra-alveolar vessels lose their support and kink, and that rise outweighs any relief in the capillaries.

Resistance follows a U-shaped, hyperbolic curve against lung volume. It is lowest at functional residual capacity and rises on either side. Below that point, the rise comes mainly from large extra-alveolar vessels kinking and from elastic recoil once their support is lost.

Sources: Miller 10eMayo review

Each lobar bronchus divides into segmental bronchi, named by their position in the lobe. The right middle lobe is a small wedge, so its bronchus splits once, into medial and lateral branches. The upper lobe segments are apical, anterior and posterior. The lower lobe has a superior segment and several basal segments resting on the diaphragm. The left lung has no middle lobe; the lingula of the left upper lobe occupies that territory and divides into superior and inferior parts.

Medial lateral segments are in middle lobe. This option contains the words medial and lateral, so it looks like the middle lobe answer. But these are medial basal and lateral basal segments, which sit with the superior segment in the right lower lobe. The word basal always means lower lobe, never middle lobe.

Right upper: apical, anterior and posterior. Right middle: medial and lateral. Lower: superior, plus basal medial, lateral, anterior and posterior. Lingula (left upper): superior and inferior.

Sources: Barash 9e