"Critical Care & Ventilator Management" — Practice

Question 1

Target tidal volume in acute respiratory distress syndrome is approximately

Accepted Answer

A

Question 2

Injury caused by repeated opening and collapse of alveoli with each breath is

Accepted Answer

C

Question 3

A 70 kg man of 170 cm with ARDS is ventilated with a tidal volume of 700 mL. What is wrong and what should it be?

Accepted Answer

The tidal volume is roughly double what it should be, and it appears to have been calculated from measured rather than predicted weight.

Low tidal volume ventilation at around 6 mL per kilogram of predicted body weight reduces mortality, and predicted body weight is derived from height because lung volume correlates with height rather than mass.

For a man of 170 cm, predicted body weight is around 66 kg, giving a target of roughly 400 mL rather than 700 mL.

The reason it matters is the baby lung concept. The lung is not uniformly affected, so consolidated dependent regions receive nothing while the small aerated fraction receives the whole tidal volume, which overdistends it and produces volutrauma and biotrauma.

Plateau pressure should be measured on an inspiratory hold and kept below about 30 cm of water, with resulting hypercapnia accepted as the price of protection.

Question 4

A severe asthmatic tachypnoeic for two hours has a carbon dioxide that has risen from 28 to 42 and is now quieter. Interpret.

Accepted Answer

This is deterioration, not improvement, and it is one of the most dangerous misreadings in emergency practice.

A patient with acute severe asthma hyperventilates, so the expected carbon dioxide is low. A normal value means alveolar ventilation has fallen to a level that only just matches a production already raised by the work of breathing, and a rising value means it is now inadequate.

Becoming quieter reflects reduced air movement rather than reduced bronchospasm, which is the same reasoning behind the silent chest, and exhaustion follows a period of maximal effort.

This patient requires urgent senior help, preparation for intubation, continued maximal bronchodilator therapy, magnesium and steroid, and intensive care involvement.

If ventilated, the strategy is deliberately unconventional: a low rate with prolonged expiratory time to allow complete exhalation, accepting hypercapnia, because dynamic hyperinflation and breath stacking cause circulatory collapse.

Question 5

A ventilated patient becomes suddenly hypotensive with high airway pressures and reduced breath sounds on one side. Diagnose and act.

Accepted Answer

Tension pneumothorax, diagnosed clinically without waiting for imaging.

Positive pressure ventilation drives air through a breach in the visceral pleura with each breath and prevents its escape, so intrapleural pressure rises progressively. That collapses the lung, shifts the mediastinum, kinks the great veins and obstructs venous return, producing hypotension.

The combination of high airway pressures, unilateral reduced breath sounds and hypotension in a ventilated patient is the pattern, and tracheal deviation is a late sign.

Immediate action is decompression followed by intercostal drain insertion. Waiting for a chest radiograph in a hypotensive ventilated patient is a recognised cause of avoidable death.

The wider differential for sudden deterioration in a ventilated patient is worth holding as a list: displaced tube, obstructed tube, pneumothorax and equipment failure.

Question 6

A patient repeatedly fails spontaneous breathing trials despite resolved pneumonia and normal gases on support. What should be considered?

Accepted Answer

Several causes beyond the lungs, and the most commonly missed is cardiac.

Positive pressure ventilation reduces venous return and reduces left ventricular afterload by lowering transmural pressure. Removing it reverses both effects simultaneously, increasing preload and afterload, which can precipitate pulmonary oedema in a patient with limited cardiac reserve. Weaning-induced cardiac failure therefore presents as respiratory failure, and echocardiography during a trial can demonstrate it.

Oversedation is next, and paired daily sedation interruption with spontaneous breathing trials is the intervention that addresses it.

Diaphragmatic weakness develops within days of controlled ventilation and is compounded by critical illness neuromyopathy, malnutrition and electrolyte disturbance including low phosphate and magnesium.

Other contributors include delirium, pain, an unnecessarily narrow tube increasing resistance, and untreated intra-abdominal pressure or pleural effusion increasing the load.

Question 7

Why is permissive hypercapnia accepted in ARDS when raised carbon dioxide causes acidosis?

Accepted Answer

Because the alternative causes more harm than the acidosis does.

Delivering enough tidal volume to normalise carbon dioxide in this syndrome requires volumes that overdistend the small aerated fraction of lung, since consolidated regions accept no ventilation. That overdistension produces volutrauma and triggers biotrauma, a systemic inflammatory response contributing to multi-organ failure and death.

The trial evidence is unambiguous: low tidal volume ventilation at around 6 mL per kilogram of predicted body weight reduces mortality compared with conventional volumes, despite higher carbon dioxide levels and lower pH.

Moderate hypercapnia is generally well tolerated. It causes vasodilatation, increased cerebral blood flow and sympathetic stimulation, and the acidosis is buffered over hours by renal bicarbonate retention.

The strategy is limited rather than unlimited. It is avoided or used cautiously with raised intracranial pressure, severe pulmonary hypertension or severe metabolic acidosis, and extremes of acidosis are corrected.

Question 8

A septic patient remains hypotensive after 4 litres of crystalloid. A further bolus is proposed. Comment.

Accepted Answer

Further fluid should not be given reflexively, and responsiveness should be assessed before committing.

Roughly half of haemodynamically unstable patients are not fluid responsive, meaning additional volume will not increase stroke volume. In those patients the fluid simply increases interstitial oedema, worsening oxygenation, gut function, renal function and wound healing, and cumulative positive balance is independently associated with worse outcome.

Assessment is straightforward. A passive leg raise autotransfuses roughly 300 mL reversibly and its effect on stroke volume predicts the response to a bolus, and in a fully ventilated patient stroke volume or pulse pressure variation across the respiratory cycle carries similar information.

If the patient is not responsive, the answer is vasopressor rather than volume, with noradrenaline as first-line in septic shock.

Two further considerations apply. The source must be controlled, since no amount of fluid or antibiotic compensates for an undrained collection. And balanced crystalloid is preferred over normal saline, which produces hyperchloraemic acidosis at this volume.

Question 9

A ventilated patient becomes agitated on day three and the nurse asks for a sedation increase. How would you approach this?

Accepted Answer

Agitation is a symptom to be explained rather than suppressed, and increasing sedation without assessment treats none of the likely causes.

The first pass looks for reversible physical causes: hypoxia, hypercapnia, hypoglycaemia, pain, a blocked or displaced tube, a distended bladder, and ventilator dyssynchrony where the machine and patient are working against each other.

Analgesia is addressed before sedation, since inadequately treated pain is a common driver and treating it reduces sedative requirement substantially.

Delirium is then screened for using a validated intensive care tool. It affects a large proportion of ventilated patients, is independently associated with mortality and long-term cognitive impairment, and its hypoactive form is commoner and routinely missed.

Management is non-pharmacological first: early mobilisation, sleep hygiene, orientation, restoring glasses and hearing aids, family presence, and removing deliriogenic drugs, particularly benzodiazepines and anticholinergics.

Deep sedation itself prolongs ventilation and increases delirium and mortality, so the aim is the lightest level compatible with safety.

Practice — "Critical Care & Ventilator Management"

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