Physiological Changes During Artificial (Mechanical) Ventilation

1. Reversal of Normal Respiratory Mechanics

2. Cardiovascular Effects

↑ Mean Intrathoracic Pressure

• The rise in intrathoracic pressure impedes venous return by diminishing the pressure gradient from peripheral capillaries to the right atrium.
• Preload falls → cardiac output (CO) decreases → blood pressure falls.
• Hypotension can occur immediately after initiating PPV, especially in hypovolaemic or vasodilated patients.

↓ Left Ventricular Afterload

• The same increased intrathoracic pressure that reduces venous return also reduces LV afterload by assisting ejection against atmospheric pressure.
• This is therapeutically beneficial in left heart failure — it improves LV function and may paradoxically improve cardiac output in these patients. Removal of PPV (weaning) can worsen LV function and precipitate weaning failure in this group.

PEEP-Related Effects

• PEEP (positive end-expiratory pressure) further raises mean intrathoracic pressure, exaggerating compromised venous return and CO, especially in states of low lung compliance (airway disease, obesity, ascites).

Catecholamine Release

• Dyspnoea, anxiety, and inadequate ventilatory support cause stress-induced catecholamine release, increasing myocardial oxygen demand and risk of dysrhythmias.

3. Pulmonary/Respiratory Effects

Ventilation–Perfusion (V/Q) Mismatch

• Spontaneous breathing preferentially ventilates dependent lung zones (which are also best perfused), optimising V/Q matching.
• PPV preferentially ventilates upper, non-dependent lung regions (which are more compliant), while blood flow remains gravity-dependent — worsening V/Q mismatch.
• As alveolar pressure rises, zone 1 (dead space) regions appear where alveolar pressure exceeds pulmonary artery pressure, increasing physiological dead space.

Change in Functional Residual Capacity (FRC)

• General anaesthesia with PPV causes reduced FRC, increased closing volume, and resultant atelectasis, particularly in dependent lung zones.
• PEEP counteracts this by maintaining alveoli open at end-expiration, increasing FRC, reducing intrapulmonary shunting, and improving oxygenation and compliance.

Barotrauma and Volutrauma

• Excessive airway pressures cause alveolar rupture (barotrauma), manifesting as pneumothorax, pneumomediastinum, pneumopericardium, or subcutaneous emphysema.
• Overdistension from large tidal volumes causes volutrauma (ventilator-induced lung injury, VILI).

Auto-PEEP / Air Trapping

• In obstructive lung disease (asthma, COPD), expiratory flow limitation causes air trapping and intrinsic PEEP (iPEEP), further raising intrathoracic pressure, increasing barotrauma risk, and causing cardiovascular depression.

Respiratory Alkalosis

• If minute ventilation is excessive, CO₂ is over-eliminated, resulting in hypocapnia and respiratory alkalosis.

4. Renal Effects

• Reduced cardiac output and increased intrathoracic pressure decrease renal blood flow and glomerular filtration rate (GFR).
• This promotes sodium and water retention — partly mediated by activation of the renin–angiotensin–aldosterone system and increased ADH secretion (impaired atrial stretch receptor signalling).
• Result: oliguria and fluid retention, especially with high PEEP.

5. Neurological Effects

• ↑ Intrathoracic pressure → ↑ Central venous pressure (CVP) → impaired cerebral venous drainage → ↑ Intracranial pressure (ICP).
• This is particularly relevant in patients with head injuries, where high airway pressures or excessive PEEP may worsen cerebral oedema.

6. Hepatic/Splanchnic Effects

• Reduced cardiac output decreases splanchnic and hepatic blood flow.
• This can impair hepatic function, reduce drug metabolism, and predispose to gut mucosal ischaemia — contributing to translocation of bacteria and systemic inflammation.

7. Hormonal/Endocrine Effects

• Reduced ANP (atrial natriuretic peptide) release due to decreased atrial stretch.
• ↑ ADH (vasopressin) secretion contributes to fluid retention.
• Catecholamine release from the adrenal medulla due to stress.

8. Lung Injury (VILI / VALI)

• Microscopic lung injury from repeated cyclic alveolar opening and closing (atelectotrauma) and overdistension (volutrauma) causes diffuse alveolar damage, increased microvascular permeability, and systemic inflammatory mediator release — potentially contributing to multi-organ dysfunction.
• Historical tidal volumes of 10–15 mL/kg are now known to cause excess mortality; lung-protective ventilation (6 mL/kg ideal body weight) reduces ARDS mortality.

Summary Table