Changes Due to Mechanical Ventilation

A. Cardiovascular Changes

1. Decreased Venous Return (Preload Reduction)

• Positive pressure during inspiration raises intrathoracic pressure, compressing the great veins and right atrium
• Venous return from the systemic circulation falls
• Right ventricular (RV) filling decreases -> RV stroke volume falls
• Left ventricular (LV) preload consequently falls after 1-2 beats (pulmonary transit time)
• Net result: Cardiac output (CO) falls

2. Increased Pulmonary Vascular Resistance (PVR)

• Lung inflation compresses alveolar capillaries
• PVR rises, increasing RV afterload
• Can cause acute RV strain or failure, especially at high PEEP

3. Hypotension

• Reduced CO + decreased left ventricle-to-aorta pressure gradient -> systemic hypotension
• Particularly dangerous in hypovolemic patients or those with vasodilatory states (e.g., sepsis, spinal anesthesia)
• Can occur immediately after initiation of MV

4. LV Afterload Effects (Unique Benefit)

• Increased intrathoracic pressure paradoxically reduces LV afterload (transmural pressure falls)
• This can actually benefit patients with LV failure - MV can improve CO in cardiogenic pulmonary edema by unloading the failing LV

5. Pulse Pressure Variation (PPV) and Stroke Volume Variation (SVV)

• These cyclic respiratory-induced changes in arterial waveform are exaggerated in hypovolemia
• PPV >13% during controlled MV predicts fluid responsiveness
• Used as a dynamic measure to guide fluid resuscitation

Viva Point: "Why can initiating MV cause cardiovascular collapse?" Answer: PPV reduces venous return and CO; if the patient is already hypovolemic or vasodilated (e.g., sepsis), this reduction unmasks haemodynamic instability. Always pre-load the patient before intubation if possible.

B. Pulmonary Changes / Ventilator-Induced Lung Injury (VILI)

1. Barotrauma

• Definition: Injury from excessive airway pressure (high peak inspiratory pressure [PIP] or plateau pressure)
• Manifestations: Pneumothorax, pneumomediastinum, subcutaneous emphysema, pneumopericardium
• Key threshold: Plateau pressure >30 cmH₂O significantly increases risk
• Volume-limited ventilation (vs. pressure-limited) is associated with decreased barotrauma incidence

2. Volutrauma

• Definition: Injury from excessive tidal volume causing alveolar overdistension
• More closely linked to VILI than barotrauma alone
• ARDSNet trial showed 6 mL/kg predicted body weight (PBW) tidal volumes reduced mortality vs. 12 mL/kg PBW

3. Atelectrauma

• Definition: Injury from repeated opening and closing (recruitment-derecruitment) of unstable alveoli with each breath cycle
• Creates shear stress at the interface of open and collapsed lung units
• PEEP is the primary strategy to prevent atelectrauma by keeping alveoli open at end-expiration
• The safe "window" lies between the lower inflection point (above which alveoli stay open) and the upper inflection point (above which overdistension begins) on the pressure-volume curve

4. Biotrauma

• Cyclic stretching of lung parenchyma releases pro-inflammatory cytokines: IL-1, IL-6, IL-8, TNF-alpha, MIP-2
• Activates phospholipase A2 -> degrades surfactant
• Causes neutrophil accumulation in lung -> pulmonary edema, hyaline membrane formation, cellular infiltration
• Can lead to systemic inflammatory response (SIRS) and multiorgan failure
• Volatile anaesthetics (sevoflurane, isoflurane) attenuate VILI partly via anti-inflammatory effects

5. Oxygen Toxicity

• FiO2 >0.5-0.6 sustained over time -> reactive oxygen species (ROS) generation
• Causes alveolar injury indistinguishable from ARDS
• Also causes absorptive atelectasis: high FiO2 washes out nitrogen that normally acts as a "splint" for alveoli

Viva Point: "Name the 4 mechanisms of VILI." Answer: Barotrauma (pressure), Volutrauma (volume), Atelectrauma (shear from cycling), Biotrauma (cytokine release). Collectively these are avoided by lung-protective ventilation: tidal volume 6 mL/kg PBW, plateau pressure <30 cmH₂O, adequate PEEP.

C. Ventilator-Induced Diaphragm Dysfunction (VIDD)

Mechanism:

• Controlled MV suppresses diaphragm activity completely
• Within 12 hours of initiating controlled MV, diaphragm atrophy commences
• Reduced diaphragm activity -> reactive oxygen species (ROS) production -> mitochondrial dysfunction
• ROS activates proteolytic pathways: calcium-dependent enzymes, ubiquitin-proteasome pathway, autophagy
• Proteolysis exceeds protein synthesis -> progressive myofibrillar atrophy and disarray
• Diaphragm-specific atrophy (peripheral skeletal muscle is relatively spared in the early phase)

Clinical consequences:

• ~50% of patients develop at least 10% diaphragm atrophy within the first few days of MV
• These patients are at much higher risk of: prolonged MV, reintubation, tracheostomy, and ICU morbidity
• Creates a vicious cycle: acute respiratory failure -> MV -> VIDD -> diaphragm weakness -> prolonged ventilator dependence

Prevention:

• Maintaining some spontaneous respiratory effort (even partial) preserves diaphragm structure
• SIMV, pressure support modes preserve drive better than pure CMV/controlled modes
• Too much pressure support also causes atrophy - optimal level uncertain but must exceed a minimum activity threshold

Viva Point: "When does VIDD begin?" Answer: Within 12 hours of initiating controlled mechanical ventilation. This is why early spontaneous breathing trials and minimising over-sedation are emphasised in modern ICU care.

D. Renal Changes

Viva Point: "How does PEEP affect the kidneys?" Answer: PEEP reduces cardiac output and venous return, activates the RAAS and sympathetic nervous system, increases ADH, reduces ANP - resulting in oliguria, sodium retention, and reduced GFR. The extent depends on mean airway pressure.

E. Haemodynamic Monitoring Changes

• PEEP elevates measured central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) artifactually - these readings must be corrected for intrathoracic pressure
• Pulse pressure variation (PPV) and stroke volume variation (SVV) are reliable dynamic preload indices only during controlled MV with regular tidal volumes
• During PPV, measurement of plateau pressure (a surrogate of transpulmonary pressure) is critical to guide lung-protective strategy

F. Other Systemic Changes

Intracranial Pressure (ICP)

• Positive pressure MV impedes cerebral venous drainage (raises jugular venous pressure)
• Can raise ICP, especially at high PEEP
• In head injury patients, brief hyperventilation (PaCO2 30-35 mmHg) remains a temporising measure to reduce ICP by cerebral vasoconstriction - but chronic hyperventilation is harmful

Gastrointestinal and Hepatic

• Reduced CO and splanchnic vasoconstriction impair gut perfusion
• Increased risk of stress ulcers -> stress ulcer prophylaxis is standard in ventilated ICU patients
• Hepatic venous congestion from raised right heart pressures

Ventilator-Associated Pneumonia (VAP)

• Defined as pneumonia developing >48 hours after intubation
• ETT bypasses upper airway defences; pooled secretions above cuff aspirate into lower airways
• Common organisms: Pseudomonas aeruginosa, Klebsiella, MRSA (late onset)
• Prevention bundle: head-of-bed elevation 30-45°, daily sedation holds, oral chlorhexidine, subglottic suctioning, early extubation

Summary Table - Exam Quick Reference

High-Yield Viva Points (Master List)

1. Why does MV reduce cardiac output? PPV raises intrathoracic pressure -> compresses venae cavae -> reduces venous return -> reduces RV preload -> reduces CO (Frank-Starling). Also raises PVR, increasing RV afterload.
2. When is reduced CO from MV actually beneficial? In acute LV failure/cardiogenic pulmonary oedema - raised intrathoracic pressure unloads the LV (reduces afterload) and helps reverse the failure.
3. Define the 4 types of VILI: Barotrauma (pressure), Volutrauma (volume/overdistension), Atelectrauma (shear from cycling), Biotrauma (cytokine/inflammatory mediator release).
4. Target settings for lung-protective ventilation: Tidal volume 6 mL/kg PBW, plateau pressure ≤30 cmH₂O, titrated PEEP, permissive hypercapnia acceptable (pH >7.2).
5. When does VIDD begin? Within 12 hours. ~50% of patients lose >10% diaphragm mass in the first few days. Mechanism: disuse -> ROS -> ubiquitin-proteasome and autophagic proteolysis.
6. How does MV affect the kidneys? Via three routes: hemodynamic (↓CO -> ↓RBF), neurohumoral (RAAS, sympathetic, ADH), and direct venous congestion (↑renal venous pressure -> ↑Na reabsorption). Result: oliguria, Na retention, risk of AKI.
7. What is atelectrauma? Shear injury from repeated opening and closing of unstable alveoli with each breath - prevented by adequate PEEP above the lower inflection point of the P-V curve.
8. Define biotrauma: Release of cytokines (IL-1, IL-6, TNF-alpha) from mechanically stressed lung tissue causing systemic inflammation that can drive multi-organ failure.
9. What is VAP? How prevented? Pneumonia >48h post-intubation. Prevention: semi-recumbent positioning (30-45°), daily sedation breaks, subglottic suctioning, early weaning.
10. PPV effect on CVP/PCWP measurements: Both are artifactually elevated by positive intrathoracic pressure - must interpret with caution; end-expiratory values are most accurate.

How Does Increased Intrathoracic Pressure Reduce LV Afterload?

The Core Concept: Transmural Pressure

Transmural pressure = Intracavitary pressure - Surrounding (intrathoracic/pericardial) pressure

Step-by-Step Physiology

During Spontaneous Breathing (normal)

• Intrathoracic pressure is negative (e.g., -5 cmH₂O at rest, -20 to -30 during distress)
• LV sits inside this negative pressure environment
• To eject blood into the aorta (which is outside the thorax at atmospheric pressure), the LV must generate pressure from, say, -5 to +120 mmHg
• Transmural pressure the LV must overcome = Aortic pressure - Intrathoracic pressure = 120 - (-5) = 125 mmHg equivalent
• The more negative the intrathoracic pressure (e.g., laboured breathing in cardiogenic pulmonary oedema), the greater this gradient the LV must overcome

During Positive Pressure Ventilation

• Intrathoracic pressure becomes positive (e.g., +10 cmH₂O)
• The positive pressure transmits through the pleura into the pericardium, surrounding the LV
• The LV cavity pressure and the aortic pressure both see a rise in their surrounding reference pressure
• Transmural pressure = Aortic pressure - Intrathoracic pressure = 120 - (+10) = 110 mmHg
• The LV now has to generate less net wall tension to eject the same stroke volume
• This is the afterload reduction

Analogy to Understand It

• Normally you squeeze against atmospheric pressure outside
• If the chamber is already pressurised, you need less effort to squeeze the same amount of paste out, because the external pressure is already "helping" push from outside

The Reverse is Also True (and Clinically Critical)

• The patient makes huge inspiratory effort against obstruction
• Intrathoracic pressure swings to -30 or -40 mmHg
• Transmural LV pressure rises dramatically: 120 - (-40) = 160 mmHg
• The failing LV must work much harder against this increased effective afterload
• This further impairs ejection, worsens pulmonary oedema, creating a vicious cycle

Summary Diagram (Conceptual)

SPONTANEOUS BREATHING (especially with distress):
  Intrathoracic pressure = -20 mmHg
  Aortic pressure        = +120 mmHg
  LV transmural pressure = 120 - (-20) = 140 mmHg  ← HIGH afterload

POSITIVE PRESSURE VENTILATION:
  Intrathoracic pressure = +10 mmHg
  Aortic pressure        = +120 mmHg
  LV transmural pressure = 120 - (+10) = 110 mmHg  ← LOWER afterload

Clinical Implications (Viva-Ready)

Viva Point: In patients with severe LV failure, removing positive pressure ventilation during weaning suddenly increases LV afterload. This is a recognised cause of weaning failure - the patient tolerates MV but decompensates when extubated. - Murray & Nadel's Textbook of Respiratory Medicine

Viva Point: The aorta exits the thorax. The LV sits inside the thorax. When intrathoracic pressure rises, the LV's surrounding pressure rises, but the aortic root's downstream (extrathoracic) pressure remains at atmospheric. The gradient the LV must overcome to eject blood decreases. This is the mechanism.