Pathophysiology of Acute Pulmonary Embolism

Part 1: Gas Exchange Abnormalities (Why patients feel breathless and have low O2)

• V = ventilation (air going in), Q = perfusion (blood flowing through)
• When a clot blocks blood flow, you get areas that are ventilated but not perfused - this is wasted ventilation called alveolar dead space
• Other areas get overperfused relative to ventilation - blood rushes through without picking up enough oxygen
• Result: low oxygen in the blood (hypoxemia)

• Because cardiac output drops (see Part 2), the tissues extract more oxygen from each unit of blood
• This means the blood returning to the lungs is already very oxygen-poor
• Any imperfect gas exchange is then magnified because you're starting from a lower baseline

• Loss of surfactant and alveolar hemorrhage cause atelectasis (lung collapse) in affected areas
• Bronchoconstriction occurs in areas of low CO2 (hypocarbia), routing even more blood through poorly ventilated zones
• Some blood passes through without picking up any oxygen at all

• Patients actually hyperventilate due to anxiety and reflex stimulation, blowing off CO2
• This causes hypocarbia (low CO2) - which paradoxically triggers bronchoconstriction in affected lung zones, worsening the shunt

• Hypoxemia triggers increased sympathetic tone
• This causes vasoconstriction and can actually increase venous return and boost stroke volume - so early on, if the heart is healthy, the body partly compensates

Part 2: Hemodynamic Alterations (What happens to the heart)

1. How much of the pulmonary vascular bed is blocked
2. Whether the patient has pre-existing heart/lung disease
3. The effects of hypoxia and neurohormonal signals on the pulmonary vasculature

Stage 1: < 20% obstruction - Compensated, no pressure rise

• The lung vasculature is like a sponge - it has reserve vessels that can open up (recruitment) and existing vessels can dilate (distension)
• Pulmonary artery pressure stays normal
• The RV maintains output by slightly increasing heart rate and stroke volume
• Patient may have minimal symptoms

Stage 2: 30-40% obstruction - Pressure starts rising

• Compensatory reserve is being used up
• Pulmonary artery pressure begins to climb
• Right atrial pressure rises slightly
• The Frank-Starling mechanism kicks in: the RV stretches more with each beat to maintain output (like stretching a rubber band harder to push more blood)

Stage 3: > 50-60% obstruction - Decompensation

• Compensatory mechanisms are overwhelmed
• Cardiac output starts to fall
• Right atrial pressure rises dramatically
• The RV dilates, wall tension increases
• RV ischemia can develop - the dilated RV needs more oxygen but gets less because coronary perfusion is reduced when systemic pressure drops
• Systemic hypotension follows

The 40 mmHg ceiling

The curve is hyperbolic - not linear

• At the low end, small increases in obstruction have little effect (reserves absorb it)
• At the high end, small additional increases cause a precipitous, cliff-like drop in cardiac output

Patients with pre-existing lung/heart disease

• Their pulmonary reserve is already depleted
• A small clot can cause severe pulmonary hypertension out of proportion to the size of the embolism
• RV hypertrophy (not just dilatation) may already be present, which is a clue the hypertension is not purely acute

Putting It All Together