What causes right ventricular (RV) ischemia in patients with pulmonary thromboembolism (PTE)?

Mechanisms of Right Ventricular Ischemia in Pulmonary Thromboembolism

Right ventricular (RV) ischemia in pulmonary thromboembolism (PTE) primarily results from an imbalance between oxygen supply and demand, with systemic hypotension being a critical element that impairs coronary driving pressure to the already overloaded right ventricle. 1

Pathophysiological Cascade Leading to RV Ischemia

Initial Hemodynamic Changes

• Acute pulmonary artery obstruction (>30-50% of cross-sectional area) causes abrupt increase in pulmonary vascular resistance (PVR) 1, 2
• This sudden increase in RV afterload results in:
  • RV dilation and increased wall tension
  • Prolonged RV contraction time
  • Increased myocyte stretch 1

Oxygen Supply-Demand Mismatch

1. Increased Oxygen Demand

   • RV workload dramatically increases due to higher afterload
   • Neurohumoral activation causes inotropic and chronotropic stimulation, further increasing oxygen requirements 1
   • RV wall tension rises, which directly increases myocardial oxygen consumption 1

2. Decreased Oxygen Supply

   • Systemic hypotension reduces coronary perfusion pressure to the RV 1
   • Unlike the left ventricle, RV coronary perfusion occurs during both systole and diastole
   • When RV pressure rises acutely, the pressure gradient driving coronary blood flow diminishes 1
   • Elevated RV end-diastolic pressure further compresses subendocardial vessels 1

Ventricular Interdependence Effects

• RV dilation causes leftward bowing of the interventricular septum
• This leads to:
  • Impaired LV filling in early diastole
  • Reduced cardiac output
  • Further systemic hypotension, creating a vicious cycle 1, 2
• Ventricular desynchronization (often with right bundle branch block) exacerbates these effects 1

Evidence of RV Ischemia in PTE

• Elevated biomarkers of myocardial injury correlate with adverse outcomes 1
• Although frank RV infarction is uncommon in PTE, cardiomyocyte damage from ischemia is well-documented 1
• Autopsy findings in fatal PTE cases have shown RV infarction despite normal coronary arteries 1
• Creatine kinase MB isoenzyme elevations confirm RV ischemic injury 1

Key Distinctions from Other Forms of RV Failure

• Unlike chronic pulmonary hypertension where RV has time to adapt through hypertrophy, acute PTE causes immediate RV deformation 3
• The acute nature of PTE triggers an inflammatory response with cytokine and chemokine release that may further amplify injury 3
• RV in PTE experiences mechanical stretch, shear force, and ischemia simultaneously 3

Clinical Implications

• RV ischemia is a critical determinant of mortality in acute PTE 1, 4
• Systemic hypotension should be promptly addressed to improve coronary perfusion to the RV 1
• Caution with fluid loading is warranted as excessive volume may worsen RV distension and further impair function 1
• Inotropic support may be necessary to maintain cardiac output and coronary perfusion 4

Monitoring Considerations

• Echocardiography can assess RV strain and monitor recovery after treatment 5
• Signs of RV dysfunction include RV dilation, wall motion abnormalities, and interventricular septal flattening 2
• Serial echocardiographic assessment helps track RV function recovery 2

RV ischemia in PTE represents a critical pathophysiological mechanism that contributes significantly to morbidity and mortality. Understanding this process is essential for appropriate management strategies that focus on improving the balance between myocardial oxygen supply and demand.