Cardiac output

Written by

in

 

Cardiac Output Variables: Mechanism & Hemodynamics

 

Variable Mechanism & Formula Factors Affecting
Stroke Volume (SV) SV = EDV – ESV
Affected by Contractility, Afterload, and Preload. The failing heart has ↓ SV.		 ↑ SV with: ↑ Contractility, ↑ Preload, ↓ and Afterload.
Stroke Work (SW) SW = SV × MAP
Work done by the ventricle to eject SV.		 Directly dependent on SV and Mean Arterial Pressure.
Contractility Ca²⁺-dependent
Via \beta_1 (cAMP/PKA pathway) or Digoxin (Na+/K+ pump block → ↑ intracellular Ca²⁺).		 ↑ with: Catecholamines, Digoxin.
↓ with: \beta_1-blockers, HF, Acidosis, Hypoxia, Non-DHP CCBs.
Preload Approximated by EDV
Dependent on venous return and blood volume.		 ↑ with: Volume loading.
↓ with: Venous vasodilators (e.g., Nitroglycerin).
Afterload Approximated by MAP
↑ Pressure → ↑ wall tension (Laplace’s Law).		 ↑ with: Hypertension.
↓ with: Arterial vasodilators (Hydralazine), ACEi, ARBs.
Cardiac O₂ Demand Wall stress = (P × r) / (2 × thickness)
O₂ consumption is proportional to work.		 ↑ with: ↑ Contractility, ↑ Afterload, ↑ HR, ↑ Ventricular diameter.

NEET PG Hint: Remember:

  • ACE inhibitors and ARBs are preferred because they reduce *both* preload and afterload.
  • Always relate myocardial O2 demand to Laplace’s Law; ventricular hypertrophy is a compensatory mechanism to normalize wall stress (T = P \times r / 2h) by increasing wall thickness (h) in the setting of chronic high afterload. For more high-yield cardiovascular protocols and free medical questions, visit mymedschool.org.