Cardiac Output — Afterload Increase

Afterload

• Load against which the muscle exerts its contractile force (Guyton)
• It is represented by the gradient of the line connecting the end-diastolic volume, to the end-systolic point
• pressure which the ventricle has to contract against (Power & Kam)

Determinants of Afterload

Modified Laplace Equation

• where
  • T represents afterload
  • P represents aortic pressure
    • Therefore, afterload increases as aortic (or pulmonary arterial) pressure increases
  • R represents ventricular radius
    • Afterload increases as ventricular radius increases
  • H represents ventricular thickness
    • Afterload decreases as the thickness of the ventricular wall increases (hypertrophy secondary to chronic hypertension and cardiac remodelling)

Modified Hagen-Poiseuille Equation

• Afterload is affected by resistance to cardiac output
  • Afterload increased by reduced radius of systemic vasculature
  • Afterload increased by increasing viscosity of blood

Resistance in parallel

• Afterload is affected by addition, or loss of large capillary networks in parallel
  • Systemic vascular resistance is increased significantly by loss of placenta, with parallel vascular networks
  • Pulmonary vascular resistance is decreased significantly by inflation of lung, causing creation of vast capillary network in parallel

Cardiovascular Effects of a sudden increase in afterload

Effects of sudden increase in afterload can be demonstrated using a Left ventricular PV loop:

• End-Systolic Volume is increased, causing a reduction in stroke volume

• Initially, Left atrial pressure decreases
• Increased End systolic volume leads to secondary increase in end diastolic volume, hence increasing ventricular filling
• This secondary increase in preload enables the ventricle to contract with greater force (Frank-Starling mechanism) which partially offsets the reduction in stroke volume
• In patients with impaired left ventricular function, the decreased in stroke volume cannot be compensated

• ventricular end-systolic pressure: increases
• ventricular end-diastolic pressure: increases

• cardiac output (=HRxSV) – remains the same
  • Initial drop in SV is compensated by increased pre-load
  • In a failing heart, the drop in SV causes subsequent stimulation of baroceptors, which in turn causes increased heart rate and can potentially return cardiac output to normal
• Increase in afterload → Anrep → Small ↑Contractility to compensate
  • Mechanism: ↑AL → sustained ↑stretch (prolonged isovolumetric contration) → ↑ Ca induced Ca release → ↑ contractility
  • Purpose: ↑AL → ↓SV and ↑ ESV
• myocardial oxygen demand and myocardial work: Increased Afterload will increase the pressure during contraction, hence increasing MVO2 for internal work. This might be partially offset by the reduction in external work (due to decreased stroke volume) depending on the cause of the increased afterload

• coronary blood flow is autoregulated to remain normal

JC 2019

Answer by JC