Effects of the sudden and sustained increase in LV Afterload

Volume

• Aortic valve closes earlier à, decreased velocity of myocyte fibre shortening à decreased stroke volume, increased left ventricular end-systolic volume
• Increased left ventricular end-systolic volume à venous return added to this volume in the ventricle à increased end diastolic volume à stroke volume therefore gradually returns to baseline with healthy left ventricle

Pressure

• The decreased velocity of myocyte fibre shortening à decreased stroke volume à increased left ventricular end-systolic pressure
• Increased left ventricular end-diastolic volume à increased left ventricular end-diastolic pressure

From: Chapter 31 – Cardiac Pressure–Volume Loops | Anesthesia Key (aneskey.com)

Work

• Myocardial oxygen demand is closely linked to afterload à increased afterload will increase myocardial oxygen demand and consumption
• Myocardial work increases

Coronary perfusion

• Autoregulated and is tightly coupled to myocardial oxygen demand, so it should remain stable acutely
• In the longer term, there is a risk of subendocardial ischaemia due to a hypertrophied left ventricle

Reflexes

• Baroreceptor: only if increased afterload is associated with an increase in arterial pressure à, stretch on carotid baroreceptors à increased firing of afferent nerves through carotid sinus and glossopharyngeal nerves to the medulla à, decreased sympathetic activity, and increased parasympathetic activity à decreased systemic vascular resistance, contractility and heart rate

Heart rate

• May increase if stroke volume remains low and results in decreased cardiac output and decreased BP (decreased BP detected by baroreceptors
• May decrease if increased afterload is associated with increased arterial pressure

Cardiac output

• Likely to remain the same with a healthy left ventricle
  • Increased afterload à increased end-diastolic volume (preload) à activates Frank-Starling mechanism, which increases contractility à compensates for the reduction in stroke volume from the increased afterload
  • Anrep effect:
    • The sudden increase in afterload causes an increased ventricular inotropy à initial increase in inotropy is via the Frank-Starling mechanism; if this is maintained for approximately 10 minutes, the contraction force increases more **thought to be secondary to increased calcium due to the activation of channels or reverse Na/Ca exchange**

Sustained effects:

• Sustained increase in afterload à, activation of genes in the ventricular muscle and then those involved in growth à left ventricle concentric hypertrophy à increased wall thickness and decreased chamber diameter à, reduces internal wall stress but decreases ventricular compliance à, can eventually lead to diastolic dysfunction, impaired myocardial blood flow during stress, and increased left atrial pressure.