Physiology of Myocardial Performance — Anaesthesia MD Exam Answer

Introduction

1. Preload

• First described by Otto Frank (1895): tension change in muscle relates directly to fibre length.
• Clinically, preload is estimated using surrogates such as central venous pressure (CVP) or pulmonary capillary wedge pressure (PCWP), though these are volume surrogates and can be inaccurate (affected by compliance, intrathoracic pressure, PEEP). More direct assessment uses echocardiographic ventricular volumes.
• Determinants of preload: venous return, total blood volume, venous tone, intrathoracic/intrapericardial pressure, atrial contraction, and ventricular compliance.

2. Afterload

• By Laplace's law: wall stress (σ) = (Pressure × Radius) / (2 × wall thickness). A dilated, thin-walled ventricle generates more wall stress for a given pressure; compensatory hypertrophy (e.g., in aortic stenosis) reduces wall stress by increasing wall thickness.
• Clinically, systemic vascular resistance (SVR) is used as a surrogate for LV afterload: SVR = 80 × (MAP − CVP) / CO (normal 900–1500 dyn·s·cm⁻⁵)
• RV afterload is governed mainly by pulmonary vascular resistance (PVR): PVR = 80 × (mean PAP − LAP) / CO (normal 50–150 dyn·s·cm⁻⁵), with PCWP substituted for LAP.
• The RV, having a thinner wall, is far more sensitive to acute increases in afterload than the LV.
• More precise (but less clinically practical) measures include aortic input impedance and effective arterial elastance (Ea), which account for arterial compliance and wave reflection — SVR alone ignores blood viscosity, vessel compliance, and pulsatile components.
• Cardiac output falls sharply with large increases in afterload, especially in the presence of pre-existing myocardial depression, ischemia, or heart failure — a key anaesthetic consideration during induction/laryngoscopy or in valvular disease.

3. Contractility (Inotropy)

• Modified by: sympathetic stimulation (mainly β1-receptor mediated, via norepinephrine/epinephrine), heart rate (force-frequency relationship), pH, temperature, and pharmacologic agents (digitalis, milrinone, catecholamines).
• Depressed by hypoxia, acidosis, catecholamine depletion, ischemia/infarction, and most volatile and IV anaesthetics/antiarrhythmics at higher doses — directly relevant to anaesthetic drug selection in patients with poor ventricular function.
• Measurement: True contractility (Vmax at zero load) cannot be measured in the intact heart. Clinically used indices include:
  • Pressure-volume loops (gold standard in intact heart, via end-systolic elastance, Ees)
  • Ejection fraction (most commonly used noninvasive index — echo, angiography, radionuclide ventriculography)
  • dP/dt max (rate of pressure rise) as an invasive index

4. The Frank-Starling Relationship

• Frank (1895) and Starling (1914) established that increasing sarcomere/muscle fibre length (end-diastolic volume) increases the force of subsequent contraction and stroke volume, up to an optimal length, due to increased actin-myosin cross-bridge interaction and Ca²⁺ sensitivity.
• Graphically depicted as ventricular function curves (stroke volume/work vs. end-diastolic volume/pressure).
• A family of curves exists — contractility changes shift the whole curve (leftward/upward = increased inotropy; rightward/downward = decreased inotropy, e.g., heart failure), whereas preload changes move the operating point along a single curve.
• This mechanism allows the heart to autoregulate output to match venous return beat-to-beat without needing neural input.

5. Heart Rate

• CO = SV × HR. Heart rate is controlled by autonomic tone (sympathetic increases rate and contractility via β1; parasympathetic/vagal decreases rate via M2 receptors on the SA node).
• Excessive tachycardia reduces diastolic filling time (lowers preload/SV) and increases myocardial O2 demand; bradycardia below a critical rate reduces CO despite compensatory increases in SV.
• The force-frequency relationship: within physiologic limits, increasing heart rate itself modestly augments contractility (Bowditch effect / treppe).

6. Myocardial Oxygen Supply-Demand Balance

• Wall stress (preload and afterload)
• Heart rate
• Contractility

7. Clinical / Anaesthetic Application