Residency · Residency · Anesthesiology
Cardiac Physiology for the Anesthesiologist
Pressure-Volume Loops
Basic PV Loop
The left ventricular pressure-volume (PV) loop plots left ventricular volume on the x-axis against left ventricular pressure on the y-axis. It encompasses four phases: isovolumetric contraction (mitral valve closes, aortic valve still closed), ejection (aortic valve opens), isovolumetric relaxation (aortic valve closes, mitral valve still closed), and filling (mitral valve opens). Stroke volume is the difference between end-diastolic volume (EDV) and end-systolic volume (ESV). The area within the loop represents stroke work.
End-Systolic Pressure-Volume Relationship (ESPVR)
The upper left corners of multiple PV loops generated at varying preloads define the ESPVR line. The slope of this line is the end-systolic elastance (Ees), which serves as a load-independent index of contractility. Increased contractility steepens the slope and shifts the loop leftward, while decreased contractility flattens the slope and shifts the loop rightward.
End-Diastolic Pressure-Volume Relationship (EDPVR)
The lower portion of the PV loop represents passive ventricular compliance. Diastolic dysfunction shifts the EDPVR upward, meaning higher pressures develop for the same volume. Compliance is defined as the change in volume divided by the change in pressure.
PV Loop Changes with Pathology
Increased afterload makes the loop taller (higher systolic pressure), narrower (reduced stroke volume), and shifted right. Increased preload shifts the loop right and makes it wider (greater stroke volume via the Frank-Starling mechanism). Increased contractility shifts the loop left with a higher ejection fraction and steeper ESPVR. Aortic stenosis produces a tall, narrow loop with high systolic pressures. Mitral regurgitation creates a volume-overloaded loop with a large total stroke volume but reduced forward stroke volume and lower peak systolic pressure.
Frank-Starling Relationship
The Law
Within physiologic limits, increasing preload (EDV or sarcomere length) increases stroke volume. The mechanism involves optimal actin-myosin overlap at greater sarcomere lengths, which increases force generation. The curve plateaus and may decline with excessive stretch (the descending limb), which is seen in acute heart failure.
Clinical Implications
Patients on the steep portion of the curve are fluid responsive — their stroke volume increases with a fluid bolus. Patients on the flat portion gain no benefit from additional fluid and risk pulmonary edema. Cardiac dysfunction shifts the entire curve downward and rightward. Inotropes shift the curve upward, producing more stroke volume for any given preload.
Determinants of Cardiac Output
Heart Rate
Cardiac output equals heart rate times stroke volume. Tachycardia increases cardiac output up to a point, beyond which reduced diastolic filling time decreases stroke volume. Heart rate is the most important determinant of myocardial oxygen consumption. The critical rate depends on diastolic function and coronary perfusion.
Preload
Preload, approximated by end-diastolic volume (or pressure as a surrogate), is determined by venous return, intravascular volume, venous tone, body position, intrathoracic pressure, atrial contraction, and ventricular compliance. CVP and PCWP are pressure surrogates but imperfect indicators of volume status.
Afterload
Afterload is the impedance to ventricular ejection. For the left ventricle, it comprises systemic vascular resistance (SVR), aortic impedance, and aortic compliance. For the right ventricle, it is pulmonary vascular resistance (PVR). Increased afterload decreases stroke volume unless compensated by increased contractility. SVR is calculated as (MAP minus CVP) divided by cardiac output, multiplied by 80, expressed in dynes-sec-cm^-5.
Contractility
Contractility is the intrinsic ability of the myocardium to generate force independent of preload and afterload. Clinical measures include ejection fraction (a load-dependent surrogate), dP/dt, and Ees (load-independent). It is increased by sympathomimetics, calcium, and digitalis. It is decreased by volatile anesthetics, propofol, beta-blockers, calcium channel blockers, acidosis, hypoxia, and myocardial ischemia.
| Determinant | Definition | Key Influencers | Anesthetic Implication |
|---|---|---|---|
| Heart Rate | Beats per minute | ANS tone, drugs, temperature | Tachycardia increases MVO2 and reduces diastolic filling |
| Preload | End-diastolic volume/pressure | Venous return, volume status, compliance | Hypovolemia reduces CO; excess causes pulmonary edema |
| Afterload | Impedance to ejection (SVR/PVR) | Vasodilators, vasoconstrictors, aortic compliance | Increased afterload reduces SV unless contractility compensates |
| Contractility | Intrinsic force generation | Sympathomimetics, volatile agents, ischemia | Volatile agents and propofol are negative inotropes |
Systolic and Diastolic Function
Systolic Function
Systolic function is the ability to eject blood, measured by ejection fraction (normal 55-70%), fractional shortening, and cardiac index. Systolic heart failure (HFrEF) is defined by an EF below 40%. In anesthesia, negative inotropes worsen systolic failure, so maintaining preload and contractility is the priority.
Diastolic Function
Diastolic function is the ability of the ventricle to fill at normal pressures. Diastolic dysfunction involves impaired relaxation and/or increased stiffness. Heart failure with preserved ejection fraction (HFpEF, EF 50% or above) is characterized by elevated filling pressures with preserved EF. Assessment tools include the E/A ratio, E/e' ratio on tissue Doppler, and LA volume. Anesthetic management of diastolic dysfunction is challenging: these patients are sensitive to preload changes (both hypovolemia and fluid overload are poorly tolerated), sinus rhythm must be maintained (the atrial kick is critical, and atrial fibrillation is poorly tolerated), tachycardia must be avoided (it shortens diastolic filling time), and afterload should be maintained because the heart is preload-dependent.
Ventricular Interdependence
Concept
The two ventricles share the interventricular septum and are enclosed in a common pericardium. Changes in one ventricle directly affect the other. Acute RV dilation shifts the septum leftward, compromising LV filling and output (both series and parallel interdependence).
Clinical Relevance
In acute pulmonary embolism, RV dilation causes septal shift, LV underfilling, and cardiogenic shock. Positive pressure ventilation increases RV afterload (compressing pulmonary vasculature) and decreases RV preload (reducing venous return) but decreases LV afterload. In pericardial tamponade, diastolic pressures equalize, both ventricles are compressed, and exaggerated interdependence produces pulsus paradoxus.
Myocardial Oxygen Supply and Demand
Oxygen Supply
Myocardial oxygen supply is determined by coronary blood flow multiplied by arterial oxygen content. Coronary blood flow occurs primarily during diastole, with subendocardial flow being especially diastolic-dependent. Coronary perfusion pressure equals aortic diastolic pressure minus LVEDP. Autoregulation maintains flow across a range of perfusion pressures (60-140 mmHg). The heart has near-maximal oxygen extraction at rest (70-80%), meaning it cannot significantly increase extraction to compensate for decreased flow — coronary blood flow is effectively everything.
Oxygen Demand
Myocardial oxygen demand is determined by heart rate (the most important factor), wall tension (which depends on preload and afterload), and contractility. Wall tension follows LaPlace's law: tension equals pressure times radius divided by twice the wall thickness. The rate-pressure product (RPP = HR times SBP) serves as a clinical surrogate for myocardial oxygen demand. An RPP above 12,000 is associated with increased ischemia risk.
Ischemia Prevention (Hemodynamic Goals)
Preventing ischemia requires maintaining coronary perfusion pressure by avoiding hypotension (especially diastolic) and elevated LVEDP. Tachycardia should be avoided because it reduces diastolic perfusion time while simultaneously increasing oxygen demand. Excessive increases in afterload or preload increase wall tension. Balancing supply and demand is the fundamental hemodynamic goal in patients with coronary artery disease.
<image>A comprehensive pressure-volume loop diagram showing: (1) the normal PV loop with all four phases labeled and valve events marked, (2) the effects of increased preload (loop shifted right, wider), (3) increased afterload (taller, narrower, shifted right), (4) increased contractility (shifted left, steeper ESPVR), and (5) pathologic examples (aortic stenosis with tall narrow loop, mitral regurgitation with volume-loaded wide loop). ESPVR and EDPVR lines drawn across multiple loops. Stroke volume, stroke work, and ejection fraction calculations annotated.</image>
<image>A diagram of the Frank-Starling relationship showing ventricular function curves: normal curve, enhanced contractility curve (shifted up and left), and depressed contractility curve (shifted down and right). X-axis is preload (LVEDV or LVEDP), Y-axis is stroke volume or cardiac output. Annotations show the steep portion (fluid responsive) and the flat portion (non-responsive). Clinical examples mapped to each curve: healthy patient, patient on inotropes, patient with systolic heart failure. Arrows show effects of vasodilators, inotropes, and fluid bolus on curve position.</image>
<image>A diagram illustrating myocardial oxygen supply and demand balance using a scale/balance metaphor. Supply side (left): coronary blood flow (determined by diastolic BP, LVEDP, coronary resistance, diastolic time), oxygen content (hemoglobin, SaO2). Demand side (right): heart rate (largest weight), wall tension (preload and afterload via LaPlace's law), contractility. Clinical interventions shown as arrows: beta-blockers reducing demand, nitroglycerin reducing preload/wall tension, maintaining diastolic BP supporting supply. The tipping point toward ischemia is highlighted.</image>
Clinical Pearls
Coronary perfusion occurs predominantly during diastole, so tachycardia is doubly harmful — it increases myocardial oxygen demand while reducing supply time. The heart has near-maximal oxygen extraction at baseline (70-80%), and unlike skeletal muscle, it cannot compensate for decreased flow by extracting more oxygen — coronary flow is everything. Diastolic heart failure (HFpEF) is challenging to manage under anesthesia: these patients need adequate preload, sinus rhythm, controlled heart rate, and maintained afterload — essentially the opposite of the classic teaching for systolic failure. Pressure-volume loops are the most fundamental framework for understanding how anesthetic agents and interventions affect cardiac function. The rate-pressure product (HR times SBP) is a bedside surrogate for myocardial oxygen demand; keeping it below 12,000 is a practical target in patients with coronary disease. Ventricular interdependence explains many hemodynamic crises: acute PE causing LV failure, tamponade causing pressure equalization, and the hemodynamic effects of positive pressure ventilation.
References
- Sagawa K, et al. Cardiac Contraction and the Pressure-Volume Relationship. Oxford University Press, 1988.
- Klabunde RE. Cardiovascular Physiology Concepts, 3rd edition. Lippincott Williams & Wilkins, 2021.
- Thiele RH, et al. Cardiac output monitoring and management of low cardiac output. In: Kaplan JA, ed. Kaplan's Cardiac Anesthesia, 7th edition.
- Miller RD, et al. Miller's Anesthesia, 9th edition. Chapter on Cardiovascular Physiology.
- Burkhoff D, et al. Assessment of systolic and diastolic ventricular properties via pressure-volume analysis. Am J Physiol Heart Circ Physiol. 2005;289(2):H501-H512.
