Residency · Residency · Cardiothoracic Surgery
Physiology of Cardiac Output and Ventricular Function
Overview
Understanding what determines cardiac output and how to assess ventricular function is fundamental to perioperative decision-making in cardiothoracic surgery. These physiologic principles translate directly into the operating room and ICU, where real-time hemodynamic management determines patient outcomes.
Determinants of Cardiac Output
Cardiac Output Equation
Cardiac output (CO) is the product of heart rate (HR) and stroke volume (SV). Normal CO ranges from 4 to 8 liters per minute. The cardiac index (CI), which normalizes CO to body surface area (BSA), has a normal range of 2.5 to 4.0 L/min/m2. Stroke volume is itself determined by three factors: preload, afterload, and contractility.
Preload
Preload refers to the end-diastolic volume, or the degree of myofiber stretch before contraction. Clinically, it is estimated by central venous pressure (CVP) for the right heart, pulmonary capillary wedge pressure (PCWP) for the left heart, and left ventricular end-diastolic volume (LVEDV) on echocardiography. Preload is governed by venous return, blood volume, venous compliance, and intrathoracic pressure. Positive pressure ventilation, for instance, reduces preload by decreasing venous return.
Afterload
Afterload is the resistance the ventricle must overcome to eject blood. For the left ventricle, this is approximated by systemic vascular resistance (SVR), calculated as (MAP - CVP) / CO x 80. For the right ventricle, it is pulmonary vascular resistance (PVR), calculated as (mPAP - PCWP) / CO x 80. Wall stress, described by LaPlace's law (stress = pressure x radius / 2 x wall thickness), provides the more complete picture. Acutely elevated afterload reduces stroke volume and increases myocardial oxygen demand.
Contractility (Inotropy)
Contractility is the intrinsic ability of the myocardium to generate force, independent of preload and afterload. The gold standard measure is the end-systolic pressure-volume relationship (ESPVR). Other measures include dP/dt max (the rate of pressure rise during isovolumetric contraction) and ejection fraction, though the latter is influenced by loading conditions and is not a pure contractility measure. Contractility is increased by sympathetic stimulation and inotropic agents (dobutamine, milrinone, epinephrine) and decreased by ischemia, cardiomyopathy, acidosis, hypoxia, and negative inotropes.
Frank-Starling Mechanism
Principle
Within physiologic limits, an increase in preload (end-diastolic volume) results in increased stroke volume. This happens because increased sarcomere length optimizes actin-myosin overlap and increases calcium sensitivity. The Frank-Starling curve plots stroke volume (or CO) against preload (LVEDV or PCWP).
Clinical Applications
In a normal heart, the curve has a steep ascending limb, meaning small increases in preload produce large increases in cardiac output. In a failing heart, the curve is flattened and depressed: further volume loading produces minimal CO increase but worsens pulmonary congestion. When the heart is supported with inotropes, the curve shifts upward and leftward, achieving higher CO at lower filling pressures.
The perioperative relevance is direct. Volume resuscitation improves CO only if the patient is on the ascending portion of the curve. Excessive volume loading in a failing heart worsens pulmonary edema without improving output. TEE-guided preload assessment is superior to pressure-based measurements alone for making these determinations in the operating room.
Pressure-Volume Loops
Components of the PV Loop
The pressure-volume loop traces four phases of the cardiac cycle. During isovolumetric contraction, the mitral valve has closed and the aortic valve has not yet opened — pressure rises at constant volume. During the ejection phase, the aortic valve is open and volume decreases as blood is ejected. During isovolumetric relaxation, the aortic valve has closed and the mitral valve has not yet opened — pressure falls at constant volume. During the filling phase, the mitral valve is open and the ventricle fills with blood.
Key Relationships in PV Loops
The ESPVR (end-systolic pressure-volume relationship) represents contractility: a steeper slope indicates higher contractility. The EDPVR (end-diastolic pressure-volume relationship) represents compliance: a steeper curve indicates a stiffer ventricle. Stroke volume is the width of the loop (EDV minus ESV). Stroke work, which approximates the external work performed by the ventricle, is the area enclosed by the loop. Ejection fraction is simply SV divided by EDV.
Effects of Loading Conditions on PV Loops
Increased preload shifts the loop rightward with a larger EDV and increased SV (if on the ascending limb). Increased afterload shifts the loop upward and leftward, with increased ESV and decreased SV. Increased contractility steepens the ESPVR slope, decreasing ESV and increasing SV. Combined effects are seen in conditions like aortic stenosis, where high afterload shifts the loop upward with compensatory hypertrophy.
Systolic Function Assessment
Ejection Fraction (EF)
Ejection fraction is calculated as (EDV - ESV) / EDV x 100. Normal LVEF is 55–70%, with mild reduction at 41–54%, moderate at 30–40%, and severe below 30%. An important limitation is that EF is load-dependent. In mitral regurgitation, for example, the ventricle ejects partly into the low-impedance left atrium, so an EF of 60% may already represent significant systolic dysfunction.
Other Systolic Measures
Fractional shortening (FS) is measured on M-mode and is normal above 25%. Global longitudinal strain (GLS), derived from speckle-tracking echocardiography, is more sensitive than EF for detecting subclinical dysfunction and is normal at more negative than -18%. dP/dt, derived from the MR jet on continuous-wave Doppler, suggests significant LV dysfunction when below 800 mmHg/s. TAPSE (tricuspid annular plane systolic excursion) measures RV systolic function, with normal values above 17 mm. S' velocity, obtained via tissue Doppler of the mitral or tricuspid annulus, provides additional assessment.
Diastolic Function Assessment
Stages of Diastolic Dysfunction
| Grade | Pattern | E/A Ratio | E/e' | Other Features |
|---|---|---|---|---|
| I | Impaired relaxation | < 0.8 | < 8 | Prolonged deceleration time |
| II | Pseudonormal | 0.8–1.5 | 9–14 | Elevated LA volume |
| III | Restrictive | > 2 | > 14 | Short deceleration time; elevated LA pressure |
Diastolic dysfunction is common after cardiac surgery and influences perioperative management strategies.
Determinants of Diastolic Function
Diastolic function depends on active relaxation (lusitropy), which is an energy-dependent process of calcium reuptake, and passive compliance, which is determined by chamber stiffness, fibrosis, and pericardial constraint. Diastolic function is impaired by hypertrophy, ischemia, fibrosis, pericardial disease, and infiltrative cardiomyopathies.
Intraoperative Hemodynamic Decision-Making
TEE-Guided Assessment
Transesophageal echocardiography provides real-time assessment of biventricular function, preload (cavity size), and valve function. Volume responsiveness can be assessed by respiratory variation in IVC or SVC diameter, or by LV cavity obliteration suggesting underfilling. New regional wall motion abnormalities suggest ischemia (from graft occlusion, air embolism, or coronary spasm). Valve function is assessed before and after repair or replacement.
Hemodynamic Management Algorithm
A systematic approach to low cardiac output begins with assessing filling pressures.
| Hemodynamic Profile | Filling Pressures | SVR | Management |
|---|---|---|---|
| Hypovolemia | Low | High | Volume resuscitation |
| Pump failure | Adequate | Normal/High | Inotropes (dobutamine, milrinone) |
| Cardiogenic shock | High | High | Inotropes + vasodilators or IABP; evaluate for mechanical cause |
| Afterload mismatch | Adequate/High | High | Afterload reduction; milrinone (inodilator) |
| Vasoplegia | Low/Adequate | Low | Vasopressors (norepinephrine, vasopressin) + inotrope if needed |
Ventricular Interdependence
The right and left ventricles share the interventricular septum and pericardial space, creating important interactions. RV dilatation shifts the septum leftward, impairing LV filling through both series and parallel interaction. After LVAD implantation, LV decompression can worsen RV function by shifting the septum. Pericardial tamponade impairs both ventricles simultaneously through external compression.
<image>A set of four pressure-volume loop diagrams showing: (1) normal PV loop with labeled phases (isovolumetric contraction, ejection, isovolumetric relaxation, filling), ESPVR, and EDPVR lines; (2) the effect of increased preload shifting the loop rightward; (3) the effect of increased afterload shifting the loop upward with decreased stroke volume; (4) the effect of increased contractility steepening the ESPVR with increased stroke volume. Each diagram is clearly annotated with color-coded phases.</image>
<image>Three Frank-Starling curves plotted on a graph with preload (LVEDV) on the x-axis and stroke volume on the y-axis, showing: (1) a normal curve with steep ascending limb and plateau; (2) a depressed curve representing heart failure with a flattened response; (3) an augmented curve shifted upward and leftward representing the effect of inotropic support. Arrows indicate the clinical effect of volume loading versus inotrope administration in each state.</image>
<image>Intraoperative transesophageal echocardiography views showing: (1) mid-esophageal four-chamber view with labeled chambers and measurement of LVEF by Simpson's biplane method; (2) transgastric short-axis view showing normal LV wall segments for regional wall motion assessment; (3) pulse-wave Doppler of mitral inflow showing E and A waves for diastolic function assessment. Each view is annotated with the clinical information obtained and normal values.</image>
Clinical Pearls
Ejection fraction is load-dependent and can be misleading: in severe mitral regurgitation, an EF of 60% may represent significant contractile impairment because the ventricle is ejecting into a low-pressure left atrium. The Frank-Starling curve explains why volume loading helps a hypovolemic patient but worsens a patient with decompensated heart failure. Pressure-volume loops are the gold standard for understanding ventricular mechanics, and contractility is best assessed by the ESPVR slope, not by EF alone. In the operating room, TEE is the most important tool for real-time hemodynamic assessment, providing simultaneous information about preload, function, and valve competence. Ventricular interdependence is critically important after LVAD implantation, where excessive LV unloading can worsen RV failure by shifting the septum. Always consider all four determinants of cardiac output (heart rate, preload, afterload, contractility) systematically when troubleshooting hemodynamic instability. GLS is more sensitive than EF for detecting early myocardial dysfunction, especially in aortic stenosis and chemotherapy-related cardiomyopathy.
References
- Burkhoff D, Mirsky I, Suga H. Assessment of systolic and diastolic ventricular properties via pressure-volume analysis: a guide for clinical, translational, and basic researchers. Am J Physiol Heart Circ Physiol. 2005;289(2):H501-H512.
- Nagueh SF, Smiseth OA, Appleton CP, et al. Recommendations for the evaluation of left ventricular diastolic function by echocardiography. J Am Soc Echocardiogr. 2016;29(4):277-314.
- Hahn RT, Abraham T, Adams MS, et al. Guidelines for performing a comprehensive transesophageal echocardiographic examination. J Am Soc Echocardiogr. 2013;26(9):921-964.
- Klabunde RE. Cardiovascular Physiology Concepts. 3rd ed. Wolters Kluwer, 2021.
