Cardiac Hemodynamic Relationships

Fundamental Relationships

The American Heart Association acknowledges that cardiac output (CO) equals heart rate (HR) multiplied by stroke volume (SV), while stroke volume is determined by the difference between end-diastolic volume (EDV) and end-systolic volume (ESV) 1
The American Thoracic Society recognizes the core equation as: CO = HR × SV, where SV = EDV - ESV 2
End-Diastolic Volume (EDV) represents the maximum blood volume in the ventricle at the end of filling (diastole), typically 100-120 mL in healthy adults 1
Stroke Volume (SV) is the amount of blood ejected per heartbeat, normally around 70-100 mL in healthy individuals at rest 1, 3
Cardiac Output (CO) is the total volume of blood pumped per minute, calculated as HR × SV, typically 4-8 L/min at rest 2

EDV directly reflects ventricular preload, which represents the initial stretching of cardiac myocytes before contraction through the Frank-Starling mechanism 4
Larger EDV increases sarcomere length, enhancing contractile force and thereby increasing stroke volume 4
In trained athletes, augmentation of stroke volume during exercise is attributable primarily to a larger end-diastolic volume 1, 3
SV increases through two mechanisms: increased EDV (preload) and decreased ESV (enhanced contractility) 1
In healthy individuals during exercise, stroke volume rises from ~70 mL at rest to ~100 mL at peak exercise 1
Enhanced systolic emptying (reduced ESV) contributes to increased SV, particularly in trained individuals 3, 5

CO increases initially through both increased SV and HR, then at moderate-to-high intensity exercise almost exclusively through HR increases 2
In healthy subjects, CO increases linearly with oxygen consumption (V̇O₂) 2
Maximal cardiac output in healthy individuals can reach 20-25 L/min during peak exercise 1

Patients with heart failure demonstrate fundamentally impaired hemodynamic relationships 1, 6
Stroke volume remains markedly reduced, rising only modestly to 50-65 mL at peak exercise compared to 100 mL in healthy subjects 1, 6
The inability to increase CO is related primarily to minimal SV increase coupled with lower maximal HR achieved at lower workload 1
EDV augmentation is blunted because the already dilated left ventricle operates near maximal volume, exhausting preload reserve 1, 6
Patients with heart failure may achieve only 50% of the maximal cardiac output attained by healthy individuals 1

Reduced ability to increase both LV preload and ejection fraction during exercise 1
Impaired intrinsic contractility and reduced β-adrenergic responsiveness 1, 6
Elevated systemic vascular resistance due to increased sympathetic and renin-angiotensin system activity 1
Exercise-induced mitral regurgitation reduces forward stroke volume 1, 6

Central venous pressure and pulmonary capillary wedge pressure are generally insensitive indicators of preload status 4
Echocardiographic measurement of EDV provides direct assessment of preload 4
In heart failure, the ventricle may be operating at maximal EDV despite "normal" filling pressures due to chamber remodeling 1, 6
Maximal heart rate achievement does not guarantee maximal effort in patients on β-blockers or with chronotropic incompetence 2

In patients with severely reduced stroke volume, cardiac output can only be maintained by increasing heart rate, as the failing heart cannot augment stroke volume adequately, according to the American College of Cardiology 7
The primary means to augment cardiac output in heart failure patients is through cardioacceleration (increased heart rate), as stated by the American Heart Association 7

A heart rate of 109 bpm for light-to-moderate intensity activity (roughly equivalent to 2-3 METs) suggests the cardiovascular system is working disproportionately hard, as indicated by the American College of Cardiology 8
Sinus tachycardia in heart failure represents a compensatory mechanism where cardiac output depends on rapid heart rate due to limited stroke volume, according to the American Heart Association 9, 7

The American Heart Association explicitly states that in compensatory tachycardias where stroke volume is limited, cardiac output becomes dependent on rapid heart rate, and attempting to reduce heart rate pharmacologically in this setting could precipitate hemodynamic collapse 9

Obtain resting heart rate and compare to this exertional value—if resting HR is already elevated (>90 bpm), this strongly suggests compensatory tachycardia, as indicated by the American College of Cardiology 7
Check for other signs of heart failure: elevated jugular venous pressure, peripheral edema, pulmonary congestion, S3 gallop, as recommended by the American College of Cardiology 7

Do not dismiss this as "normal sinus tachycardia" simply because the rate is <150 bpm—in the context of severely low SVI and low-intensity activity, this represents significant pathology, as warned by the American Heart Association 9