Cardiac Output

Because cardiac output increases with body size. A 5 L/min output is perfectly normal for a 70 kg man, but it would be too low for a 150 kg man and dangerously high for a 5 kg infant. Dividing by the body surface area (BSA) removes this variation and gives the cardiac index (CI = CO/BSA), which is comparable across the whole range of human sizes. The normal range for CI is 2.5–4.0 L/min/m² for adults, with values below 2.2 indicating severe hypoperfusion and values above 4.2 indicating a high-output state. Body surface area is usually estimated from height and weight using a nomogram or a formula — the Mosteller formula BSA = √(height × weight / 3600) is the simplest and most widely used, with height in cm and weight in kg.

Stroke volume is set by preload, contractility and afterload. Preload is the end-diastolic volume — the amount of blood in the ventricle just before it contracts. By the Frank–Starling mechanism, more filling produces a more forceful contraction and a larger stroke volume, up to a plateau beyond which further filling does not help. Contractility is the intrinsic strength of the myocardium independent of preload or afterload, increased by sympathetic stimulation and by inotropic drugs such as dobutamine, and reduced by ischaemia, acidosis and heart failure. Afterload is the resistance the ventricle must overcome to open the aortic valve and eject — approximated by the systemic vascular resistance — and it is inversely related to stroke volume for a given preload and contractility. Manipulating these three determinants — with fluids, inotropes and vasoactive drugs — is the core of cardiovascular critical care.

There are four main methods. The Fick principle measures oxygen consumption and the arteriovenous oxygen difference and computes CO = VO₂ / (CaO₂ − CvO₂); this is the gold standard but requires a metabolic cart. Thermodilution uses a pulmonary artery catheter to inject cold saline and measure the temperature change downstream; the Stewart–Hamilton equation then gives the CO. Echocardiography measures the cross-sectional area of the left ventricular outflow tract and the velocity–time integral of flow through it, and CO = area × VTI × HR. Pulse contour analysis uses the arterial waveform from a peripheral line and a calibration factor to estimate stroke volume continuously. Each method has its own accuracy, precision and failure modes, but all of them measure the same physiological quantity — the flow rate of the circulation.

Because the ventricle needs time to fill. The cardiac cycle is divided into systole, during which the ventricle contracts and ejects, and diastole, during which it relaxes and fills. As the heart rate rises, both phases shorten, but diastole shortens much more — at 180 bpm the diastolic filling time is less than 100 ms, which is barely enough for the ventricle to receive blood from the atrium. As filling time falls, the end-diastolic volume falls, and by the Frank–Starling mechanism the stroke volume falls with it. Eventually the loss of stroke volume exactly offsets the gain from the higher rate, and the cardiac output stops rising. The plateau heart rate is about 160–180 bpm in young adults and lower in the elderly, whose ventricles relax more slowly. This is why the linear formula CO = SV × HR over-predicts output at extreme rates.

Systemic vascular resistance (SVR) is the resistance the left ventricle must overcome to eject blood into the aorta. It is the ratio of the pressure gradient across the systemic circulation to the flow through it, with a constant of 80 to convert between clinical units: SVR = 80 × (MAP − CVP) / CO, where MAP is the mean arterial pressure in mmHg, CVP is the central venous pressure in mmHg, and CO is the cardiac output in L/min. The result is in dyne·s·cm⁻⁵, the traditional unit; dividing by 80 gives the value in Wood units (mmHg·min/L). Normal SVR is 900–1,400 dyne·s·cm⁻⁵ at rest. It is low in distributive shock (sepsis, anaphylaxis, cirrhosis), high in cardiogenic and hypovolaemic shock, and elevated in chronic hypertension.

Yes. A persistently elevated cardiac output — above about 8 L/min at rest, or a cardiac index above 4.2 L/min/m² — is abnormal and is described as a high-output state. It occurs in sepsis (where vasodilatation forces the heart to pump more to maintain pressure), severe anaemia (where the reduced oxygen-carrying capacity is compensated by increased flow), thyrotoxicosis (where metabolic rate and sympathetic tone are both increased), arteriovenous fistulae (where blood bypasses the capillary bed), and in the late stages of cirrhosis. A sustained high output is not benign: it increases myocardial oxygen demand, places the heart under chronic volume overload, and eventually leads to high-output cardiac failure. The treatment is to identify and correct the underlying cause, not to try to reduce the cardiac output directly.

Exercise increases cardiac output through both determinants, but the relative contribution changes with intensity and with training. At low-intensity exercise, stroke volume rises first — from sympathetic stimulation increasing contractility, and from the muscle pump and venoconstriction increasing venous return and preload. As intensity increases, heart rate rises steeply and contributes progressively more, until at maximal exercise the heart rate accounts for about 70–80 % of the increase in cardiac output. In an untrained adult, maximal cardiac output is typically 15–20 L/min; in a trained endurance athlete it can reach 30–35 L/min, mostly because the athlete's heart has a larger stroke volume at every intensity, including maximal exercise. This is why training bradycardia (a low resting heart rate) is a marker of cardiovascular fitness.