Cardiac output is the product of stroke volume and heart rate. Stroke volume is determined by three variables that are central to the understanding and management of all forms of shock:

Preload

Preload is the degree of myocardial fibre stretch at end-diastole — essentially the filling volume of the heart. The Frank-Starling relationship describes how stroke volume increases as preload increases, up to a point beyond which further filling reduces contractile efficiency. The SICS module uses the elastic band analogy: the further you pull it back, the harder it fires. In clinical practice, low preload from hypovolaemia or relative hypovolaemia is the commonest reversible cause of low cardiac output in critically ill patients and responds to fluid resuscitation. The converse — over-filling a failing heart — worsens cardiac function and causes pulmonary oedema.

Contractility

Contractility refers to the intrinsic force-generating capacity of the myocardium at a given preload. It determines the slope of the Starling curve — a more contractile heart generates a greater stroke volume for any given filling. Inotropes work by increasing contractility, shifting the Starling curve upward. Crucially, inotropes are most effective in a heart that is adequately filled — administering inotropes to a volume-depleted patient is both futile and potentially harmful.

Afterload

Afterload is the resistance against which the ventricle must pump to generate cardiac output — in practical terms, the systemic vascular resistance (SVR). High afterload reduces cardiac output. This is why vasodilators (GTN, sodium nitroprusside) improve cardiac output in cardiogenic shock by reducing the resistance the failing ventricle must overcome. Conversely, vasopressors increase SVR and can reduce cardiac output in the patient with myocardial dysfunction.