Aetiology

Shock can be classified into four major types.

Hypovolaemic

Associated with decreased cardiac preload (blood return to the right ventricle due to low vascular volume), which could be due to:

Haemorrhage

  • Overt, as in gastrointestinal bleeding or trauma

  • Concealed, such as aortic aneurysm rupture, retroperitoneal bleeding, soft tissue bleeding associated with long-bone fractures, or traumatic body cavity bleeds.

Fluid depletion

  • Gastrointestinal losses, such as diarrhoea, vomiting

  • Insensible losses, such as burns

  • Third-space losses, such as major surgery, pancreatitis, intestinal obstruction

  • Excessive heat or exercise exposure without fluid replacement.

Decreased preload results in decreased cardiac output due to ineffective heart filling. The physiological reaction to this condition is diversion of blood from the splanchnic (peripheral) circulation areas to vital organs by increasing systemic vascular resistance (SVR).

Cardiogenic

Results from heart pump dysfunction (more commonly left-sided) causing a decrease in cardiac output. Compensatory surges in catecholamines lead to increased SVR. However, in some instances (especially acute coronary syndrome), decreased SVR may be observed.​[10][11]​​ Early, aggressive management can lead to improved outcome.[12] Myocardial infarction, viral and alcoholic cardiomyopathies, congestive heart failure, and cardiac valvular lesions are some of the main contributors.

Patients with a history of hypertension or heart disease who are being treated with a beta-blocker, a calcium-channel blocker, or a class 1c anti-arrhythmic such as flecainide may be at risk due to pharmacological suppression of cardiac contractility and alteration of electrical depolarisation of automatic myocardial contraction mechanisms.

Obstructive

Secondary to an obstruction to cardiac flow or filling

  • Flow restriction: pulmonary embolism or severe pulmonary hypertension. Usually accompanied by decreased oxygenation with very minimal physical signs.

  • Filling restriction: cardiac tamponade or tension pneumothorax. Classically cardiac tamponade presents with raised jugular venous pressure, muffled heart sounds, and low blood pressure. Pulsus paradoxus or electrical alternans may also be apparent. Physical findings with tension pneumothorax may include decreased unilateral breath sounds, hyper-resonance to percussion on the affected side, and tracheal deviation to the opposite side from the pneumothorax. These conditions require immediate attention.

Distributive

This is associated with significant vasodilation resulting in relative hypovolaemia (decreased cardiac preload) and decreased SVR. The classic description of distributive shock includes an elevated cardiac output. However, in a substantial percentage of septic shock patients with secondary distributive shock, depression of cardiac contractility is observed.[13] Causes of distributive shock include sepsis, neurogenic shock, adrenal insufficiency, anaphylaxis, thiamine deficiency, and arterial-venous fistula.

Combination

While the above classification can guide evaluation, a combination of the above processes can co-exist. For example, septic shock may include a cardiogenic component (myocardial depression), an obstructive component (disseminated intravascular coagulation with systemic microthrombosis), and a hypovolaemic element (diffuse capillary leak).[11]

Nevertheless, the goals of resuscitation are the same for any type of shock: restoring oxygen delivery and reversing the tissue oxygen debt, thus normalising mixed venous oxygen levels (SVO₂). Timely resuscitation, restoring the circulating volume,and addressing the underlying cause for shock leads to much improved outcomes.[12][14][15][16]

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