All causes of shock lead to generalised hypo-perfusion of tissues and thus share common clinical features.

Signs of poor tissue perfusion include:

Tachycardia and tachypnoea are relatively early signs of shock whereas a lactic acidosis and hypotension are late signs. Two of the earliest organs to suffer the effects of tissue hypo-perfusion are the kidneys and brain. Decreased urine output and decreased conscious level are therefore early indicators of hypo-perfusion and end organ disorder.

Hypovolaemic shock

If there is volume depletion the patient may complain of thirst and have cold and clammy peripheries and a decreased capillary refill time. The jugular venous pressure (JVP) will be reduced. There may be a history of blood loss (e.g. gastrointestinal bleed, recent surgery or trauma) with a resultant drop in haemoglobin levels, or evidence of increased fluid losses (e.g. diarrhoea, vomiting or losses due to small bowel obstruction). Iatrogenic factors may contribute to hypovolaemia due to inadequate fluid prescription or inappropriate use of diuretics.

Septic shock

Septic shock will have many of the features common to other types of shock but with some important differences, which will help to differentiate it from other causes. Patients with sepsis often present with a fever, tachycardia, and hypotension but feel warm to touch with a bounding pulse due to the raised cardiac output in the early stages. Common sources for sepsis include chest, abdomen, soft tissues, wounds, urine and intravascular lines.

Cardiogenic shock

The clinical features of cardiogenic shock are similar to hypovolaemic shock. There is loss of cardiac output due to reduced contractility (rather then reduced preload seen in hypovolaemic shock) with a resultant increase in SVR due to circulating catecholamines. Therefore features include cold clammy peripheries, reduced capillary refill and other signs of reduced tissue perfusion. The notable difference is that the JVP will be raised in cardiogenic shock and there may be signs of pulmonary oedema in patients with left ventricular failure. Causes include myocardial infarction, acute arrhythmias and cardiac contusion from trauma. A careful history and examination will help to elicit the cause with additional information gained from an ECG or echocardiogram.

Obstructive shock

Tension pneumothorax or a pulmonary embolus (PE), may well be diagnosed during your assessment of the Breathing part of ABCDE, but often hypotension is a predominant feature. Cardiac tamponade is rare and difficult to diagnose. It occurs when fluid accumulates within the pericardial space faster than the sac can stretch, causing pressure on the heart. Findings include tachycardia, hypotension, muffled heart sounds, raised JVP and distended neck veins. Immediate decompression with pericardiocentesis may be necessary.

Cardiovascular changes in shock

  Hypovolemic Distributive
Cardiogenic Obstructive Neurogenic
HR ↑↓ →↓
JVP/CVP (Preload)
SVR (Afterload) ↑→