Causes

Due to an intrinsic heart problem

• Myocardial infarction (MI).
• Myocardial contusion (often from steering wheel impact).
• Acute dysrhythmia compromising cardiac output.
• Acute mitral regurgitation (usually as a complication of MI due to ruptured chordae tendinae).
• Ventricular septal rupture (usually occurring as post-MI complication).
• Cardiac rupture (rupture of the wall of the left ventricle can occur post-MI or due to cardiac trauma).
• Hypertrophic obstructive cardiomyopathy or end-stage cardiomyopathy of other cause.
• Myocarditis.
• Post-cardiac surgery requiring prolonged cardioplegia and cardiopulmonary bypass.
• Severe valvular heart disease, particularly aortic stenosis.

Due to other causes

• Acute, severe pulmonary embolism.
• Pericardial tamponade or severe constrictive pericarditis.
• Tension pneumothorax.
• Myocardial suppression due to bacteraemia or sepsis (although, strictly speaking, this may be defined as septic shock).
• Suppression of myocardial contractility by drugs, eg betablockers, or due to metabolic disturbance, eg acidosis, hypokalaemia or hyperkalaemia, hypocalcaemia.
• Thyrotoxic crisis.

Risk factors

• It is more likely to develop in the elderly and in diabetics.^[3]
• Anterior and right-ventricular MI are associated with an increased risk.
• History of previous infarction, peripheral vascular disease, cerebrovascular disease and multi-vessel atheroma increases the likelihood of the development of cardiogenic shock.

Presentation

Shock is due to an inability to perfuse vital organs and tissues adequately. The skin, brain, heart and kidneys are usually most severely affected by this. The symptoms and signs can present abruptly or develop insidiously over the course of many hours.

Symptoms

As many patients with cardiogenic shock have had an acute myocardial infarction (MI), symptoms can include:

• Chest pain
• Nausea and vomiting
• Dyspnoea
• Profuse sweating
• Confusion/disorientation
• Palpitations
• Faintness/syncope

Signs

• Pale, mottled, cold skin with slow capillary refill and poor peripheral pulses.
• Hypotension (remember to check BP in both arms in case of aortic dissection).
• Tachycardia/bradycardia.
• Raised JVP/distension of neck veins.
• Peripheral oedema.
• Quiet heart sounds or presence of third and fourth heart sounds.
• Heaves, thrills or murmurs may be present and may indicate the cause, such as valve dysfunction.
• Bilateral basal pulmonary crackles or wheeze may occur.
• Oliguria (catheterisation is a useful early monitoring intervention).
• Altered mental state.

Assessment and initial management

• Assess 'Airway and Breathing':
  • Intubation and mechanical ventilation may be needed; provide oxygen as adequate.
• 'Circulation':
  • Gain venous access; patients often require central venous access as peripherally shut down - send bloods (see 'Investigations', below).
  • Intravenous fluids: 250 ml boluses should be used if any coexistent depletion of intravascular volume is present.
• Monitoring:
  • Cardiac monitoring.
  • BP monitoring (usually via an arterial line).
  • Venous pressure monitoring via central venous pressure (CVP).
  • Insertion of a Swan-Ganz catheter (not performed routinely): allows monitoring of CVP and pulmonary capillary wedge pressure. This can guide the need for fluid resuscitation. Haemodynamic monitoring using a Swan-Ganz catheter can help to differentiate cardiogenic shock from other causes of shock such as hypovolaemia. (Arterial line, simple central venous line for CVP monitoring and a PiCCO® line are alternatives to a Swan-Ganz catheter.)
  • Urinary catheter.
• Investigations:
  • U&Es and creatinine can assess renal function.
  • Urine pregnancy test in women.
  • LFTs.
  • FBC to exclude anaemia.
  • Cardiac enzymes, including troponins.
  • Arterial blood gases.
  • Brain natriuretic peptide (BNP): low BNP levels may help to rule out cardiogenic shock in the setting of hypotension but a high BNP level isn't diagnostic of cardiogenic shock (eg there may be high BNP levels in PE, atrial fibrillation and sepsis);^[5] BNP levels may be more practical in monitoring progression in CCU/ICU.
  • Perform an ECG early: this can show acute myocardial infarction (MI). ECG may be normal in other causes of cardiogenic shock.
  • CXR: can show tension pneumothorax, widened mediastinum in aortic dissection, signs of left ventricular failure.
  • CT pulmonary angiography (CTPA) or ventilation/perfusion lung scan (also known as V/Q scanning) to look for PE may be appropriate but only once patient is stabilised (D-dimer is likely to be raised so less useful).
  • Echocardiography: this can establish the cause of cardiogenic shock, eg acute ventricular septal defect, pericardial tamponade.
• Consider pharmacological inotropic support (see directly below).
• Provide symptom relief if needed, eg opiate analgesia.
• Treat any electrolyte abnormalities.
• Treat any arrhythmias.
• Treat any underlying causes, eg usual management of acute MI, urgent valve repair.

Pharmacological inotropic support

• Vasopressor/inotropic support with dopamine, dobutamine, or epinephrine may be needed. However, one study suggested that dopamine might be associated with increased mortality.^[6]
• These agents may lead to increased heart rate which could worsen myocardial ischaemia. A risk-benefit analysis has to be made but they are useful in the short-term until the underlying cause can be corrected.
• Phosphodiesterase inhibitors, eg milrinone, are also available but more rarely used.

Intra-aortic balloon pump (IABP) counterpulsation

• IABP counterpulsation increases cardiac output and improves coronary artery blood flow.
• It can help to stabilise patients so that a diagnosis can be established and treatment initiated. It is not, in itself, definitive therapy.
• Its impact on long-term survival is controversial.^[7]

Revascularisation

• Revascularisation with thrombolysis, percutaneous intervention or coronary artery bypass surgery should be considered.
• The SHOCK trial (= SH ould we emergently revascularize O ccluded C oronaries for cardiogenic shocK) found that early revascularisation (angioplasty or coronary artery bypass graft) improves 1-year survival in patients under the age of 75 with acute MI and cardiogenic shock when compared with medical treatments (including thrombolysis and IABP).^[8] This survival advantage seems to persist at 3 and 6 years.^[9]
• The American College of Cardiology and American Heart Association Guidelines suggest that patients who arrive at hospital in cardiogenic shock, or who develop it after arrival, be transferred to a centre where revascularisation can take place.^[10]

See separate article Acute Myocardial Infarction Management for further details.

Other management options

• Ventricular assist devices: these are essentially prosthetic ventricles that can support right and left ventricle performance. They may allow survival to cardiac transplantation. They are generally used when medical treatment and IABP fail and the cause of the cardiogenic shock is potentially reversible. A recent study has found them to be a safe and effective therapy.^[11]
• Non-invasive positive pressure ventilation (NIPPV) may be helpful in mild-to-moderate cases of cardiogenic shock (provided the BP can support it).

Prognosis

• Cardiogenic shock is the leading cause of death in acute myocardial infarction (MI).^[4]
• Mortality rates may be 70-90%, reduced to 40-60% if patients are treated aggressively.^[7]
• A recent study showed that, among patients with cardiogenic shock who survive for 30 days after an ST-segment elevation myocardial infarction (MI), annual mortality rates of 2% to 4% are approximately the same as those of patients without shock. Percutaneous revascularisation was associated with a reduced risk of death.^[12]

Prevention

• Early coronary revascularisation in patients post-myocardial infarction (MI) and adequate treatment of patients with structural heart disease may help to prevent cardiogenic shock.
• Better treatment of acute coronary syndrome seems to be reducing the rates of cardiogenic shock.^[13]