Cardiogenic Shock

Cardiogenic shock occurs when there is failure of the pump action of the heart resulting in reduced cardiac output. This leads to acute hypoperfusion and hypoxia of the tissues and organs, despite the presence of an adequate intravascular volume. Cardiogenic shock can be defined as the presence of the following (despite adequate left ventricular filling pressure):

• Sustained hypotension (systolic blood pressure < 90 mmHg for more than 30 minutes)
• Tissue hypoperfusion (cold peripheries, or oliguria < 30 ml/hour, or both)¹

Cardiogenic shock most commonly occurs as a complication of acute myocardial infarction. It occurs in 7% of patients with ST segment elevation myocardial infarction and 3% with non-ST segment elevation myocardial infarction.² It is a medical emergency requiring immediate resuscitation.

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/cardiopulmonary bypass
• Severe valvular heart disease, particularly aortic stenosis

Due to other causes

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

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

Shock is due to an inability to adequately perfuse vital organs and tissues. 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, 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
• 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
• Bibasal pulmonary crackles or wheeze may occur
• Oliguria (catheterisation is a useful early monitoring intervention)
• Altered mental state

• Assess Airway, Breathing and Circulation.
  • Initiate oxygen/ventilatory support: intubation and mechanical ventilation may be needed.
  • Insertion of a Swan-Ganz catheter: allows monitoring of central venous pressure (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.)
• Opiate analgesia such as diamorphine 2.5–5mg can be given if sufficient respiratory effort/rate and if blood pressure can support it.
• Treat any electrolyte abnormalities.
• Treat any arrhythmias.
• Perform an ECG early: this can show acute MI. ECG may be normal in other causes of cardiogenic shock.
• Chest X-ray: can show tension pneumothorax, widened mediastinum in aortic dissection, signs of LVF.
• Blood tests:
  • Urea, electrolytes and creatinine can assess renal function
  • Liver function tests
  • Full blood count 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 (e.g. there may be high BNP levels in pulmonary embolism, atrial fibrillation and sepsis);⁵ BNP levels may be more practical in monitoring progression in CCU/ICU
• Echocardiography: this can establish the cause of cardiogenic shock, e.g. acute ventricular septal defect, pericardial tamponade

Usual management of acute myocardial infarction

This should also take place including:

• Aspirin ± clopidogrel
• Heparin
• Glycoprotein IIb/IIIa inhibitors (for high-risk patients with non-ST-segment-elevation myocardial infarction).^6,7
• Glycaemic control
• Nitrates may be a useful treatment as they can effectively lower preload and afterload, provided the blood pressure can support them. Care must be taken as vasodilators and beta-blockers usually used in the treatment of MI may cause hypotension and worsen tissue perfusion.

Pharmacological inotropic support

• Vasopressor/inotropic support with dopamine, dobutamine, levosimendan or epinephrine may be needed.
• However, one study suggested that dopamine might be associated with increased mortality.⁸
• Another study suggested that levosimendan improves haemodynamic performance when compared to dobutamine and may lower mortality in patients with low-output heart failure.⁹

Intra-aortic balloon pump counterpulsation

• Intra-aortic balloon pump counterpulsation (IABP) 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.¹⁰

Revascularisation

• Revascularisation with thrombolysis, percutaneous intervention or coronary artery bypass surgery should be considered.
• The SHOCK trial found that early revascularisation (angioplasty or coronary artery bypass graft) improves 1-year survival in patients under the age of 75 with acute myocardial infarction and cardiogenic shock when compared to medical treatments (including thrombolysis and intra-aortic balloon counterpulsation).¹¹ This survival advantage seems to persist at 3 and 6 years.¹²
• 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, are transferred to a centre where revascularisation can take place.¹³

See Acute Myocardial Infarction Management for further details.

• 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 fails and the cause of the cardiogenic shock is potentially reversible. A recent study has found them to be a safe and effective therapy.¹⁴
• Non-invasive positive pressure ventilation (NIPPV) may be helpful in mild-moderate cases of cardiogenic shock (provided the blood pressure can support it).

• Cardiogenic shock is the leading cause of death in acute myocardial infarction.⁴
• Mortality rates may be 70-90%, reduced to 40-60% if patients are treated aggressively.¹⁰
• A recent study showed that among patients with cardiogenic shock who survive for 30 days after an ST-segment elevation myocardial infarction, 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.¹⁵

• Early coronary revascularisation in patients post-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.¹⁶