Cardiogenic shock

What is cardiogenic shock?

Cardiogenic shock occurs when there is failure of the pump action of the heart, resulting in a decrease in cardiac output causing reduced end-organ perfusion^{1 2} . 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 (BP) <90 mm Hg for more than 30 minutes)³ .

• Tissue hypoperfusion (cold peripheries, or oliguria <30 ml/hour, or both).

Cardiogenic shock most commonly occurs as a complication of acute myocardial infarction (MI). It occurs in 7% of patients with ST-segment elevation MI and 3% with non ST-segment elevation MI⁴ . It is a medical emergency requiring immediate resuscitation.

Cardiogenic shock causes

Cardiogenic shock is most often caused by acute MI, particularly affecting the anterior wall of the heart⁵ .

Due to an intrinsic heart problem

• 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 (PE).

• 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, beta-blockers) or due to metabolic disturbance (eg, acidosis, hypokalaemia or hyperkalaemia, hypocalcaemia).

• Thyrotoxic crisis.

Risk factors for cardiogenic shock

• It is more likely to develop in the elderly and in those with diabetes⁶ .

• 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.

Cardiogenic shock symptoms

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.

As many patients with cardiogenic shock have had an acute 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.

Cardiogenic shock treatment

• 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 co-existent 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)⁷ . BNP levels may be more practical in monitoring progression in CCU/ICU.

  • Perform an ECG early: this can show acute 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 the 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 medications used include dopamine, dobutamine, enoximone, and milrinone.

• Although inotropes increase cardiac output, they may also increase mortality due to increased tachycardia and myocardial oxygen consumption leading to arrhythmia and myocardial ischaemia⁸ .

• At present, there are no convincing data supporting any specific inotropic or vasodilating therapy to reduce mortality in haemodynamically unstable patients with cardiogenic shock and low cardiac output⁹ .

Intra-aortic balloon pump (IABP) counterpulsation

• IABP counterpulsation increases cardiac output and improves coronary artery blood flow.

• Although evidence suggests that IABP may have a beneficial effect on some haemodynamic parameters, there is no strong evidence of survival benefits to support the use of IABP in infarct-related cardiogenic shock¹⁰ .

Revascularisation

• Revascularisation with thrombolysis, percutaneous intervention or coronary artery bypass surgery should be considered.

• The SHOCK trial (= SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK) found that early revascularisation (angioplasty or coronary artery bypass graft) improves one-year survival in patients under the age of 75 with acute MI and cardiogenic shock when compared with medical treatments (including thrombolysis and IABP). This survival advantage seems to persist at three and six years¹¹ .

See the separate Acute Myocardial Infarction Management article.

Other treatment options

• Percutaneous mechanical support can provide substantial haemodynamic improvement in refractory cardiogenic shock¹² .

• A Cochrane review found no evidence of a benefit from mechanical assist devices in improving survival for people with acute cardiogenic shock¹³ .

• Non-invasive positive pressure ventilation (NIPPV) may be helpful in mild-to-moderate cases of cardiogenic shock (provided the BP can support it).

• Moderate hypothermia may improve parameters of cardiac function¹⁴ .

Prognosis

• Despite improving survival in recent years, patient morbidity and mortality remain high¹ .

• The mortality rate of post-infarction cardiogenic shock was 80.0-90.0%. However more recent studies have shown a significant reduction of hospital mortality to approximately 50.0%¹⁵ .

• A 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 death¹⁶ .

Cardiogenic shock prevention

• 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 shock¹⁷ .