Kardiogen chock

Bakgrund¹²

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. 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):

• Clinical criteria:

  • Sustained hypotension (systolic BP <90 mmHg) for more than 30 minutes, or

  • Support needed to maintain systolic BP at 90 mmHg or

  • Urine output 30 mL per hour or less or

  • Cool extremities.

• Haemodynamic criteria:

  • Depressed cardiac index (2.2 L per minute per square metre of body surface area or less) and

  • Pulmonary-capillary wedge pressure >15 mmHg.

Etiologi¹

Cardiogenic shock most commonly occurs as a complication of acute myocardial infarction (MI). It occurs in 5-8% of patients with ST-segment elevation MI and 2-3% with non ST-segment elevation MI. It is a medical emergency requiring immediate resuscitation. Other causes are as follows:

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.

• Myokardit.

• 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.

Riskfaktorer

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

• 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.

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

• Bröstsmärtor.

• Illamående och kräkningar.

• Dyspnoea.

• Profuse sweating.

• Confusion/disorientation.

• Palpitations.

• Faintness/syncope.

Skyltar

• 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.

Ledning

• Cardiogenic shock is a medical emergency, always treated in hospital.

• The broad areas of treatment are as follows:

  • Assess airway, breathing and circulate - intubate and ventilate if needed, gain intravenous access and give fluids if necessary.

  • Ongoing monitoring of vital signs, including urinary catheterisation to monitor fluid balance.

  • Investigations to look at current function and possible cause -eg, U&E, LFT, FBC, cardiac enzymes, troponin, brain natriuretic peptide (BNP), pregnancy test in a woman of reproductive age, ECG, CXR.

  • Further imaging as guided by the clinical picture.

  • Inotropic support and symptom relief.

  • Treat the underlying cause, for example with revascularisation after an MI.

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Prognos¹³

• Cardiogenic shock carries a mortality rate over 50%, with some sources quoting mortality as high as 80%.

• Factors increasing the risk of early mortality include age of 75 or over, peripheral arterial disease, chronic kidney disease and female sex.

• 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 death.⁴

Förebyggande

• 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 shock¹ and better management of cardiovascular risk factors and thus a reduction in MI should also reduce rates.