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Cardiogenic Shock

Synonyms: Acute left ventricular failure with hypotension, acute hypotensive heart failure, hibernating myocardium, myocardial stunning

Acute hypoperfusion of the tissues and organs, usually with associated hypotension, due to a primary failure of the pump action of the heart, where the circulating blood volume is adequate. Commonest cause is myocardial death/stunning after infarction or critical ischaemia. This scenario often becomes a self-perpetuating downward spiral. Ongoing myocardial ischaemia causes further deterioration in cardiac function and coronary hypoperfusion, leading to worsening ischaemia. The condition can also arise where there is a relatively minor worsening in cardiac function, superimposed on previously impaired cardiac reserve.

Other causes include:

• Acute dysrhythmia compromising cardiac output, eg ventricular tachyarrhythmia, fast AF, or severe bradycardia due to complete heart block
• Acute mitral regurgitation (usually late post-MI complication due to ruptured chordae tendinae)
• Rupture of interventricular septum (again, usually occurring as late post-MI complication)
• Rupture of free cardiac wall (late post-MI or cardiac trauma)
• Myocardial contusion (often post-RTA from steering wheel impact)
• 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
• Suppression of myocardial contractility by drugs, eg ß-blockers; or metabolic disturbance, eg acidosis, hypo or hyperkalaemia, hypocalcaemia
• Pericardial tamponade/severe constrictive pericarditis
• Acute, severe pulmonary embolism
• Myocardial suppression due to bacteraemia/sepsis (although, strictly speaking, this would be defined as septic shock)

Epidemiology
Incidence Occurs in 5-10% of patients who suffer myocardial infarction.¹ At initial presentation after MI, before treatment, the rate may be as high as 29%.² There are no reliable figures for the community incidence of cardiogenic shock due to non-ischaemic causes.

Risk factors It is more likely to develop in the elderly and diabetics.³ Anterior and right-ventricular 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.

Presentation 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

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

Signs It is important to conduct a calm, yet rapid and thorough assessment. The patient should be sat upright and given high-flow oxygen (even if pre-existing airways disease; hypoxia kills in minutes but hypercapnea takes hours and can be corrected later). It is wise to establish early intravenous access. Pulse, temperature and BP should be recorded immediately and initial investigations such as ECG and CXR commenced whilst the examination is being conducted. Potentially correctable underlying causes of the state of shock such as tension pneumothorax, massive PE, occult haemorrhage or hypovolaemia, sepsis, pericardial tamponade, anaphylaxis or respiratory failure should be kept in mind whilst the assessment is carried out.

• Pale, mottled, cold skin
• Hypotension, eg. systolic BP<90, or 30mmHg below baseline for >30mins, with a cardiac index <2.2, associated with signs of hypoperfusion
• Tachycardia/bradycardia
• Raised JVP/distension of neck veins
• Peripheral oedema may be present if pre-existing congestive cardiac failure
• Quiet heart sounds± S₃, S₄
• Check for heaves, thrills and murmurs
• Bibasal pulmonary crackles will often be evident but are not pathognomonic or necessary to make the diagnosis
• Wheeze may occur and should not necessarily be taken as a sign that airflow limitation is the major problem
• Oliguria (catheterisation is a useful early monitoring intervention)

Differential Diagnosis Other causes of shock:

• Metabolic
• Hypovolaemic
• Septic
• Anaphylactic
• Addisonian crisis
• Post-anaesthesia
• Cocaine/MDMA (ecstasy)/amphetamine toxicity

Investigations Initiate first line tests as soon as possible during assessment

• ECG, CXR, arterial blood gases, U&E, creatinine, FBC, cardiac enzymes inc. troponins
• Echocardiography can confirm diagnosis and rule out other causes
• Cardiac catheterisation– pulmonary capillary occlusion pressure >15mm Hg, cardiac index >2.2 l/min/m.⁵

Management
General

• Airway protection/maintenance
• Oxygen
• Diamorphine analgesia 2.5–5mg if sufficient respiratory effort/rate
• IV furosemide 40–80 mg if systolic BP>100 mmHg
• Treat any underlying diagnosis, electrolyte abnormalities, arrhythmias
• Vasopressor agents such as dopamine,and vasopressin and inotropes such as dobutamine, adrenaline and noradrenaline are often used. There is very little empirical evidence to support their efficacy in terms of survival,¹¹ but their use is widespread, according to individual clinical experience
• Intra-aortic balloon counterpulsation (IABP) and artificial ventilation are established and efficacious treatments for severe cardiogenic shock¹²
• In patients with adequate systolic BP, vasodilators such as nitrates or sodium nitroprusside have been shown to be effective¹³
• Ventricular assist devices may allow survival to transplantation, and like IABP, may be used when medical treatment fails and the cause of the cardiogenic shock is potentially irreversible..

Caused by myocardial ischaemia/infarction The highest priority must be given to ameliorating or removing the condition, to allow recovery of sufficient myocardium to perfuse vital organs.

• Chewed aspirin 150–300mg (if no contraindication)
• Corrective therapy for ischaemia/infarction, ie thrombolysis (check indications & contraindications) or PTCA ± stenting or if no ST-elevation/other indicators of MI: intravenous nitrates (if systolic BP>100 mmHg)± heparin
• Use of glycoprotein IIb/IIIa inhibitors¹⁴

Thrombolysis or PTCA?
It has been shown that early mechanical percutaneous coronary revascularisation in cases of acute MI complicated by cardiogenic shock is a strategy that reduces mortality compared to thrombolysis.^8,9,10 It has been a Class I recommendation of guidelines issued by The American College of Cardiology and The American Heart Association for some years. Resource and manpower issues mean that it is an extremely difficult acute therapy to administer. This situation is changing in the US,⁸ and may do so in the UK over the coming years.

Prognosis Mortality rate 50-80%.

Prevention Early coronary revascularisation with angioplasty or coronary surgery gives best results.

References Used

1. eMedicine Sharma S and Zevitz M, Cardiogenic shock
2. Babaev A, Frederick PD, Pasta DJ, et al; Trends in management and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock.;JAMA 2005 Jul 27;294(4):448-54.[abstract]
3. Casella G, Savonitto S, Chiarella F, et al; Clinical characteristics and outcome of diabetic patients with acute myocardial infarction. Data from the BLITZ-1 study.;Ital Heart J 2005 May;6(5):374-83.[abstract]
4. Hollenberg SM Kavinsky CJ, Parillo JE. Cardiogenic Shock. Ann Intern Med. 1999; 131: 47-59.
5. Hollenberg SM. Cardiogenic shock. Crit Care Clin. 2001;17(2): 391-410.
6. SIGN Guideline No. 35, Diagnosis and Treatment of Heart Failure due to Left Ventricular Systolic Dysfunction
7. SIGN Guideline No. 36, Antithrombotic Therapy
8. Babaev A, Frederick PD, Pasta DJ, et al; Trends in management and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock.;JAMA 2005 Jul 27;294(4):448-54.[abstract]
9. Clinical Evidence Early invasive cardiac revascularisation for MI with cardiogenic shock
10. Sleeper LA, Ramanathan K, Picard MH, et al; Functional status and quality of life after emergency revascularization for cardiogenic shock complicating acute myocardial infarction.;J Am Coll Cardiol 2005 Jul 19;46(2):266-73.[abstract]
11. Yazbek NF, Kleiman NS; Therapeutic Strategies for Cardiogenic Shock.;Curr Treat Options Cardiovasc Med 2004 Feb;6(1):29-41.[abstract]
12. Duvernoy CS, Bates ER; Management of cardiogenic shock attributable to acute myocardial infarction in the reperfusion era.;J Intensive Care Med 2005 Jul-Aug;20(4):188-98.[abstract]
13. Cotter G, Moshkovitz Y, Milovanov O, et al; Acute heart failure: a novel approach to its pathogenesis and treatment.;Eur J Heart Fail 2002 Jun;4(3):227-34.[abstract]
14. NICE Acute coronary syndromes - glycoprotein IIb/IIIa inhibitors (review) (No. 47)

Internet and further reading

• Kohsaka S, Menon V, Lowe AM, et al; Systemic inflammatory response syndrome after acute myocardial infarction complicated by cardiogenic shock.;Arch Intern Med 2005 Jul 25;165(14):1643-50.[abstract]
• Spencer FA, Meyer T; Heart failure and shock complicating acute coronary syndromes.;Curr Cardiol Rep 2005 Jul;7(4):276-82.[abstract]
• Yazbek NF, Kleiman NS; Therapeutic Strategies for Cardiogenic Shock.;Curr Treat Options Cardiovasc Med 2004 Feb;6(1):29-41.[abstract]
• Bouki KP, Pavlakis G, Papasteriadis E; Management of cardiogenic shock due to acute coronary syndromes.;Angiology 2005 Mar-Apr;56(2):123-30.[abstract]
• NICE Ischaemic heart disease - coronary artery stents (No. 71)
• Cochrane Collaboration Primary stenting versus primary balloon angioplasty for treating acute myocardial infarction [abstract and plain language summary]

Acknowledgements EMIS is grateful to Dr Sean Kavanagh for rewriting and updating this article. The final copy has passed peer review of the independent Mentor GP authoring team. ©EMIS 2006.

Last issued 08 May 2006