Dr Clare Colebourne MRCP DICM
SpR in ICU medicine, John Radcliffe hospital, Oxford
Focus on Assessment and Initial Management
While the definitive treatment of cardiogenic shock depends on the cause the initial management and assessment are essential to limit the damage due to global tissue hypoperfusion.
Initial treatment with supplemental high flow oxygen and opiate analgesia will go some way to reducing the tissue hypoxia and early recourse to mechanical ventilation will help by reducing the work of breathing and reduce the preload and afterload. Treatment of associated arrhythmia and electrolyte abnormalities is essential. Drugs commonly used in acute myocardial infarction such as vasodilators and beta-blockers will cause hypotension and may worsen tissue perfusion.
Electrocardiography and early echocardiography are essential to determine the cause of the cardiogenic shock and help guide further treatment. For example, right ventricular infarction characteristically requires higher filling pressures to maintain cardiac output; evidence of papillary muscle rupture or ventricular septal defect may need surgical intervention.
In cardiogenic shock due to myocardial infarction it may be necessary to augment cardiac output by one of three ways:
- Pharmacological inotropic support
- Intra-aortic balloon counterpulsation
- Revascularisation with:
- percutaneous intervention or
- coronary artery bypass surgery
Focus on Pharmacological agents
Ventricular filling needs to be optimised to make the diagnosis of cardiogenic shock and this may need to be guided with the insertion of a pulmonary artery catheter. In situations where the systolic BP is above 80mmHg, dobutamine has traditionally been the drug of choice. It is a pure beta-1-adrenergic agonist with direct inotropic effects to improve cardiac contractility and cardiac output with little purported chronotropic effects. However, dobutamine can have peripheral vasodilatory effects leading to worsening hypotension and in addition can cause arrhythmias and increase myocardial oxygen demand and worsen ischaemia. It should only been seen as a bridging measure to definitive treatment.
If the cardiogenic shock is associated with a systolic blood pressure below 80mmHg dopamine is an option in view of its mixed vasopressor/inotropic effects. In refractory cases, noradrenaline may be needed for its vasopressor effects to maintain vital organ perfusion. Other agents include the phosphodiesterase inhibitors Milrinone and Amrinone (so called "ino-dilators"). These can be used as add on agents as they work via a different pathway to the other inotropes.
The novel calcium filament sensitiser Levosimendan has been the subject of interest in recent years. This drug stabilises the troponin C – Ca2+ binding and reduces the inhibitory effects of troponin I. Its use has been well studied in acute exacerbations of chronic heart failure and there is increasing data supporting its use in cardiogenic shock.
Clearly all the above agents are all supportive measures to stabilise the patient prior to some form of definitive therapy, and it is important to emphasise that all these pharmacological agents are associated with potentially significant side effects.
Focus on intra-aortic balloon counter-pulsation
Mechanical augmentation of cardiac output has the advantage of improving haemodynamics with no concomitant increase in myocardial oxygen demand. Intra-aortic balloon counterpulsation (IABC) works to reduce the afterload on the left ventricle reducing myocardial work and in addition augments diastolic coronary blood flow (Table 1).
Table 1. Effects of Intra Aortic Balloon Conterpulsation
| Reduced left ventricular filling pressure|
| Reduced left ventricular wall stress|
| Reduced myocardial lactate production|
| Reduced myocardial oxygen extraction|
| Augmented diastolic coronary blood flow|
The IABC device is inserted by Seldinger technique or cut down through the femoral artery. A 35-50cc balloon inflates and deflates in time with the aortic waveform. Helium is used as the inflation gas as its low viscosity allows rapid inflation and deflation. The balloon is positioned just distal to the left subclavian artery and this is confirmed radiographically as the tip is radio-opaque.
Timing is essential and this can be synchronised with the intra-aortic pressure or with the electrocardiogram. The optimal timing is for balloon inflation to occur with the dicrotic notch to maximise diastolic coronary flow. Deflation occurs as late in diastole as possible just prior to ventricular ejection. The aim is to ensure that the end-diastolic pressure in the aorta is lower than in the left ventricular cavity to reduce the afterload.
No trial to date has shown a mortality benefit from IABC in cardiogenic shock secondary to acute myocardial infarction. However in the GUSTO trial, patients in shock who had IABP placed early did show a trend towards an improved mortality. The SHOCK trial also showed a trend towards an improved mortality but it was not a primary outcome measure and is difficult to dissect out the effects of subsequent coronary intervention.
It would appear that IABC is a useful bridging method to revascularisation. However, it is important to determine that there is a reversible cause to the cardiogenic shock and it is also important to remember that the morbidity associated with an indwelling IABC can be substantial (see table 2).
Table 2. Morbidity associated with Intra Aortic Balloon Conterpulsation
| Limb ischaemia (5-15%)|
| Balloon rupture|
Focus on revascularisation
The role of revascularisation in cardiogenic shock appears intuitive. In spite of this
until the early 1990’s there were no randomised controlled trials with clinical end-points designed to assess the mortality benefit of intervening in patients with cardiogenic shock complicating acute myocardial infarction.
There had been small non-randomised studies demonstrating markedly improved mortality rates in patients with cardiogenic shock complicating acute myocardial infarction who underwent revascularisation. However, there was clear selection bias.
In 1999 a prematurely terminated randomised controlled trial comparing angioplasty with conventional therapy in 55 patients reported no difference in mortality (‘SMASH’). The trial suffered from poor recruitment rates and was criticised for low rates of use of support such as intra-aortic balloon pumps, ventilatory strategies and thrombolysis.
A 1999 landmark trial conducted in 30 American centres by Hochman et al finally produced meaningful results. The group took five years to recruit 302 patients having screened over 1000. Patients with acute myocardial infarction complicated by cardiogenic shock were randomised to receive either intensive medical therapy alone or medical therapy with revascularisation within six hours of diagnosis (coronary artery by-pass grafting or percutaneous intervention). Those randomised to receive intensive medical therapy had high levels of intensive care support, thrombolysis and use of the intra-aortic balloon pump. They were also able to undergo revascularisation at more than 54 hours from diagnosis. Eligibility was determined from pulmonary artery catheter data except in those with anterior myocardial infarction in whom it was not deemed necessary. Patients were well matched. The average age of the patients was 66 years and 32% of the group were women. The trial was powered to detect an absolute difference of 20% in the 30 day mortality rate where n=300.
The primary outcome measure of 30 day mortality was negative with a rate of 56% in the intensive medical therapy group and 46% in the early revascularisation group however the secondary end-point of mortality at six months, showed a significant absolute mortality reduction of 12.8%. In a six year follow up study this benefit appeared to be sustained. These data would suggest that the benefit of revascularisation early could improve the outcome later by a salvage effect on left ventricular function. Similar results were shown in the ‘GUSTO’ trial of early revascularisation after myocardial infarction that included patients with cardiogenic shock.
It appears that immediate survival following cardiogenic shock is not dependent on early revascularisation but may well be dependent on good medical and intensive care. This is supported by the less than expected mortality rate in both groups in the SHOCK trial. The cause of the benefit over a longer period is difficult to dissect but could represent attrition from worse left ventricular function after recovering from the initial episode.
Key Learning Points
- Early echocardiography is important to establish the cause of cardiogenic shock
- Pharmacological inotropes have a bridging role due to the significant increase in myocardial oxygen demand
- Intra-aortic balloon conunterpulsatio is a useful measure to increase coronary flow and reduce afterload
- Intensive medical treatment improves outcome
- Revascularisation appears to have no immediate effect on mortality but confers a long-term survival benefit
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Annals of Internal Medicine 1999; 131(1):47-59
Advances in positive inotropic threrapy: Levosimendan.
Crit Care Med 2003;31:2408-2409
Hochman JS, Sleeper LA, Webb JG, Sanborn TA, White HD, Talley JD et al.
Early revascularisation in acute myocardial infarction complicated by cardiogenic shock.
Hibbard MD, Holmes DR Jr, Bailey KR, Reeder GS, Bresnahan JF, Gersh BJ.
Percutaneous transluminal coronary angioplasty in patients with cardiogenic shock.
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Urban P, Stauffer JC, Bleed D et al.
A randomised evaluation of early revascularisation to ttreat shock compliacating acute myocardial infarction: the (Swiss) multicentre trial of angioplasty for shock – (S)MASH.
Eur Heart J 1999;20:1030-8.
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Extended mortality benefit of early postinfarction reperfusion. GUSTO-I Angiographic Investigators. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries Trial.
Hochman JS, Sleeper LA, Webb JG, Dzavik V, Buller CE, Aliward P et al.
Early revasularisation and long-term survival in cardiogenic shock complicating acute myocardial infarction.