INTENSIVE CARE

Ischaemic cardiogenic shock

Learning objectives

Ida-Fong Ukor
After reading this article you should be able to:

Lisen E Hockings

Abstract
Ischaemia is the most common underlying cause of cardiogenic shock.
Cardiogenic shock occurs in up to 10% of patients presenting with
acute myocardial infarction and is the leading cause of death. Myocardial
ischaemia results in both systolic and diastolic dysfunction and triggers a
maladaptive feedback loop that can ultimately result in tissue hypoxia,
multi-organ dysfunction and death. Myocardial dysfunction can be complicated by a systemic inflammatory response syndrome (SIRS) as a result of
systemic hypoxia. Echocardiography is key to diagnosis and to exclude
conditions requiring urgent surgical intervention. Serial assessment can
be used to monitor response to interventions and/or complications.
Resuscitative aims are immediate cardiorespiratory stabilization to facilitate urgent revascularization. Both pharmacological and mechanical supportive techniques are used. Mortality rates for patients who develop
ischaemic cardiogenic shock remain high, and further research into strategies to prevent and treat the condition is required.

and a significantly decreased cardiac index (CI) (<1.8

litres/minute/kg without support or <2.0 litres/minute/kg
with support) and

adequate or excessive filling pressures (e.g. central venous
pressure (CVP) >10e15 mmHg or pulmonary artery occlusion pressure (PAOP) >15e18 mmHg)1e4
Clinical correlates suggestive of cardiogenic shock include:
cool, mottled peripheries; oliguria; elevated jugular venous
pressure; and altered mental state. Elevated serum lactate (2
mmol/litre) suggests inadequate cellular oxygen supply.1,2,5
Ischaemia is the most common underlying cause of cardiogenic shock. Other potential causes include end-stage cardiomyopathy, pericardial tamponade, myocarditis, myocardial
contusion, valvular heart disease, left ventricular outflow tract
obstruction, dysrhythmia and septic shock with severe myocardial depression.2
Advances in early intervention and revascularization (percutaneous coronary intervention (PCI) and coronary artery bypass
grafting (CABG)) for myocardial infarction (MI) have seen a
dramatic fall in overall mortality rates for all patients presenting
with MI over recent decades. However, in the subset who
develop cardiogenic shock, mortality has remained high at
approximately 50%.1e3,5
Cardiogenic shock occurs in up to 10% of patients presenting
with acute myocardial infarction and is the leading cause of
death. The vast majority of patients who develop ischaemic CS
will have suffered ST elevated myocardial infarction (STEMI),
but it is also seen after non-ST elevated myocardial infarction
(NSTEMI). Patients who develop CS after NSTEMI tend to do so
later in the course of their hospital admission, and are older with
more significant comorbid diseases. The mortality rate for CS is
not different between STEMI and NSTEMI patients.2

Keywords Acute myocardial infarction/ischaemia; cardiogenic shock;

myocardial revascularization
Royal College of Anaesthetists CPD matrix: 1B04, 2C01, 2C03, 2C04, 3C00

Definition and incidence

Shock is a clinical state in which there is an imbalance between
cellular oxygen supply and demand resulting in tissue hypoxia.
Cardiogenic shock (CS) is shock occurring as a result of primary
cardiac pathology with inadequate cardiac output. It can be
thought of as persistent hypotension and tissue hypoperfusion
induced by heart failure after adequate correction of preload and
major arrhythmia. It is defined primarily on the basis of haemodynamic parameters:

persistent systemic hypotension
 systolic blood pressure (SBP) <90 mmHg for 30 min or
 mean arterial pressure (MAP) 60 mmHg or 30 mmHg
below baseline
 the need for vasopressors or intra-aortic balloon counterpulsation (IABP) to achieve these targets

Pathophysiology

Ida-Fong Ukor BMedSci MBBS is an Intensive Care Registrar and

Anaesthetic Trainee at the Austin Hospital in Melbourne, Australia.
Competing interest: none declared.

Ischaemic CS can result from a large primary MI or may develop

in the setting of delayed extension of the original infarction. Of
patients who develop CS after MI, registry data suggest that only
up to 30% are in CS at hospital presentation. More than 70%
develop CS after presentation to hospital with a median time to
onset of 7e10 hours after MI in STEMI, and over 70 hours after
MI in NSTEMI.2,6,7

Lisen E Hockings MBBS(Hons) FANZCA FCICM PGDipEcho is a Consultant

Anaesthetist and Intensivist at Papworth Hospital in Cambridge, UK,
and an Honorary Intensivist at The Alfred Hospital in Melbourne,
Australia. Competing interest: none declared.

ANAESTHESIA AND INTENSIVE CARE MEDICINE 15:2

define cardiogenic shock according to both clinical and haemodynamic parameters

explain the pathophysiological processes that can cause or
contribute to cardiogenic shock in the setting of myocardial
ischaemia
explain the processes of acute resuscitation of patients in
ischaemic cardiogenic shock as they relate to pharmacotherapy,
mechanical support and revascularization
recognize the need for urgent revascularization in the setting of
myocardial ischaemia

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Infarction or necrosis of large areas of myocardial tissue leads

to impaired contractility, a fall in stroke volume (SV), and hence
cardiac output and systemic MAP. The fall in MAP e particularly
diastolic blood pressure (DBP) e further compromises myocardial perfusion. These changes provoke a host of neurohormonal
responses aimed at rectifying the fall in cardiac output by
attempting to increase circulating blood volume and perfusion
pressure. Sympathetic nervous system activation and stimulation
of the reninangiotensinealdosterone system cause tachycardia,
widespread vasoconstriction and retention of salt and water.
These compensatory responses are ultimately maladaptive. In
addition to disordered systolic contraction, myocardial ischaemia
also results in impaired diastolic relaxation with an increase in
left ventricular end-diastolic volume (LVEDV) (systolic heart
failure) and pressure (LVEDP) (diastolic heart failure), increased
ventricular wall stress, a further fall in coronary artery perfusion
and ischaemia or infarction of already compromised myocardium. Increased LVEDP may result in pulmonary oedema with
resultant increased work of breathing (and oxygen consumption)
and hypoxaemia. The combination of systolic and diastolic
dysfunction and maladaptive responses results in a feedback
loop that cycles towards ongoing systemic hypotension, worsening tissue hypoxia and lactic acidosis, multi-organ failure, and
eventual death.2,3
An important component of the pathophysiology of ischaemic
CS is the systemic inflammatory response syndrome (SIRS).
Inadequate cardiac output results in widespread tissue hypoxia
and triggers the release of inflammatory mediators that generate
a SIRS response. There is evidence to suggest that the SIRS
response contributes significantly to vascular endothelial
dysfunction and ischaemiaereperfusion injury and results in
further myocardial damage in areas of hypoperfusion. Strong
associations have been demonstrated between higher levels of
baseline inflammatory markers and increased incidence of CS or
death in the setting of STEMI.6
Mechanical complications of myocardial ischaemia that result
in cardiogenic shock are less common in the era of early revascularization. They occur in a bimodal distribution with most
occurring within 24 hours of the onset of MI, and the remainder
within the first week. Mechanical complications can include
mitral regurgitation (MR) e either due to papillary muscle rupture
or post-infarction LV remodelling; ventricular septal rupture; LV
free wall rupture with tamponade; and LV aneurysm.7

oliguria is frequently present. Distended jugular veins, chest

crepitations and hypoxia are indicative of predominantly left
ventricular (LV) failure, while a clear chest and the presence of
Kussmauls sign* suggest right ventricular (RV) failure. A third
or fourth heart sound is often heard on auscultation of the
praecordium, and there may be a systolic murmur in the setting
of ischaemic mitral regurgitation (MR) or ventricular septal
defect (VSD). Initial bedside investigations must include a 12lead ECG looking for signs of myocardial ischaemia, a chest X-ray
to determine evidence of pulmonary oedema (and exclude other
causes of shock), and rapid focused echocardiographic assessment of cardiac function (looking particularly at biventricular
function and volume status; and for regional wall motion abnormalities (RWMA); mechanical complications of MI; or alternative cause of shock, e.g. pulmonary embolus, aortic
dissection). An arterial blood gas, electrolyte panel, full blood
count, coagulation profile and cardiac enzyme measurement
complete the initial evaluation.2,3 A group and screen should be
taken in case of alternative diagnosis or complication requiring
urgent transfusion.
Monitoring should include continuous ECG and oxygen
saturation, invasive arterial and central venous pressures (central venous access also facilitates administration of potent vasoactive agents), and urine output assessment via an in-dwelling
urinary catheter. Pulmonary artery catheterization is not recommended routinely in the management of patients with
ischaemic CS but may be considered in a minority of patients e
particularly in the setting of persistent hypotension despite
inotropic support.8

Management
Reperfusion
The goal of early resuscitation and stabilization is to treat
emergent threats to life and facilitate and expedite (not delay)
reperfusion. Early revascularization of the occluded coronary
vessel(s) is paramount to effective management of ischaemic CS
with demonstrable mortality benefit. In settings where primary
PCI (pPCI) or cardiothoracic surgical interventions are not
readily available, both in-hospital and pre-hospital thrombolysis
should be considered.6,7,9
Mechanical
complications
require
urgent
surgical
intervention.
Resuscitation and stabilization
The principles of resuscitation and stabilization of the patient in
CS are the same as those of any shocked patient e aiming to
alleviate symptoms, stabilize haemodynamics and respiratory
function, and identify and treat the underlying cause. Intubation and mandatory ventilation are often necessary to manage
hypoxia, respiratory distress or obtundation, as well as to
reduce the work of breathing. The haemodynamic effects of
positive pressure ventilation (PPV) may assist by decreasing
afterload in LV failure. However, the implications of PPV for the
RV should also be considered (reduced preload and increased
afterload). Furthermore, the choice of intubation drugs should

Assessment and evaluation

Prompt assessment of the shocked patient and diagnosis of CS is
critical to enable rapid implementation of appropriate life-saving
therapy. As with the approach to all critically ill patients,
assessment and management should proceed simultaneously e
ideally in a fully equipped resuscitation area, and using a teambased approach. A short focused history, with concurrent
resuscitation, should be obtained however this may not be
possible as cerebral hypoperfusion and an acute confusional
state or coma is common. Collateral history is often required.
Other aetiologies of a shocked state should be considered.
Clinical assessment in CS usually reveals evidence of global
hypoperfusion and end organ failure. A combination of pallor or
cyanosis, cool peripheries, dysrhythmias, tachypnoea and

ANAESTHESIA AND INTENSIVE CARE MEDICINE 15:2

Kussmauls sign: a paradoxical rise in jugular venous pressure on

inspiration in the spontaneously breathing patient.

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Levosimendan is a novel inodilator with calcium sensitizing

and K-channel opening properties that provides inotropy and
lusitropy without increasing myocardial oxygen demand. Systemic vasodilatation may result in hypotension or the need for
concomitant vasopressor administration. Despite the theoretical
pharmacological benefit of this agent on myocardial oxygenation, the majority of trials to date have excluded patients with
cardiogenic shock. Further research is needed.

take into consideration a significantly prolonged circulation

time in the shocked patient, and the likely haemodynamic
consequences of the agents. Blunting of the sympathetic nervous system response to shock will result in a fall in endogenous circulating catecholamines regardless of the induction
agent used. Non-invasive ventilation (NIV) may be considered
to alleviate symptoms in the conscious patient, but neither
continuous positive airway pressure (CPAP) nor non-invasive
positive pressure ventilation (NIPPV) have been shown to
reduce mortality or the rate of intubation in patients in pulmonary oedema.8
Careful fluid resuscitation if hypovolaemia is identified can be
of benefit in restoring adequate filling pressures, particularly in
the setting of RV infarction/failure. Persistent cardiac
dysrhythmia should be aggressively managed with defibrillation
(for atrial or ventricular tachyarrhythmias) or temporary pacing
(for bradyarrhythmias) in conjunction with electrolyte replacement and pharmacological therapy in accordance with published
guidelines.7,10 Blood sugar should be monitored and controlled.
Acidosis may further depress myocardial function and should be
avoided or treated where possible.

Non-pharmacological therapy
Persistent haemodynamic instability despite titration of vasoactive agents may necessitate consideration of additional nonpharmacological supports such as IABP and extracorporeal
membrane oxygenation (ECMO).
IABP is the most widely utilized mechanical support measure
in the setting of refractory CS. It works on the principles of
augmentation of DBP and hence improved diastolic coronary
perfusion pressure, and reduction of LV afterload with concomitant reduction of myocardial oxygen consumption. The use of
IABP has become controversial with the advent of early revascularization techniques for acute MI and CS. A recent metaanalysis supports the use of IABP for CS where thrombolysis is
the primary mode of revascularization however no benefit was
found post-pPCI/-bypass surgery with the suggestion of worsened outcome.12
Veno-arterial or cardiac ECMO is an emerging form of mechanical circulatory support (MCS) for the management of refractory circulatory failure due to CS. Conceptually analogous to
cardiopulmonary bypass used for cardiothoracic surgery, ECMO
can be inserted centrally (through a sternotomy) or peripherally
via central venous access cannulation (typically femoral or jugular) and return arterial cannulation (typically femoral, but
occasionally axillary). Due to the highly specialized and
resource-intensive nature of ECMO support, this is a treatment
largely confined to major tertiary and quaternary referral centres.
In those who would otherwise succumb to CS, ECMO provides a
feasible bridging therapy to consideration of implantation of
ventricular assist device (VAD), cardiac transplantation (bridge
to decision); or meaningful clinical recovery.

Pharmacotherapy
Immediate, resuscitative cardiovascular support is generally
attempted pharmacologically:
Oxygen: oxygen should be administered to patients who are
hypoxaemic (SpO2 <90%). The role of oxygen supplementation
in patients who are not hypoxaemic remains controversial and
further research is needed.7,8
Exogenous catecholamines, inotropes and vasopressors: in the
acute setting exogenous catecholamines are used to increase
MAP with the hope of providing adequate end organ perfusion e
both coronary and systemic. However, excessive increases in
systemic vascular resistance (SVR) may result in increased
afterload and worsen cardiac failure. Nearly all inotropes in
clinical use improve cardiac contractility at the cost of increasing
myocardial oxygen consumption in a condition where myocardial oxygen demand already exceeds supply. Furthermore, they
are potent chronotropes and may induce tachycardia that reduces diastolic coronary perfusion time, or a more malignant
tachydysrhythmia.
There are no clear guidelines to inform the use of exogenous
catecholamines in cardiogenic shock and clinical evidence is
limited. Dopamine has previously been recommended as a first
line agent in the management of CS. However, recent randomized control trial evidence suggests that noradrenaline is the
safest first line vasopressor in this setting.1,7,11 Predominantly
inotropic agents including adrenaline, dobutamine, milrinone
and enoximone are all employed in the setting of ischaemic
cardiogenic shock. Pharmacokinetic data suggest that first-line
treatment in the setting of resuscitation should begin with
adrenaline or dobutamine due to the more rapid onset of action
without the need for a loading dose. The choice of inotropes in a
given setting tends to be based on individual experience, pathophysiological understanding and institutional protocols.1
Whichever agent(s) is/are chosen, careful titration to clinical
and haemodynamic end-points is required and the agent(s)
should be weaned and ceased as soon as practicable.

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Conclusion
Ischaemic CS remains a challenging condition to treat and continues to be the primary cause of death after MI. Rapid diagnosis
and early revascularization are the keys to improving outcomes,
particularly mortality. New pharmacological and nonpharmacological interventions are required. Ongoing research
into the role of SIRS in the pathophysiology of the shock state
after MI, the potential role of stem cells in promoting myocardial
regeneration post-infarction, and support of the systemic circulation (mechanical and pharmacological) is required, in addition
to preventative and public health measures to minimize the
incidence of myocardial ischaemia.
A

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