BJA Education, 23(5): 172e181 (2023)
doi: 10.1016/j.bjae.2023.01.006
Matrix codes: 1A02;
2A04; 2C01; 2C03;
2C04; 3C00; 3G00
Management of cardiogenic shock after acute
coronary syndromes
B. Milne1,*, J.R. Dalzell2 and G. Kunst1
1
King’s College Hospital NHS Foundation Trust, London, UK and 2NHS Golden Jubilee, Glasgow, UK
*Corresponding author: Benjamin.milne@kcl.ac.uk
Keywords: acute coronary syndrome; anaesthesia; cardiac procedures; shock; cardiogenic
Learning objectives
By reading this article you should be able to.

Define cardiogenic shock and understand its
pathophysiology after acute coronary syndromes
(ACS).

Assess the patient with, or at risk of cardiogenic
shock after ACS.

Discuss the key therapeutic and supportive steps
in managing patients with cardiogenic shock af-
ter ACS.
Cardiogenic shock (CS) represents a spectrum of potential
clinical presentations characterised by end-organ hypo-
perfusion and tissue hypoxia caused by primary cardiac
dysfunction, which can result in multiorgan failure and
death.1e3 It is the most common cause of in-hospital death
after acute coronary syndromes (ACS) (CS after acute
myocardial infarction [AMI]; CS-AMI) with a mortality rate of
40e70%.3,4
Benjamin Milne BSc FRCA is a specialty registrar in anaesthesia and
intensive care medicine at King’s College Hospital NHS Foundation
Trust and a NIHR academic clinical fellow. He is a core committee
member of the Pan-London Perioperative Audit & Research Network.
Jonathan R. Dalzell MD FRCP FESC FACC is a consultant cardiolo-
gist at NHS Golden Jubilee and the clinical lead for the Scottish Na-
tional Advanced Heart Failure Service.
Gudrun Kunst MD PhD EDAIC FRCA FFICM is a consultant
anaesthetist at King’s College Hospital NHS Foundation Trust and
professor of cardiovascular anaesthesia at King’s College London.
She serves as treasurer of the Association for Cardiothoracic
Anaesthesia & Critical Care and is the South London NIHR Clinical
Research Network lead for Anaesthesia, Perioperative Medicine &
Pain.
Accepted: 27 January 2023
© 2023 British Journal of Anaesthesia. Published by Elsevier Ltd. All rights reserved.
For Permissions, please email: permissions@elsevier.com
Advance Access Publication Date: 27 March 2023
Key points

Cardiogenic shock is the most common cause of
in-hospital death after acute coronary
syndromes.

Myocardial dysfunction triggers a compensatory
systemic vascular response.

The key to diagnosis is demonstration of end-
organ hypoperfusion.

Myocardial revascularisation by percutaneous
coronary intervention is the only evidence-based
treatment shown definitively to improve
outcome.

Pharmacological and mechanical circulatory
support enables revascularisation, advanced
therapies and recovery.
Traditionally, CS has been defined by haemodynamic
criteria derived from invasive monitoring, but recent defini-
tions describe a recognisable clinical phenotype (Table 1).1,3
However, oversimplistic classifications with arbitrary sys-
tolic arterial pressure (SAP) thresholds have inherent weak-
nesses, with a wide interpatient variability as to the SAP at
which hypoperfusion develops. Furthermore, compensatory
vasoconstriction may result in a spuriously reassuring SAP
despite clinically obvious peripheral hypoperfusion. Versatile
clinical and diagnostic skills are therefore required when
assessing such patients.
Aetiology
Acute myocardial infarction with subsequent left ventricular
(LV) dysfunction accounts for most cases of CS, and recent UK
registry data reveal that 8.9% of patients with ST-elevation
myocardial infarction (STEMI) develop CS-AMI.2,4 At coro-
nary angiography in the Culprit Lesion Only PCI vs Multivessel
PCI in Cardiogenic Shock (CULPRIT-SHOCK) study, 42% of
172

patients had left anterior descending (LAD) artery lesions,
with left circumflex (LCx) artery (21%), left mainstem (LMS)
artery (8%) and right coronary artery (RCA) (28%) representing
the majority of other causative lesions. The majority of pa-
tients (63%) had triple-vessel disease, whereas 23% had at
least one chronic total occlusion.5
Pathophysiology
Thrombotic total or subtotal occlusion of an epicardial coro-
nary artery obstructs, or restricts, perfusion to a region of
myocardium. Ischaemia and infarction ensue, characterised
by myocyte necrosis and acute myocardial dysfunction.6
Reduced contractility may result in declining cardiac output
(CO) and arterial pressure, and elevated LV filling pressures
(Fig 1). High LV end-diastolic pressure (LVEDP) reduces coro-
nary perfusion pressure (CPP), further exacerbating myocar-
dial ischaemia, and causes pulmonary congestion with
resultant worsening hypoxaemia and ischaemia.1
The pathophysiology of CS extends beyond a state of simple
‘pump failure’ and is characterised by multisystem dysfunc-
tion, which promotes its development and progression.
Reduced CO is detected by carotid arterial baroreceptors and
the renal juxtaglomerular apparatus, with consequent activa-
tion of the renineangiotensinealdosterone and sympathetic
nervous systems. The sequelae are intense peripheral vaso-
constriction and avid sodium and water retention, resulting in
a clinical syndrome of hypoperfusion with cool extremities,
rising lactate and, usually, fluid overload with high filling
pressures and congestion (‘cold and wet’ phenotype; Table 2).2,7
Acidosis, hypoperfusion and congestion exacerbate myocardial
dysfunction with resultant augmentation of adverse neuro-
hormonal activation resulting in a self-perpetuating spiral of
reduced CPP, increased myocardial ischaemia, worsening car-
diac function and circulatory collapse.6
Diagnosis and classification
Deciphering the temporal relationship between the onset of a
recognisable shocked state and the ischaemic precipitant is
complex. For example, patients with LMS or proximal LAD dis-
ease may present in profound shock, pulmonary oedema or
cardiac arrest. Similarly, proximal RCA disease can drive a shock
presentation secondary to high-grade atrioventricular block.
Other patients may present with ischaemic chest pain, which
can be insidious and protracted, before developing CS. A high
Table 1 Haemodynamic and clinical definitions of cardiogenic shock. LVEDP, left ventricular end-diastolic pressure; RVEDP, right
ventricular end-diastolic pressure; SAP, systolic arterial pressure. Haemodynamic definition e Reynolds and Hochman1; clinical
definition e Thiele and colleagues3
Haemodynamic definition Clinical definition
Persistent Cardiac index (<1.8 L SAP <90 mmHg
hypotension (SAP min1 m2 with adequate
<80e90 mmHg, or unsupported, or <2.0 volume and:
MAP 30 mmHg e2.2 L min1 m2 with
below baseline) support)
with: and:
Adequate/elevated
filling pressures
(LVEDP >18 mmHg or
RVEDP >10e15 mmHg
Cardiogenic shock management after ACS
degree of vigilance is thus required, to consider an ischaemic
cause in the patient with shock, and to prepare for potential CS
in the patient with more classical symptoms of ACS, especially
those with ECG evidence of a proximal LAD or LMS lesion.
Routine initial assessment of the CS-AMI patient should
include a focused clinical history, if possible, and examina-
tion, which alone may enable diagnosis by demonstration of
significant hypotension, clinical signs of inadequate end-
organ perfusion, or both (Table 1). Echocardiography will
help confirm suspected myocardial ischaemia, indicate the
region involved and can guide prediction of LV recovery or the
need for advanced heart failure therapies by the development
of Q waves (i.e. transmural irreversible infarction) in the
affected coronary territory. Echocardiography is essential to
assess for regional wall motion abnormalities; evaluate the
extent of LV dysfunction, right ventricular (RV) dysfunction, or
both; screen for mechanical complications (including ischae-
mic mitral regurgitation [MR] and ventricular septal rupture
[VSR]) and for pericardial or pleural effusions, which may
contribute to cardiorespiratory impairment.
Arterial (ABG) or venous blood-gas analysis is required to
assess the extent of hypoperfusion and shock severity, by
demonstration of a metabolic acidaemia and hyper-
lactataemia. Laboratory blood tests should include renal and
liver function tests (LFTs), which may provide further evi-
dence of end-organ hypoperfusion, and serum troponin, for
diagnostic purposes, and to indicate degree of cardiac muscle
loss. Pulmonary artery catheterisation (PAC) can assist initial
diagnosis, yielding highly useful quantitative information
with increasing value for increasing severity of illness, but
should not delay primary revascularisation.8
A readily applicable classification tool has been proposed
for patients across the risk/severity spectrum, with increasing
class associated with increasing mortality (Table 3).9
Management
Revascularisation
Myocardial revascularisation is the only evidence-based inter-
vention to reduce mortality in CS-AMI with the consensus
backing of numerous international guidelines. Therefore,
emergent angiography must be prioritised in any shocked pa-
tient with evidence of myocardial ischaemia on ECG.
Immediate revascularisation has been shown to signifi-
cantly reduce mortality at 6, 12 and 72 months, compared
with initial medical management, whereas delayed
Clinical signs of Cool peripheries
hypoperfusion Oliguria
Impaired mentation
Narrow pulse pressure
Laboratory signs of Metabolic acidaemia
hypoperfusion Increased serum
lactate
Increased serum
creatinine
BJA Education - Volume 23, Number 5, 2023 173
Cardiogenic shock management after ACS

Thrombotic (total or subtotal) occlusion

of epicardial coronary artery

Myocardial ischaemia
with or without infarction

Acute myocardial dysfunction

Pulmonary Increased end-
- reduced contractility
congestion diastolic pressure
- impaired relaxation

Reduced
Reduced coronary
cardiac
perfusion pressure
output

Systemic
Acidaemia
hypoperfusion

Neurohormonal response:

SNS RAAS
hyperactivation hyperactivation

Intense Sodium &

peripheral water
vasoconstriction retention

Fig 1 Pathophysiology of cardiogenic shock after acute myocardial infarction (CS-AMI) RAAS, renineangiotensinealdosterone system; SNS, sympathetic nervous
system.

Table 2 Physiological characteristics of cardiogenic shock phenotypes. Alternative shock phenotypes, include normotensive cardio-
genic shock (CS) (likely a compensatory pre-shock phase) and isolated right ventricular CS

Phenotype Cardiac Systemic Pulmonary capillary Notes

index vascular wedge pressure
resistance

‘Cold and wet’ Reduced Increased Increased The predominant (‘classic’) phenotype
Peripheral vasoconstriction and
intravascularly replete
‘Cold and dry’ Reduced Increased Normal Minority of patients
Euvolaemic
‘Wet and warm’ Reduced Reduced/normal Increased Minority of patients
Myocardial injury causes a predominate systemic
inflammatory response. Inflammatory mediators
cause vasodilation, impair mitochondrial function,
depress myocardial contractility and reduce
catecholamine sensitivity

174 BJA Education - Volume 23, Number 5, 2023

 Cardiogenic shock management after ACS

Table 3 Society for Cardiovascular Angiography & Interventions cardiogenic shock stages. Features typical for stage are in bold. CI,
cardiac index; CHF, chronic heart failure; CPR, cardiopulmonary resuscitation; CRT, capillary refill time; CS, cardiogenic shock; GCS,
Glasgow coma scale; JVP, jugular venous pressure; MCS, mechanical circulatory support; MI, myocardial infarction; NT-proBNP, N-
terminal pro-brain natriuretic peptide; PCWP, pulmonary capillary wedge pressure; SAP, systolic arterial pressure; UO, urine output.
Adapted with permission from Naidu and colleagues9

Stage Description Clinical findings

A At risk of developing CS, but without Normal JVP

At risk current signs or symptoms, e.g. large Warm and well perfused
acute MI, or new MI with prior Serum lactate <2.0 mmol L¡1
infarction/CHF SAP ≥100 mmHg
Reassuring invasive haemodynamics
B Evidence of haemodynamic Increased JVP
Beginning CS instability (i.e. hypotension or Warm and well-perfused
tachycardia) without hypoperfusion May have crepitations
Serum lactate <2.0 mmol L¡1
SAP <90 mmHg/MAP <60 mmHg/>30
mmHg decrease from baseline
Heart rate  100 beats min¡1
C Evidence of hypoperfusion Volume overload
Classic CS requiring single intervention Altered GCS, cool extremities,
(beyond fluid resuscitation) delayed CRT, UO <30 ml h1
Extensive crepitations
Lactate  2.0 mmol L¡1
Deranged renal/liver function
Increased NT-proBNP
CI <2.2 L min1 m2
PCWP >15 mmHg
D Failure of initial intervention Deteriorating signs/symptoms
Deteriorating to restore perfusion of hypoperfusion (as in C)
Increasing serum lactate
Deteriorating renal/liver function
Escalating doses/number of vasoactive
therapies/use of MCS device
E Circulatory collapse Unconscious
Extremis (actual or impending) Weak pulse
(A) Modifier e cardiac Profound hypotension despite maximal support
arrest with suspected Requiring multiple defibrillations/CPR
hypoxic brain injury Serum lactate ≥8 mmol L¡1
pH <7.2

revascularisation adversely affects outcomes.10,11 Subsequent
RCT evidence favours the prioritisation of immediate revascu-
larisation by percutaneous coronary intervention (PCI) of the
culprit lesion only in CS-AMI, with reduced all-cause mortality
at 30 days and 1 yr.5 Patients with multi-vessel disease should
thus receive a staged revascularisation strategy.
In the UK, angiography with follow-on primary PCI is per-
formed for STEMI patients if presenting within 12 h of symp-
toms (if deliverable within 120 min), or if presenting more
than 12 h after symptom onset with continuing myocardial
ischaemia or CS-AMI. Similarly, although PCI for non-STEMI
(NSTEMI) is usually guided by risk-stratification tools, imme-
diate angiography is offered in CS-AMI.12 Immediate angiog-
raphy and follow-on PCI is also indicated in patients
resuscitated from out-of-hospital cardiac arrest and ST
elevation on ECG; or with no ST elevation but a high proba-
bility of acute coronary occlusion (usually evidenced by hae-
modynamic or electrical instability).13
Surgical management of CS-AMI
Surgical revascularisation is largely reserved for patients in
whom PCI is not possible or there has been a procedural
complication such as coronary dissection or tamponade not
amenable to percutaneous drainage. Such intervention in a
patient with CS-AMI is clearly extremely high-risk and re-
quires careful individualised consideration.
Surgery is the primary therapy for mechanical complica-
tions of AMI such as acute severe ischaemic MR or VSR.
Without intervention, these complications are associated
with a dire prognosis. Where possible, it is current practice to
attempt to stabilise patients with short-term mechanical cir-
culatory support (MCS) such as an intra-aortic balloon pump
(IABP) or venoarterial extracorporeal membrane oxygenation
(VA-ECMO) before surgery. This allows resolution of end-
organ dysfunction and for friable areas of necrotic myocar-
dium to fibrose before subsequent surgical manipulation,
which increases the chances of successful repair.
Airway and breathing
Patients with emerging or evolving CS-AMI are likely to
require invasive ventilation, owing to altered mentation,
haemodynamic instability, impaired gas exchange and,
potentially, to facilitate PCI. Use of non-invasive continuous
positive airway pressure (CPAP) can be considered in patients
not appropriate for invasive ventilation, or those with less
severe shock state, but for this latter group preparation should

BJA Education - Volume 23, Number 5, 2023 175

Cardiogenic shock management after ACS
be made for emergent tracheal intubation. Mechanical venti-
lation should adhere to lung protective principles, including
low pressure and low tidal volume ventilation, to reduce the
release of inflammatory mediators, reduce the burden of
superimposed iatrogenic lung injury and optimise pulmonary
blood flow.14
The benefits of positive pressure ventilation should be
considered (improved oxygenation, reduced LV afterload and
work of breathing), alongside the detrimental effects (reduced
venous return and therefore preload, reduced RV output and
CO), in the context of the anatomical region of AMI. Lung
protective ventilation should be used with careful selection of
appropriate PEEP. This is particularly important in isolated RV
failure because of the harmful effect on RV afterload of
increased intrathoracic pressure.
Circulation
The aim of management in perioperative and intensive care is
to restore haemodynamic stability by reversing the patho-
physiological spiral described and providing end-organ sup-
port where necessary. No robust evidence exists for any
specific agent, and choice is guided by the clinician’s famil-
iarity and the presence of significant renal impairment. The
potential for all vasopressor and inotropic drugs to cause ar-
rhythmias needs to be considered, especially if shock has
already been associated with significant arrhythmias.
Hypotension is a common clinical feature requiring inten-
sive care input. Assessment of fluid status can be challenging,
especially in younger patients when the typical clinical signs of
congestion seen in older patients will be absent owing to more
effective compensatory mechanisms. The pathophysiological
mechanisms of CS-AMI do not leave the patient volume
deplete, doing the opposite, and so pursuing fluid resuscitation
is potentially hazardous. Furthermore, pharmacological man-
agement of hypotension often commences with noradrenaline
(norepinephrine) infusion. However, this is contentious as CS-
AMI is overwhelmingly associated with intense intrinsic
vasoconstriction and high systemic vascular resistance (SVR).
Extremely careful titration is required, with invasive moni-
toring, to avoid a clinically significant increase in LV afterload
secondary to a predominant vasopressor effect. In contrast,
inodilation can be beneficial in reducing LV afterload, imposed
by the adverse neurohormonal activation of the CS-AMI syn-
drome. Commonly used vasopressors and inotropes are
compared in Table 4.
Vasoactive management should be guided by invasive
monitoring, including an arterial catheter, and although there
is little in the way of specific evidence, a MAP between 60 and 65
mmHg is commonly targeted. Vascular access via the radial
artery is preferred for PCI, which should be considered when
siting arterial catheters or ABG sampling if the patient has yet to
undergo cardiac catheterisation. Arterial blood-gas moni-
toring, including serial lactate concentrations, can guide
resuscitation. A central venous catheter (CVC) may yield some
relevant information if there is an abnormal central venous
waveform or grossly increased central venous pressure. Echo-
cardiography can also be used as a haemodynamic monitor in
the ICU, guiding drug therapy, by assessment of trends in
intracardiac pressures and individual ventricular function in
response to drug titration. It can also inform ventilator man-
agement, particularly PEEP titration for optimal RV function.
Pulmonary artery catheterisation provides a large amount
of crucial data. Left and right heart filling pressures, CO/
176 BJA Education - Volume 23, Number 5, 2023
cardiac index (CI), SVR and pulmonary artery (PA) oxygen
saturation can be monitored continuously. This allows titra-
tion of vasopressor, inodilator, diuretic drugs and MCS. In
contrast, minimally invasive CO monitors based on arterial
waveform analysis have limited use in CS-AMI, because of
intense peripheral vasoconstriction and possible concomitant
use of IABP.
Sedation
Adequate sedation to enable optimal ventilation, reduce ox-
ygen consumption and avoid psychological harm must be
ensured, whilst minimising possible adverse effects from the
sedative agents. There is no robust evidence for or against the
use of specific drugs. The agents chosen should be used within
the context of the haemodynamic status of the patient and
taking care to avoid the harms of oversedation.15
Renal
More than one third of patients with CS-AMI will develop
acute kidney injury (AKI).16 Standard renal monitoring,
including hourly urine output and regular serum creatinine
should continue. Renal replacement therapy (RRT) can be
used to manage severe metabolic acidaemia and optimise
intravascular status. Continuous haemodynamically stable
methods, such as ultrafiltration or haemodiafiltration, are
most appropriate. Circuit heparinisation is useful if systemic
anticoagulation is required but may be inappropriate in
postoperative patients and risks development of thrombocy-
topenia. Alternatives, such as regional anticoagulation with
citrate, are increasingly being used.
Gastrointestinal and hepatic
Liver function tests should be assessed daily, with derange-
ment occurring in more than 50%, often indicating RV
congestion. Increased transaminase enzymes can indicate
hepatic hypoperfusion, and mandate further attempts to
stabilise haemodynamics.17 General ICU practice for glycae-
mic control and ulcer prophylaxis should be followed. In the
initial phase of shock, enteral perfusion is likely to be poorand
it may be appropriate to delay initiation of nutrition, or
consider early parenteral nutrition.18 Similarly, poor enteral
perfusion and use of opioids may impair uptake of enteral
antiplatelet agents, and intravenous alternatives may be
required.
Patient blood management
Twice-daily measurement of full blood count and coagulation
is appropriate. Patients will necessarily be given antiplatelet
and anticoagulant agents and these must be considered as
part of appropriate patient blood management (PBM). Routine
PBM principles apply, including the restrictive use of individ-
ual products, guided by viscoelastic testing, and using
adjunctive agents, such as tranexamic acid. There is little
evidence for specific transfusion thresholds for CS-AMI
beyond the general ICU target haemoglobin 70 g L1,
although cardiac ICU practice tends to aim for higher
thresholds, and expert consensus has suggested a threshold
of 9e10 g L1.3,19 Furthermore, the potential role of trans-
plantation as a destination therapy should be considered
when administering blood products given possible anti-HLA
(human leucocyte antigen) antibody generation and the
impact upon transplant candidacy.
 Table 4 Comparison of vasopressor and inotropic drugs commonly used in CS-AMI. AF, atrial fibrillation; AS, aortic stenosis; AV, atrioventricular; cAMP, cyclic adenosine mono-
phosphate; CBF, coronary blood flow; CO, cardiac output; COMT, catechol-O-methyltransferase; CS, cardiogenic shock; MAO, monoamine oxidase; PCWP, pulmonary capillary wedge
pressure; PDE, phosphodiesterase; PVR, pulmonary vascular resistance; SVR, systemic vascular resistance; t1/2, half-life

Class Drug Site of action Usual dose Metabolism Mechanism of Beneficial effects Adverse effects
action

Catecholamines Dobutamine b1 agonism Infusion: 0.5e20 t1/2: 2 min Synthetic Overall effect Increases myocardial
(b1>b2) mg kg1 min1 Metabolised by catecholamine counteracts oxygen consumption
COMT Increases cAMP pathophysiology of Increased AV
Inactive metabolites production, CS: increases conduction may
Renal excretion increasing myocardial cause tachycardia or
myocardial performance and proarrhythmic effect,
contractility reduces therefore caution
vasoconstriction with AF
Increased CO Caution with use in
Reduced PCWP fixed cardiac outflow
Reduced SVR/PVR obstruction (e.g. AS)
Caution with
vasoconstriction at
higher doses
Dopamine b1 agonism b1: 5e10 mg kg1 t1/2: 3 min Endogenous Increased CO and CBF Increased myocardial
(Lower dose: D1/ min1 Metabolised by precursor of Debated effect of low oxygen consumption,
D2 Agonism; D1/D2: <5 mg kg1 MAO and COMT in noradrenaline dose infusion to tachycardia,
Higher dose min1 liver, kidneys and Predominant b1 increase renal proarrhythmic
range: a1 a1: >10 mg kg1 plasma agonism increases perfusion (via Higher doses can
agonism min1 Inactive metabolites cAMP, increasing vasodilation of cause systemic and
Renal excretion myocardial splanchnic vessels) e pulmonary
contractility effect may relate to vasoconstriction
improved CO and Increases
BJA Education - Volume 23, Number 5, 2023

enhanced natriuresis endogenous

owing to inhibition of noradrenaline
proximal tubule release, which may
sodium reabsorption increase SVR,
independent of a-

Cardiogenic shock management after ACS

agonism
Adrenaline b1 agonism (<0.1 0.05e0.5 mg kg1 t1/2: 2 min Endogenous Increased CO and Increased myocardial
mg kg1 min1) min1 Metabolised by catecholamine coronary artery oxygen consumption,
Higher dose: a1 COMT and MAO b1 Agonism dilatation proarrhythmic,
agonism Inactive metabolites increases cAMP tachycardia.
Renal excretion production, Increased SVR and
increasing PVR at higher doses
myocardial Increased plasma
contractility, and glucose and lactate,
coronary artery and ketogenesis
dilation
a1 Agonism
increases
availability of
intracellular
calcium, increasing
177

SVR
(continued on next page)
 Table 4 (continued )
178

Cardiogenic shock management after ACS

Class Drug Site of action Usual dose Metabolism Mechanism of Beneficial effects Adverse effects
action

Mainly a1 0.01e1.0 mg kg1

BJA Education - Volume 23, Number 5, 2023

Noradrenaline t1/2: 2 min Endogenous Minimal impact on Increases myocardial

agonism, with min1 Metabolised by catecholamine myocardial oxygen consumption,
some b1 agonism COMT a1 Agonism contraction, in the but CO likely to
Inactive metabolites increases context of markedly decrease owing to
Renal excretion intracellular increased systemic increased SVR/PVR
calcium availability vascular resistance Reflex bradycardia,
Peripheral Venoconstriction can proarrhythmic
vasoconstriction increase venous Reduced splanchnic
return blood flow
Coronary artery
dilatation
PDE III inhibitors Milrinone Non-receptor- Slow bolus 25 t1/2: 1e2 h Bipyridine Increased CO by Reduces myocardial
mediated e75 mg kg1, Renal excretion derivative increased myocardial refractory period,
inhibition of PDE infusion 0.375 (unchanged, so Increased contractility, with causing tachycardia
III e0.75 mg kg1 adjust dose in renal intracellular cAMP, vasodilation and is proarrhythmic
min1 failure) increasing calcium (pulmonary and Effect on vascular
for contractility systemic) owing to smooth muscle can
effect on vascular cause hypotension
smooth muscle
Improved myocardial
oxygen balance
owing to reduced
ventricular wall
tension and
enhanced CBF

Enoximone Non-receptor- Slow bolus 0.5 t1/2: 7.5 h Imidazole As for milrinone As for milrinone
mediated e1.0 mg kg1, Hepatic metabolism derivative
inhibition of PDE Infusion 5e20 mg Active metabolite Increased
III kg1 min1 Renal excretion intracellular cAMP,
(reduce dose in increasing calcium
renal failure) for contractility

Calcium Levosimendan Non-receptor- Optional slow t1/2: 80 h Pyridazoline Increases CO by Risks of hypotension
Sensitisers mediated bolus: 12 mg kg1 Hepatic metabolism edinitrile derivative increased myocardial and proarrhythmic
increase in Infusion: 0.1 mg Active metabolites Increases contractility, without Prolonged t1/2 means
calcium kg1 min1 Renal excretion sensitivity of increasing that adverse effects
sensitivity (decrease to 0.05 troponin C to myocardial oxygen can persist
or increase to 0.2 calcium, increasing demand
if required) myocardial Reduced PVR and SVR
contractility owing to action on
Increased CBF vascular smooth
muscle
Reduces PCWP
Increased CBF
 Cardiogenic shock management after ACS

Management during procedures in the catheterisation laboratory. However, a brief period of

Goals of management are similar to those for other patients in
the ICU: ensuring coronary perfusion, reducing myocardial
oxygen demand and increasing end-organ perfusion.
Anaesthesia for primary PCI is often amenable to the use of
conscious sedation; however, if the patient is shocked, general
anaesthesia with a definitive airway is more likely to be
required. The decision for tracheal intubation is usually made
because of significant cardiorespiratory or neurological
compromise. General considerations will include the
requirement for emergency airway management in the pa-
tient who is not fasted, and for remote-site and time-critical
anaesthesia.
Early referral to the anaesthetist should be emphasised to
enable rapid preoperative assessment, which should consider
the shock phenotype and the current level of cardiovascular
support. The requirements for the procedure should be dis-
cussed with cardiology colleagues, including the possibility of
needing MCS. Advanced pharmacological knowledge should
be applied to the individual patient to ensure safe conduct of
anaesthesia. Even relatively ‘cardiostable’ induction agents
can reduce sympathetic tone, and careful titration should
occur, considering a likely reduction in volume of distribution
and a slow onset of clinical effect from intravenous agents
because of low CO. Balanced anaesthesia should be pursued,
with careful titration of either intravenous or volatile anaes-
thetic agents, and supplemented with short-acting opioids.
Postoperative patients will likely need ICU admission.
Patients with emerging or evolving CS-AMI will be hae-
modynamically unstable, and will need to remain intubated
and ventilated after the procedure. If haemodynamic stability
and metabolic status is much improved, for example in pa-
tients with stage A or B CS, and a relatively short, percuta-
neous procedure has been performed, extubation could be
considered, if equipment and personnel make it safe to do so
mechanical ventilation with further optimisation of haemo-
dynamic and metabolic status before controlled extubation in
ICU should be considered.
Referral to a specialist centre
The location for care should be commensurate to the
complexity of the case and the requirement for specialist
services. Management in a specialist cardiac ICU is preferred,
particularly given the high incidence of multiorgan failure.
Given current regionalised organisation of primary PCI cen-
tres, patients with STEMI should be taken to ‘heart attack
centres’, and peripheral units will have tertiary referral cen-
tres for the onward transfer of patients requiring emergency
revascularisation.
Even within this framework, the provision of specialist
services may vary by location. Specialist cardiology and car-
diac intensive care advice should be sought early, as emer-
gency transfer may be required for refractory CS-AMI.
Furthermore, patients likely to require MCS should be referred
early to facilitate consideration of the appropriate destination.
The key priority in the setting of STEMI remains patient
transfer for emergent angiography, with follow-on PCI, and
IABP insertion if required. The need for higher degree of MCS,
the involvement of surgical teams and the need for advanced
heart failure involvement can then be reviewed again.
Mechanical circulatory support
Percutaneous temporary MCS devices (Table 5) are used in the
management of refractory CS-AMI, to offer a high degree of
CO augmentation, while attempting to minimise the dose, and
thus deleterious effects, of catecholamines, without signifi-
cantly increasing the risk of ischaemia, and favourably

Table 5 Examples of percutaneous temporary mechanical circulatory support devices. LV, left ventricle; PA, pulmonary artery; RA,
right atrium; RV, right ventricle; VA-ECMO, venoarterial extracorporeal membrane oxygenation. Adapted with permission from Thiele
and colleagues3 and Mebazaa and colleagues20

Support Device Access Physiological benefit Maximal degree of Maximum

cardiac output recommended
augmentation duration of use

LV Intra-aortic balloon Femoral artery Minor LV unloading 0.8 L min1 Usually short term
pump but can be in for
months depending
on scenario and
insertion site.
Impella 2.5/3.5/5.0 Femoral artery LV unloading 2.5e5.0 L min1 Varies by device: 7
(Abiomed, Danvers, e10 days, up to 2e3
MA, USA) weeks
TandemHeart Femoral artery/ LV unloading 4.0 L min1 2e3 weeks
(Cardiac Assist Inc., femoral vein
Pittsburgh, PA, USA)
RV Impella RP Femoral vein RV unloading Up to 4.0 L min1 2e3 weeks
(Abiomed)
TandemHeart RA- Internal jugular RV unloading Up to 4.0 L min1 2e3 weeks
PA (Cardiac Assist vein
Inc., Pittsburgh, PA,
USA)
LV þ RV VA-ECMO Femoral artery/ RV unloading Up to 7.0 L min1 3e4 weeks
femoral vein

BJA Education - Volume 23, Number 5, 2023 179

Cardiogenic shock management after ACS
altering the myocardial oxygen supplyedemand
relationship.3,14,20,21 In CS-AMI, the most frequently used
percutaneous support devices are the IABP and a microaxial
LV assist device (LVAD).22
The principles of MCS mirror those for pharmacological
therapies, ensuring the correct ‘dose’ and using the least sup-
port that is required. Greater CO augmentation comes at the
cost of increased risk with regard to both complexity of im-
plantation and risk of complication while on support. Higher
forms of support should therefore only be used when clearly
necessary. This is especially true in patients who have under-
gone PCI and are therefore committed to dual antiplatelet
therapy alongside any MCS-mandated anticoagulation.
Although large registry data suggest early MCS improves
outcomes, RCT data are sparse and comprehensively nega-
tive. However, these devices are not intended as a cure for CS-
AMI and standard study endpoints may not enable appro-
priate evaluation. Mechanical circulatory support is a tem-
porising strategy to give the multidisciplinary team time to
alter prognosis, reserved for refractory CS-AMI. This is by
allowing revascularisation or surgical intervention, promoting
myocardial recovery, or instituting advanced heart failure
therapies (long-term MCS or transplant). Only 40e50% of pa-
tients are likely to require MCS, which includes 25e35% of
patients that are unlikely to benefit, and 15e25% of patients
that may benefit.3 Identifying this cohort is crucial.
Intra-aortic balloon pump
The physiological benefits of IABP use include augmentation
of aortic diastolic pressure and diastolic pressureetime index
(increasing coronary blood flow), and reduced LV afterload
and tensionetime index (reducing myocardial oxygen de-
mand).23 IABP can be rapidly deployed, and there is extensive
clinical experience in its use. However, augmentation is
modest (0.8e1.0 L min1), requires native cardiac contractility,
and as it is ECG-gated its efficacy can be limited by tachycardia
(although practically introduction of an IABP often induces a
reduction in sinus rate).24 Contraindications include aortic
dissection and significant aortic regurgitation (AR), which the
IABP will exacerbate. Evidence for use in CS-AMI for patients
undergoing revascularisation is contentious, but use remains
commonplace, and has value in reducing LV afterload in in-
stances of mechanical complications of ACS and in decom-
pressing the LV during VA-ECMO support.
Microaxial LVAD
The Impella axial flow pumps (Abiomed, Danvers, MA, USA)
are inserted via the femoral or axillary artery, passing retro-
gradely across the aortic valve into the LV, directly augment-
ing CO (by 2.5e5.0 L min1) by pumping blood into the
proximal aorta.24 Action is independent of native heart func-
tion and rhythm, and LV offloading (reducing LVEDP and wall
tension) reduces myocardial oxygen consumption with
favourable LV-aortic uncoupling. Early insertion can enable
more complex coronary interventions to occur, and may be
associated with better outcomes.14,25 There is also a role for
use alongside VA-ECMO to promote LV unloading and prevent
LV dilatation, aortic valve closure and consequent worsening
pulmonary oedema and thrombus formation. Insertion can
cause a degree of AR, and pre-existing significant AR is a
contra-indication, as is a metallic aortic valve replacement
and presence of mural LV thrombus.
180 BJA Education - Volume 23, Number 5, 2023
Venoarterial extracorporeal membrane oxygenation
Venoarterial extracorporeal membrane oxygenation is
increasingly used in the management of CS and the principles
have previously been reviewed. Peripheral cannulae insertion
(via the ipsilateral or contralateral femoral artery and vein) has
reduced the complications of surgical access; however, there is
an increase in LV afterload (with inadequate unloading) which
may be minimised with concomitant use of IABP or LVAD.
Venoarterial extracorporeal membrane oxygenation-
ECMO can be initiated relatively rapidly and can provide a
high degree of cardiorespiratory support (output: 50e100 ml
kg1 min1). Full support is not sought as it is essential to
maintain intrinsic LV ejection to prevent LV and pulmonary
thrombosis. Inotropes and IABP/LVAD have an increasing role
to play in this regard. There are significant risks of systemic
thromboembolic events and limb ischaemia.3,20
Conclusions
CS complicates almost 10% of all cases of AMI and is the pri-
mary cause of in-hospital death after ACS. Emergent angiog-
raphy and revascularisation is the sole evidence-based
therapy. Management requires prompt and effective
involvement of members of a multidisciplinary team, which
includes cardiologists, cardiothoracic surgeons, perfusionists
anaesthetists and intensivists. Timely, decisive and patient-
centred decision-making is essential for a successful
outcome. The failing myocardium, the consequent haemo-
dynamic instability and resultant end-organ dysfunction
must be addressed in parallel, using vasoactive pharmaco-
logical agents and appropriate MCS, before, during and after
revascularisation.
Declaration of interests
The authors declare that they have no conflicts of interest.
MCQs
The associated MCQs (to support CME/CPD activity) will be
accessible at www.bjaed.org/cme/home by subscribers to BJA
Education.
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