C a rdi o g e n i c Sh o c k

Semhar Z. Tewelde, MDa, Stanley S. Liu, MDb, Michael E. Winters, MDc,*

KEYWORDS
 Cardiogenic shock  Hypoperfusion  Inotropic medications  Vasopressor medications
 Percutaneous coronary intervention  Echocardiography  Dobutamine
 Intra-aortic balloon pump counterpulsation

KEY POINTS
 Bedside echocardiography should be performed in the initial evaluation of patients with cardiogenic
shock (CS) to assess intravascular volume, determine the left ventricular ejection fraction, and di-
agnose a pericardial effusion or obstructive lesions.
 Initial resuscitation of the patient with CS is aimed at restoring cardiac output and tissue perfusion.
 Management of the patient with CS includes a combination of medical therapies, reperfusion ther-
apy, and mechanical support.
 Vasopressor and inotrope medications can increase myocardial oxygen consumption and increase
the risk of arrhythmias.
 Consider mechanical support devices in patients with CS who are not responding to pharmacologic
therapy.

INTRODUCTION
Cardiogenic shock (CS) is commonly defined as a
physiologic state in which cardiac pump function
is inadequate to perfuse the tissues. If CS is not
rapidly recognized and treated, tissue hypoperfu-
sion can quickly lead to organ dysfunction and pa-
tient death. Patients with CS can present with a
myriad of symptoms and physical examination
findings that range from subtle hemodynamic al-
terations to overt cardiovascular collapse. Once
diagnosed, patients with CS require rapid initiation
of therapy to prevent unnecessary increases in
morbidity and mortality. Treatment of patients
with CS is challenging, as many will require a com-
bination of vasoactive medications and mechani-
cal support. This article reviews the most
common etiologies of CS, along with critical com-
ponents in the diagnostic evaluation of patients
with CS. Medical management and mechanical
support of patients with CS also is discussed.
DIAGNOSIS
Commonly accepted hemodynamic criteria for the
diagnosis of CS are listed in Box 1. In addition to
these hemodynamic criteria, patients with CS
also exhibit signs and symptoms of pulmonary
congestion and tissue hypoperfusion. These signs
and symptoms can include dyspnea, rales,
elevated jugular venous pressure (JVP), altered
mental status, narrow pulse pressure, reduced
urine output (less than 20 mL/h), cool and clammy
skin, and elevated lactate levels.1,2
EPIDEMIOLOGY
Many patients with CS die before hospital arrival.
As a result, it is difficult to determine the true
incidence of CS. What is clear, however, is that
the proportion of intensive care unit admissions
with CS has doubled from 4% to 8% over
the past 15 years.3 Currently, CS complicates
cardiology.theclinics.com

Disclosure: The authors have no relevant financial relationships to disclose.

a
Department of Emergency Medicine, University of Maryland School of Medicine, 110 South Paca Street, 6th
Floor, Suite 200, Baltimore, MD 21201, USA; b Division of Cardiovascular Medicine, University of Maryland
School of Medicine, 110 South Paca Street 7-N-127, Baltimore, MD 21224, USA; c Emergency Medicine/Internal
Medicine/Critical Care Program, University of Maryland School of Medicine, 110 South Paca Street, 6th Floor,
Suite 200, Baltimore, MD 21201, USA
* Corresponding author.
E-mail address: mwinters@em.umaryland.edu

Cardiol Clin 36 (2018) 53–61

https://doi.org/10.1016/j.ccl.2017.08.009
0733-8651/18/Ó 2017 Elsevier Inc. All rights reserved.
54 Tewelde et al

Box 1 Table 1
Diagnostic criteria for cardiogenic shock Nonischemic etiologies of cardiogenic shock

 Hypotension Etiology Examples

 Systolic blood pressure less than 90 mm Hg Pharmacologic Beta blockers
OR Calcium channel blockers
 A reduction in mean arterial pressure of Digoxin toxicity
30 mm Hg or more from the patient’s Primary Acute myocarditis
baseline ventricular Stress cardiomyopathy (ie,
 Reduced Cardiac Index dysfunction Takatsubo
cardiomyopathy)
 Less than 2.2 L/min/m2 body surface area Nonischemic
for patients receiving vasoactive or me- cardiomyopathy (eg,
chanical support sarcoidosis, amyloidosis,
 Less than 1.8 L/min/m2 body surface area hemochromatosis)
for patients not receiving vasoactive or me- Outflow Valvular stenosis
chanical support obstruction Left ventricular outflow
obstruction (eg, in
 Adequate Filling Pressure
hypertrophic
 Pulmonary artery wedge pressure greater cardiomyopathy)
than 15 mm Hg Acute valvular Trauma
Adapted from Reynolds HR, Hochman JS. Cardiogenic
regurgitation Degenerative disease
shock: current concepts and improving outcomes. Cir- Endocarditis
culation 2008;117:686; with permission. Endocrine Severe hypothyroidism
Pericardial Cardiac tamponade
disease Pericardial constriction
approximately 8% to 9% of patients with an ST- Tachyarrhythmias Supraventricular/atrial
segment elevation myocardial infarction (STEMI), tachyarrhythmias
Monomorphic VT
whereas the incidence of CS in patients with a
Polymorphic VT (ie,
non-ST-segment myocardial infarction (NSTEMI) Torsades de Pointes)
is approximately 2.5%.4–6 Mortality for patients
Bradyarrhythmias Sinus node dysfunction (eg,
with CS is unchanged in recent years and
sick sinus syndrome)
remains unacceptably high at approximately AV node dysfunction (eg,
50%.7 AV nodal block)

Abbreviations: AV, atrioventricular; VT, ventricular

ETIOLOGIES
The SHOCK Trial Registry is the largest data set
from which to assess the various cardiac etiol-
ogies of CS.8 By far, the most common cardiac
cause of CS is acute left ventricular failure in
the setting of an STEMI.8 Most often this is due
to anterior wall myocardial infarction and
accounts for almost 79% of patients with CS.8
Mechanical complications of ischemic heart dis-
ease include severe mitral regurgitation (7%),
ventricular septal rupture (4%), right ventricular
failure (3%), and tamponade (1.4%).8 Of these
cardiac causes, ventricular septal rupture carries
the highest mortality.
CS can also result from nonischemic cardiac
conditions. These conditions are listed in Table 1.
It is important to consider these nonischemic etiol-
ogies in patients presenting with typical signs and
symptoms of CS but with nonspecific findings on
the electrocardiogram (ECG) and negative labora-
tory values for myocardial infarction.
tachycardia.
INITIAL EVALUATION
Emergent evaluation of the patient with suspected
CS is critical. The immediate goals of the initial
evaluation are to identify signs of tissue hypoper-
fusion and determine the etiology of shock. Select
findings from the physical examination, ECG,
chest radiograph (CXR), laboratory studies, and
bedside echocardiogram are extremely helpful in
achieving these initial goals.
Physical Examination
A focused physical examination should be per-
formed in patients with suspected CS. Pertinent
findings from the examination are listed in Box 2.
Although physical examination findings of
abnormal cardiac function often lack sensitivity,
the presence of an elevated JVP, an S3, and a

Box 2
Physical examination findings
 Signs of abnormal cardiac function
 S3 or S4 heart sounds
 Bibasilar rales
 Murmurs of valvular disease or mechanical
complication of ischemia
 Signs of decreased organ perfusion
 Altered mental status
 Oliguria
 Decreased capillary refill
 Cool, clammy extremities
 Signs of elevated intravascular volume
 Elevated jugular venous pressure
 Hepatojugular reflex
 Pedal edema
displaced cardiac apex are strongly suggestive of
acute heart failure.9 Jugular venous pressure can
be used to estimate central venous pressure
(CVP), but can be challenging to measure in criti-
cally ill patients. Recall that the jugular venous
wave is a 2-part wave that rises and falls with
inspiration. In nonsupine patients, the distance
from the right atrium to sternal angle is approxi-
mately 8 cm.10 A JVP of more than 3 cm above
the sternal angle has a positive likelihood ratio of
10.4 for a CVP above 12 cm H2O.11 Application
of pressure to the patient’s right upper quadrant,
termed the hepatojugular reflex (HJR), can be
used to confirm the JVP location. In fact, a positive
HJR has a positive likelihood ratio of 8.0 for eleva-
tions in left heart filling pressure.9 Rather than esti-
mating a true CVP value, it is more practical to
determine whether the JVP is elevated, normal,
or low. Bedside ultrasound can be used to assess
the central veins and estimate filling pressures
when JVP measurements cannot be performed
(ie, obese patients).
Electrocardiogram
An ECG should be performed as soon as possible
in patients with suspected CS to evaluate for the
presence of an acute coronary syndrome. In addi-
tion to evaluating for a STEMI, the ECG can pro-
vide valuable prognostic information. For patients
with an inferior myocardial infarction, a right-
sided ECG that demonstrates at least 0.5 mm
ST-segment elevation in lead V4R has
been shown to be an independent predictor of
Cardiogenic Shock 55
increased in-hospital mortality.12,13 Similarly, ST-
segment depression in leads V1, V2, and/or V3 in
the setting of an inferior myocardial infarction sug-
gests posterior wall involvement and is associated
with increased morbidity and mortality.14
The ECG can also suggest nonischemic cardiac
etiologies of CS, such as cardiac tamponade.
Although the findings of low QRS voltage, electri-
cal alternans, and PR depression have limited
specificity and negative predictive value for tam-
ponade, the presence of these abnormalities can
prompt bedside ultrasound evaluation.15,16
Chest Radiography
A CXR should be obtained in all patients with sus-
pected CS to evaluate for pulmonary edema.
However, acute heart failure cannot be excluded
based on the absence of pulmonary congestion
on the CXR.17,18
Laboratory Studies
Laboratory studies commonly obtained in the
evaluation of patients with shock include a com-
plete blood count, comprehensive metabolic
panel, coagulation factors, lactate, troponin, and
venous blood gas. Values are often abnormal in
all forms of shock due to hypoperfusion. For pa-
tients with CS, hepatic congestion due to cardiac
failure can cause abnormal liver enzyme and coag-
ulation levels. In addition, it is important to identify
electrolyte abnormalities in patients with CS who
present with arrhythmias. Natriuretic peptide
levels can be valuable in patients with suspected
CS, as elevated levels have high sensitivity for
acute heart failure. In contrast, a B-type natriuretic
peptide level less than 100 pg/mL, or an N-termi-
nal B-type peptide level less than 300 pg/mL,
exclude the diagnosis of acute heart failure.18
Echocardiography
Echocardiography should be performed as part of
the initial evaluation of patients with suspected CS
to assess intravascular volume status, left ventric-
ular ejection fraction, and pericardial effusion or
obstructive lesion.19 Echocardiography can be
performed by an emergency physician, cardiolo-
gist, or sonographer with training in point-of-care
ultrasound.
Echocardiography assessment of the inferior
vena cava (IVC) can be used to determine intravas-
cular volume status and estimate right atrial pres-
sure (RAP). Specifically, an IVC diameter that is
less than 2.1 cm and collapses more than 50%
with inspiration suggests hypovolemia and an
RAP between 0 and 5 mm Hg (Fig. 1).20 An IVC
diameter greater than 2.1 cm with more than
56 Tewelde et al
50% collapse with inspiration suggests an RAP
between 5 and 10 mm Hg, whereas an IVC diam-
eter greater than 2.1 cm with less than 50%
collapse with inspiration suggests an RAP greater
than 10 mm Hg (Fig. 2).20 It is important to note
that these IVC measurements are estimates of
RAP. Some patients can still respond to additional
intravenous fluid (IVF) even in the setting of high
RAPs. In addition, patients receiving positive pres-
sure ventilation will have a dilated IVC that does
not collapse with inspiration.20 In these patients,
the Distensibility Index should be used to assess
intravascular volume and the need for additional
intravenous fluids.
It is critical to estimate the left ventricular ejec-
tion fraction with echocardiography in patients
with suspected CS. The ejection fraction can sim-
ply be categorized as normal, poor, or hyperkinet-
ic. Normal, or hyperkinetic, left ventricular systolic
function in the absence of valvular disease,
Fig. 2. B-mode ultrasound image of dilated IVC with
no respiratory variation.
Fig. 1. M-mode ultrasound image
of IVC with greater than 50%
collapse between inspiration and
expiration.
tamponade, or arrhythmias essentially excludes
the diagnosis of CS. Unfortunately, poor systolic
function alone does not establish the diagnosis
of CS. Rather, a poor ejection fraction should be
interpreted in the overall context of the patient.
Finally, echocardiography can be used to eval-
uate for a pericardial effusion and obstructive le-
sions. Echocardiography can diagnose a
pericardial effusion and determine whether it is
circumferential or localized. Signs of cardiac tam-
ponade include end-diastolic right atrial collapse
and early right ventricular diastolic collapse. In
addition, an IVC diameter greater than 2.1 cm is
highly sensitive, but not specific, for tamponade.
A greater than 30% inspiratory decrease in
mitral-inflow velocity, measured by pulse-wave
Doppler, is also associated with cardiac tampo-
nade.21 Obstructive lesions (ie, aortic stenosis,
mitral stenosis, left ventricular outflow tract
obstruction) can be with 2-dimensional (2-D) and
color Doppler echocardiography. Similarly, acute
valvular regurgitation can be diagnosed with
these modalities and prompt emergent surgical
evaluation.
INITIAL RESUSCITATION AND MANAGEMENT
The initial resuscitation of the patient with CS
should be focused on restoring cardiac output
and tissue perfusion. This is accomplished
through a combination of medical therapies,
reperfusion therapy, and mechanical support.
Medical Therapies
Medical management of the patient with CS in-
cludes IVFs, inotropes, and vasopressor medica-
tions. Importantly, the role of these therapies is

primarily supportive, as there are no randomized
data that demonstrate improved patient outcomes
when used alone for the management of CS.2
Similar to septic shock, medical therapies should
be used to target a mean arterial blood pressure
(MAP) between 65 and 70 mm Hg.1
Intravenous fluids
Intravenous fluids should be administered to the
patient with CS to optimize cardiac filling pres-
sures and maintain euvolemia.1,2 The number of
IVFs should be individualized and based on hemo-
dynamic parameters, clinical assessment, and
echocardiography findings. There are currently
no data to support a specific type of IVF for pa-
tients with CS. Similar to other shock states,
isotonic crystalloid solutions are the most
commonly administered IVF.
Vasopressors
Common vasopressor medications used in the
treatment of CS are listed in Table 2. These
include norepinephrine, epinephrine, dopamine,
and vasopressin. It is important to note that,
although these agents increase MAP, they can
also increase myocardial oxygen demand and in-
crease the risk of arrhythmias. Thus, these agents
should be administered at the lowest dose to
achieve the goal MAP and for the shortest period
possible.
Norepinephrine (NE) stimulates the alpha adren-
ergic receptor and, to a lesser extent, beta adren-
ergic receptors. As a result, NE increases MAP
primarily through an increase in systemic vascular
resistance (SVR). Heart rate and contractility are
only minimally increased, given the weaker beta
adrenergic receptor stimulation. NE is often the
first-line vasopressor medication chosen to
augment MAP in patients with CS, usually in com-
bination with dobutamine.22,23 Side effects of NE
include reduced renal and splanchnic blood
flow.22
Table 2
Vasoactive medication
Vasopressors Clinical Effect
Epinephrine Increase HR, SV, CO
Vasoconstriction at higher doses
Norepinephrine Increase vasoconstriction
Mild increase in HR, CO
Dopamine Increase CO
Vasoconstriction at high doses
Vasopressin Increase vasoconstriction
Abbreviations: CO, cardiac output; HR, heart rate; SV, stroke volume; SVR, systemic vascular resistance.
Cardiogenic Shock 57
Epinephrine strongly stimulates both alpha and
beta adrenergic receptors. As a result, it increases
MAP through increases in heart rate, contractility,
and SVR.2 Epinephrine can also increase pulmo-
nary vascular resistance and right ventricular after-
load.2 Due to its strong effects on heart rate and
contractility, epinephrine can markedly increase
myocardial oxygen demand. Epinephrine will also
elevate both lactate and blood glucose levels.22
Given these profound side effects, epinephrine is
less frequently used in the treatment of CS
compared with NE.23
Dopamine is the endogenous precursor to both
NE and epinephrine. Its effects on the various
adrenergic receptors are dose-dependent. At
low doses, dopamine stimulates the D2 receptor,
which results in vasodilation of the splanchnic and
renal vascular beds.2 At intermediate doses,
dopamine stimulates beta-2 adrenergic receptors
and causes an increase in contractility and heart
rate.2 At high doses, dopamine stimulates the
alpha adrenergic receptor, resulting in vasocon-
striction and an increase in SVR.2 Dopamine has
historically been the first-line vasopressor of
choice for patients with CS. However, recent liter-
ature has demonstrated that dopamine may be
less favorable for patients with CS when
compared with NE.24 In a trial of more than
1600 patients with shock, De Backer and col-
leagues24 demonstrated an increase in arrhyth-
mogenic events in patients treated with
dopamine compared with those treated with NE.
Furthermore, in the subgroup of patients with
CS, dopamine was associated with a higher 28-
day mortality when compared with NE.24 As a
result of this trial, dopamine is no longer recom-
mended as the first-line vasopressor medication
for CS.
Vasopressin causes peripheral vasoconstriction
through stimulation of V1 receptors in vascular
smooth muscle.2,22 Although vasopressin is
commonly used as a second-line vasopressor in
Dose
0.05–0.5 mg/kg/min
0.05–0.5 mg/kg/min
1–20 mg/kg/min
0.01–0.04 units/min
58 Tewelde et al
patients with septic shock, there is little to no liter-
ature on its use in CS. In fact, there are no random-
ized trials on the use of vasopressin in CS.22
Nevertheless, vasopressin has been recommen-
ded by some clinicians for use in patients
with CS due to right ventricular failure, as it does
not significantly increase pulmonary vascular
resistance.2
Phenylephrine should be avoided in patients
with CS. It increases MAP through strong activa-
tion of the alpha adrenergic receptor. The marked
increase in SVR can decrease cardiac contractility
and may cause a reflex bradycardia. As a result,
cardiac output decreases and tissue hypoperfu-
sion may worsen.
Inotropes
The 2 most common inotrope medications used
in CS are listed in Table 3. These medications
increase cardiac output primarily through an in-
crease in cardiac contractility. Inotropic medica-
tions are critical in the medical management of
CS to bridge patients to reperfusion therapy or
mechanical support. Similar to vasopressor med-
ications, both dobutamine and milrinone increase
myocardial oxygen consumption and increase
the risk of arrhythmias. At present, there is no
literature that demonstrates the superiority of
either dobutamine or milrinone in the treatment
of CS.
Dobutamine stimulates both beta adrenergic re-
ceptors and is the most common inotrope used in
CS.23 The recommended initial infusion rate of
dobutamine in CS is 2.5 mg/kg per minute. The
infusion is then increased by 2.5 mg/kg per minute
every 10 minutes until clinical improvement occurs
or a dose of 20 mg/kg per minute is reached.
Dobutamine does not require adjustment for renal
function. Although dobutamine primarily aug-
ments cardiac contractility and cardiac output
through stimulation of the beta-1 receptor, it is
important to note that hypotension can worsen
through stimulation of the beta-2 receptor. As a
result, a vasopressor medication (ie, NE) is often
used with dobutamine.23
Table 3
Vasoactive medication
Inotropes Clinical Effect
Dobutamine Increase SV, CO
Increase vasodilation
Milrinone Increase diastolic relaxation, CO
Increase vasodilation
Abbreviations: CO, cardiac output; SV, stroke volume.
Milrinone is a phosphodiesterase-3 inhibitor
that increases cyclic adenosine monophosphate
levels. The result is an increase in cardiac
contractility without the significant increase in
heart rate seen with other vasoactive medica-
tions. In addition, milrinone can cause vasodila-
tion of both the pulmonary and systemic
circulations.25 Importantly, milrinone can take
several hours to take effect and must be adjusted
for renal impairment.25
Reperfusion Therapy
Since acute coronary syndrome is the most com-
mon cause of CS, emergent reperfusion therapy
with either percutaneous coronary intervention
(PCI) or coronary artery bypass grafting (CABG)
is critical. For appropriate patients, emergent PCI
or CABG reduces mortality.26 The American Col-
lege of Cardiology (ACC) and the American Heart
Association (AHA) recommend emergent PCI for
patients with an STEMI and CS.27 Unfortunately,
in-hospital mortality remains high for patients
with CS who undergo emergent PCI.28 This may
be due to the relative increase in patients over
the past decade with an NSTEMI compared with
those who have an STEMI.29–31 The latest ACC/
AHA Guideline for the management of NSTEMI
specifically references hemodynamic instability
(ie, shock) as a criterion for emergent PCI.32 Data
from the SHOCK trial demonstrated no difference
in hospital mortality in patients with an NSTEMI
compared with those with an STEMI.33 More
recent trials, however, have suggested that there
may be mortality differences between patients
with STEMI and NSTEMI.34,35 Nevertheless, PCI
or CABG is preferred over fibrinolytic therapy for
patients with CS. Fibrinolytic therapy can be
administered to patients with an STEMI and CS
in the event that transport to the cardiac catheter-
ization laboratory is delayed or the patient is not a
candidate for emergent PCI or CABG.27 Patients
who fail PCI, are found to have severe triple vessel
disease or left main coronary artery disease at the
time of PCI, or have a mechanical complication of
Dose
2.5–20 mg/kg/min
Loading dose: 50 mg/kg
Infusion: 0.375–0.75 mg/kg/min
 Cardiogenic Shock 59

an acute coronary syndrome (ie, papillary muscle
rupture, ventricular septal rupture, free wall
rupture) are candidates for emergent cardiac
surgery.27,36–38
Mechanical Support
Mechanical devices used to support the circula-
tion are being used with increased frequency in
patients with CS. These devices include the
intra-aortic balloon pump (IABP), percutaneous
ventricular assist device (pVAD), and extracorpo-
real life support (ECLS). These devices are
pictured in Fig. 3. At present, there are no data
to suggest the superiority of any mechanical
support device. In fact, mortality rates have
been shown to be relatively equal among all
devices.
The IABP remains the most commonly used me-
chanical device in patients with CS, despite the
lack of evidence to support improved patient out-
comes.39 IABPs decrease afterload and improve
diastolic coronary blood flow. The most recent
ACC/AHA STEMI Guidelines recommend IABP
for patients who are not quickly improving with
the use of pharmacologic therapy (ie, vasopressor,
inotropes).27 Importantly, this recommendation
has been downgraded from class I to class IIa,
based primarily on the study by Thiele and
colleagues.1,25,27,39
The pVAD devices are now more accessible
and may provide more robust circulatory support
compared with the IABP.40 Two of the most
common pVAD used in clinical practice are the
micro-axial flow catheter (Impella, Abiomed,
Inc, Danvers, MA) and the centrifugally driven
right to left femoral artery bypass device (Tan-
demHeart, Cardiac Assist, Inc, Pittsburgh, PA).
These pVADs can deliver 2.5 to 4 L/min of flow
and may be best for patients with left ventricular
failure without pulmonary compromise. Impor-
tantly, pVADs are temporary and must be
replaced by an implantable VAD or the patient
must undergo CABG.
ECLS is a novel mechanical support therapy
that is being used in many acute care settings
with impressive results. In a single-center series
of approximately 200 patients with STEMI and
CS, the use of ECLS during cardiac catheterization
demonstrated a 33% decrease in 30-day mortality
compared with patients who did not receive
ECLS.41 The most common type of ECLS is extra-
corporeal membrane oxygenation (ECMO). The 2
types of ECMO are veno-venous ECMO and
veno-arterial ECMO (VA-ECMO). VA-ECMO is
used in the patient with CS to provide full cardio-
pulmonary support. Importantly, ECMO is
currently limited to select centers, as this therapy
is very labor intensive. Patients who do not
respond to pharmacologic therapy can be consid-
ered for ECMO as a bridge to emergent reperfu-
sion therapy or cardiac transplantation. In most
of these cases, transfer to a center with expertise
in ECMO will be needed.

Fig. 3. Percutaneous mechanical support devices. (A) Intra-aortic balloon counterpulsation. (B) The Impella is in-
serted percutaneously and positioned across the aortic valve in the left ventricle. (C) The TandemHeart ventricular
assist device, which is placed in the left ventricle using a trans-septal cannula. (D) The venous access is connected
to an ECMO system with an integrated centrifugal pump and membrane oxygenator (artificial lung) and con-
nected to the arterial inflow access. (From Werdan K, Gielen S, Ebelt H, et al. Mechanical circulatory support
in cardiogenic shock. Eur Heart J 2013;35(3):156–67; with permission.)
60 Tewelde et al
SUMMARY
Patients with CS are critically ill and can rapidly
decompensate. If CS is not recognized and
treated, tissue hypoperfusion can quickly lead to
organ dysfunction and patient death. In addition
to a focused history and physical examination,
the initial evaluation of patients with suspected
CS should include an ECG, CXR, laboratory
studies, and a point-of-care echocardiogram.
The initial resuscitation of patients with CS is
directed toward restoring cardiac output and tis-
sue perfusion. This is accomplished through the
administration of intravenous fluids and a combi-
nation of inotropic and vasopressor medications.
Mechanical circulatory support is indicated for pa-
tients with CS who do not respond to pharmaco-
logic therapy. These patients should undergo
emergent reperfusion therapy with either PCI or
CABG.
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