REVIEW

URRENT
C
OPINION

Pharmacologic therapies for acute cardiogenic

shock
Jose Nativi-Nicolau a,b, Craig H. Selzman c, James C. Fang a, and
Josef Stehlik a,b

Purpose of review
The natural history of cardiogenic shock has improved significantly with the utilization of revascularization
and mechanical circulatory support. Despite the interest in identifying new pharmacological agents, the
medical therapy to restore perfusion is limited by their side-effects and no solid evidence about improving
outcomes. In this article, we review the current pharmacological agents utilized during cardiogenic shock.
Recent findings
Inotropes and vasopressors are widely used to improve hemodynamics acutely; however, reliable
information regarding comparative efficacy of individual agents is lacking. A subanalysis of a prospective
randomized trial suggested that norepinephrine may be preferred over dopamine in patients with
cardiogenic shock. Levosimendan is a new inotrope with calcium sensitization properties that improves
acute hemodynamics, but with uncertain effects in mortality. Diuretics are used to decongest patients;
however, mortality data are not available. Inhibition of inflammation during cardiogenic shock seems to be
a potential therapeutic target; however, initial clinical studies in this area have not shown benefit.
Summary
The current pharmacological treatment for cardiogenic shock includes inotropes, vasopressors and
diuretics. The information about comparative effective outcomes is limited and their use should be limited as
a temporary measure as a bridge to recovery, mechanical circulatory support or heart transplantation.
Keywords
inotropes, shock, vasopressors

INTRODUCTION
Cardiogenic shock is a stage of heart failure characterized by decreased tissue perfusion from cardiac
pump failure. Clinically, cardiogenic shock presents
with an evidence of congestion (dyspnea, orthopnea, high jugular venous pressure, rales, edema,
ascites) and low perfusion (hypotension, narrow
pulse pressure, pulsus alternans, cool forearms and
legs, obtunded mental status, oliguria), a clinical
scenario commonly described as a wet and cold
patient [1]. Hemodynamically, cardiogenic shock is
defined as persistent hypotension (systolic blood
pressure <8090 mmHg or mean arterial pressure
30 mmHg lower than baseline) with severe
reduction in cardiac index (<1.8 l/min/m2 without
support or <2.02.2 l/min/m2 with support) and
adequate or elevated filling pressures (e.g., left ventricular end-diastolic pressure >18 mmHg or right
ventricular end-diastolic pressure >1015 mmHg)
[2 ]. Hemodynamic definition of cardiogenic shock
is as follows:
&&

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(1) Persistent hypotension

(a) Systolic blood pressure <8090 mmHg or
(b) Mean arterial pressure 30 mmHg lower than
baseline
(2) Severe reduction in cardiac index
(a) <1.8 l/min/m2 without support (support
indicates use of vasoactive drugs or mechanical circulatory support) or

a
Division of Cardiovascular Medicine, Department of Medicine, University
of Utah School of Medicine, bCardiology Section, Veterans Affairs Salt
Lake City Healthcare System and cDivision of Cardiothoracic Surgery,
Department of Surgery, University of Utah School of Medicine, Salt Lake
City, Utah, USA

Correspondence to Jose Nativi-Nicolau, MD, University of Utah Health

Sciences Center 30 North 1900 East, Room 4A100 Salt Lake City, UT
84132, USA. Tel: +1 801 213 4060; fax: +1 801 587 3039; e-mail:
jose.nativi@hsc.utah.edu
Curr Opin Cardiol 2014, 29:250257
DOI:10.1097/HCO.0000000000000057
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Number 3
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Pharmacologic therapy for cardiogenic shock Nativi-Nicolau et al.

KEY POINTS

Medical therapies for cardiogenic shock include
inotropes, vasopressors and diuretics.

There is limited information about comparative efficacy
among pharmacological agents.

The utilization of inotropes, vasopressors and diuretics
is limited by their adverse event profile and limited
improvement in outcomes.

The utilization of inotropes and vasopressors is
recommended as a temporary measure as a bridge to
recovery, mechanical circulatory support or heart
transplantation.

transplantation. In this article, we will review the

current pharmacological strategies available for the
treatment of acute cardiogenic shock.

INOTROPES AND VASOPRESSORS

Inotropes and vasopressors increase myocardial
contractility and modify vascular tone through
the activation of adrenergic pathways. The effects
vary depending on the interaction with the specific
receptors in the myocardium and the smooth
muscle (Table 1). Table 2 provides a summary of
the inotropes and vasopressors commonly used in
cardiogenic shock.

Dobutamine
(b) <2.02.2 l/min/m2 with support (support
indicates use of vasoactive drugs or mechanical circulatory support)
(3) Adequate or elevated filling pressures
(a) Left ventricular end-diastolic pressure
>18 mmHg or
(b) Right ventricular end-diastolic pressure
>1015 mmHg (Adapted from [2 ])
&&

This general definition includes a fairly large

spectrum of patients as far as acuity of onset of
hemodynamic derangements, treatment considerations and expected prognosis. Therefore, for heart
failure patients, who are failing optimal medical
therapy, additional clinical stratification into the
Interagency Registry for Mechanically Assisted Circulatory Support INTERMACS profiles has been
proposed [3 ]. Patients with cardiogenic shock are
assigned profiles 13: INTERMACS Profile 1 encompasses patients with life-threatening hypotension
despite rapidly escalating inotropic support and
critical organ hypoperfusion, often confirmed by
worsening acidosis; INTERMACS Profile 2 is characterized by a progressive decline despite inotropic
support, and INTERMAC Profile 3 designates a more
stable but inotrope-dependent patient [3 ].
Any reversible cause of cardiogenic shock should
be treated emergently, for example revascularization
in acute coronary syndromes, pericardial drainage in
tamponade, or surgery for acute valvular heart disease or mechanical complications of myocardial
infarction. Medical management to restore tissue
perfusion is limited by potential complications of
pharmacologic therapies and the lack of evidence
of improved survival with medical management
alone. In the absence of a reversible underlying cause
of cardiogenic shock, the role of medical management is mainly supportive, serving as a bridge to
recovery, mechanical circulatory support or heart
&&

Dobutamine is a predominantly b1-adrenergic

agonist, with weak b2 and a1 activity. In patients
with heart failure, dobutamine increases the heart
rate, stroke volume and cardiac output with a concomitant decrease in the left ventricular filling
pressures, and a modest decrease in blood pressure
and systemic vascular resistance (SVR) [4]. The
positive effects on the cardiac output and filling
pressures make dobutamine an ideal medication
for cardiogenic shock. However, the beneficial
effects are limited by an increase in heart rate and
myocardial oxygen consumption [4], which can
precipitate and accelerate tachyarrhythmias, worsen
myocardial ischemia and increase mortality. An
analysis from the Acute Decompensated Heart
Failure National Registry demonstrated that, in
4226 patients with decompensated heart failure
treated with dobutamine, the inhospital mortality
was 14%, raising significant concerns about safety
[5]. The mortality is also high in other clinical
Table 1. Adrenergic receptors location and responses
Receptor

Location

Response to activation

b1

Heart

Increase force and rate

of contraction

&&

Increase AV nodal
conduction velocity
b2

Smooth muscle
(vascular, bronchial,
GI and GU)

Relaxation

a1

Vascular smooth muscle

Contraction

Heart

Increase force of
contraction

a2

Vascular smooth muscle

Contraction

D1

Vascular smooth
muscle (renal)

Relaxation

AV, atrio-ventricular; GI, gastrointestinal; GU, genitourinary.

Adapted from [25].

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Cardiac failure
Table 2. Inotropes and vasopressors for cardiogenic shock
Medication

Mechanism/receptor

Therapeutic dose

BP

HR

CO

SVR

Dobutamine

b1 > b2 > a

215 mg/kg/min

"

""

Milrinone

PDE-3 inhibitor

0.3750.75 mg/kg/min

##

"

""

##

Levosimendan

Calcium sensitizer

0.050.2 mg/kg/min

""

##

Epinephrine

b1 b2 > a

0.010.03 mg/kg/min, max 0.10.3 mg/kg/min

"

"

"""

Norepinephrine

b1 > a > b2

0.010.03 mg/kg/min, max 0.1 mg/kg/min

""

0 or #

""

Dopamine

Moderate dose b

25 mg/kg/min

""

"

""

0 or #

Dopamine

High dose a

515 mg/kg/min

""

""

"

""

Phenylephrine

a1

4060 mg/min

""

"

Vasopressin

V1

0.010.04 units/min

""

""

BP, blood pressure; CO, cardiac output; HR, heart rate; PDE, phosphodiesterase; SVR, systemic vascular resistance.

scenarios, including intermittent [6] and continuous intravenous (i.v.) infusions [7]. The recommended dose is from 2 to 15 mg/kg/min [8] and
does not require renal adjustment.

and should be adjusted for renal insufficiency. A

loading dose of 50 mg/kg can be used to accelerate
the onset of milrinones hemodynamic effects.

Milrinone

Levosimendan is a calcium-sensitizing agent that

binds to cardiac troponin C in a calcium-dependent
manner. It also has a vasodilatory effect in the
vascular smooth muscle by opening adenosine
triphosphate-sensitive potassium channels. Several
trials have evaluated the effects of levosimendan
in severe decompensated heart failure [1013].
The Survival of Patients With Acute Heart Failure
in Need of Intravenous Inotropic Support trial
compared levosimendan with dobutamine in 1327
patients with decompensated heart failure. After
180 days, there was no difference in all-cause
mortality [12]. The Randomized Multicenter Evaluation of Intravenous Levosimendan Efficacy trial
randomized 600 patients to 24-h levosimendan
infusion vs. placebo. At 5 days after randomization
patients in the levosimendan group had better
symptoms, lower serum B-type natriuretic peptide
levels and shorter length of hospital stay compared
with placebo. However, at 90 days after randomization, patients assigned to levosimendan experienced more hypotension, cardiac arrhythmias and
higher mortality (14 vs. 11% deaths, P 0.29) [13].
As hypotension was an exclusion criterion in these
trials, the role of levosimendan in cardiogenic shock
remains uncertain and limited to case reports
describing successful outcomes of patients with
refractory cardiogenic shock treated with levosimendan [1417]. Delle Karth et al. [18] reported
on the hemodynamic effects of levosimendan
0.1 mg/kg/min in 10 patients with refractory cardiogenic shock. At 24 h, cardiac index increased from
1.8  0.4 to 2.4  0.6 l/min/m2, P 0.023, and SVR
decreased from 1559  430 to 1109  202 dyn/s/
cm5, P 0.001. There were no changes in heart rate

Milrinone is a phosphodiesterase-3 inhibitor that

prevents the degradation of cyclic adenosine monophosphate (cAMP). In the myocardium, elevated
levels of cAMP activate protein kinase A, which then
phosphorylates calcium channels, increasing the
influx of calcium into the cardiomyocyte, and promotes contractility. In the smooth muscle, elevated
cAMP inhibits myosin light chain kinase, producing
arterial and venous vasodilation. In patients with
heart failure, milrinone increases heart rate, stroke
volume and cardiac output. It is also likely to
decrease mean arterial pressures, SVR and left
ventricular filling pressures [4]. Milrinone increases
myocardial oxygen consumption, but to a lesser
degree than dobutamine (Fig. 1) Although milrinone improves hemodynamics acutely, there are
concerns regarding its safety as far as longer-term
outcomes. The Outcomes of a Prospective Trial of
Intravenous Milrinone for Exacerbations of Chronic
Heart Failure study randomized 951 patients with
decompensated heart failure (not in shock) to
milrinone vs. placebo for a total of 48 h. There
was no significant difference in the primary endpoint of cumulative days of hospitalisation;
however, there was a nonsignificant increase in
inhospital mortality in the milrinone group vs.
the placebo group (3.8 vs. 2.3%, P 0.19). There
were also more adverse events in the milrinone
group compared with placebo, including new atrial
fibrillation or flutter (4.6 vs. 1.5%, P 0.004) and
sustained hypotension (10.7 vs. 3.2%, P <0.001)
[9 ]. Because of safety concerns, milrinone is recommended only for refractory cardiogenic shock.
Recommended doses are 0.3750.75 mg/kg/min [8]
&

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Calcium sensitizers

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30
10

LVDP
(mm/Hg)

Heart rate
(beats/min)

Pharmacologic therapy for cardiogenic shock Nativi-Nicolau et al.

00

Stroke volume index

(ml/mm/m2)

00

90

80

70

40

30

20
60

Peak positive dp/dt

(% change)

Systemic vascular resistance

(dyness. sec cm3)

Mean arterial pressure

(mm/Hg)

90

20

800

1400

1000

600

20

0 2 5 8 11 14 RC 125 25 50 75
Dobutamine
mcg/kg/min

40

Milrinone
mcg/kg

0 2 5 8 11 14 RC125 25 50 75
Dobutamine
mcg/kg/min

Milrinone
mcg/kg

From [5] with permission

FIGURE 1. Hemodynamic effects of dobutamine vs. milrinone in heart failure. The effects of dobutamine and milrinone are
dose-dependent. Compared with dobutamine, milrinone produces lower mean arterial pressure, lower systemic vascular
resistance, lower left ventricular end diastolic pressure and lower peak positive dP/dt. dP/dt, index of left ventricle pressure
rise in early systole; LVDP, left ventricular diastolic pressure.

or blood pressure. There was a small and nonsignificant decrease in the pulmonary capillary wedge
pressure and pulmonary vascular resistance. Six of
the 10 patients died, four from refractory cardiogenic shock, one from intracerebral bleed and one
from mesenteric embolization.
The role of levosimendan in cardiogenic shock
remains unclear. The recommended dose is 0.05
0.2 mg/kg/min, but levosimendan is not recommended in systolic blood pressures <90 mmHg [19].

Epinephrine
Epinephrine (adrenaline) is a strong agonist of a and
b receptors. Its use results in the elevation of
systemic blood pressure through positive inotropic
effect, positive chronotropic effect and vasoconstriction in the cutaneous and renal vascular beds.
Epinephrine increases stroke volume and cardiac
output and decreases SVR by stimulating b2

receptors in the skeletal smooth muscle [20]. It also

increases pulmonary vascular resistance and right
ventricular afterload [21]. As epinephrine increases
myocardial oxygen consumption, it is rarely used
for the management of acute decompensated heart
failure. Epinephrine is commonly used after cardiac
surgery, however, to overcome myocardial stunning
and raise systemic blood pressure. The increase in
myocardial oxygen demand is less of a concern in
this scenario, where the cardiac abnormality leading
to cardiogenic shock was corrected or alleviated
surgically. The recommended starting dose is
0.010.03 mg/kg/min; maximum suggested doses
are 0.10.3 mg/kg/min [8].

Norepinephrine
Norepinephrine differs from epinephrine only in
the methyl substitution in the amino group. It is
a potent a agonist, and also stimulates b1 receptors.

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Cardiac failure

Norepinephrine increases systemic blood pressure,

pulse pressure, peripheral vascular resistance and
stroke volume. In response to norepinephrine
therapy, the cardiac output is unchanged or
decreased, and there is a compensatory vagal reflex
that slows the heart rate [20]. In clinical practice,
norepinephrine is commonly used as a first-line
agent to provide blood pressure support in hypotension, and it is suggested as a better choice than
dopamine for the initial management of hypotension [22 ]. The recommended starting dose is from
0.01 to 0.03 mg/kg/min; maximum suggested dose is
0.1 mg/kg/min [8].
&&

Dopamine
Dopamine is an endogenous catecholamine with
cardiovascular effects that are dose-dependent. At
low doses (2 mg/kg), it causes vasodilation by stimulating dopaminergic receptors on smooth muscle
and by stimulating D2 receptors, which are dominant in splanchnic and renal artery beds. At intermediate doses (25 mg/kg/min), it stimulates b
receptors in the heart and on vascular sympathetic
neurons. At higher doses (515 mg/kg/min), alpha
adrenergic stimulation occurs, with peripheral arterial and venous constriction [20]. The effects of
dopamine in cardiogenic shock include an elevation
in the heart rate (11%), cardiac output (40%),
stroke volume (30%) and left ventricular end diastolic pressures (2.4 mm Hg), with a reduction in
SVR (20%) [20]. In animal models, high doses of
dopamine increase mean pulmonary artery pressures without changes in pulmonary vascular resistance [23].
The effects of dopamine and norepinephrine in
the treatment of shock of different causes were
recently examined in a randomized trial. Patients
assigned to dopamine and norepinephrine had
similar mortality during intensive care (50 vs.
46%, P 0.07), during overall hospital stay (59 vs.
57%, P 0.24) and at 12 months (66 vs. 63%,
P 0.34). Patients assigned to dopamine had higher
rate of arrhythmias compared with patients on
norepinephrine, including atrial fibrillation (20.5
vs. 11%, P 0.001), ventricular tachycardia (2.4
vs. 1.0%, P <0.001) and ventricular fibrillation
(1.2 vs. 0.5%, P <0.001). A subgroup analysis in
patients with cardiogenic shock demonstrated that
patients treated with dopamine had a higher 28-day
mortality rate compared with norepinephrine
[22 ]. The reasons for this finding are unclear,
but could be related to higher heart rate with dopamine or to pharmacological differences between the
two drugs, with norepinephrine causing higher
elevations in SVR compared with dopamine. The
&&

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use of low-dose dopamine (2 mg/kg/min) in patients

with acutely decompensated heart failure did not
result in reduced incidence of renal dysfunction or
other clinical outcomes compared with nesiritide or
placebo [24].

Phenylephrine
Phenylephrine differs little from epinephrine in
chemical structure but is an a1 selective agonist
[20]. It increases peripheral vascular resistance and
blood pressure. The elevation in blood pressure
stimulates baroreceptors with activation of the vagal
reflex with significant bradycardia. Because of the
decreased heart rate, the cardiac output also
decreases, but to a lower degree compared with
the heart rate, secondary to an increase in venous
return and stroke volume [25]. Because of its negative effect on the cardiac output, utilization in cardiogenic shock is rare and it is more frequently
utilized for vasodilatory shock. The recommended
dose is 4060 mg/min.

Vasopressin
Vasopressin in high doses activates vascular smooth
muscle V1 and oxytocin receptors, causing vasoconstriction [26]. Vasopressin is most commonly
used in vasodilatory septic shock, in which it has
been best studied [2731]. In patients with refractory cardiogenic shock complicating myocardial
infarction, a retrospective analysis of 36 patients
showed that vasopressin increased the mean arterial
pressure from 56 to 73 mmHg without affecting
pulmonary capillary wedge pressure, cardiac index
or the urine output [32]. Vasopressin is considered
to be a reasonable vasopressor choice for cardiogenic
shock from right ventricular failure as experimental
data have shown that it does not increase pulmonary vascular resistance [33]. Vasopressin also
effectively reverses hypotension when vasoplegia
complicates left ventricular assist device and transplant surgery due to a relative vasopressin-deficient
state [34,35]. A combination of milrinone and
vasopressin can be considered to counteract the
systemic vasodilatory effects of milrinone. The
recommended dose is 0.010.04 units/min.

INTRAVASCULAR VOLUME OPTIMIZATION

Optimization of filling pressures will enhance
hemodynamic improvement in cardiogenic shock.
Hypovolemia should be treated with volume resuscitation with crystalloids, colloids and blood products (discussion of these strategies is out of the scope
of this review).
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Pharmacologic therapy for cardiogenic shock Nativi-Nicolau et al.

Cardiogenic shock is more often associated

with hypervolemia, and diuretics are used to
decrease the elevated filling pressures and relieve
pulmonary and peripheral edema. Acute kidney
injury is a common complication of cardiogenic
shock from a ST-elevation myocardial infarction
[36 ,37], and results in diuretic resistance and
increased need for renal replacement therapy. In
the setting of hypotension with clear signs of congestion, efforts should be made to restore adequate
perfusion of the kidneys.
&&

Loop diuretics
Furosemide is a loop diuretic that blocks the
sodium-potassium-chloride transporter, and therefore increases urinary excretion of Na and Cl.
Furosemide also acutely increases the systemic
venous capacitance, decreasing left ventricular
filling pressures independently of its diuretic effect
[3840]. The oral bioavailability of furosemide can
be markedly reduced during congestion, making
the i.v. route preferred in cardiogenic shock. The
response to furosemide is decreased when underlying renal function is abnormal. There are no
clinical trials of diuretics in cardiogenic shock, but
the Diuretic Strategies in Patients with Acute
Decompensated Heart Failure trial evaluated the
outcomes of high (2.5 outpatient oral dose) vs.
low dose (outpatient oral dose) and intermittent vs.
continuous infusion of furosemide in patients
with decompensated heart failure. After 72 h, there
were no differences in the co-primary end-point of
global assessment of symptoms and change in
serum creatinine level when diuretics were administered by bolus compared with continuous infusion
or at high dose compared with a low dose. However,
the higher dose group compared with the low dose
group was associated with greater weight loss
(8.7 vs. 6.1 pounds, P 0.011), and greater net
volume loss at 72 h (4.8 vs. 3.6 l, P 0.001) but with
a transient increase in serum creatinine (23 vs. 14%,
P 0.041) [41]. Bumetanide and torsemide are other
commonly used loop diuretics.

Sequential nephron blockade

Diuretic resistance is common in advanced heart
failure. In cardiogenic shock, it can be related to low
cardiac output, low renal perfusion pressure and
acute kidney injury. It can also be related to the
braking phenomenon a decrease in the efficacy
of loop diuretics due to multiple dosing [42]. This
can sometimes be overcome by increasing the dose
or frequency of the loop diuretic. Another strategy is
sequential nephron blockade combining loop and

a thiazide diuretic which results in a synergistic

blocking of sodium absorption in different sections
of the nephron. The only randomized clinical trial
of sequential nephron blockade compared addition
of metolazone 10 mg daily or bendrofluazide 10 mg
daily to furosemide 80 mg i.v. twice daily. Both
treatment arms achieved similar median weight
loss (5.6 vs. 5.1 kg), but patients on metolazone
had higher loss of potassium compared with bendrofluazide (0.7 vs. 0.3 mmol/l) [43]. Because of
the risk of hypokalemia and acute kidney injury
with the combination therapy, low doses of thiazides are recommended.

ANTI-INFLAMMATORY AGENTS
SVR is typically elevated in cardiogenic shock. However, some patients present with profound hypotension and normal or decreased SVR. The proposed
mechanisms for this vasoplegic state include activation of KATP channels in the vascular smooth
muscle, vasopressin deficiency and the release of
cytokines and nitric oxide due to an underlying
inflammatory process [44,45]. Inflammatory modulators have been identified as potential targets for
therapy.

Tilarginine
Nitric oxide is a proinflammatory mediator
that stimulates guanylate cyclase, increasing
cyclic guanosine monophosphatase (cGMP) and
smooth muscle relaxation. It has been shown
that nitric oxide synthase (NOS) is upregulated
in acute myocardial infarction [46,47]. As the
vasodilatory effect of NOS can contribute to hypotension in shock, NOS inhibition has been proposed as a therapeutic target. In the Tilarginine
Acetate Injection in a Randomized International
Study in Unstable Acute Myocardial Infarction
Patients with Cardiogenic Shock trial, 398 patients
with acute coronary syndrome, percutaneous
revascularization and cardiogenic shock refractory
to vasopressor therapy were randomized to NOS
inhibitor tilarginine (1 mg/kg bolus 1 mg/kg/h
5-h infusion) vs. placebo. Enrolment was terminated early, however, after an interim analysis
showed no differences between the treatment
groups in 30-day and 6-month mortality, shock
duration and resolution [48].

Methylene blue
Methylene blue is a guanylate cyclase inhibitor that
decreases cGMP and circumvents its vasodilatory
effects in the smooth muscle [49]. In patients with

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Cardiac failure

catecholamine-refractory vasoplegia, methylene

blue administered at 2 mg/kg i.v. for 20 min
increases mean arterial pressure and SVR, with a
consequent decrease in cardiac output. The mean
pulmonary artery pressure and the right atrial and
left atrial pressures remain unchanged [50]. Methylene blue has been suggested to improve morbidity
and mortality in vasoplegic syndrome after cardiopulmonary bypass, defined as mean arterial pressure
lower than 50 mmHg, cardiac index higher than
2.5 l/min/m2, right atrial pressure lower than
5 mmHg, left atrial pressure lower than 10 mmHg
and SVR less than 800 dynes/s/cm5 during norepinephrine infusion (0.5 mg/kg/min) [49,51]. Methylene blue is, in general, avoided in cardiogenic
shock of other causes due to its negative effect on
cardiac output.

CONCLUSION
There has been limited progress in pharmacological
approaches in the treatment of cardiogenic shock.
Vasoactive medications inotropes and vasopressors are widely used to acutely improve hemodynamics; however, reliable information regarding
comparative efficacy of individual agents is lacking.
A common clinical practice in the setting of cardiogenic shock is to initiate therapy with inotropes and
to add, or transition to, vasopressors, if hypotension
persists. Nevertheless, this approach has not been
tested in prospective trials. A subanalysis of a lone
prospective randomized trial suggested that norepinephrine may be preferred over dopamine in
patients with cardiogenic shock [22 ]. Diuretics
are used to decongest patients in cardiogenic shock
and volume overload; however, mortality data are
also not available for this group of medications.
Inhibition of inflammation during cardiogenic
shock seems to be a potential therapeutic target;
however, initial clinical studies in this area have
not shown benefit.
In summary, vasoactive therapies have predictable favorable acute effect on hemodynamics in
most patients; however, their use is accompanied
by significant adverse events and possibly increased
mortality. Other strategies, including early introduction of mechanical circulatory support, may
improve survival in cardiogenic shock, and this
hypothesis should be tested in clinical trials. In
the meantime, the use of vasoactive agents should
be limited to the dose and time necessary to restore
tissue perfusion before recovery of myocardial function takes place (where this can be accomplished), or
before advanced therapies, including mechanical
circulatory support or heart transplantation, can
be implemented.
&&

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Acknowledgements
None.
Conflicts of interest
There are no conflicts of interest.

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