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Review Article

Pediatric cardiogenic shock: Current perspectives

Subhranshu Sekhar Kar
Department of Paediatrics, Ras al-Khaimah (RAK) Medical and Health Sciences University, Al Qusaidat, Ras al-Khaimah,
United Arab Emirates

ABSTRACT
Cardiogenic shock is a pathophysiologic state where an abnormality of cardiac function is responsible for the failure of the
cardiovascular system to meet the metabolic needs of the body tissues.Though it is less common than hypovolemia as the primary
etiology in paediatric shock, eventually myocardial function is affected because of reduced perfusion in all forms of shock. Myocardial
malfunction, in other forms of shock, is secondary to ischemia, acidosis, drugs, toxins or inflammation. Cardiogenic shock is a low
output state characterized by elevated filling pressures, neurohormonal activation with the evidence of end-organ hypoperfusion.
The management is challenging and consists of a combination of conventional cardio-respiratory support, vasoactive medications
with correction of the anatomic cardiac defects. Treatment options like Extracorporeal membrane oxygenation and Ventricular assist
devices provide a bridge to recovery, surgery or transplant. As cardiogenic shock in children carries a high risk of morbidity and
mortality, emphasis should be placed on expedient management to arrest the pathophysiological cascade and avoid hypotension.
This article aims to review the aetio-pathophysiological basis of pediatric cardiogenic shock, diagnostic options, recent advances in
management modalities and outcome.

Key Words: Cardiac transplant, congenital heart disease, congestive cardiac failure (CCF), extracorporeal membrane oxygenation,
inotropes, myocardial dysfunction, myocarditis, pediatric cardiogenic shock, ventricular assist device (VAD)

Introduction in the management of shock, cardiogenic shock continues to

The major function of the cardiovascular system (CVS) is to
provide oxygen and energy substrates to the tissues, failing
which the body is unable to meet the metabolic demands of
the tissues. Worldwide, shock is a leading cause of morbidity
and mortality in children.[1-3] Cardiogenic shock, where cardiac
dysfunction is the primary derangement, is the third most
common type of shock in children in Western countries,
following septic and hypovolemic shock.[4] Despite advances
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remain a challenge requiring efficient treatment approaches. In
most cases, myocardial malfunction is secondary to ischemia,
acidosis, drugs, toxins, or myocardial inflammation.[5,6]
Definition
Myocardial dysfunction is frequently a common final event
seen as a late manifestation of shock of any etiology.
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License, which allows others to remix, tweak, and build upon the
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DOI:
10.4103/2321-4848.171917 How to cite this article: Kar SS. Pediatric cardiogenic shock: Current
perspectives. Arch Med Health Sci 2015;3:252-65.

Corresponding Author:
Dr. Subhranshu Sekhar Kar, Department of Paediatrics, Ras al-Khaimah (RAK) Medical and Health Sciences University, Al Qusaidat,
Ras al-Khaimah, United Arab Emirates. E-mail: drsskar@gmail.com

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Kar, et al.: Cardiogenic shock

Cardiogenic shock is defined as decreased cardiac output (CO) Equation III

and evidence of tissue hypoxia with adequate intravascular
volume.[7] This low-output state is characterized by elevated
ventricular filling pressures, low CO, systemic hypotension,
and end-organ hypoperfusion. The hemodynamic criteria
for diagnosis are persistent hypotension [systolic blood
pressure (SBP) <2 standard deviation (SD) for age for at
least 1 h] not responsive to fluids or requiring inotrope or
vasopressor support to maintain blood pressure (BP) and a
reduced cardiac index (CI ≤2.2 L/min/m2) in the presence
of high left-sided filling pressures (pulmonary congestion,
elevated pulmonary capillary wedge pressure ≥15 mmHg).
Systemic vascular resistance (SVR) may be high in patients
with cardiogenic shock, although this is a not a requirement
for diagnosis.[8] Clinical signs include oliguria, cyanosis,
cold extremities, altered mentation, and hypotension. In
most patients these signs may persist after attempts have
been made to correct hypovolemia, arrhythmia, hypoxia,
and acidosis.
Pathophysiology
Physiologic determinants
Parameters that determine adequate oxygen delivery
(DO 2 ) to tissues include blood flow to tissues, the
regional balance between blood flow and metabolic
demand, and the oxygen content of blood [hemoglobin
(Hb) concentration and percentage of Hb saturated with
oxygen).[1,9,10]
• DO2 is defined as the amount of oxygen delivered to
the tissues of the body per minute. It depends on the
amount of blood pumped per minute (that is, CO) and
the arterial oxygen content of that blood (CaO2).
Equation I
DO2 (mL O2/min) = CaO2 (mL O2/L blood) × CO (L/min)
• The CaO2 depends on how much oxygen-carrying
capacity is available in terms of Hb content and depends
on how much oxygen the patient’s Hb contains, defined
as the arterial oxygen saturation (SaO2). A small amount
of oxygen is directly dissolved in the blood that is not
bound to Hb.
CO = SV × HR
• SV is determined by preload, cardiac contractility, and
afterload.
• Children with compensated shock typically have
normal BP [Table 1 shows the cutoff values for defining
hypotension based on systolic BP according to age]
despite signs of poor perfusion (such as decreased
peripheral pulses and tachycardia). [11-14] While
decreased perfusion directly reflects decreased CO,
the increased CO observed in hyperdynamic shock
states is also associated with decreased effective tissue
perfusion.[13] This decreased effective perfusion derives
from a complex interaction of numerous humoral and
microcirculatory processes resulting in patchy, uneven
local regional blood flow and a derangement of cellular
metabolic processes.[14]
Equation IV
BP = CO × SVR
Hemodynamic response and cardiovascular mechanics
[Figure 1]
The principal mechanical defect identified in cardiogenic
shock is the rightward shift of the left ventricular (LV)
end-systolic pressure-volume curve due to a marked
reduction in contractility.[15] Thus, as the ventricle ejects
less blood per beat at a similar or even lower systolic
pressure, the end-systolic volume is usually greatly
increased and SV is decreased. As a compensatory
mechanism to the decreased SV, a rightward shift of
the curvilinear diastolic pressure-volume curve occurs,
Table 1: Definition of hypotension based on age[11,12]
Age Systolic BP (mmHg)
0-28 days <60
1 month-12 months <70
1-10 years <70+(2× age in years)
>10 years <90
Figure 1: Hemodynamic response and cardiovascular mechanics

Equation II
CaO2 (mL/100 mL) = Hb (g/100 mL) × SaO2 × 1.34
mLO2/g + (0.003 × Partial pressure of oxygen in
arteries (PaO2))
A state of clinical shock may occur when CaO2 is impaired.
• CO is the product of stroke volume (SV) multiplied by
heart rate (HR). Hence, tachycardia is a common sign
of decreased perfusion and early shock. Infants have
relatively fixed SV and are particularly dependent upon
HR to increase CO.

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Kar, et al.: Cardiogenic shock
resulting in a decreased diastolic compliance. This causes
increase in diastolic filling with resultant increase in end-
diastolic pressure. The attempt to increase CO to maintain
tissue perfusion by this mechanism comes at the cost of
elevated LV diastolic filling pressure, which increases
myocardial oxygen demand and results in pulmonary
edema.[16-18] However, owing to decrease in contractility,
the left and right ventricular (RV) filling pressures
increase and CO decreases. Significant arterial oxygen
desaturation often occurs in cardiogenic shock as a result
of decrease in mixed venous oxygen saturation (SVO2)
and intrapulmonary shunting. SVO2 decrease occurs as
a result of increased tissue oxygen extraction because of
the low CO.[17,18] In Figure 1, the Frank-Starling mechanism
is explained, and it plays an important compensatory role
in the early stages of heart failure. Point “a” represents a
healthy patient where cardiac performance increases as
preload increases (the amount of stretch on the ventricle
before contraction due to an increase in volume). Point
“b” represents the same individual after developing
LV systolic dysfunction. As the heart is no longer able
to contract as effectively as it did before, SV falls with
elevation of the preload. Because point “b” is on the
ascending portion of the curve, the increased end-diastolic
volume initially serves a compensatory role by leading to
a subsequent increase in SV (i.e., more diastolic stretch
causes greater contractility and thus the greater is the
SV — the Frank-Starling mechanism). However, this is
less than the increase a normal patient would experience.
As the heart failure progresses (represented by point
“c”), which is on the relatively flat portion of the curve,
SV only increases slightly relative to further increases
in end-diastolic volume (preload). Here the ability of the
Frank-Starling mechanism to compensate for worsening
LV function is nearly exhausted. In such circumstances,
marked elevation of the end-diastolic volume and
end-diastolic pressure results in pulmonary congestion,
while decreasing CO leads to increasing fatigue and
exercise intolerance. Eventually, the curve starts downward
due to decompensation of the heart muscle. When cardiac
resynchronization therapy is implemented, the heart failure
patient is put back on top of the curve rather than on the
downward slope.[15-18]
Clinical effects
As the myocardial perfusion is compromised, tachycardia
becomes the major compensatory mechanism to improve
the systemic perfusion. The myocardial pump failure results
in the rise of ventricular diastolic pressures, with increase
in wall stress and myocardial oxygen requirement. Decrease
in systemic perfusion, due to decreased CO, augments
254 Archives of Medicine and Health Sciences / Jul-Dec 2015 / Vol 3 | Issue 2
anaerobic metabolism with the formation of lactic acid,
which again compromises the systolic performance of the
myocardium.[17,18] This triggers compensatory mechanisms
such as sympathetic stimulation, which causes tachycardia,
increased cardiac contractility, and renal fluid retention.
These compensatory responses may be counterproductive.
As renal fluid retention again increases the LV preload,
tachycardia with increased cardiac contractility causes
additional rise of demand for myocardial oxygen, worsening
of myocardial ischemia, pulmonary venous congestion, and
hypoxemia.[17,18] Sympathetically mediated vasoconstriction
increases not only systemic BP but the myocardial afterload
as well, which causes additional deterioration of cardiac
performance.
Etiology
Causes of cardiogenic shock in patients can be categorized
as systolic dysfunction, diastolic dysfunction, valvular
dysfunction, cardiac arrhythmias, coronary artery disease,
and mechanical complications [Tables 2 and 3].[11,19-32] Signs
and symptoms develop in patients when pulmonary venous
pressure is increased to critical levels or tissue perfusion
is severely limited [Tables 3 and 4].[11,19-32] Cardiogenic
shock is diagnosed after excluding other possible causes
of hypotension and after establishing the presence of
myocardial dysfunction. It is important to recognize certain
physical examination findings that differentiate cardiogenic
shock from other causes of shock [Table 5].[11,19-32]
It is imperative to note that congestive cardiac failure
(CCF) is not synonymous with cardiogenic shock. CCF is
a chronic process where the body adapts to low ejection
fraction (EF) by increasing HR and augmenting the
preload and afterload. These patients are usually well
compensated, although they may be symptomatic in terms
of edema, low BP, respiratory distress, or fatigability.
Symptoms improve with oral decongestive therapy and
correction of aggravating factors. In cardiogenic shock,
the decreased CO occurs more abruptly and there is
acute decompensation with features of shock, tissue
hypoperfusion, and acidosis. BP may be normal or low,
and these patients need rapid, more intensive therapeutic
measures to reestablish adequate perfusion and oxygen
delivery to end organs.
Diastolic dysfunction is suspected if shock persists
despite adequate filling and echocardiography (echo)
shows preserved EF. Features of pulmonary edema occur
even with small-volume resuscitation, the central venous
pressure (CVP) is usually high, and large increments
occur with filling. The echo with Doppler studies are
confirmatory.
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Kar, et al.: Cardiogenic shock

Table 2: Etiology of cardiogenic shock[11,19-32]

Congenital heart lesions
Left ventricular outflow tract obstruction (LVOTO) Hypoplastic left heart syndrome, critical aortic stenosis, coarctation of the aorta, and hypertrophic cardiomyopathy
Large left-to-right shunts, Physiologic or (HCM)
pathologic pulmonary steal Atrial-septal defect, ventricular-septal defect, patent ductus arteriosus, and atrioventricular septal defect
Inflammatory disorders of the heart
Infectious myocarditis Viral: Enteroviruses (esp. Coxsackie B), adenoviruses, influenza, Epstein-Barr virus, parvoviruses, mumps, West Nile virus, human herpes
virus-6 (HHV-6), human immunodeficiency virus (HIV), Cytomegalovirus (CMV), Herpes Simplex Virus-2 (HSV-2), Hepatitis C
Bacterial: Campylobacter jejuni, Chlamydophila psittaci, Corynebacterium diphtheriae, Borrelia spp., Neisseria meningitides, Mycoplasma
pneumoniae, Spirillium minus
Parasitic: Trypanosoma cruzi, Trypanosoma brucei (gambiense), Trypanosoma brucei (rhodesiense), Toxocara canis/cati, Toxoplasma
gondii, Trichinella spiralis
Metabolic Hypo- or hyperthyroidism, hypoglycemia, pheochromocytoma, glycogen storage diseases (e.g., Pompe disease), mucopolysaccharidoses,
carnitine deficiency, Fabry disease, disorders of fatty acid metabolism, acidosis, hypothermia, and hypocalcemia
Toxic Sulfonamides, penicillins, and anthracyclines
Autoimmune/connective tissue derangements Systemic lupus erythamatosus (SLE), juvenile rheumatoid arthritis, polyarteritis nodosa, Kawasaki disease, and acute rheumatic
fever
Neuromuscular disorders/ inherited cardiomyopathies Duchenne muscular dystrophy, myotonic dystrophy, limb-girdle dystrophy, spinal muscular atrophy, and Friedreich’s ataxia
Hypoxic-ischemic events leading to cardiac failure Cardiac arrest and cardiopulmonary bypass, head injury, prolonged shock, and carbon monoxide poisoning
Dysrhythmias
Prolonged, unrecognized supraventricular tachycardia (SVT); bradyarrhythmias; complete heart block; tachyarrhythmias such as
ventricular tachycardia (with or without pulse) or ventricular fibrillation; conditions that could predispose a patient to developing a
dysrhythmia, such as hypothermia and drug intoxications
Obstructive lesions
Cardiac tamponade
Acute severe pulmonary embolus
Other disorders
Acute valvular regurgitation
Trauma: Commotio cordis and contusio cordis

Table 3: Specific pathologic mechanisms of cardiogenic shock[11,19-32] Table 4: Physiological mechanisms of symptoms and signs of
Systolic dysfunction (decreased contractility) cardiogenic shock[11,19-32]
Ischemia/infarction
Symptomatology Pathophysiology
Global hypoxemia
Valvular disease Dyspnea Pulmonary congestion
Myocardial depressant drugs (e.g., beta-blockers, calcium channel blockers, antiarrhythmics) Compression of bronchi by dilated pulmonary arteries or atria
Myocardial contusion Pulmonary edema
Respiratory acidosis Tachypnea Reflex response to rise in pulmonary venous pressure, left
Metabolic derangements (e.g., acidosis, hypophosphatemia, hypocalcemia) ventricular volume, and pressure. Caused by stimulation of vagus
Diastolic dysfunction/increased myocardial diastolic stiffness nerve or J receptors in pulmonary interstitium
Ischemia Increase in capillary permeability and slower lymphatic drainage
Ventricular hypertrophy implicated as factors responsible for the predominance of this
Restrictive cardiomyopathy symptom in infancy
Consequence of prolonged hypovolemic or septic shock Irritability Reduced O2 transport to brain
Ventricular interdependence Feeding difficulty Lack of energy to suck and tiring quickly
External compression by pericardial tamponade Failure to thrive Inadequate calories due to poor intake and extra work of
Increased afterload breathing cause increased metabolic demand
Aortic stenosis Sweating Increased sympathetic activity
Hypertrophic cardiomyopathy Reduced urine output Impaired renal perfusion
Dynamic aortic outflow tract obstruction Tachycardia Increased sympathetic activity as a compensatory means to
Coarctation of the aorta increase O2 delivery to tissues
Malignant hypertension Gallop sounds Increased afterload, reduced compliance
Pulmonary embolism Precordial heave Chamber dilatation
Pulmonary vascular disease (e.g., pulmonary arterial hypertension, venoocclusive disease) Crepitation Alveolar edema
Hypoxic pulmonary vasoconstriction Hepatomegaly and edema Systemic venous congestion
Peak end-expiratory pressure Reduced capillary filling Reduced tissue perfusion
High alveolar pressure
Acute respiratory distress syndrome
Pulmonary fibrosis Investigations
Sleep-disordered breathing
Chronic obstructive pulmonary disease Though essentially the diagnosis of cardiogenic shock
Valvular or structural abnormality is clinical, certain laboratory tests are required to
Mitral stenosis
Endocarditis
define the nature of specific diseases, functional status
Mitral aortic regurgitation of the myocardium, and other comorbid features
Obstruction due to atrial myxoma or thrombus
Papillary muscle dysfunction or rupture
[Table 6]. [33-38] To assess the therapeutic response,
Ruptured septum or free wall however, serial laboratory investigations are required
Arrhythmia from time to time.

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Kar, et al.: Cardiogenic shock

Chest radiography Blood gas and electrolytes

Chest radiography is required to diagnose air leak
syndrome for the assessment of pulmonary vasculature
and to exclude other causes of shock or chest pain.
Cardiomegaly may provide an important clue toward
etiological diagnosis. A widened mediastinum points
toward aortic dissection.
Electrocardiography (ECG)
It helps to identify rhythm disturbances and structural
diseases, such as the anomalous origin of the left coronary
artery arising from the pulmonary artery (ALCAPA).[33]
Echocardiography (echo)
For diagnosis of anatomic abnormalities, to ascertain
functional status, and for follow-up assessment of response
to therapy, echo is extremely useful. Serial measurements
of systolic and diastolic functions help in deciding particular
therapy and its efficacy. Another value that is calculated is
the myocardial performance index (MPI).[34] MPI is a simple,
reproducible, and noninvasive measure of combined systolic
and diastolic ventricular function and is a comparison of the
isovolumetric contraction (ICT) and relaxation times (IRT)
to the ventricular ejection time (VET).
MPI = (ICT+IRT)/VET
As systolic function worsens, ICT lengthens, and VET
shortens, the MPI is increased. With worsened diastolic
function, IRT lengthens and MPI is similarly increased. A
benefit of MPI is that it is not limited by the geometric
shape of the ventricle.[35] Various echo parameters help in
differentiating abnormal loading conditions of the heart
from alteration in contractility.[36] Antenatal echo can help
in diagnosing fetal CCF, which usually manifests as fetal
hydrops.
Table 5: Differentiating physical examination findings of cardiogenic
shock[11,19-32]
Irregular pulse
Narrow pulse pressure
Distended jugular vein
Distant heart sound
Presence of S3, S4
Presence of murmur
Crackles in chest
Blood gas analysis in patients with acute CCF with low
CO usually shows metabolic acidosis and lactic acidemia,
while in chronic CCF, partial pressure of carbon dioxide
(PaCO2) is low and pH is usually normal.[37] In patients on
diuretic therapy, hyponatremia and hypochloremia should
be monitored by regular electrolyte analysis. Hypokalemia
and lactic acidemia can develop owing to reduced tissue
perfusion. SVO2 is a measure of CO, and serial measurements
can help in directing therapy.
Cardiac catheterization
Functional data from the failing myocardium can be obtained
by this procedure. Myocardial biopsy with histological
analysis and polymerase chain reaction (PCR) testing aid in
diagnosing underlying causes such as myocarditis. Coronary
abnormalities and Kawasaki disease can be identified by
coronary angiography. Hemodynamic data usually reveal
elevated LV and RV end-diastolic pressures. A structural
abnormality causing cardiogenic shock can also be identified.
Other tests
Electrolytes, renal function tests, and liver function tests help
reveal the adequacy of end-organ perfusion. Complete blood
count will reveal anemia that may be worsening the clinical
picture. If Hb is low, it can increase left-to-right shunting
by reducing the pulmonary vascular resistance (PVR) and
aggravate the failure. Hypoglycemia and hypocalcemia should
be ruled out in neonatal LV failure. Creatine phospho kinase-
MB (CPK-MB) and troponin I levels should be done in case of
coronary insufficiency and asphyxia. B-type natriuretic protein
(BNP) is a well-studied diagnostic test in diagnosing early heart
disease in adults. Recently, its role is increasing in the diagnosis
of congenital heart disease and heart failure, monitoring
postoperative hemodynamics in cardiac surgery patients,
predicting the progression of disease in cardiomyopathy,
and even in posttransplant monitoring.[38] Anti-dsDNA and
antinuclear antibody (ANA) assays can be done in autoimmune
disorders. Blood levels of carnitine, lactate, and glucose
may be done to diagnose mitochondrial cardiomyopathies.
Albuminuria, increase in urine specific gravity, and microscopic
hematuria may be detected on urine analysis. The presence of
methylglutamic aciduria implies a metabolic cause.

Table 6: Relevant investigations in cardiogenic shock[33-38]

Chest radiography Cardiomegaly, pulmonary venous congestion, Kerley B lines, pleural effusion, alveolar edema (B/L parahilar distribution), and to rule out tension pneumothorax/
pneumomediastinum
ECG Arrhythmia, heart block, chamber hypertrophy, features of ALCAPA
Echo Preload, contractility, RV and LV systolic and diastolic function (EF, SVR, CI), pulmonary artery pressures, coronary anatomy (Kawasaki, ALCAPA), structural
problems, tamponade, assessment of response to therapy
Blood gas and electrolytes Metabolic acidosis, lactic acidosis, dyselectrolytemia (sodium, potassium, chloride)
Cardiac catheterization Chamber pressure, myocardial biopsy, assessment of coronary vessels
Others Glucose, calcium, magnesium, cardiac enzymes, routine urine examination, complete blood count, blood urea nitrogen (BUN), creatinine, liver function tests, BNP

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Management
If a patient presents with shock, an early working diagnosis
must be made and urgent resuscitation should be done.
The working diagnosis is confirmed subsequently with
investigations. First-line treatment in any form of shock
involves stabilizing the airway, breathing, and circulation
with the establishment of vascular access. There are,
however, some conditions where oxygen can be detrimental
to the patient. Oxygen is a pulmonary vasodilator, thus in
single-ventricle physiology, dilating the pulmonary vascular
bed can worsen pulmonary overcirculation and systemic
“steal.”[39]
Fluid resuscitation to correct hypovolemia and hypotension
is the most important and initial step unless pulmonary
edema is present.[40] It is advisable to give small fluid boluses
(5-10 mL/kg) rather than large volumes to avoid precipitation
of pulmonary edema. Central venous and arterial lines should
be inserted. Multiparameter monitor is necessary for proper
monitoring of the patients with cardiogenic shock. Blood
gas analysis and correction of electrolyte and acid-base
abnormalities, such as hypokalemia, hypomagnesemia, and
acidosis are critical [Table 7].[41,42] Goal-directed therapy is
a bundle of care that includes intensive care monitoring,
fluids, blood products, inotropy, and rapid turn-around time
in laboratory evaluation for maximizing patient care.[41,42] In
addition, patients with cardiogenic shock mostly have low
SVO2, which is associated with poor prognosis, but those
with relatively high saturation levels fare better.[43]
Supportive therapy
Bed rest
It helps in reduction of the myocardial work load. Activity
can be increased gradually according to the response to
treatment and patient tolerability.
Position
To improve the pulmonary function by easing respiration and
reducing pulmonary pooling, the patient should be placed in
semi-Fowler position either by modified cardiac chair or by
elevating the head end and the shoulders to 45°.
Temperature
Normothermia should be maintained to minimize myocardial
oxygen demand.
Table 7: Goals of treatment[41,42]
General supportive care to maintain systemic perfusion and relieve pulmonary and systemic congestion
Optimizing the preload: Use of diuretics and vasodilators, and aggressive fluid management (depending on the clinical assessment of volume status)
Improving myocardial contractility and performance: Correction of metabolic derangements including adequate serum ionized calcium and providing inotropic support
Reduction of afterload by providing sedation and pain control and by using the appropriate pharmacologic agents
Treatment of the underlying cause, and prevention of disease progression
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Oxygen administration
It can be started through mask or nasal prongs with adequate
humidification. However, for duct-dependent cardiac defects,
oxygen should be administered with great caution during
the neonatal period.
Assisted ventilation
To improve blood gas tension and reduce the work of
breathing, intubation and mechanical ventilation is instituted
in cardiogenic shock. Its usefulness is established in patients
with LV dysfunction, where ventilation causes reduction
in afterload. Sedation and paralysis of the mechanically
ventilated patient eliminates the movement of skeletal
muscles, which is a source of oxygen consumption.
Prostaglandin (PGE1) infusion
It helps to maintain the ductal patency in duct-dependent
systemic circulation and improves systemic perfusion
with reduction in pulmonary congestion. Doses as high
as 0.05-0.1 mcg/kg/min have been used, but significant
hypotension and apnea can occur as side effects.[35]
Nutrition and other therapies
The recommended daily calorie and protein intake should
be maintained. The calorie requirement in infants can be up
to 130-170 cal/kg/day. Individualized salt restriction should
be done in the presence of severe systemic congestion or
edema. Use of low-solute formula with 7-12 meq/L may
be required in infants. Iron supplement 2-3 mg/kg should
be started as it benefits by improving anemia. L-carnitine
supplementation should be done in patients with dilated
cardiomyopathy at a dose of 20-35 mg/kg/dose orally
three times a day. In severely symptomatic children,
nasogastric tube feeds can help to improve calorie intake
and weight gain. Correction of metabolic acidosis or other
electrolyte abnormalities, transfusion of blood products (if
anemic), administration of vitamin K, and cryoprecipitate
or fresh frozen plasma if coagulation defects are present
are other adjunct therapies, depending on the underlying
condition.[41]
Specific therapy
Diuretics [Table 8][44]
These drugs relieve systemic and pulmonary vascular
congestion. The common classes of drugs used are
loop diuretics, thiazide, and aldosterone antagonists.
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Kar, et al.: Cardiogenic shock

Furosemide is the most commonly used diuretic. It Inotropes and vasopressors [Table 9][11]
has a rapid onset of action (2-5 min) with duration of Dopamine
action of about 3 h. Use of continuous infusion results It is very effective in acute cardiac failure and cardiogenic
in lowered hemodynamic instability and electrolyte shock, particularly when a postoperative patient has low
imbalances.[44,45] Common adverse effects of furosemide CO. The half-life (t 1/2) is only 3-4 min and the major effects
include hypokalemia, metabolic alkalosis, hypocalcemia, are increase in contractility, vasoconstriction, increase in
hyponatremia, and hyperuricemia. Ototoxicity is a rare HR, and increase in PVR. The effect of dopamine varies
reversible complication in neonates and infants. Thiazides with the dose infused. It has the best dopaminergic action
have a slower onset of action and are commonly used for at the dose range of 3-5 μg/kg/min, which improves
chronic CCF. The aldosterone antagonist spironolactone renal flow and natriuresis. Hence, it is a preferred agent
is a weak diuretic and is rarely used alone. It is usually in cardiogenic shock following cardiopulmonary bypass.
added to loop diuretics or thiazides to antagonize the At 5-15 μg/kg/min it has inotropic effect (β effect). At
kaliuretic action. It is given orally, and the onset of action doses higher than 20 μg/kg it may compromise renal
takes 2-3 days. flow and increase PVR, oxygen demand, and ventricular

Table 8: Pharmacology of diuretics[44]

Type Agent
Loop diuretics Furosemide
Torsemide
Thiazide diuretics Hydrochlorothiazide
Carbonic anhydrase Acetazolamide
inhibitors
Osmotic diuretics Mannitol
Potassium- sparing Sodium channel inhibitors:
diuretics Amiloride, triamterene
Aldosterone antagonists:
Spironolactone, eplerenone
Site of action
Loop of Henle:
Thick ascending limb
Distal convoluted tubule
Proximal tubule
Loop of Henle, Proximal
tubule
Cortical collecting tubule
Cortical collecting tubule
Mechanism Dose range Side effects/special consideration
Inhibition of sodium-potassium- 1 mg/kg/dose per oral (PO) or IV Hypokalemia, hypomagnesemia, metabolic
2 chloride symport alkalosis, hyperuricemia, dehydration, ototoxicity
Inhibition of Sodium-chloride 2 mg/kg/day PO divided BID Hypokalemia, hyponatremia, metabolic
symport alkalosis, hyperglycemia, dehydration,
hypercholesterolemia, hyperuricemia
Inhibition of carbonic anhydrase 5 mg/kg/dose once daily Hypokalemia
Metabolic Acidosis
Not used in hypertension/heart failure
Osmotic action 0.5-1 gm/kg/dose Dehydration
Hypernatremia
Not commonly used in hypertension/heart failure
Inhibition of sodium channel 0.4-0.6 mg/kg/day Hyperkalemia, metabolic acidosis, gynecomastia
(aldosterone antagonists), gastric problem
(peptic ulcer)
Inhibition of aldosterone 1-3 mg/kg/day
receptor

Table 9: Pharmacology of inotropes and vasopressors[11]

Drugs Site of action (receptors they act on) Clinical effect Dose range Major side effects
Dopamine Beta 1 agonist; increasing alpha effect with increasing Increases contractility, 1-20 mcg/kg/min Severe hypertension (especially in patients taking
dose— vasoconstricts, increases HR, nonselective
At dose range of 1-5 mcg/kg/min: Dopaminergic effect increases PVR B-blockers), ventricular arrhythmias, cardiac ischemia,
At dose range of 6-10 mcg/kg/min: Beta 1 agonist tissue ischemia/gangrene (high doses or due to tissue
At dose range of 11-20 mcg/kg/min: Alpha agonist extravasation)
Dobutamine Beta 2 > Beta 1 effect Alpha agonist Increases contractility, vasodilates 1-20 mcg/kg/min Tachycardia, increased ventricular response rate in
(Beta 2), decreases PVR patients with atrial fibrillation, ventricular arrhythmias,
cardiac ischemia, hypertension (especially nonselective
Inotropes

B-blocker patients), hypotension

Epinephrine Beta > Alpha effect Increases contractility and HR, 0.01-1 mcg/kgmin Ventricular arrhythmia, severe hypertension resulting in
vasoconstricts cerebrovascular hemorrhage, cardiac ischemia, sudden
cardiac death
Norepinephrine Alpha > Beta effect Vasoconstricts, increases SVR, 0.01-1 mcg/kg/min Arrhythmias, bradycardia, peripheral (digital) ischemia,
increases contractility and HR hypertension (with nonselective B-blocker patients)
Isoproterenol Beta 1 and 2 agonist Increases contractility and HR 2-10 mcg/kg/min Ventricular arrhythmia, cardiac ischemia, hypertension,
hypotension
Milrinone Phosphodiesterase inhibitor Inodilator, increases contractility 0.1-1 mcg/kgmin Ventricular arrhythmia, hypotension, cardiac ischemia,
with no increase in HR, decreases Torsades de pointes
SVR and PVR
Phenylephrine Pure alpha agonist Vasoconstricts, increases SVR 0.1-0.5 mcg/kgmin Reflex bradycardia, hypertension, (especially with
nonselective B-blockers), severe peripheral and visceral
Vasopressors

vasoconstriction, tissue necrosis with extravasation

Vasopressin V1 vascular receptor Vasoconstricts, vasodilates circle of 0.0003-0.008 U/ Arrhythmia, hypertension, decreased CO (at doses
Willis, stimulates cortisol secretion kg/min >0.4 U/min), cardiac ischemia, severe peripheral
vasoconstriction causing ischemia (especially skin),
splanchnic vasoconstriction

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Kar, et al.: Cardiogenic shock
afterload. It should not be mixed with sodium bicarbonate
infusion.[46-48]
Dobutamine
Dobutamine is a preferred drug in perioperative cases as it is
less arrhythmogenic and augments CO. It acts predominantly
on β1 rather than β2 and also on α receptors. It does not
depend on norepinephrine stores to produce the desired
effects. When used at a dose of 2-20 μg/kg/min, it causes
mild vasodilatation, increases the CO, and reduces the
SVR, with minimal alteration of BP and HR. It has a short
t 1/2 of 2-3 min and does not alter or impair renal flow.[46-52]
In patients with postoperative failure, a combination of
3-5 μg/kg/min of dopamine with dobutamine 5-10 μg/kg/min
and afterload-reducing agents such as milrinone produces
excellent results.
Epinephrine
It acts on both β and α receptors. Improvement of CO is
noted in patients with cardiogenic shock and in postoperative
situations because of intense vasoconstriction.[46,52] It has
a short t 1/2 of 2-3 min. It is arrhythmogenic because of its
excessive chronotropic action and causes downregulation
of β receptors on long-term use. It should be used as
short-term treatment for patients unresponsive to other
drugs and should be tapered off as early as possible.
Epinephrine should be administered preferably through the
central venous catheter.
Norepinephrine
It acts on both α1  and α2  adrenergic receptors to cause
vasoconstriction. Because of its deleterious effects on
afterload, renal flow, and myocardial demand, caution
regarding its use is warranted. Although generally reserved as
a second-line agent or used in addition to other vasopressors
in cases of severe distributive shock, norepinephrine is
emerging as an agent of choice for the management of
hypotension in hyperdynamic septic shock. It has a short
t 1/2 of 2-3 min.[52]
Isoproterenol
It is a very good drug in patients with acute heart failure
complicated by increased reactive PVR or complete
heart block. Because of its β1 and β2 effects, it improves
contractility and HR along with vasodilatation without
altering renal blood flow. Thus, normovolemia should be
ensured during its infusion.[52]
Phosphodiesterase III inhibitors
These nonglycosidal, noncatecholamine agents are one of
the most effective types of drugs, which help to augment
the SV in shock. They act by improving the contractility
Archives of Medicine and Health Sciences / Jul-Dec 2015 / Vol 3 | Issue 2 259
and simultaneously reducing the afterload (inodilators).
Amrinone and milrinone are the two most well-studied drugs
in this group. Their onset of action is slower than adrenergic
agents. Milrinone is used widely as it is free of the harmful
side effects of amrinone, e.g., hypotension, ventricular
ectopy, and thrombocytopenia.[53-59]
Phenylephrine
It induces predominantly α effects and causes vasoconstriction
with increase in SVR. The dose range is 0.1-0.5 μg/kg/min.
The elimination half-life of phenylephrine is about 2.5-3.0 h.[52]
It is especially useful in counteracting the hypotensive effect
of epidural and subarachnoid anesthetics as well as the
vasodilating effect of bacterial toxins and the inflammatory
response in sepsis. It should preferably be infused through
the central line.
Vasopressin
It acts on the V1 vascular receptor and causes systemic
vasoconstriction, but vasodilates the circle of Willis and also
stimulates cortisol secretion. The dose used is 0.0003-0.008
Units/kg/min.[52]
Digoxin
The efficacy of digoxin is well established in CCF. However, in
cardiogenic shock, because of the risk of increased toxicity,
its use is limited. Digoxin acts by inhibiting sarcolemmal
Na+K+-ATPase activity, thereby increasing intracellular
calcium and augmenting ventricular contractility. HR and
conduction are slowed as well. Most commonly, it is used
where improvement in myocardial contractility is needed.
Digoxin use in large left-to-right shunts is controversial. In
patients with systolic dysfunction, it provides a subjective
benefit through its neurohormonal modulating effect. It is
also used in fetal CCF induced by excessive tachycardia.[60]
Vasodilators
These are mostly used along with inotropes and diuretics
to improve cardiac function by favorably altering afterload
and preload in cardiogenic shock secondary to left-to-
right shunt, postoperative low CO, severe atrioventricular
valve regurgitation, and dilated cardiomyopathy. Drugs
such as prazosin and hydralazine are not widely used in
children in the acute setting except in cases of scorpion
sting poisoning. The patients should be monitored for SBP
and filling pressures.[61]
Angiotensin-converting enzyme (ACE) inhibitors
Captopril and enalapril are the common ACE inhibitors that
act by favorably altering the maladaptive mechanism of
the renin-angiotensin system. Thus, hemodynamic status
improves by ventricular remodeling, reduction of SVR, and
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Kar, et al.: Cardiogenic shock
increase in venous capacitance. Monitoring of BP and the
neutrophil count is necessary. However, these have limited
use in the acute stage.[61]
Angiotensin II receptor blockers (ARBs)
These are as effective as ACE inhibitors in the treatment
of heart failure. Their adverse-effect profile is similar to
that of ACE inhibitors with regard to renal insufficiency
or hyperkalemia, but they do not cause potentiation of
bradykinin and do not cause cough. Losartan is an ARB that
blocks the vasoconstrictor and aldosterone-secreting effects
of angiotensin II. It may induce a more complete inhibition of
the renin-angiotensin system than ACE inhibitors. It is used
for patients unable to tolerate ACE inhibitors.[61]
Sodium nitroprusside
It is often used in acute cases and in postoperative patients
needing afterload reduction as it effectively reduces afterload
and decreases filling pressures, SVR, and PVR. Hypotension
is a common side effect. Thiocyanate toxicity is a possible
side effect when the drug is used for longer than 72 h.[61]
Nitroglycerin
It is mostly used in conditions with increased preload
and pulmonary venous congestion as it increases venous
capacitance and reduces filling pressures. If the patient’s
CO is compromised, side effects are increased.[61]
Newer drugs
Levosimendan
It is a new inotrope, which has properties of both calcium
sensitization and phosphodiesterase inhibition. It stabilizes
the interaction between calcium and troponin C by binding
to troponin C in a calcium-dependent manner, thereby
improving inotropy without any adverse effect on lusitropy.
The vasodilatory effect is related to the activation of
several potassium channels. The combined inotropic
and vasodilatory actions result in an increased force of
contraction and decreased preload and afterload. By opening
the mitochondrial (ATP)-sensitive potassium channels in
cardiomyocytes it also exerts its cardioprotective effect.
Unlike other inotropes, its use does not result in significant
increase in myocardial oxygen consumption, arrhythmia,
and neurohormonal activation. In large controlled trials
in patients with decompensated heart failure, intravenous
(IV) levosimendan was found to be more effective than
dobutamine for overall hemodynamic improvement. The
pharmacokinetic profile of this drug in children is similar
to that in adult patients with CCF.[61] The pharmacokinetics
of levosimendan are linear at the therapeutic dose range of
0.05-0.2 μg/kg/min. Its short half-life (about 1 h) enables
fast onset of drug action but the effects are long-lasting due
260 Archives of Medicine and Health Sciences / Jul-Dec 2015 / Vol 3 | Issue 2
to the active metabolite, which has an elimination half-life
of 70-80 h in patients with heart failure. Although further
studies are needed, current clinical evidence suggests that
levosimendan is more effective than classical inotropes
in improving cardiac mechanical efficiency and reducing
congestion in acute HF patients without hypotension. The
European guidelines recommend using it very cautiously
and in special circumstances.[62-68]
Nesiritide
It is the recombinant form of human BNP, which is normally
produced by the ventricular myocardium in response
to pressure and volume elevation. Nesiritide facilitates
cardiovascular fluid homeostasis through counterregulation
of the renin-angiotensin-aldosterone system, stimulating
cyclic guanosine monophosphate, leading to smooth muscle
cell relaxation. Thus it compensates for deteriorating cardiac
function by causing preload and afterload reductions,
natriuresis, diuresis, suppression of the renin-angiotensin-
aldosterone system, and lowering of norepinephrine. It
results in clinically significant balanced vasodilatation of
arteries and veins. In clinical trials, this drug has been shown
to decrease pulmonary capillary wedge pressure, pulmonary
artery pressure, right atrial pressure, and SVR as well as
increase CI and SV index. HR variability also improved with
nesiritide.[69,70] Its use has consistently shown symptomatic
improvement owing to its unique mechanism of improvement
in hemodynamics. It was shown in the acute study of clinical
effectiveness of nesiritide and decompensated heart failure
(ASCEND-HF) trial that nesiritide did not affect renal function
in patients with acute decompensated heart failure.[71,72] It
is given by continuous IV infusion of 0.01 μg/kg/min, which
may be increased every 3 h to a maximum of 0.03 μg/kg/min.
Inotropic treatment strategy in different clinical
situations
• In low-CO states with hypotension (Presentation:
Increased HR, low-volume pulse, delayed capillary
refill, oliguria, hyperlactatemia, hypotension:
• Optimization of preload by giving small saline bolus
(5 mL/kg) over 1 h, with careful monitoring for
hepatomegaly and basal crepitations.
• Dopamine (10 ug/kg/min) and dobutamine
(10-15 ug/kg/min) infusions.
• Mechanical ventilation to be started in case of
respiratory distress or in a critically ill child.
• In low-CO states with normotension:
• Furosemide infusion 0.05-0.1 mg/kg/h to be added.
• Inodilators (milrinone/levosimendan) to be added.
• In increased afterload states (Presentation: HR settling,
good central pulses, weak peripheral pulses, cold
peripheries, BP normal to high, hyperlactatemia:
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Kar, et al.: Cardiogenic shock
• Milrinone needs to be started or the infusion rate
has to be increased if already added.
• If there is tachycardia, good pulses, warm
peripheries, decreased urine output, slightly low
BP, and hyperlactatemia after milrinone infusion,
hypovolemia due to vasodilation should be thought
of, which should be treated with fluid bolus.
• When optimal CO is achieved, as evident from good
normal pulses, warm extremities, good urine output,
normal BP, and normal lactate:
• The same inotropic support needs to be maintained,
and weaning from ventilation should be started. In
a stepwise manner, extubation is planned, and slow
and gradual inotrope tapering should be initiated
after adding digoxin and vasodilators (enalapril).
Mechanical afterload reduction
Intraaortic balloon pump (IABP)
Though not commonly used in children, it has been effectively
used in cases with coronary artery disease (Kawasaki
disease or ALCAPA) and in a postoperative setting with
reduced CO to achieve diastolic augmentation of BP. IABP
both provides mechanical afterload reduction and improves
coronary artery perfusion. It may be considered as an option
for end-stage failure.[73-75]
Extracorporal membrane oxygenation (ECMO)
ECMO is a complex system designed to circumvent the
lungs and heart in cases of severe cardiac and/or pulmonary
failure. It has truly revolutionized the survival of critically
sick children with cardiogenic shock and is currently the
most commonly used mechanical support system for
infants and young children. It has distinct advantages over
other support mechanisms.[76,77] ECMO can be used for
two broad categories of patients: Refractory hypoxemic
respiratory failure and refractory circulatory failure. The
most commonly used support method for cardiac failure
and cardiogenic shock is the venoarterial (VA) ECMO where
the right atrium is drained by venous cannulation, allowing
desaturated venous blood to be removed from the body.
This desaturated blood is pumped to the oxygenator, where
gas exchange occurs. Gas exchange in the membrane
oxygenator depends on the permeability of the membrane
to oxygen and carbon dioxide, the available surface area,
the pressure gradient, and the interface time. Viscosity,
temperature, and pH of the blood can also affect gas
exchange. After oxygenation, blood is rewarmed to body
temperature and returned to the patient via an arterial
cannula. Because the adequacy of flow depends on the
volume of deoxygenated blood, removed venous return
must be maintained for ECMO to be effective. In severely
depressed myocardial function, left atrial decompression
Archives of Medicine and Health Sciences / Jul-Dec 2015 / Vol 3 | Issue 2 261
may be required via atrial septostomy. Without left atrial
decompression, pulmonary edema develops. To deal
with the ECMO circuit resistance met at the cannula
site, a large-bore cannula is preferred. Any process that
limits right atrial filling, such as a pneumothorax or
pneumopericardium, will also hinder venous drainage.
Similar problems can occur on the arterial side. Less
commonly, venovenous (VV) ECMO can be used, employing
only central venous access and no central arterial access.
Candidates for VV ECMO must have isolated hypoxemic
respiratory failure with largely preserved cardiac function.
Though neonates with congenital diaphragmatic hernia had
similar outcomes for both VA and VV ECMO, in patients
with cardiac failure VA ECMO is preferred. It is effective at
bridging nearly half of eligible children to transplant.[77,78]
However, the most common significant complications
encountered with ECMO are hemorrhagic complications
associated with the requirement for anticoagulation and
organ failure related to the nonphysiologic, nonpulsatile
arterial flow patterns.[79]
Ventricular assist device (VAD)
These are mechanical pumps that take over the function
of one or both ventricles in an attempt to restore normal
hemodynamics. This treatment modality is rapidly evolving
in the treatment of children and may be used as a bridge to
transplant or if there is difficulty in weaning from bypass.[79]
In cases of fulminant myocarditis, VADs may help in
stabilization of patients till the time the myocardium
starts recovering. Currently, centrifugal pump and pulsatile
VADs have grown in popularity for pediatric support and
have been used even in children weighing less than 6
kg.[80] There are advantages of VAD use over the use of
ECMO. VADs allow for direct decompression of the left
ventricle and can provide pulsatile blood flow; as they
do not require an oxygenator in circuit, trauma to blood
elements is reduced, which decreases the requirement
for excessive transfusion and the development of
sensitivity to human leukocyte antigen (HLA) surface
antigen. In addition, VADs allow a decreased dose of
systemic anticoagulation, thereby reducing the risk of
hemorrhagic complications. [77-81] VAD support is best
used when isolated LV failure is the only indication for
assistance, and it can be used for a longer amount of time
than ECMO, as well.[79,80,82] However, a major disadvantage
of VAD support is that it requires direct cannulation
of the heart via sternotomy and four cannulation sites
compared to ECMO’s two cannulation sites.[80] Pulmonary
hypertension, respiratory failure, biventricular cardiac
failure, and residual intracardiac shunts are all other
relative contraindications for VAD support.[79] VAD therapy
should not be offered to a patient with advanced HF until all
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Kar, et al.: Cardiogenic shock

the medical options have been explored. On the other hand,
it should be implemented before profound hemodynamic
decompensation and end-organ failure occurs.[83] They
can be used as short-term support (days) or as long-term
support (weeks or months) [Table 10].[84-86] The short-
term VADs are usually used in patients who present in
cardiogenic shock after an acute myocardial infarction or
acute myocarditis or postcardiotomy shock. The long-term
VADs are again classified into first-generation, second-
generation, and third-generation devices [Table 11].[87-92]
Abdominal compression devices
To reduce right heart volume overload with right heart
failure, antishock trousers or ventilator reservoir bags can
be used, but experience with these modalities is limited in
children.
support.[79] A major limitation of pediatric heart transplant
is the unavailability of a suitable donor pool due to the
size restrictions of a small child’s thoracic cavity. Hence,
dilated cardiomyopathy patients match better in the
selection process because of the larger native heart size.
In addition, prognosis for pediatric patients awaiting
transplant is guarded, with high short-term mortality up
to 20% overall for children and 31% in young children
(less than 6 months).[94] Therefore, better pretransplant
therapies in the form of pediatric-sized VADs are needed.
More recent survival data are, however, more reassuring.
High pretransplant PVR, RV, and restrictive cardiomyopathy
were poor prognostic factors for survival after transplant.
On long-term follow-up, acute rejection and infection were
the most common causes of mortality.[95]

Cardiac transplantation
Management of “HFPEF-Heart
Heart transplantation is the last therapeutic option for
Failure with Preserved Ejection
children suffering from terminal heart failure refractory
Fraction” (Previously Called
to medical therapy who are dependent on mechanical “Diastolic Cardiac Failure”)
supportive interventions.[93] If after 72 h of mechanical
ECMO support there is no recovery of myocardial function, When there is an increase in end-diastolic pressures with
a decision should be made concerning transplant, longer- normal ventricular volume, diastolic failure is thought to be
term assist device implementation, or termination of present. Medications used for the management of diastolic
failure include low-dose diuretics, beta-blockers, calcium
channel blockers, and ACE inhibitors, but their effectiveness
Table 10: Classification and characteristics of short-term VADs[84-86]
is limited. Constrictive pericarditis must be ruled out in these
Types and qualities of the pump Disadvantages
Pulsatile: Available widely Requires trained personnel cases and the prognosis remains poor.
Placement extracorporeal Need for anticoagulation and risk of
Uni- or biventricular support thromboembolic events Management of Other Underlying
Conditions
Examples: Limited potential of deambulation
Abiomed BVS 5000, Abiomed AB 5000
Nonpulsatile: Good clinical experience Patient has to be bedridden
Axial flow Need for anticoagulation and risk of
Uni-or biventricular support thromboembolic events
In critical aortic stenosis or coarctation, transcatheter
Simple cannulation or implantation No potential for deambulation interventions may be needed. Early surgical correction of large
Examples: left-to-right shunt is warranted. Dynamic cardiomyoplasty
ECMO, Impella LP, TandemHeart, Levitronix,
CentriMag may also be useful in some patients. Supportive treatments
such as the control of infection, anemia, arrhythmias,
hypertension, and metabolic deficiencies are essential.
Table 11: Classification and characteristics of long-term VADs[87-92]
Types and qualities of the pump Disadvantages IV immunoglobulin can be tried in patients with myocarditis.
First-generation devices: Pulsatile with volume displacement Large size
Thoratec pVAD or IVAD, Placement intra- or extracorporeal Percutaneous lead
Administration of digoxin in the antenatal period can control
HeartMate, IP1000,VE or Uni- or biventricular support Audible pump operation supraventricular tachycardia causing failure in the fetus.
XVE, Novacor, LionHeart High incidence of device Discussion of the problem, genetic implications, treatment
malfunction
Second-generation devices: Rotary-axial flow Percutaneous lead modalities, and the prognosis with the parents forms an
HeartMate II, Jarvik 2000, LVAD Contact bearings important part of management.
DeBakey Thrombus formation and

Outcome
need for anticoagulation
Risk of ventricular suction
Third-generation devices: Rotary with centrifugal flow Large size
VentrAssist, DuraHeart, LVAD Percutaneous lead
HVAD, EVAHEART Noncontact bearings Risk of ventricular suction
Depending on the etiology and treatment, highly variable
Lack of enough clinical outcomes are noted in pediatric cardiogenic shock. The outcomes
evidence depend on the extent and nature of the myocardial inflammation

262 Archives of Medicine and Health Sciences / Jul-Dec 2015 / Vol 3 | Issue 2
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Kar, et al.: Cardiogenic shock
and overall reversibility of the diseased myocardium. ECMO has
poor neurologic outcome as compared with those supported
with VAD.[80] Intracranial hemorrhage and thromboembolic
cerebral events occur in 3-6% of patients regardless of the mode
of support.[79] Fewer than 33% survived to the transplantation
stage.[77] Myocarditis has the highest survival rate of 58-80%
among children requiring ECMO or VAD.[80] The experimental
use of paracorporeal VAD has successfully bridged patients to
transplant 60% of the time.[96] Despite the limited availability
of organs, cardiac transplantation outcomes have been rapidly
improving in recent years.
Conclusion
The clinical syndrome of shock is one of the most dynamic
life-threatening problems. Though untreated shock is
uniformly lethal, mortality can be substantially reduced
with early recognition and management. The most common
causes of cardiogenic shock remain congenital heart diseases
and infections of the heart. With better prenatal diagnosis of
congenital heart diseases, there is a reduction in the number
of undiagnosed structural heart defects. However, we have
a long way to go in properly anticipating and diagnosing
infectious causes of myocarditis, whose diagnosis still
remains essentially clinical. The clinical presentation of
cardiogenic shock greatly overlaps with other types of shock.
The mainstay of management consists of a combination
of supportive cardiorespiratory therapies and vasoactive
medications, with subsequent correction of the anatomic
cardiac defects. Treatment options such as ECMO and VADs
provide a bridge to recovery, surgery, or transplant. Though
cardiac transplant outcomes in children are improving, the
major limiting factor is the lack of an adequate donor pool.
However, multispecialty care involving the pediatrician,
the pediatric cardiologist, the pediatric intensivist, and the
cardiothoracic surgeon is invariably required for proper
management.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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