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 Table of Contents  
Year : 2015  |  Volume : 3  |  Issue : 2  |  Page : 252-265

Pediatric cardiogenic shock: Current perspectives

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

Date of Web Publication16-Dec-2015

Correspondence Address:
Subhranshu Sekhar Kar
Department of Paediatrics, Ras al-Khaimah (RAK) Medical and Health Sciences University, Al Qusaidat, Ras al-Khaimah
United Arab Emirates
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2321-4848.171917

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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.

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

How to cite this article:
Kar SS. Pediatric cardiogenic shock: Current perspectives . Arch Med Health Sci 2015;3:252-65

How to cite this URL:
Kar SS. Pediatric cardiogenic shock: Current perspectives . Arch Med Health Sci [serial online] 2015 [cited 2023 Feb 2];3:252-65. Available from: https://www.amhsjournal.org/text.asp?2015/3/2/252/171917

  Introduction Top

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],[2],[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 in the management of shock, cardiogenic shock continues to 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 Top

Myocardial dysfunction is frequently a common final event seen as a late manifestation of shock of any etiology. Cardiogenic shock is defined as decreased cardiac output (CO) 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/m 2 ) 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 Top

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]

  • DO 2 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 (CaO 2 ).

Equation I

DO 2 (mL O 2 /min) = CaO 2 (mL O 2 /L blood) × CO (L/min)

  • The CaO 2 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 (SaO 2 ). A small amount of oxygen is directly dissolved in the blood that is not bound to Hb.
Equation II

CaO 2 (mL/100 mL) = Hb (g/100 mL) × SaO 2 × 1.34 mLO 2 /g + (0.003 × Partial pressure of oxygen in arteries (PaO 2 ))

A state of clinical shock may occur when CaO 2 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.

Equation III

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],[12],[13],[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]
Table 1: Definition of hypotension based on age[11,12]

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Equation IV


Hemodynamic response and cardiovascular mechanics [Figure 1]
Figure 1: Hemodynamic response and cardiovascular mechanics

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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, 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],[17],[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 (SVO 2 ) and intrapulmonary shunting. SVO 2 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],[16],[17],[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 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.


Causes of cardiogenic shock in patients can be categorized as systolic dysfunction, diastolic dysfunction, valvular dysfunction, cardiac arrhythmias, coronary artery disease, and mechanical complications [Table 2] and [Table 3]. [11],[19],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30],[31],[32] Signs and symptoms develop in patients when pulmonary venous pressure is increased to critical levels or tissue perfusion is severely limited [Table 3] and [Table 4]. [11],[19],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30],[31],[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],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30],[31],[32]
Table 2: Etiology of cardiogenic shock[11,19-32]

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Table 3: Specific pathologic mechanisms of cardiogenic shock[11,19-32]

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Table 4: Physiological mechanisms of symptoms and signs of cardiogenic shock[11,19-32]

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Table 5: Differentiating physical examination fi ndings of cardiogenic shock[11,19-32]

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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.


Though essentially the diagnosis of cardiogenic shock is clinical, certain laboratory tests are required to define the nature of specific diseases, functional status of the myocardium, and other comorbid features [Table 6]. [33],[34],[35],[36],[37],[38] To assess the therapeutic response, however, serial laboratory investigations are required from time to time.
Table 6: Relevant investigations in cardiogenic shock[33-38]

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Chest radiography

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).


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.

Blood gas and electrolytes

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 (PaCO 2 ) 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. SVO 2 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.


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 SVO 2 , which is associated with poor prognosis, but those with relatively high saturation levels fare better. [43]
Table 7: Goals of treatment[41,42]

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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.


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°.


Normothermia should be maintained to minimize myocardial oxygen demand.

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]
Table 8: Pharmacology of diuretics[44]

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These drugs relieve systemic and pulmonary vascular congestion. The common classes of drugs used are loop diuretics, thiazide, and aldosterone antagonists. Furosemide is the most commonly used diuretic. It has a rapid onset of action (2-5 min) with duration of action of about 3 h. Use of continuous infusion results in lowered hemodynamic instability and electrolyte imbalances. [44],[45] Common adverse effects of furosemide include hypokalemia, metabolic alkalosis, hypocalcemia, hyponatremia, and hyperuricemia. Ototoxicity is a rare reversible complication in neonates and infants. Thiazides have a slower onset of action and are commonly used for chronic CCF. The aldosterone antagonist spironolactone is a weak diuretic and is rarely used alone. It is usually added to loop diuretics or thiazides to antagonize the kaliuretic action. It is given orally, and the onset of action takes 2-3 days.

Inotropes and vasopressors [Table 9] [11]
Table 9: Pharmacology of inotropes and vasopressors[11]

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It is very effective in acute cardiac failure and cardiogenic shock, particularly when a postoperative patient has low CO. The half-life (t 1/2 ) is only 3-4 min and the major effects are increase in contractility, vasoconstriction, increase in HR, and increase in PVR. The effect of dopamine varies with the dose infused. It has the best dopaminergic action at the dose range of 3-5 mg/kg/min, which improves renal flow and natriuresis. Hence, it is a preferred agent in cardiogenic shock following cardiopulmonary bypass. At 5-15 mg/kg/min it has inotropic effect (b effect). At doses higher than 20 mg/kg it may compromise renal flow and increase PVR, oxygen demand, and ventricular afterload. It should not be mixed with sodium bicarbonate infusion. [46],[47],[48]


Dobutamine is a preferred drug in perioperative cases as it is less arrhythmogenic and augments CO. It acts predominantly on b1 rather than b2 and also on a receptors. It does not depend on norepinephrine stores to produce the desired effects. When used at a dose of 2-20 mg/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],[47],[48],[49],[50],[51],[52] In patients with postoperative failure, a combination of 3-5 mg/kg/min of dopamine with dobutamine 5-10 mg/kg/min and afterload-reducing agents such as milrinone produces excellent results.


It acts on both b and a 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 b 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.


It acts on both a1 and a2 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]


It is a very good drug in patients with acute heart failure complicated by increased reactive PVR or complete heart block. Because of its b1 and b2 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 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],[54],[55],[56],[57],[58],[59]


It induces predominantly a effects and causes vasoconstriction with increase in SVR. The dose range is 0.1-0.5 mg/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.


It acts on the V 1 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]


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]


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 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]


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


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 mg/kg/min. Its short half-life (about 1 h) enables fast onset of drug action but the effects are long-lasting due 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],[63],[64],[65],[66],[67],[68]


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 mg/kg/min, which may be increased every 3 h to a maximum of 0.03 mg/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:

  • 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],[74],[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 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],[78],[79],[80],[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 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],[85],[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],[88],[89],[90],[91],[92]
Table 10: Classification and characteristics of short-term VADs[84-86]

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Table 11: Classification and characteristics of long-term VADs[87-92]

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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.

Cardiac transplantation

Heart transplantation is the last therapeutic option for children suffering from terminal heart failure refractory to medical therapy who are dependent on mechanical supportive interventions. [93] If after 72 h of mechanical ECMO support there is no recovery of myocardial function, a decision should be made concerning transplant, longer-term assist device implementation, or termination of 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]

[TAG:2]Management of "HFPEF-Heart Failure with Preserved Ejection Fraction" (Previously Called "Diastolic Cardiac Failure")[/TAG:2]

When there is an increase in end-diastolic pressures with normal ventricular volume, diastolic failure is thought to be present. Medications used for the management of diastolic failure include low-dose diuretics, beta-blockers, calcium channel blockers, and ACE inhibitors, but their effectiveness is limited. Constrictive pericarditis must be ruled out in these cases and the prognosis remains poor.

  Management of Other Underlying Conditions Top

In critical aortic stenosis or coarctation, transcatheter interventions may be needed. Early surgical correction of large left-to-right shunt is warranted. Dynamic cardiomyoplasty may also be useful in some patients. Supportive treatments such as the control of infection, anemia, arrhythmias, hypertension, and metabolic deficiencies are essential.

IV immunoglobulin can be tried in patients with myocarditis. Administration of digoxin in the antenatal period can control supraventricular tachycardia causing failure in the fetus. Discussion of the problem, genetic implications, treatment modalities, and the prognosis with the parents forms an important part of management.

  Outcome Top

Depending on the etiology and treatment, highly variable outcomes are noted in pediatric cardiogenic shock. The outcomes depend on the extent and nature of the myocardial inflammation 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 Top

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


Conflicts of interest

There are no conflicts of interest.

  References Top

Chameides L, Samson RA, Schexnayder SM, Hazinski MF. Pediatric Advanced Life Support Provider Manual. Dallas: American Heart Association, Subcommittee on Pediatric Resuscitation; 2011. p. 69.  Back to cited text no. 1
Bell LM. Shock. In: Fleisher GR, Ludwig S, Henretig FM, editors. Textbook of Pediatric Emergency Medicine. 6 th ed. Philadelphia: Lippincott Williams & Wilkins; 2010. p. 46.  Back to cited text no. 2
Tobin RT, Wetzel RC. Shock and multiple system organ failure. In: Rogers MC, editor. Textbook of Pediatric Intensive Care. Baltimore: Lippincott Williams & Wilkins; 1996. p. 555.  Back to cited text no. 3
Fisher JD, Nelson DG, Beyersdorf H, Satkowiak LJ. Clinical spectrum of shock in the pediatric emergency department. Pediatr Emerg Care 2010;26:622-5.  Back to cited text no. 4
Court O, Kumar A, Parrillo JE, Kumar A. Clinical review: Myocardial depression in sepsis and septic shock. Crit Care 2002;6:500-8.  Back to cited text no. 5
Domico M, Liao P, Anas N, Mink RB. Elevation of brain natriuretic peptide levels in children with septic shock. Pediatr Crit Care Med 2008;9:478-83.  Back to cited text no. 6
O'Laughlin MP. Congestive heart failure in children. Pediatr Clin North Am 1999;46:263-73.  Back to cited text no. 7
Annabel AC, Michael AF. Mechanical complications of myocardial infarction. In: Irwin RS, Rippe JM, editors. Irwin and Rippe's Intensive Care Medicine. 6 th ed. Philadelphia: Lippincott Williams & Wilkins; 2008. p. 444.  Back to cited text no. 8
Vallet B, Tavernier B, Lund N. Assessment of tissue oxygenation in the critically-ill. Eur J Anaesthesiol 200;17: 221-9.  Back to cited text no. 9
Epstein D, Randall CW. Cardiovascular physiology and shock. In: Nichols DG, Cameron DE, Ungerleider RM, Nichols DG, Spevak PJ, Greeley WJ, et al., editors. Critical Heart Disease in Infants and Children. 2 nd ed. Philadelphia, PA: Mosby; 2006. p. 17-72.  Back to cited text no. 10
McKiernan CA, Lieberman SA. Circulatory shock in children: An overview. Pediatr Rev 2005;26:451-60.  Back to cited text no. 11
Zubrow AB, Hulman S, Kushner H, Falkner B. Determinants of blood pressure in infants admitted to neonatal intensive care units: A prospective multicenter study. Philadelphia Neonatal Blood Pressure Study Group. J Perinatol 1995;15: 470-9.  Back to cited text no. 12
Chittock DR, Russell JA. Oxygen delivery and consumption during sepsis. Clin Chest Med 1996;17:263-78.  Back to cited text no. 13
Hinshaw LB. Sepsis/septic shock: Participation of the microcirculation: An abbreviated review. Crit Care Med 1996;24:1072-8.  Back to cited text no. 14
Artman M, Parrish MD, Graham TP Jr. Congestive heart failure in children and adolescence: Recognition and management. Am Heart J 1983;105:471-80.  Back to cited text no. 15
Artman M, Graham TP Jr. Congestive heart failure in infancy: Recognition and management. Am Heart J 1982;103:1040-55.  Back to cited text no. 16
Freed MD. Congestive heart failure. In: Nadas' Pediatric Cardiology. 1 st ed. Philadelphia:Hanley and Belfus 1994. p. 63-72.  Back to cited text no. 17
Erickson LC, Burg FD, Polin RA, Ingelfinger JR, Wald ER. Congestive Heart Failure in Current Pediatric Therapy. Vol. 16. Philadelphia, PA: WB Saunders; 1997. p. 10.  Back to cited text no. 18
Radermecker M, Canivet JL, Lancellotti P, Limet R. The usual causes of left ventricular outflow tract obstruction below the aortic valve in normal ventriculoarterial connection: Review of the physiopathology and surgical implications. Acta Chir Belg 2005;105:475-81.  Back to cited text no. 19
Mann D, Qu JZ, Mehta V. Congenital heart diseases with left-to-right shunts. Int Anesthesiol Clin 2004;42:45-58.  Back to cited text no. 20
Kane JM, Rossi J, Tsao S, Burton BK. Metabolic cardiomyopathy and mitochondrial disorders in the pediatric intensive care unit. J Pediatr 2007;151:538-41.  Back to cited text no. 21
Hsing DD, Madikians A. True-true, unrelated: A case report. Pediatr Emerg Care 2005;21:755-9.  Back to cited text no. 22
Rathe M, Carlsen NL, Oxhoj H, Nielsen G. Long-term cardiac follow-up of children treated with anthracycline doses of 300 mg/m 2 or less for acute lymphoblastic leukemia. Pediatr Blood Cancer 2010;54:444-8.  Back to cited text no. 23
Hartmann M, Bode C, Zirlik A. Anaphylactic shock-associated cardiomyopathy. Int J Cardiol 2008;127:e136-7.  Back to cited text no. 24
Jain D, Halushka MK. Cardiac pathology of systemic lupus erythematosus. J Clin Pathol 2009;62:584-92.  Back to cited text no. 25
Fayssoil A, Nardi O, Orlikowski D, Annane D. Cardiomyopathy in Duchenne muscular dystrophy: Pathogenesis and therapeutics. Heart Fail Rev 2010;15:103-7.  Back to cited text no. 26
Bouhouch R, Elhouari T, Oukerraj L, Fellat I, Zarzur J, Bennani R, et al. Management of cardiac involvement in neuromuscular diseases: Review. Open Cardiovasc Med J 2008;2:93-6.  Back to cited text no. 27
Distefano G, Sciacca P, Parisi MG, Parano E, Smilari P, Marletta M, et al. Heart involvement in progressive spinal muscular atrophy. A review of the literature and case histories in childhood. Pediatr Med Chir 1994;16:125-8.  Back to cited text no. 28
Casazza F, Morpurgo M. The varying evolution of Friedreich's ataxia cardiomyopathy. Am J Cardiol 1996;77:895-8.  Back to cited text no. 29
Pandolfo M. Friedreich ataxia: The clinical picture. J Neurol 2009;256 (Suppl 1):3-8.  Back to cited text no. 30
Gucev Z, Tasic V, Jancevska A, Popjordanova N, Koceva S, Kuturec M, et al. Friedreich ataxia (FA) associated with diabetes mellitus type 1 and hyperthrophic cardiomyopathy. Bosn J Basic Med Sci 2009;9:107-10.  Back to cited text no. 31
Yanir Y, Shupak A, Abramovich A, Reisner SA, Lorber A. Cardiogenic shock complicating acute carbon monoxide poisoning despite neurologic and metabolic recovery. Ann Emerg Med 2002;40:420-4.  Back to cited text no. 32
Johnsrude CL, Perry JC, Cecchin F, Smith EO, Fraley K, Friedman RA, et al. Differentiating anomalous left main coronary artery originating from the pulmonary artery in infants from myocarditis and dilated cardiomyopathy by electrocardiogram. Am J Cardiol 1995;75:71-4.  Back to cited text no. 33
Smith KA, Bigham MT. Cardiogenic shock. Open Pediatr Med Journal 2013;7 (Suppl 1:M5):19-27.  Back to cited text no. 34
Fesseha AK, Eidem BW, Dibardino DJ, Cron SG, McKenzie ED, Fraser CD Jr, et al. Neonates with aortic coarctation and cardiogenic shock: Presentation and outcomes. Ann Thorac Surg 2005;79:1650-5.  Back to cited text no. 35
Colan SD, Borow KM, Neumann A. Left ventricular end-systolic wall stress-velocity of fibre shortening relation: A load-independent index of myocardial contractility. J Am Coll Cardiol 1984;4:715-24.  Back to cited text no. 36
Talner NS, Sanyal SK, Halloran KH, Gardner TH, Ordway NK. Congestive heart failure in infancy. I. Abnormalities in blood gases and acid-base equilibrium. Pediatrics 1965;35: 20-6.  Back to cited text no. 37
Das BB, Raj S, Solinger R. Natriuretic peptides in cardiovascular diseases of fetus, infants and children. Cardiovasc Hematol Agents Med Chem 2009;7:43-51.  Back to cited text no. 38
Gupta A, Mogos C, Schmer V, Gudavalli M. One day old infant with acyanotic congenital heart disease: Critical aortic stenosis. J Perinat Med 1999;27:292-4.  Back to cited text no. 39
Balaguru D, Artman M, Auslender M. Management of heart failure in children. Curr Probl Pediatr 2000;30:1-35.  Back to cited text no. 40
Gordon A, Russell JA. Goal directed therapy: How long can we wait? Crit Care 2005;9:647-8.  Back to cited text no. 41
Rossi AF, Khan DM, Hannan R, Bolivar J, Zaidenweber M, Burke R. Goal-directed medical therapy and point-of-care testing improve outcomes after congenital heart surgery. Intensive Care Med 2005;31:98-104.  Back to cited text no. 42
Hainsworth R. Mixed venous oxygen content and its meaning. Intensive Care Med 1981;7:153-5.   Back to cited text no. 43
Brater DC. Diuretic therapy. N Engl J Med 1998;339:387-95.  Back to cited text no. 44
Singh NC, Kissoon N, al Mofada S, Bennett M, Bohn DJ. Comparison of continuous versus intermittent furosemide administration in postoperative pediatric cardiac patients. Crit Care Med 1992;20:17-21.   Back to cited text no. 45
Scholz H. Inotropic drugs and their mechanism of action. J Am Coll Cardiol 1984;4:389-97.  Back to cited text no. 46
Eldadah MK, Schwartz PH, Harrison R, Newth CJ. Pharmacokinetics of dopamine in infants and children. Crit Care Med 1991;19:1008-11.  Back to cited text no. 47
Colluci WS, Wright RF, Braunwald E. New positive inotropic agents in the treatment of congestive heart failure. Mechanisms of action and recent clinical developments. 2. N Engl J Med 1986;314:349-58.  Back to cited text no. 48
Driscoll DJ, Gillette PC, Duff DF, Nihill MR, Gutgesell HP, Vargo TA, et al. Hemodynamic effects of dobutamine in children. Am J Cardiol 1979;43:581-5.  Back to cited text no. 49
Habib DM, Padbury JF, Anas NG, Perkin RM, Minegar C. Dobutamine pharmacokinetics and pharmacodynamics in pediatric intensive care patients. Crit Care Med 1992;20: 601-8.  Back to cited text no. 50
Berg RA, Donnerstein RL, Padbury JF. Dobutamine infusions in stable, critically ill children: Pharmacokinetics and hemodynamic actions. Crit Care Med 1993;21:678-86.  Back to cited text no. 51
Cooper BE. Review and update on inotropes and vasopressors. AACN Adv Crit Care 2008;19:5-15.  Back to cited text no. 52
Alousi AA, Johnson DC. Pharmacology of bipyridines: Amrinone and milrinone. Circulation 1986;73:III10-24.  Back to cited text no. 53
Edelson J, Stroshane R, Benziger DP, Cody R, Benotti J, Hood WB Jr, et al. Pharmacokinetics of the bipyridines amrinone and milrinone. Circulation 1986;73:III145-55.  Back to cited text no. 54
Laitinen P, Ahonen J, Olkkola KT, Peltola K, Rautiainen P, Räsänen J. Pharmacokinetics of amrinone in neonates and infants. J Cardiothorac Vasc Anesth 2000;14:378-82.  Back to cited text no. 55
Teshima H, Tobita K, Yamamura H, Takeda A, Motomura H, Nakazawa M. Cardiovascular effects of a phosphodiesterase III inhibitor, amrinone, in infants: Non-invasive echocardiographic evaluation. Pediatr Int 2002;44:259-63.  Back to cited text no. 56
Hoffman TM, Wernovsky G, Atz AM, Bailey JM, Akbary A, Kocsis JF, et al. Prophylactic intravenous use of milrinone after cardiac operation in pediatrics (PRIMACORP) study. Prophylactic intravenous use of milrinone after cardiac operation in pediatrics. Am Heart J 2002;143:15-21.  Back to cited text no. 57
Hoffman TM, Wernovsky G, Atz AM, Kulik TJ, Nelson DP, Chang AC, et al. Efficacy and safety of milrinone in preventing low cardiac output syndrome in infants and children after corrective surgery for congenital heart disease. Circulation 2003;107:996-1002.  Back to cited text no. 58
Friedman WF, George BL. Treatment of congestive heart failure by altering loading conditions of the heart. J Pediatr 1985;106:697-706.  Back to cited text no. 59
Alpert BS, Barfield JA, Taylor WJ. Reappraisal of digitalis in infants with left-to-right shunts and heart failure. J Pediatr 1985;106:66-8.  Back to cited text no. 60
Artman M, Graham TP Jr. Guidelines for vasodilator therapy of congestive heart failure in infants and children. Am Heart J 1987;113:994-1005.  Back to cited text no. 61
Ng TM. Levosimendan, a new calcium-sensitizing inotrope for heart failure. Pharmacotherapy 2004;24:1366-84.  Back to cited text no. 62
Mebazaa A, Erhardt L. Levosimendan: A new dualaction drug in the treatment of acute heart failure. Int J Clin Pract 2003;57:410-6.  Back to cited text no. 63
Nieminen MS. Levosimendan compared with dobutamine in low output patients. Minerva Anestesiol 2003;69: 258-63.  Back to cited text no. 64
Turanlahti M, Boldt T, Palkama T, Antila S, Lehtonen L, Pesonen E. Pharmacokinetics of levosimendan in pediatric patients evaluated for cardiac surgery. Pediatr Crit Care Med 2004;5:457-62.   Back to cited text no. 65
Ebade AA, Khalil MA, Mohamed AK. Levosimendan is superior to dobutamine as an inodilator in the treatment of pulmonary hypertension for children undergoing cardiac surgery. J Anesth 2013;27:334-9.  Back to cited text no. 66
Yilmaz MB, Yontar C, Erdem A, Karadas F, Yalta K, Turgut OO, et al. Comparative effects of levosimendan and dobutamine on right ventricular function in patients with biventricular heart failure. Heart Vessels 2009;24:16-21.  Back to cited text no. 67
Revermann M, Schloss M, Mieth A, Babelova A, Schröder K, Neofitidou S, et al. Levosimendan attenuates pulmonary vascular remodeling. Intensive Care Med 2011; 37:1368-77.   Back to cited text no. 68
Mahle WT, Cuadrado AR, Kirshbom PM, Kanter KR, Simsic JM. Nesiritide in infants and children with congestive heart failure. Pediatr Crit Care Med 2005;6:543-6.  Back to cited text no. 69
Feingold B, Law YM. Neseritide use in pediatric patients with congestive heart failure. J Heart Lung Transplant 2004;23: 1455-9.   Back to cited text no. 70
DeWald TA, Hernandez AF. Efficacy and safety of nesiritide in patients with acute decompensated heart failure. Expert Rev Cardiovasc Ther 2010;8:159-69.  Back to cited text no. 71
van Deursen VM, Hernandez AF, Stebbins A, Hasselblad V, Ezekowitz JA, Califf RM, et al. Nesiritide, renal function, and associated outcomes during hospitalization for acute decompensated heart failure: Results from the Acute Study of Clinical Effectiveness of Nesiritide and Decompensated Heart Failure (ASCEND-HF). Circulation 2014;130:958-65.  Back to cited text no. 72
Pollock JC, Charlton MC, Williams WG, Edmonds JF, Trusler GA. Intra aortic balloon pumping in children. Ann Thorac Surg 1980;29:522-8.  Back to cited text no. 73
Veasy LG, Blalock RC, Orth JL, Boucek MM. Intra aortic balloon pumping in infants and children. Circulation 1983;68:1095-107.  Back to cited text no. 74
Park JK, Hsu DT, Gersony WM. Intraaortic balloon pump management of refractory congestive heart failure in children. Pediatr Cardiol 1993;14:19-22.  Back to cited text no. 75
Raithel SC, Pennington DG, Boegner E, Fiore A, Weber TR. Extracorporeal membrane oxygenation in children after cardiac surgery. Circulation 1992;86 (Suppl):II305-10.  Back to cited text no. 76
Fynn-Thompson F, Almond C. Pediatric ventricular assist devices. Pediatr Cardiol 2007;28:149-55.  Back to cited text no. 77
Kugelman A, Gangitano E, Pincros J, Tantivit P, Taschuk R, Durand M. Venovenous versus venoarterial extracorporeal membrane oxygenation in congenital diaphragmatic hernia. J Pediatr Surg 2003;38:1131-6.  Back to cited text no. 78
Deiwick M, Hoffmeier A, Tjan TD, Krasemann T, Schmid C, Scheld HH. Heart failure in children - mechanical assistance. Thorac Cardiovasc Surg 2005;53 (Suppl 2):S135-40.  Back to cited text no. 79
Duncan BW. Mechanical circulatory support for infants and children with cardiac disease. Ann Thorac Surg 2002;73:1670-7.  Back to cited text no. 80
McMullan DM, Emmert JA, Permut LC, Mazor RL, Jeffries HE, Parrish AR, et al. Minimizing bleeding associated with mechanical circulatory support following pediatric heart surgery. Eur J Cardiothorac Surg 2011;39:392-7.  Back to cited text no. 81
Vatta M, Stetson S, Perez-Verdia A, Entman ML, Noon GP, Torre-Amione G, et al. Molecular remodeling of dystrophin in patients with end-stage cardiomyopathies and reversal in patients on assistance-device therapy. Lancet 2002;359: 936-41.  Back to cited text no. 82
Lietz K, Long JW, Kfoury AG, Slaughter MS, Silver MA, Milano CA, et al. Outcomes of left ventricular assist device implantation as destination therapy in the post-REMATCH era: Implications for patient selection. Circulation 2007;116:497-505.   Back to cited text no. 83
Delgado DH, Rao V, Ross HJ, Verma S, Smedira NG. Mechanical circulatory assistance: State of art. Circulation 2002;106:2046-50.  Back to cited text no. 84
Goldstein DJ, Oz MC, Rose EA. Implantable left ventricular assist devices. N Engl J Med 1998;339:1522-33.  Back to cited text no. 85
Rao V, Oz MC, Edwards NM, Naka Y. A new off-pump technique for thoratec right ventricular assist device insertion. Ann Thorac Surg 2001;71:1719-20.   Back to cited text no. 86
Lietz K, Miller LW. Destination therapy: Current results and future promise. Semin Thorac Cardiovasc Surg 2008;20: 225-33.   Back to cited text no. 87
Crow S, John R, Boyle A, Shumway S, Liao K, Colvin-Adams M, et al. Gastrointestinal bleeding rates in recipients of nonpulsatile and pulsatile left ventricular assist devices. J Thorac Cardiovasc Surg 2009;137:208-15.   Back to cited text no. 88
Morgan JA, John R, Rao V, Weinberg AD, Lee BJ, Mazzeo PA, et al. Bridging to transplant with the HeartMate left ventricular assist device: The Columbia Presbyterian 12-year experience. J Thorac Cardiovasc Surg 2004;127:1309-16.   Back to cited text no. 89
Miller LW, Pagani FD, Rusell SD, John R, Boyle AJ, Aaronson KD, et al.; HeartMate II Clinical Investigators. Use of continuous-flow device in patients awaiting heart transplantation. N Engl J Med 2007;357:885-96.   Back to cited text no. 90
John R, Kamdar F, Liao K, Colvin-Adams M, Boyle A, Joyce L, et al. Improved survival and decreasing incidence of adverse events using the HeartMate II left ventricular assist device as a bridge-to-transplant. Ann Thorac Surg 2008;86:1227-35.   Back to cited text no. 91
Pagani FD. Continuous-flow rotary left ventricular assist devices with "3 rd generation" design. Semin Thorac Cardiovasc Surg 2008;20:255-63.  Back to cited text no. 92
Groetzner J, Reichart B, Roemer U, Tiete A, Sachweh J, Kozlik-Feldmann R, et al. Results of pediatric cardiac transplantation - long-term results of a 15-year experience. Thorac Cardiovasc Surg 2005;53 (Suppl 2):S149-54.  Back to cited text no. 93
Jatene MB, Miana LA, Pessoa AJ, Riso A, Azeka E, Tanamati C, et al. Pediatric heart transplantation in refractory cardiogenic shock: A critical analysis of feasibility, applicability and results. Arq Bras Cardiol 2008;90:329-33.  Back to cited text no. 94
Hoskote A, Carter C, Rees P, Elliott M, Burch M, Brown K. Acute right ventricular failure after pediatric cardiac transplant: Predictors and long-term outcome in current era of transplantation medicine. J Thorac Cardiovasc Surg 2010;139:146-53.  Back to cited text no. 95
Malaisrie SC, Pelletier MP, Yun JJ, Sharma K, Timek TA, Rosenthal DN, et al. Pneumatic paracorporeal ventricular assist device in infants and children: Initial Stanford experience. J Heart Lung Transplant 2008;27:173-7.  Back to cited text no. 96


  [Figure 1]

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9], [Table 10], [Table 11]


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