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Shock in Pediatrics Medication

  • Author: Eric A Pasman, MD; Chief Editor: Timothy E Corden, MD  more...
Updated: Mar 03, 2015

Medication Summary

A variety of therapeutic treatments may be required for pediatric patients in shock. Possible therapies may include the following:

  • Inotropic medications
  • Dextrose
  • Electrolytes and calcium stabilization
  • Prostaglandin E1
  • Corticosteroids

Inotropic agents

Class Summary

Inotropic agents increase myocardial contractility and have variable effects on peripheral vascular resistance. First-line inotropic agents in pediatric shock include dopamine and epinephrine. On the basis of cardiac output (CO) and systemic vascular resistance (SVR), other vasoactive agents indicated in the treatment of shock may include vasoconstrictors (eg, norepinephrine, phenylephrine) or vasodilators (eg, dobutamine, milrinone).[50, 51] Which agents are indicated and which are effective in patients with any given etiology of shock depends on the end-diastolic volume and contractile state of the patient's cardiovascular system.



Dopamine is used for refractory hypotension following adequate volume resuscitation. It stimulates beta1- and alpha1-adrenergic and dopaminergic receptors in a dose-dependent fashion. In low doses, dopamine acts on dopaminergic receptors in renal and splanchnic vascular beds, causing vasodilatation in these beds. In midrange doses, it acts on beta-adrenergic receptors to increase heart rate and contractility, improve cardiac output, and enhance conduction (increasing sinoatrial rate) in the heart. In high doses, it acts on alpha-adrenergic receptors to increase systemic vascular resistance and raise blood pressure.



Sympathomimetic agent with primarily beta1-agonist effects, increasing heart rate and blood pressure. Some weak beta2-mediated peripheral vasodilation. Little effect on alpha receptors. May precipitate ventricular dysrhythmias, although potentially less likely to do so than epinephrine.

Epinephrine (Adrenalin)


Epinephrine is used for hypotension refractory to dopamine. Its alpha-agonist effects include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Its beta2-agonist effects include bronchodilation, chronotropic cardiac activity, and positive inotropic effects.

Norepinephrine (Levophed)


Norepinephrine is used for protracted hypotension following adequate fluid-volume replacement. This agent stimulates beta1- and alpha-adrenergic receptors, thereby increasing cardiac muscle contractility and heart rate, as well as vasoconstriction.



Strong alpha-receptor stimulant with little beta-adrenergic activity that produces vasoconstriction of arterioles in the body, helping increase systemic vascular resistance.


Phosphodiesterase Enzyme Inhibitor

Class Summary

Milrinone is the primary phosphodiesterase (PDE) inhibitor used in pediatrics, and it works via a different mechanism than that of the catecholamines. Milrinone inhibits PDE III, producing an increase in intracellular cyclic adenosine monophosphate (cAMP), which raises intracellular calcium levels and thereby improving cardiac inotropy and peripheral vasodilation.

Milrinone may be used together with catecholamines to further increase myocardial contractility while reducing systemic vascular resistance (SVR) and afterload. It can be useful in improving perfusion in patients who remain in compensated shock with poor peripheral perfusion but a normal central blood pressure and adequate intravascular volume. Milrinone is also often a useful adjunct in patients who have low cardiac output syndrome following congenital heart corrective surgeries.[52]

Adverse effects of milrinone may include arrhythmias and thrombocytopenia.[53, 54] Care must be taken when choosing to start phosphodiesterase inhibitors because of their vasodilator effects and their long half-life.



Milrinone is a selective PDE III inhibitor that acts as a positive inotrope and vasodilator with little chronotropic activity.


Prostaglandins, Endocrine

Class Summary

Neonates who present with shock associated with a large liver, enlarged cardiac silhouette, or heart murmur may have obstructive shock that develops because of closing of the ductus arteriosus. Prior to closure, the ductus arteriosus allows sufficient systemic blood flow to bypass the obstructive lesion. In patients in whom the ductus arteriosus has closed, initiation of prostaglandin E1 to maintain or reestablish its patency may be lifesaving. Adverse effects may include fever, apnea, or hypotension due to vasodilation. Evaluation of cardiac anatomy with echocardiography, performed by a pediatric cardiologist, should be obtained as soon as possible.

Alprostadil IV (Prostin VR)


Alprostadil is a synthetic prostaglandin E1 and induces vascular smooth muscle and ductus arteriosus vasodilation. This agent is beneficial in infants with congenital defects that restrict pulmonary or systemic blood flow and in patients who depend on a patent ductus arteriosus for adequate oxygenation and perfusion.



Class Summary

The use of corticosteroids in shock is controversial. However, it is possible that patients in severe septic shock have inadequate levels of circulating glucocorticoids and may benefit from stress dosing of steroids.

Hydrocortisone (Solu-Cortef, Cortef)


Hydrocortisone is a glucocorticoid with complex and varied metabolic effects when given systemically. It is the corticosteroid of choice in vasopressor-refractory shock because of its mineralocorticoid activity and glucocorticoid effects.

Contributor Information and Disclosures

Eric A Pasman, MD Resident Physician, Department of Pediatrics, National Capital Consortium, Walter Reed National Military Medical Center

Eric A Pasman, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics

Disclosure: Nothing to disclose.


Christopher M Watson, MD, MPH Assistant Professor, Department of Pediatrics, Uniformed Services University of the Health Sciences; Adjunct Assistant Professor, Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine

Christopher M Watson, MD, MPH is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Medical Association, Association of Pediatric Program Directors, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Chief Editor

Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, Wisconsin Medical Society

Disclosure: Nothing to disclose.


Barry J Evans, MD Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center

Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Adam J Schwarz, MD Consulting Staff, Critical Care Division, Pediatric Subspecialty Faculty, Children's Hospital of Orange County

Adam J Schwarz, MD is a member of the following medical societies: American Academy of Pediatrics and Phi Beta Kappa

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.


The views expressed are those of the authors and do not reflect the official policy or position of the US Navy, Department of Defense, or the US Government.

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Chest radiograph in a patient with cardiomegaly, which may accompany cardiogenic shock.
Determinants of cardiac function and oxygen delivery to tissues. FiO2 = fraction of inspired oxygen. Adapted from Strange GR. APLS: The Pediatric Emergency Medicine Course. 3rd ed. Elk Grove Village, Ill: American Academy of Pediatrics; 1998:34.
Hemodynamic response to shock hemorrhage model (based on normal data). Adapted from Schwaitzberg SD, Bergman KS, Harris BH. A pediatric trauma model of continuous hemorrhage. J Pediatr Surg. Jul 1988;23(7):605-9.
Pediatric shock management algorithm. ACTH = adrenocorticotropic hormone; CI = cardiac index; ECMO = extracorporeal membrane oxygenation; MAP-CVP = mean arterial pressure-central venous pressure; PALS = Pediatric Advanced Life Support; PDE = phosphodiesterase; PICU = pediatric intensive care unit; SVC O2 = superior vena cava oxygen saturation.
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