Pediatric Circulatory Failure

Authors

Erin Tromble, MD, Resident, Departments of Pediatrics and Emergency Medicine, University of Arizona, Tucson, AZ

Aaron Leetch, MD, Assistant Professor, Departments of Emergency Medicine and Pediatrics; Associate Program Director, Emergency Medicine/Pediatrics Residency, University of Arizona, Tucson, AZ

Dr. Tromble and Dr. Leetch report no financial relationships relevant to this field of study.

Pediatric Cardiogenic Failure/Shock

Etiology

Cardiogenic failure or shock encompasses a wide array of processes that result in insufficient oxygen and nutrient supply to meet the body’s metabolic needs. Shock is defined as insufficient delivery of oxygen or nutrients to tissues. If uncorrected, this state leads to development of anaerobic metabolism,lactate production, metabolic acidosis, and, ultimately, multisystem organ failure and death. Respiratory failure is the most common cause of cardiogenic failure and arrest in children. Other etiologies include sepsis, metabolic derangements, trauma, and intrinsic cardiac disease.

Pathophysiology

Shock ultimately develops with either impairment of cardiac output (CO), systemic vascular resistance (SVR), or both.

There are several categories of shock, which include the following:

• Hypovolemic – Decreased intravascular volume, (either hemorrhagic or non-hemorrhagic). Volume loss results in decreased pre-load and stroke volume, causing decreased cardiac output (CO).
• Septic – Caused by an infectious insult (bacterial, viral, fungal) resulting in inflammatory responses that cause increased metabolic demand and impaired perfusion. Pediatric presentation is variable. The classic adult presentation of low SVR and high CO is present in the minority of pediatric patients.
• Distributive – Results from a peripheral vasodilatory state leading to low SVR. Two major causes include anaphylaxis (allergic reaction leading to massive histamine release) and neurogenic (CNS injury causing loss of autonomic tone).
• Cardiogenic – CO is impaired by myocardial dysfunction, dysrhythmias, or congenital malformations
• Obstructive – Preload is restricted due to obstruction of venous return. Shock develops from decreased CO. Two major causes include tension pneumothorax and pericardial tamponade.

Table 1: Types of Shock

Type	Pathophysiology	Signs & Symptoms
Hypovolemic	Intravascular volume loss, ↓ CO	Tachycardia, ↓ pulses, ↓ capillary refill, hypotension (late in pediatric patients)
Septic	Infectious insult, varying pediatric presentation of CO and SVR	Tachycardia, variable blood pressure, ↓ capillary refill
Distributive	↓ SVR, ↑ CO in anaphylaxis, ↓ CO in neurogenic shock	Anaphylaxis: angioedema, respiratory distress, tachycardia Neurogenic: normal or low heart rate, hypotension, paralysis
Cardiogenic	↓ CO, normal or ↑ SVR	Normal to elevated heart rate, hepatomegaly, cardiomegaly, normal to low blood pressure
Obstructive	↓ CO, normal or ↑ SVR	Jugular venous distention, Tension pneumothorax: Absent breath sounds Pericardial Tamponade: Muffled heart sounds

Pediatric shock is a unique entity, distinct from that of adults, and must be evaluated with attention to the qualities that make pediatric shock.

Table 2: Characteristics of Pediatric Shock

Increased metabolic rate and insensible fluid losses, and decreased renal concentrating ability greater sensitivity to hypoperfusion Greater ability to maintain SVR hypotension is late finding Hypoperfusion, once developed, is generally profound Less myocardial mass and less ability to increase stroke volume dependent on tachycardia to maintain CO

Diagnosis

Shock can be challenging to identify in the pediatric patient. Clinical signs are often subtle and may be limited to tachycardia in the early compensated phase.Careful attention to appearance, work of breathing and color may identify early clues. (See Table 3.) Irritability, lethargy, and fluctuations in mental status may indicate poor perfusion. Increased respiratory effort may be due to respiratory distress or due to increased metabolic demand. End-organ perfusion can be assessed in the form of capillary refill (skin), urine output (kidneys), mental status (CNS), and heart rate (cardiac). In the setting of a normal blood pressure, poor perfusion indicates compensated shock, which may quickly progress into decompensated shock without intervention. Hypotension is generally a late, and often ominous, finding.

Table 3: Rapid Assessment of Pediatric Patients (“Pediatric Assessment Triangle”)

Appearance	Level of alertness Interaction Response to stimuli
Work of Breathing	Respiratory rate Respiratory effort (retractions, nasal flaring, grunting, abdominal breathing)
Color	Cyanosis Pallor Mottling

Figure: A Child with Mottling and Poor Perfusion

Diagnostic Evaluation

Laboratory data should be obtained and interpreted in the context of the patient at hand. Arterial or venous blood gas analysis and serum lactate measurement may reveal a metabolic acidosis secondary to hypoxemia and anaerobic metabolism. CBC, comprehensive metabolic profile (CMP), blood glucose level, and coagulation studies may be non-specific but should be interpreted in the context of the clinical picture. Blood and fluid cultures should be obtained, if an infectious etiology is suspected.

Table 4: Classic Laboratory Findings in Shock

	Classic Laboratory Findings
Septic Shock	WBC: ↑ Lactate: ↑ ScvO2: ↓ Glucose: ↑
Hypovolemic	WBC: generally ↑ Lactate: ↑ Hgb/HCT: ↓ (hemorrhagic – may be nl initially) PTT, PT/INR: ↑ (hemorrhagic) Glucose: ↑
Distributive	Neurogenic: WBC: generally ↑ Lactate: nl early, ↓ late Anaphylactic: WBC: ↑ Glucose: ↑
Cardiogenic	WBC: varies with etiology, but generally ↑ ScvO2: ↓ Lactate: ↑

WBC = white blood cell count, ScvO₂ = central venous oxygen saturation, Hgb = hemoglobin, HCT = hematocrit, nl = normal, PTT =partial thromboblastin time, PT = prothrombin time, INR = international ratio

Management

Early recognition and aggressive intervention is essential and should be in accordance with the American Heart Association Guidelines for Pediatric Advanced Life Support (PALS). In undifferentiated shock, intervention should include the following:

• Venous access
  • Two proximal large bore IVs.
  • Intraosseous access, if the above cannot be established quickly.
  • Central venous access may be indicated in advanced, refractory cases of shock.

• Continuous monitoring
  • Patients should be placed on cardiac monitoring throughout the resuscitation to monitor for dysrhythmias, including bradycardia.
  • Continuous pulse oximetry can aid in monitoring and titrating respiratory support.

• Respiratory support:
  • Supplemental oxygen should be administered to all patients in shock.
  • Consider intubation if there is impaired mental status or concern for airway protection.
  • If signs of respiratory failure are present, intubation should not be delayed.

• Fluid resuscitation
  • 20 mL/kg boluses of isotonic fluid, repeated up to 60 mL/kg or more until perfusion improves or hepatomegaly, rales, or other signs of congestive heart failure develop.
  • Patients should be frequently reassessed for response to fluids and to guide further resuscitation.
  • Blood products should be transfused if there are signs of hemorrhagic shock, symptomatic anemia, or DIC.

• Vasoactive medications
  • Used in the setting of persistent hypotension despite adequate fluid resuscitation.
  • Dopamine (starting dose: 5mcg/kg/min) is the recommended first line agent for septic shock. Infusion should be titrated to establish and maintain adequate perfusion.
  • Alternative or additive therapy with norepinephrine, epinephrine, milrinone, and vasopressin should be based on the patient’s clinical picture.

• Adrenal insufficiency
  • Hydrocortisone should be administered in catecholamine resistant shock, history of CNS abnormality (hypopituitarism), or history of recent steroid use.
  • Hydrocortisone should be given empirically in cases of vasopressor refractory shock.
  • Cortisol levels should be checked prior to administration when possible.

National Guideline/Academic Resources

http://www.aacn.org/WD/CETests/Media/ACC2344.pdf

http://pediatrics.aappublications.org/content/126/5/e1361.full

References

Dellinger RP, Levy MM, Carlet JM, et al. Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock. Intensive Care Med 2008;34:17-60.

Goldstein B, Zimmermann JJ. New horizons, the science and practice of acute medicine: Critical care of pediatric shock. Crit Care Med 1998;6:S120-S154.

Tabbutt S. Heart failure in pediatric septic shock: Utilizing inotropic support. Crit Care Med2001;29:S231-236.

Circulatory failure