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SHOCK IN CHILDREN. Definition. Circulatory system failure to supply oxygen and nutrients to meet cellular metabolic demands. Other Definitions. Blood Pressure BP = CO x SVR Cardiac Output CO = SV X HR Vascular Tone (SVR) Regulated by several mechanisms. Oxygen Delivery.

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Circulatory system failure to supply

oxygen and nutrients to meet cellular

metabolic demands

other definitions
Other Definitions
  • Blood Pressure


  • Cardiac Output


  • Vascular Tone (SVR)
    • Regulated by several mechanisms
oxygen delivery
Oxygen Delivery
  • DO2 = CO x CaO2 x 10
    • Remember: CO depends on HR, preload, afterload, and contractility
  • CaO2 = Hgb x 1.34 x SaO2 + (PaO2 x 0.003)
    • Remember: hemoglobin carries more than 99% of oxygen in the blood under standard conditions

Textbook of Pediatric Advanced Life Support, 1988

defending the blood pressure
Neural Sympathetic


Carotid Body

Aortic Arch

Volume receptors

Right Atrium

Pulmonary vascular


Aortic and carotid


Cerebral ischemic response


Adrenal medulla


Hypothalamopituitary response

Adrenocorticotropic hormone


Renin-angiotensin-aldosterone system

Defending the blood pressure
cardiovascular function
Cardiovascular function
  • Cardiac Output
    • Clinical Assessment
      • peripheral perfusion, temperature, capillary refill, urine output, mentation, acid-base status
    • CO = HR x SV
      • HR responds the quickest
      • SV is a function of three variables
        • preload, afterload, and myocardial contractility
      • A noncompliant heart cannot increase SV
stroke volume
Stroke Volume
  • Preload (LVEDV)
    • Reflects patient’s volume status
    • CVP or PCWP
    • Starling curve
  • Afterload
    • The resistance to ventricular ejection
    • Two variables:
      • vascular tone and transmural pressure
  • Myocardial Contractility (“squeeze”)
    • Many factors including coronary perfusion, baseline myocardial function, use of cardiotonic medications
classification of shock
Classification of Shock
    • blood flow is normal or increased and may be maldistributed; vital organ function is maintained
    • microvascular perfusion is compromised; significant reductions in effective circulating volume
    • inadequate perfusion of vital organs; irreparable damage; death cannot be prevented
other classifications
Other Classifications
  • Hypovolemic or Hemorrhagic
  • Cardiogenic
  • Obstructive
  • Distributive
cardiovascular changes in shock
Cardiovascular Changes in Shock

TypePreload AfterloadContractility

Cardiogenic 

Hypovolemic  No change

Distributive 


early 

late 

  • Regardless of the cause: ABC’s
    • First assess airway patency, ventilation, then circulatory system
  • Respiratory Performance
    • Respiratory rate and pattern, work of breathing, oxygenation (color), level of alertness
  • Circulation
    • Heart rate, BP, perfusion, and pulses, liver size
    • CVP monitoring may be helpful
  • Early Signs of Shock
    • sinus tachycardia
    • delayed capillary refill
    • fussy, irritable
  • Late Signs of Shock
    • bradycardia
    • altered mental status (lethargy, coma)
    • hypotonia, decreased DTR’s
    • Cheyne-Stokes breathing
    • hypotension is a very late sign
    • Lower limit of SBP = 70 + (2 x age in years)
cardiovascular assessment
Heart Rate

Too high: 180 bpm for infants, 160 bpm for children >1year old

Blood Pressure

Lower limit of SBP = 70 + (2 x age in years)

Peripheral Pulses


Strength (diminished, normal, bounding)

Skin Perfusion

Capillary refill time




CNS Perfusion

Recognition of parents

Reaction to pain

Muscle tone

Pupil size

Renal Perfusion

UOP >1cc/kg/hr

Cardiovascular Assessment

Airway management

  • Always provide supplemental oxygen
  • Endotracheal intubation and controlled ventilation is suggested if respiratory failure or airway compromise is likely
    • elective is safer and less difficult
    • decrease negative intrathoracic pressure
    • improved oxygenation and O2 delivery and decreased O2 consumption
    • can hyperventilate if necessary


  • Based on presumed etiology
  • Rapid restoration of intravascular volume
    • PIV-if unstable you have 60-90 seconds
    • I.O. if less than 4-6 years old
    • Central venous catheter
    • Use isotonic fluid: NS, LR, or 5% albumin
    • PRBC’s to replace blood loss or if still unstable after 60cc/kg of crystalloid
      • anemia is poorly tolerated in the stressed, hypoxic, hemodynamically unstable patient
vasoactive cardiotonic agents
Vasoactive/Cardiotonic Agents
  • Dopamine
    • 1-5 mcg/kg/min: dopaminergic
    • 5-15 mcg/kg/min: more beta-1
    • 10-20 mcg/kg/min: more alpha-1
    • may be useful in distributive shock
  • Dobutamine
    • 2.5-15 mcg/kg/min: mostly beta-1, some beta-2
    • may be useful in cardiogenic shock
  • Epinephrine
    • 0.05-0.1 mcg/kg/min: mostly beta-1, some beta-2
    • > 0.1 to 0.2 mcg/kg/min: alpha-1
vasoactive cardiotonic agents18
Vasoactive/Cardiotonic Agents
  • Norepinephrine
    • 0.05-0.2mcg/kg/min: only alpha and beta-1
    • Use up to 1mcg/kg/min
  • Milrinone
    • 50mcg/kg load then 0.375-0.75mcg/kg/min: phosphodiesterase inhibitor; results in increased inotropy and peripheral vasodilation (greater effect on pulmonary vasculature)
  • Phenylephrine
    • 0.1-0.5mcg/kg/min: pure alpha
  • # 1 cause of death in children worldwide
  • Causes
      • Water Loss (diarrhea, vomiting with poor PO intake, diabetes, major burns)
      • Blood Loss (obvious trauma; occult bleeding from pelvic fractures, blunt abdominal trauma, “shaken baby”)
  • Low preload leads to decreased SV and decreased CO.
  • Compensation occurs with increased HR and SVR
hypovolemic shock
Hypovolemic Shock
  • Mainstay of therapy is fluid
  • Goals
    • Restore intravascular volume
    • Correct metabolic acidosis
    • Treat the cause
  • Degree of dehydration often underestimated
    • Reassess perfusion, urine output, vital signs...
  • Isotonic crystalloid is always a good choice
    • 20 to 50 cc/kg rapidly if cardiac function is normal
    • NS can cause a hyperchloremic acidosis

Solution Na+ Cl- K+ Ca++ Mg++ Buffer

NS 154 154 0 0 0 None

LR 130 109 4 3 0 Lactate

Plasmalyte 140 98 5 0 3 Acetate & Gluconate

  • Inotropic and vasoactive drugs are not a substitute for fluid, however...
    • Can have various combinations of hypovolemic and septic and cardiogenic shock
    • May need to treat poor vascular tone and/or poor cardiac function
hemorrhagic shock
Hemorrhagic Shock
  • Treatment is PRBCs or whole blood
    • Treat the cause if able (stop the bleeding)
    • Transfuse if significant blood loss is known or if patient unstable after 60cc/kg crystalloid
      • In an emergency can give group O PRBCs before cross matching is complete or type specific non-cross-matched blood products
  • Low CO and high systemic vascular resistance
  • Result of primary cardiac dysfunction:
      • A compensatory increase in SVR occurs to maintain vital organ function
      • Subsequent increase in LV afterload, LV work, and cardiac oxygen consumption
      • CO decreases and ultimately results in volume retention, pulmonary edema, and RV failure
cardiogenic shock etiologies
Congenital heart disease


Ischemic heart disease


Myocardial injury

Acute and chronic drug toxicity

Late septic shock

Infiltrative diseases


glycogen storage diseases



Cardiogenic ShockEtiologies
cardiogenic shock
Cardiogenic Shock
  • Initial clinical presentation can be identical to hypovolemic shock
  • Initial therapy is a fluid challenge
  • If no improvement or if worsens after giving volume, suspect cardiogenic shock
  • Usually need invasive monitoring, further evaluation, pharmacologic therapy
  • Balancing fluid therapy and inotropic support can be very difficult.
    • Call an intensivist and/or a cardiologist
obstructive shock
Obstructive Shock
  • Low CO secondary to a physical obstruction to flow
  • Compensatory increased SVR
  • Causes:
    • Pericardial tamponade
    • Tension pneumothorax
    • Critical coarctation of the aorta
    • Aortic stenosis
    • Hypoplastic left heart syndrome
obstructive shock27
Obstructive Shock
  • Initial clinical presentation can be identical to hypovolemic shock
  • Initial therapy is a fluid challenge
  • Treat the cause
    • pericardial drain, chest tube, surgical intervention
    • if the patient is a neonate with a ductal dependent lesion then give PGE
  • Further evaluation, invasive monitoring, pharmacologic therapy, appropriate consults
distributive shock
Distributive Shock
  • High CO and low SVR (opposite of hypovolemic, cardiogenic, and obstructive)
  • Maldistribution of blood flow causing inadequate tissue perfusion
  • Due to release of endotoxin, vasoactive substances, complement cascade activation, and microcirculation thrombosis
  • Early septic shock is the most common form
distributive shock29
Distributive Shock
  • Goal is to maintain intravascular volume and minimize increases in interstitial fluid (the primary problem is a decrease in SVR)
    • Use crystalloid initially
    • Additional fluid therapy should be based on lab studies
    • Can give up to 40cc/kg without monitoring CVP
    • Vasoactive/Cardiotonic agents often necessary
    • Treat the cause (i.e.. antimicrobial therapy)
distributive shock etiologies
Distributive ShockEtiologies
  • Anaphylaxis
  • Anaphylactoid reactions
  • Spinal cord injury/spinal shock
  • Head injury
  • Early sepsis
  • Drug intoxication
    • Barbiturates, Phenothiazines, Antihypertensives
metabolic issues acid base
Metabolic IssuesAcid-Base
  • Metabolic acidosis develops secondary to tissue hypoperfusion
  • Profound acidosis depresses myocardial contractility and impairs the effectiveness of catecholamines
  • Tx: fluid administration and controlled ventilation
  • Buffer administration
    • Sodium Bicarbonate 1-2meq/kg or can calculate a 1/2 correction = 0.3 x weight (kg) x base deficit
    • hyperosmolarity, hypocalcemia, hypernatremia, left-ward shift of the oxyhemoglobin dissociation curve
metabolic issues electrolytes
Metabolic IssuesElectrolytes
  • Electrolytes
    • Calcium is important for cardiac function and for the pressor effect of catecholamines
    • Hypoglycemia can lead to CNS damage and is needed for proper cardiovascular function
    • Check the BUN and creatinine to evaluate renal function
    • Hyperkalemia can occur from renal dysfunction and/or acidosis
metabolic issues special topics
Metabolic IssuesSpecial Topics

Congenital adrenal hyperplasia

  • Infant presents in shock, usually in the second week of life, typically a boy, with metabolic acidosis, hyponatremia, hypoglycemia, and hyperkalemia


  • mild elevations are common with shock
  • levels > 1000 are consistent with inborn errors of metabolism
  • consider Reye Syndrome, toxins, hepatic failure
other studies
Other Studies
  • Look for etiology of shock
  • Evaluate hemoglobin, hematocrit, and platelet count
    • Should be followed as these values may drop after fluid resuscitation
  • Shock from any etiology can lead to DIC and end organ damage
    • CBC, PT, INR, PTT, Fibrinogen, Factor V, Factor VIII, D-dimer, and/or FDPs
    • Check LFT’s, follow CNS and pulmonary status
other studies ii
Other Studies II
  • Think about inborn errors of metabolism
    • Lactate and pyruvate
    • Ammonium, LFTs
    • Plasma amino acids, urine organic acids
    • Urinalysis with reducing substances
    • Urine tox screen
  • Goal of therapy is identification, evaluation, and treatment of shock in its earliest stage
  • Initial priorities are for the ABC’s
  • Fluid resuscitation begins with 20cc/kg of crystalloid or 10cc/kg of colloid
  • Subsequent treatment depends on the etiology of shock and the patient’s hemodynamic condition
  • Successful resuscitation depends on early and judicious intervention