Pediatric Shock

Recognition and Classification

Introduction

Shock is a syndrome of cardiovascular dysfunction cause inability of circulatory system to provide adequate oxygen and nutrient to meet the metabolic demands of vital organs. Oxygen delivery (DO2 ) is less than Oxygen Consumption (< VO2) Untreated this leads to metabolic acidosis, organ dysfunction and death

Shock

Transition between life and death Failure to oxygenate & nourish the body adequately Mortality > 20%

Hemodynamics
Myocardial Contractility Stroke Volume Cardiac Output Blood Pressure Systemic Vascular Resistance Preload Afterload

Heart Rate

Oxygen Delivery

Oxygen delivery = Cardiac Output x Arterial Oxygen Content

(DO2 = CO x CaO2)

Art Oxygen Content = Oxygen content of the RBC + the oxygen dissolved in plasma
(CaO2 = Hb X SaO2 X 1.34 + (.003 X PaO2)

Defending the blood pressure

Neural Sympathetic
Baroreceptors Carotid Body Aortic Arch
Volume receptors Right Atrium Pulmonary vascular Chemoreceptors Aortic and carotid Medullary Cerebral ischemic

Humoral
Adrenal medulla
Catecholamines

Hypothalamopituitary

response Adrenocorticotropic hormone Vasopressin Renin-angiotensinaldosterone system

response

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

Preload (LVEDV)
Reflects patients volume status CVP or PCWP

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

Pathophysiology & Biochemistry in shock

Pathophysiology

Shock affects mitochondria first Without oxygen mitochondria convert fuels to lactate lactic acid Failure of the krebs cycle
Oxygen is the final electron accepter to form

water

Lactic Acid

Early shock
Skeletal muscle and splanchnic organs 1st

affected Lactic acid production

Resuscitation
Pyruvate delivery from glycolysis can

overwhelm Krebs cycle

Systemic Response

Decreased vascular wall tension increases sympathetic stimulation (blocked in sepsis)

Increased epi, norepi, corticosteroids, renin,

and glucagon Increased glycogenolysis and lipolysis

Increased glucose and FFAs to TCA can overwhelm it

Immune Response

Neutrophil and macrophage activation due to hypoxia

Enzymatic organ damage Capillary plugs causing micro ischemia

TNF and Interleukins released

Cardiac Physiology
Inflammatory actions of TNF, Interleukins, and NO decrease contractility Acidosis can decrease contractility but effect is minimal Gregg Phenomenon

Contractile strength decreases with decreased

coronary perfusion

Decreased coronary perfusion in shock Decreased workload due to lower SVR Very minimal cardiac ischemia even in severe shock

Classification of Shock
COMPENSATED blood flow is normal or increased and may be maldistributed; vital organ function is maintained

UNCOMPENSATED microvascular perfusion is compromised; significant reductions in effective circulating volume

IRREVERSIBLE inadequate perfusion of vital organs; irreparable damage; death cannot be prevented

Classification:

Hypovolumic Cardiogenic Obstructive

Distributive

Hemodynamic Variables in Different Shock States

CO SVR MAP Wedge CVP Or Hypovolemic Cardiogenic Or Or Obstructive Or Or Or Distributive Septic: Early Or or Septic: Late

Clinical Presentation
Early

diagnosis requires a high index of suspicion is made through the physical examination focused on tissue perfusion
hypotension is a late and premorbid sign

Diagnosis

Abject

Initial Evaluation: Physical Exam Findings of Shock

Neurological: Fluctuating mental status, sunken fontanels Skin and extremities: Cool, pallor, mottling, cyanosis, poor cap refill, weak pulses, poor muscle tone. Cardio-pulmonary: Hyperpnoea, tachycardia. Renal: Scant, concentrated urine

Evaluation

Early Signs of Shock sinus tachycardia delayed capillary refill fussy, irritable Late Signs of Shock bradycardia altered mental status (lethargy, coma) hypotonia, decreased DTRs 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

Skin Perfusion

infants, 160 bpm for children >1year old

Blood Pressure
Lower limit of SBP =

Capillary refill time Temperature Color Mottling

CNS Perfusion
Recognition of

70 + (2 x age in years)

Peripheral Pulses
Present/Absent Strength (diminished,

parents Reaction to pain Muscle tone Pupil size

normal, bounding)

Renal Perfusion
UOP >1cc/kg/hr

Neonate in Shock: Include in differential:

Congenital adrenal hyperplasia Inborn errors of metabolism Obstructive left sided cardiac lesions: Aortic stenosis Hypo plastic left heart syndrome Coarctation of the aorta Interrupted aortic arch

Hypovolemic Shock
Most common form of shock world-wide Results in decreased circulating blood volume, decrease in preload, decreased stroke volume and resultant decrease in cardiac output. Etiology: Hemorrhage, renal and/or GI fluid losses, capillary leak syndromes

Hypovolemic Shock
Clinically, history of vomiting/diarrhea or trauma/blood loss Signs of dehydration: dry mucous membranes, absent tears, decreased skin turgor Hypotension, tachycardia without signs of congestive heart failure, CRT delayed.

Hemorrhagic Shock
Most common cause of shock (due to trauma) Patients present with an obvious history (but in child abuse history may be misleading) Site of blood loss obvious or concealed (liver, spleen, intracranial, GI, long bone fracture) Hypotension, tachycardia and pallor

Septic Shock
SIRS/Sepsis/Septic shock

Mediator release: exogenous & endogenous

Maldistribution of blood flow

Cardiac dysfunction

Imbalance of oxygen supply and demand

Alterations in metabolism

Septic Shock: Warm Shock

Early, compensated, hyperdynamic state Clinical signs
Warm extremities with bounding pulses,

tachycardia, tachypnea, confusion.

Physiologic parameters
widened pulse pressure, increased cardiac

ouptut and mixed venous saturation, decreased systemic vascular resistance.

Biochemical evidence:
Hypocarbia, elevated lactate, hyperglycemia

Septic Shock: Cold Shock

Late, uncompensated stage with drop in cardiac output. Clinical signs
Cyanosis, cold and clammy skin, rapid thready

pulses, shallow respirations.

Physiologic parameters
Decreased mixed venous sats, cardiac output

and CVP, increased SVR, thrombocytopenia, oliguria, myocardial dysfunction, capillary leak

Biochemical abnormalities
Metabolic acidosis, hypoxia, coagulopathy,

hypoglycemia.

Septic Shock

Cold Shock rapidly progresses to mutiorgan system failure or death if untreated. Multi-Organ System Failure: Coma, ARDS, CHF, Renal Failure, Ileus or GI hemorrhage, DIC. More organ systems involved, worse the prognosis

Cardiogenic Shock
Etiology:
Dysrhythmias Infection (myocarditis) Metabolic Obstructive Drug intoxication Congenital heart disease Trauma

Cardiogenic Shock
Differentiation from other types of shock:
History Exam:
Enlarged liver Gallop rhythm Murmur Cold extremitis, altered mental status, oliguria. Tachypnea tachycardia

CXR:
Enlarged heart, pulmonary venous congestion

Distributive Shock
Due to an abnormality in vascular tone leading to peripheral pooling of blood with a relative hypovolemia.

Etiology
Anaphylaxis Drug toxicity Neurologic injury Early sepsis

Obstructive Shock

Mechanical obstruction to ventricular outflow.

Etiology: Congenital heart disease, massive pulmonary embolism, tension pneumothorax, cardiac tamponade.

Inadequate C.O. in the face of adequate preload and contractility

Dissociative Shock

Inability of Hemoglobin molecule to give up the oxygen to tissues. Etiology: Carbon Monoxide poisoning, methemoglobinemia, dyshemoglobinemias. Tissue perfusion is adequate, but oxygen release to tissue is abnormal.

Differential Diagnosis of Shock

Cardiogenic
Myocardial dysfunction Dysrrhythmia Congenital heart

Hypovolemic
Hemorrhage Fluid loss Drugs

disease

Distributive
Anaphylactic Neurogenic Septic

Obstructive
Pneumothorax,

CardiacTamponade, Aortic Dissection

Dissociative
Heat, Carbon

monoxide, Cyanide Endocrine

Recognition and Classification

Initial Management of Shock

Final Thoughts
Recognize compensated shock quickly- have a high index of suspicion, remember tachycardia is an early sign. Hypotension is late and ominous. Gain access quickly- if necessary use an intraoseous line. Fluid, fluid, fluid - Administer adequate amounts of fluid rapidly. Remember ongoing losses. Correct electrolytes and glucose problems quickly. If the patient is not responding the way you think he should, broaden your differential, think about different types of shock.

References, Recommended Reading, and Acknowledgments

Uptodate:

Initial Management of Shock in Pediatric patients Nelsons Textbook of Pediatrics Some slides based on works by Dr. Lou DeNicola and Dr. Linda Siegel for PedsCCM American Heart Association PALS guidelines