dr. Shirley L A, Sp.A23 November 2011

SHOCK

• An acute dramatic syndrome• Characterized by inadequate circulatory

provision of oxygen

Metabolic demands of vital organs and tissues are not met

SHOCK

If inadequate tissue perfusion continues…

Epidemiology• Shock occurs in approximately 2% of

all hospitalized children & adults in US• Mortality rate is 20 - 50%• Multiple organ dysfunction increases

the probability of death 1 organ system involved – 25% 2 - 60% 3 or > - 85%

• There are 5 major types of shock: hypovolemic, septic, cardiogenic,

distributive, and obstructive

• Hypovolemic (diarrhea-dehydration, hemorrhage) and septic shock are the most common causes of shock in children

Clinical classification of shockType of Shock

Septic Cardiogenic Distributive

Characteristics Infectious organisms release toxins that affect fluid distribution, cardiac output & so on

Primary pump failure produces inadequate tissue perfusion;resultant metabolic acidosis further impairs cardiac function

Neurologic disturbance may cause uneven distribution of fluids, leading to acidosisOverdose of drug can alter fluid distribution

Sample causes

BacterialViral Fungal(all are more likely in immunocompromised)

Ischemic insultCardiomyopathyCHD

Neurogenic (disturbance of vasomotor tone)AnaphylaxisToxinsAllergic reactions

Clinical classification of shockType of Shock Hypovolemic Obstructive

Characteristics Reduced fluid volume Reduces cardiac output; metabolic acidosis can result from low intravascular volume and poor tissue perfusion; serious electrolyte abnormalities may occur

Poor cardiac output, cyanosis, hypotension, narrow pulse pressure

Sample causes EnteritisHemorrhageExtensive burnsDiabetes insipidusAdrenal insufficiency

Tension pneumothorax, pericardial tamponade

Pathophysiology• An initial insult triggers shock thus disrupting blood

flow to end-organs leading to inadequate tissue perfusion

• The body's compensatory mechanisms are initiated to maintain perfusion to vital organs, leading to compensated shock

• If treatment is not introduced during this period of compensated shock, decompensated shock develops, causing tissue damage that leads to multisystem organ dysfunction and death

Algorithm for decompensated shock

Initial insult

Triggers shock

Decreased perfusion

Body’s compensatory mechanisms

Compensated shock

Decompensated shock

Tissue damage

Multiple organ failure

Death

• In early phases of shock, a number of compensatory physiologic mechanisms act to maintain BP and preserve tissue perfusion

increase HR, stroke volume & vascular smooth muscle tone, regulated through neurohormonal changes in sympathetic

nervous system activation and other hormonal responses to help preserve blood flow to vital organs such as brain, heart, and kidneys

RR ↑ to promote the excretion of CO2 to compensate for increased CO2 production and the metabolic acidosis that occurs due to poor tissue perfusion. Increased renal excretion of hydrogen ions and retention of bicarbonate occurs in an effort to maintain normal pH

Maintenance of vascular volume is facilitated by the renin-angiotensin-aldosterone & atrial natriuretic factor axes (through regulation of sodium), cortisol & catecholamine synthesis and release, and secretion of ADH

Despite these compensatory mechanisms, intravascular fluid leaks into the interstitial extracellular space because of vascular endothelial cell injury and loss of tight junctions

Pathophysiology of Shock

• EXTRACORPOREAL FLUID LOSS Hypovolemic shock may be due to direct blood loss through hemorrhage or abnormal loss of body fluids (diarrhea, vomiting, burns, diabetes mellitus or insipidus, nephrosis)

• LOWERING PLASMA ONCOTIC FORCES Hypovolemic shock may also result from hypoproteinemia (liver injury, or as a progressive complication of increased capillary permeability)

• ABNORMAL VASODILATION Distributive shock (neurogenic, anaphylaxis, or septic shock) occurs when there is loss of vascular tone— venous, arterial, or both (sympathetic blockade, local substances affecting permeability, acidosis, drug effects, spinal cord transection)

Pathophysiology of Shock

• INCREASED VASCULAR PERMEABILITY Sepsis may change the capillary permeability in the absence of any change in capillary hydrostatic pressure (endotoxins from sepsis, excess histamine release in anaphylaxis)

• CARDIAC DYSFUNCTION Peripheral hypoperfusion may result from any condition that affects the heart's ability to pump blood efficiently (ischemia, acidosis, drugs, constrictive pericarditis, pancreatitis, sepsis)

Sepsis, pancreatitis, and SIRS can produce direct myocardial depressant effects adding a cardiogenic component to patients with

septic shock

All forms of shock affect heart rate

Fluid loss (vomiting, diarrhea,

hemorrhagic trauma,severe

burns)

initial ↑ in vascular

resistance

maintain BP & restore circulating

intravascular volume

hypotension develops &

produces tissue ischemia

Significant electrolyte alterations

pre-existing low plasma oncotic

pressure (nephrotic syndrome,

malnutrition, hepatic dysfunction, acute

severe burns)

greater capillary leaking

intravascular volume,more

edema, potentially

worsens the respiratory

status

SHOCK

Distributive shock• Abnormal vasodilation results in vasodilatory

shock and is usually caused by sepsis, hypoxia, poisonings (carbon monoxide, cyanide, metformin), anaphylaxis, neurogenic events, or mitochondrial dysfunction

• The lower systemic vascular resistance (SVR) is usually accompanied by an increase in cardiac output and a redistribution of blood flow away from vital organs to nonvital organs; hence, the term distributive shock

• shock occurs only with low BP (hypotension)

• Through various compensatory mechanisms, hypotension is often a late finding

• Hypotension is an advanced state of decompensated shock and has a high mortality rate

Tachycardia, with or without tachypnea, may be the 1st or

only sign of early compensated shock

• Shock may be present with normal BP if other factors do not permit the patient to maintain adequate tissue oxygen delivery

• Anemia and hypoxia result in reduced oxygen delivery at any given cardiac output

• Fever and trauma may increase tissue oxygen and metabolic requirements

• Progression of any of the mechanisms that lead to shock results in hypoxia and lactic acidosis

• Conversely, if blood pressure is low, but tissue perfusion is adequate to meet the metabolic demands of the body, shock may not be present

• vital signs• physical examination findings• laboratory studies• presence or absence of acidosis

to determine if the pediatric patient is in shock

CLINICAL MANIFESTATIONS

ORGAN SYSTEM ↓PERFUSION ↓↓PERFUSION ↓↓↓PERFUSIONCentral nervous system — Restless, apathetic,

anxiousAgitated/confused, stuporous, coma

Respiration — ↑Ventilation ↑↑VentilationMetabolism — Compensated metabolic

acidemiaUncompensated metabolic acidemia

Gut — ↓Motility IleusKidney ↓Urine volume Oliguria (<0.5 mL/kg/hr) Oliguria/anuria

  ↑Urinary specific gravity    

Skin Delayed capillary refill Cool extremities Mottled, cyanotic, cold extremities

Cardiovascular system ↑Heart rate ↑↑Heart rate ↑↑Heart rate, ↓blood pressure, central pulses only

Hypovolemic shock• usually presents as changes in mental status,

tachypnea, tachycardia, hypotension, poor peripheral pulses, cool extremities, and oliguria

• Supine hypotension and tachycardia are hallmarks of hypovolemia

• Neonates and infants may also have poor urine output. Dry mucous membranes, dry axillae, and poor skin turgor are variably present

• Hypovolemic shock may initially present with normal or only slightly cool distal extremities

Septic shock• has 2 phases: 1. Early, or warm, shock is diagnosed by low SVR2. late, or cold, shock is diagnosed by high SVR

Septic shock may present initially with :- warm extremities (from peripheral vasodilation secondary to low SVR)- bounding pulses (from high stroke volume and widened pulse

pressure)- tachycardia- tachypnea- adequate urination- mild metabolic acidosis

Cardiogenic shock• cool extremities• delayed (>2–3 sec) capillary filling time• hypotension• poor peripheral or central pulses• tachypnea• increasing obtundation• decreased urination

all caused by peripheral vasoconstriction & decreased COUncompensated shock (high vascular resistance, decreased CO,

obtundation, oliguria) occurs late in the progression of shock, regardless of its etiology

Compensated shock

decompensated shock

- ↑ in lactic acid production - very low mixed venous 02 sat indicating inadequate oxygen delivery

Measurement of the oxygen saturation of central mixed venous blood (Mvo2)

- from the PA, RV, RA, SVC, or IVC can determine if overall peripheral oxygen delivery (the true standard for such measurements is the pulmonary artery) is adequate

- Mvo2 should be 20–25% < the arterial 02 sat (N Mvo2 is 75–80%)

- A low Mvo2 suggests poor perfusion- This can guide caregivers in the use of fluid support and

inotropic agents to improve cardiac output in the treatment of shock

Treatment • Initial management : ABCs of resuscitation (airway, breathing, & circulation)

• Neonates and infants in particular may also have profound hypoglycemia associated with shock; it maybe helpful to recognize the ABCDs, with the D standing for dextrose in the pediatric population

In most patients with early shock…

Cardiogenic shock ? the fluid bolus should be held or a smaller volume given over a longer period to avoid

exacerbating heart failure

Children in severe hypovolemic, septic, or anaphylactic shock may

require additional fluid boluses (60–80 mL/kg within the 1st 1–2 hr of

presentation)

Fluid therapy should be titrated until improvements are noted

Cardiovascular Drug Treatment of Shock

DRUG EFFECT(S) DOSE RANGE COMMENTSDopamine Strengthens contractions

(throughout dose range)Intermediate dose = 5–15 μg/kg/min

increasing risk of dysrhythmias at high dose

   increases renal blood flow (low/intermediate doses)

High dose = 15–25 μg/kg/min

Should be administered in a central vein

  Vasoconstriction (high doses)    

Epinephrine Increases heart rate and strength of contractions

0.05–3.0 μg/kg/min May lessen renal perfusion

  Potent vasoconstrictor   Causes high O2 consumption in the heart

      High risk of dysrhythmiaDobutamine Increases strength of heart

contraction1–20 μg/kg/min Very weak vasoconstriction (high dose)

  Little effect on heart rate   Good for cardiogenic shock; strengthens heart contraction and produces afterload reduction

  Peripheral vasodilator, especially in vessels to viscera

   

Cardiovascular Drug Treatment of Shock

DRUG EFFECT(S) DOSE RANGE COMMENTSNorepinephrine Strong vasoconstrictor 0.05–1.5 μg/kg/min Produces short-term rise in

blood pressure (high systemic vascular resistance)

  Weak effect on strength of heart contraction

  Causes increase in O2 consumption, tendency for dysrhythmias

Phenylephrine Strong vasoconstrictor 0.5–2.0 μg/kg/min Can cause sudden hypertension

  Can be used to slow tachycardia through reflex cardiac slowing

  Causes increase in O2 consumption

Milrinone Potent inotrope Load 50 μg/kg over 15 min

Phosphodiesterase inhibitor—slows cyclic adenosine monophosphate breakdown

  Potent chronotrope 0.5–1 μg/kg/min    Peripheral vasodilator