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SHOCK
By : O. Ahmadi, MD. Professor Assistant
of Esfahan medical School, Emergency
Department of Al-Zahra Hospital
Shock is defined as circulatory
insufficiency that creates an imbalance
between tissue oxygen supply and oxygen
demand
Nutrient requirements are not fulfilled
Toxic metabolites are not removed
If untreated, inevitable progression from
inadequate perfusion to organ dysfunction
and ultimately to death
Shock is classified into four
categories by etiology
(1) Hypovolemic (caused by inadequate
circulating volume)
(2) Cardiogenic (caused by inadequate
cardiac pump function)
(3) Distributive (caused by peripheral
vasodilatation and maldistribution of
blood flow)
(4) Obstructive (caused by extra cardiac
obstruction to blood flow)
Effect of cytokine exposure, arterial
hypotension, and acidosis on cardiac
function can be generalized
Indirectly depressed in shock conditions
by coronary hypotension
The contribution of acidosis to depressed
heart function is probably minimal
Hemorrhagic Shock
Rapid reduction in blood volume
Baroreceptor activation
Vasoconstriction
Strength of cardiac contraction
Heart rate
The first clinical manifestations of
hemorrhage are tachycardia, then a slight
increase in the diastolic BP
Causing the pulse pressure (difference
between systolic and diastolic BP) to
narrow.
The base deficit is defined as the amount of
strong base that would have to be added
to 1 L of blood to normalize the pH.
Distinguish simple hemorrhage from
hemorrhagic shock occurs when the base
deficit worsens (the total body base deficit
increases)
Arterial hypotension
Systolic arterial BP less than 90 mm Hg
Systolic arterial BP less than 100 mm Hg in
patients with known systemic hypertension
and in patients older than age 60 years
The second phase of organ injury from
hemorrhagic shock occurs during
resuscitation
Septic shock
Septic shock causes three major effects that
must be addressed during resuscitation:
Hypovolemia, Cardiovascular depression,
and Induction of systemic inflammation
More recently the incidence of gram-positive
infections has increased to a frequency
equal to that of gram-negative infections
Hypoxemia is more severe with septic shock
than hemorrhagic shock
Cardiogenic Shock
Results when more than 40% of the
myocardium becomes necrosed from
ischemia
Severe left ventricular dysfunction is evident
on echocardiography early in the course of
cardiogenic shock
Anaphylactic Shock
IgE-mediated systemic response to an
allergen
IgE
mast cells to release histamine
vascular smooth muscle relaxation +
bronchial smooth muscle constriction +
capillary leak of plasma into interstitial
spaces
• Platelets
PAF
peripheral
vasodilation + bronchial constriction +
pulmonary arterial and coronary
vasoconstriction
• PAF an important mediator of anaphylaxis
that is refractory to antihistamine
treatments.
CLINICAL FEATURES
• Shock can be strongly supported by the
presence of a worsening base deficit or
lactic acidosis
• Arterial BP as a sole measurement
remains an unreliable marker of circulatory
status
• The HR-to-systolic BP ratio (a normal ratio
is less than 0.8 )
• Excellent indicator of organ perfusion
Urine output
• Measuring urine output requires at least
30 minutes, however, to determine
accurately if output is normal (>1mL/kg/hr),
reduced (0.5 to 1 mL/kg/hr), or severely
reduced (<0.5 mL/kg/hr)
1-Empiric Criteria for Diagnosis
of Circulatory Shock
• Ill appearance or altered mental status
• Heart rate >100 beats/min
• Respiratory rate >22 breaths/min or
PaCO2 <32 mm Hg
• Arterial base deficit <−5 mEq/L or lactate
>4 mM/L
• Urine output <0.5 mL/kg/hr
• Arterial hypotension >20 minutes duration
Regardless of cause. Four criteria should be met
2-Classify the cause of shock
• Rectal temperature should be performed on
every patient with suspected shock.
• A hemoglobin level less than 8 g/dL strongly
suggests the need for blood transfusion if other
criteria for shock are present
• Some emergency departments have bedside
ultrasound capability, and cardiac and abdominal
scanning can be performed rapidly at the
bedside
Septic Shock
Systemic inflammatory response syndrome (SIRS)
Two or more of the following:
1. Temperature >38° C or <36° C
2. Heart rate >90 beats/min
3. Respiratory rate >20 breaths/min or PaCO2 <32 mm Hg
4. While blood cell count >12,000/mm3, <4000/mm3, or >10% band
neutrophilia
Sepsis syndrome
SIRS associated with organ dysfunction or hypotension; organ dysfunction
may include presence of lactic acidosis, oliguria, or altered mental status
Septic shock
SIRS with hypotension despite adequate fluid resuscitation; septic shock
should still be diagnosed if vasopressor therapy has normalized blood
pressure
Hemorrhagic Shock
• Simple hemorrhage
Suspected bleeding with pulse <100 beats/min,
normal respiratory rate, normal blood pressure,
and normal base deficit
• Hemorrhage with hypoperfusion
Suspected bleeding with base deficit <−5 mEq/L
or persistent pulse >100 beats/min
• Hemorrhagic shock
Suspected bleeding with at least four criteria
Cardiogenic Shock
• Cardiac failure
Clinical evidence of impaired forward flow
of the heart
presence of dyspnea,
tachycardia, pulmonary rales, peripheral
edema, or cyanosis
• Cardiogenic shock
Cardiac failure plus four criteria
Goal-directed therapy
• Resuscitation should continue until the
lactate concentration decreases to less
than 2 mM/L
Hemorrhagic Shock
Ensure adequate ventilation/oxygenation
Provide immediate control of hemorrhage, when possible (e.g., traction
for long bone fractures, direct pressure)
Initiate judicious infusion of lactated Ringer's solution (10-20 mL/kg) or
5% hydroxyethyl starch (5 mL/kg)
With evidence of poor organ perfusion and 30-minute anticipated delay
to hemorrhage control, begin packed red blood cell (PRBC) infusion
(5-10 mL/kg)
With suspected central nervous system trauma or Glasgow Coma
Scale score <9, immediate PRBC transfusion may be preferable as
initial resuscitation fluid
Treat severe acidosis (pH <6.8)
Treat coincident dysrhythmias (e.g., atrial fibrillation with synchronized
cardioversion)
Cardiogenic Shock
Ameliorate increased work of breathing; provide oxygen
and positive end-expiratory pressure (PEEP) for
pulmonary edema
Begin inotropic support; dobutamine(5µg/kg/min) is
common empiric agent
Seek to reverse the insult (e.g., initiate thrombolysis,
arrange percutaneous transluminal angioplasty, or
administer charcoal for drug overdose)
Consider intra-aortic balloon pump counterpulsation for
refractory shock
Septic Shock
Ensure adequate oxygenation; remove work of breathing.
Administer 20 mL/kg of crystalloid or 5 mL/kg of colloid,
and titrate infusion to adequate urine output
Begin antimicrobial therapy; attempt surgical drainage or
debridement
If volume restoration fails to improve organ perfusion, begin
vasopressor support; initial choice includes dopamine,
infused at 5-15µg/kg/min, or norepinephrine, infused at
0.1-1µg/kg/min
Anaphylactic Shock
Control airway and ventilation
Administer 10-20 mL/kg of crystalloid
Test an intravenous bolus of epinephrine (50100µg), then mix 5 mg of epinephrine in 500 mL
of normal saline. Begin infusion at 10 cc/hr, and
titrate to arterial blood pressure response
Administer 5-10 mg/kg of hydrocortisone or 1-2
mg/kg of methylprednisolone