SHOCKBy : 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 fulfilledToxic metabolites are not removedIf 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 syndromeSIRS associated with organ dysfunction or hypotension; organ dysfunction may include presence of lactic acidosis, oliguria, or altered mental status

Septic shockSIRS with hypotension despite adequate fluid resuscitation; septic shock should still be diagnosed if vasopressor therapy has normalized blood pressure

Hemorrhagic Shock

• Simple hemorrhageSuspected bleeding with pulse <100 beats/min, normal respiratory rate, normal blood pressure, and normal base deficit

• Hemorrhage with hypoperfusionSuspected bleeding with base deficit <−5 mEq/L or persistent pulse >100 beats/min

• Hemorrhagic shockSuspected bleeding with at least four criteria

Cardiogenic Shock

• Cardiac failureClinical evidence of impaired forward flow of the heart presence of dyspnea, tachycardia, pulmonary rales, peripheral edema, or cyanosis

• Cardiogenic shockCardiac 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/oxygenationProvide 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 outputBegin antimicrobial therapy; attempt surgical drainage or

debridementIf 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 ventilationAdminister 10-20 mL/kg of crystalloidTest an intravenous bolus of epinephrine (50-

100µg), 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