Shock Management, by Ayman Raweh

8/4/2019 Shock Management, by Ayman Raweh

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Shock

Done by

Ayman RawehJordan University of Science &

Technology

April 22, 2004


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Shock Seminar, Ayman Raweh 2

MECHANISM/DESCRIPTION

Supply of blood flow to tissues inadequate to meet

the demands of the tissuesNutrient requirements are not fulfilledToxic metabolites are not removed

Main components of blood flowCardiac outputBlood volumePeripheral resistance of arteriolar and venous

system (systemic vascular resistance)

Clinical shock is usually accompanied byhypotension, i.e., a mean arterial pressure


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General Picture of Shock Hypotension

Decreased peripheral pulsesTachycardia

TachypneaDecreased urine outputDiaphoresis

Anxiety

ObtundationLethargy


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1. Hypovolemic shock Cold and clammy extremities

Pallor

Flattened neck veinsDecreased capillary refillNarrowed pulse pressure

2. Cardiogenic shock Chest pain/pressure

DyspneaOrthopneaJugular venous distentionCool, clammy, sweaty extremitiesRalesWheezesDullness at lung bases

S3 gallop


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3. Septic shock Warm flushed extremities

Strong pulses

HyperthermiaHypothermiaPurpura or petechial rash

4. Anaphylactic shock Warm flushed extremities

UrticariaStridorThroat tightnessHoarsenessWheezing

5. Neurogenic shockFlaccid paralysisLoss of rectal toneHypotension with bradycardia


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Diagnosis


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LABORATORY TESTS Hemoglobin/hematocrit Low hemoglobin and hematocrit

hemorrhageVery high hematocritdehydration

Poor marker with acute hemorrhage White blood cell count Highnonspecific marker of infection

Lowneutropenic infection Electrolytes Low CO 2acidosis

Increased BUN (GI hemorrhage)

Increased Na, K, Cl, BUN/CR (dehydration) Blood glucose High (DKA or septic shock)

PT/PTT Increased in DIC, septic shock , and liver disease Cardiac enzymes Urinalysis High glucose/ketones (DKA or septic shock )

WBCs and bacteria when uroseptic

Beta-HCG Women of childbearing age at risk for a ruptured ectopicpregnancy Lactic acid level Anaerobic metabolism of lactic acids when organ demands

exceed nutrient supplyGood surrogate marker of shock state


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IMAGING/SPECIAL TESTS EKG Assess for ischemia and other disorders of cardiac muscle

Electrical alternans with cardiac tamponadeRight heart strain with pulmonary embolism

Chest x-rayPneumonia

Pulmonary edemaPneumothorax

HemothoraxPulmonary infarctionTraumatic injuries

EchocardiographyTamponade

Wall motion abnormalities (myocardial ischemia)LV collapse (pulmonary embolus)Aortic dissection

Abdominal ultrasound Use to assess for intraperitoneal hemorrhageEctopic pregnancy

CT abdomenRequires that the patient first be stabilized

In the setting of abdominal trauma and in search for suspicion of abdominalcatastrophes and trauma


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Treatment

INITIAL STABILIZATION ABCs

Large-bore IV access

When possible central venous access andmonitoring

Fluid resuscitation in noncardiogenicshock patients

Control bleeding with temporary measuresDirect pressureLong bone tractionExternal fixation of pelvis


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FURTHER TREATMENTHypovolemic Shock

Identify source of volume depletion Aggressive fluid resuscitation keeping SBP >100 mm Hg

until definitive treatment 23 L crystalloid initiallyTransfuse packed red blood cells (O-negative if typespecific unavailable) if 23 crystalloids do not correct

pressure Identify source of bleeding and rapidly move toward

definitive treatment Dopamine and epinephrine in refractory shock after

maximal fluid and blood product resuscitation with

delayed hemorrhage control Thoracotomy and aortic cross-clamping in refractory

shock with penetrating torso trauma


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Cardiogenic Shock

Ease work of breathing with intubation

A PCWP of 15 to 20 mmHg should be theinitial goal

Insult specific therapy (e.g., thrombolyticsfor MI, pericardiocentesis for pericardialtamponade)

Treat dysrhythmias


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Septic Shock

Aggressive volume expansion with acrystalloid solution to a PCWP ofapproximately 15 mmHg

Titrate fluid to urine output >30 cc/h Blood product transfusion to maintain Hct

3035%

Early antimicrobial therapy Inotropic support as needed Dopamine

infusion or Norepinephrine infusion


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Anaphylactic Shock

Intubation for airway compromise

H-1 blockers (diphenhydramine)

H-2 blockers (cimetidine)

Corticosteroids (hydrocortisone or

methylprednisolone) Nebulized 2-antagonists for

bronchospasm

Epinephrine Subcutaneous in noncriticalsettings

Intravenous drip for immediate life threats

or refractory hypotension


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Neurogenic Shock Supportive therapy

Traction and fracture stabilization

Corticosteroids

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Shock Management, by Ayman Raweh