Shock Management, by Ayman Raweh

Shock
Done by
Ayman Raweh
Jordan University of Science & Technology

April 22, 2004
MECHANISM/DESCRIPTION
Supply of blood flow to tissues inadequate to meet the demands of the tissues Nutrient requirements are not fulfilled Toxic metabolites are not removed Main components of blood flow Cardiac output Blood volume Peripheral resistance of arteriolar and venous system (systemic vascular resistance) Clinical shock is usually accompanied by hypotension, i.e., a mean arterial pressure <60 mmHg in previously normotensive persons
Shock Seminar, Ayman Raweh 2
General Picture of Shock Hypotension Decreased peripheral pulses Tachycardia Tachypnea Decreased urine output Diaphoresis Anxiety Obtundation Lethargy
Shock Seminar, Ayman Raweh
1. Hypovolemic shock
Cold and clammy extremities Pallor Flattened neck veins Decreased capillary refill Narrowed pulse pressure
2. Cardiogenic shock
Chest pain/pressure Dyspnea Orthopnea Jugular venous distention Cool, clammy, sweaty extremities Rales Wheezes Dullness at lung bases S3 gallop
3. Septic shock
Warm flushed extremities Strong pulses Hyperthermia Hypothermia Purpura or petechial rash
4. Anaphylactic shock
Warm flushed extremities Urticaria Stridor Throat tightness Hoarseness Wheezing
5. Neurogenic shock
Flaccid paralysis Loss of rectal tone Hypotension with bradycardia
Diagnosis
Hemoglobin/hematocrit Low hemoglobin and hematocrithemorrhage Very 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 ectopic pregnancy Lactic acid level Anaerobic metabolism of lactic acids when organ demands exceed nutrient supply Good surrogate marker of shock state
LABORATORY TESTS
IMAGING/SPECIAL TESTS

EKG Assess for ischemia and other disorders of cardiac muscle Electrical alternans with cardiac tamponade Right heart strain with pulmonary embolism Chest x-ray Pneumonia Pulmonary edema Pneumothorax Hemothorax Pulmonary infarction Traumatic injuries Echocardiography Tamponade Wall motion abnormalities (myocardial ischemia) LV collapse (pulmonary embolus) Aortic dissection Abdominal ultrasound Use to assess for intraperitoneal hemorrhage Ectopic pregnancy CT abdomen Requires that the patient first be stabilized In the setting of abdominal trauma and in search for suspicion of abdominal catastrophes and trauma
Treatment INITIAL STABILIZATION

ABCs Large-bore IV access When possible central venous access and monitoring Fluid resuscitation in noncardiogenic shock patients Control bleeding with temporary measures Direct pressure Long bone traction External fixation of pelvis
Hypovolemic Shock

FURTHER TREATMENT
Identify source of volume depletion Aggressive fluid resuscitation keeping SBP >100 mm Hg until definitive treatment 23 L crystalloid initially Transfuse packed red blood cells (O-negative if type specific 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 the initial goal Insult specific therapy (e.g., thrombolytics for MI, pericardiocentesis for pericardial tamponade) Treat dysrhythmias
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Septic Shock
Aggressive volume expansion with a crystalloid solution to a PCWP of approximately 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
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 noncritical settings Intravenous drip for immediate life threats or refractory hypotension
Neurogenic Shock
Supportive therapy
Traction and fracture stabilization Corticosteroids
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Shock

Jordan University of Science & Technology

Shock Seminar, Ayman Raweh

Warm flushed extremities Urticaria Stridor Throat tightness Hoarseness Wheezing

Flaccid paralysis Loss of rectal tone Hypotension with bradycardia

Shock Seminar, Ayman Raweh

Shock Seminar, Ayman Raweh

Shock Seminar, Ayman Raweh

Shock Seminar, Ayman Raweh

Treatment INITIAL STABILIZATION

Shock Seminar, Ayman Raweh

Shock Seminar, Ayman Raweh

Shock Seminar, Ayman Raweh

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