Shock

Definition

Condition of severe impairment of tissue perfusion leading to cellular injury

and dysfunction. Cell membrane dysfunction is a common end stage for various

forms of shock. Rapid recognition and treatment are essential to prevent irreversible

organ damage. Common causes are listed in Table 14-1.

Clinical Manifestations

• Hypotension (systolic bp _ 90, mean bp _ 60), tachycardia, tachypnea,

pallor, restlessness, and altered sensorium.

Table 14-1

Common Forms of Shock

Oligemic shock

Hemorrhage

Volume depletion (e.g., vomiting, diarrhea, diuretic over-usage,

ketoacidosis)

Internal sequestration (ascites, pancreatitis, intestinal obstruction)

Cardiogenic shock

Myopathic (acute MI, dilated cardiomyopathy)

Mechanical (acute mitral regurgitation, ventricular septal defect, severe

aortic stenosis)

Arrhythmic

Extracardiac obstructive shock

Pericardial tamponade

Massive pulmonary embolism

Tension pneumothorax

Distributive shock (profound decrease in systemic vascular tone)

Sepsis

Toxic overdoses

Anaphylaxis

Neurogenic (e.g., spinal cord injury)

Endocrinologic (Addison’s disease, myxedema)

Signs of intense peripheral vasoconstriction, weak pulses, cold clammy extremities

[in distributive (e.g., septic) shock, vasodilatation predominates and

extremities are warm].

• Oliguria (_20 mL/h) and metabolic acidosis common.

Approach to the Patient

Tissue perfusion must be restored immediately (see below); also obtain history

for underlying cause, including

• Known cardiac disease (coronary disease, CHF, pericarditis)

• Recent fever or infection (leading to sepsis)

• Drugs, i.e., excess diuretics or antihypertensives

• Conditions predisposing for pulmonary embolism (Chap. 135)

• Possible bleeding from any site, particularly GI tract.

Physical Examination

• Jugular veins are flat in oligemic or distributive shock; jugular venous distention

(JVD) suggests cardiogenic shock; JVD in presence of paradoxical pulse

(Chap. 117) may reflect cardiac tamponade (Chap. 121).

• Look for evidence of CHF (Chap. 126), murmurs of aortic stenosis, acute

regurgitation (mitral or aortic), ventricular septal defect.

• Check for asymmetry of pulses (aortic dissection) (Chap. 127).

• Tenderness or rebound in abdomen may indicate peritonitis or pancreatitis;

high-pitched bowel sounds suggest intestinal obstruction. Perform stool guaiac

to rule out GI bleeding.

• Fever and chills usually accompany septic shock. Sepsis may not cause fever

in elderly, uremic, or alcoholic patients.

• Skin lesion may suggest specific pathogens in septic shock: petechiae or

purpura (Neisseria meningitidis), erythyma gangrenosum (Pseudomonas aeruginosa), generalized erythroderma (toxic shock due to Staphylococcus aureus

or Streptococcus pyogenes).

Laboratory

• Obtain hematocrit, WBC, electrolytes. If actively bleeding, check platelet

count, PT, PTT, DIC screen.

• Arterial blood gas usually shows metabolic acidosis (in septic shock, respiratory

alkalosis precedes metabolic acidosis). If sepsis suspected, draw blood

cultures, perform urinalysis, and obtain Gram stain and cultures of sputum,

urine, and other suspected sites.

• Obtain ECG (myocardial ischemia or acute arrhythmia), chest x-ray (CHF,

tension pneumothorax, aortic dissection, pneumonia). Echocardiogram may be

helpful (cardiac tamponade, CHF).

• Central venous pressure or pulmonary capillary wedge (PCW) pressure measurements

may be necessary to distinguishbetween different categories of shock

(Table 14-2): Mean PCW _ 6 mmHg suggests oligemic or distributive shock;

PCW _ 20 mmHg suggests left ventricular failure. Cardiac output (thermodilution)

is decreased in cardiogenic and oligemic shock, and usually increased

initially in septic shock.

TREATMENT

See Fig. 14-1.

Aimed at rapid improvement of tissue hypoperfusion and respiratory impairment:

• Serial measurements of bp (intraarterial line preferred), heart rate, continuous

ECG monitor, urine output, pulse oximetry, blood studies: Hct, electrolytes,

creatinine, BUN, ABGs, calcium, phosphate, lactate, urine Na concentration

(_20 mmol/L suggests volume depletion). Continuous monitoring of

CVP and/or pulmonary artery pressure, withserial PCW pressures.

• Insert Foley catheter to monitor urine flow.

• Assess mental status frequently.

• Augment systolic bp to _100 mmHg: (1) place in reverse Trendelenburg

position; (2) IV volume infusion (500- to 1000-mL bolus), unless cardiogenic

shock suspected (begin with normal saline, then whole blood, dextran, or

packed RBCs, if anemic); continue volume replacement as needed to restore

vascular volume.

• Add vasoactive drugs after intravascular volume is optimized; administer

vasopressors (Table 14-3) if systemic vascular resistance (SVR) is decreased

(begin with norepinephrine or dopamine; for persistent hypotension add

phenylephrine or vasopressin).

• If CHF present, add inotropic agents (usually dobutamine) (Table 14-3);

aim to maintain cardiac index _ 2.2 (L/m2)/min [_4.0 (L/m2)/min in septic

shock].

• Administer 100% O2; intubate withmech anical ventilation if PO _ 70 2

mmHg.

• If severe metabolic acidosis present (pH _ 7.15), administer NaHCO3

(44.6–89.2 mmol).

• Identify and treat underlying cause of shock. Cardiogenic shock in acute

MI is discussed in Chap. 123. Emergent coronary revascularization may be

lifesaving if persistent ischemia is present. Consider cardiac tamponade (see

Chap. 121).