Condition of severe impairment of tissue perfusion leading to cellular injury and dysfunction. Rapid recognition and treatment are essential to prevent irreversible organ damage and death. Common causes are listed in Table 12-1.
TABLE 12-1 COMMON FORMS OF SHOCK
• Hypotension (mean arterial bp <60 mmHg), tachycardia, tachypnea, pallor, restlessness, and altered sensorium.
• Signs of intense peripheral vasoconstriction, with weak pulses and cold clammy extremities. In distributive (e.g., septic) shock, vasodilatation predominates and extremities are warm.
• Oliguria (<20 mL/h) and metabolic acidosis common.
• Acute lung injury and acute respiratory distress syndrome (ARDS; see Chap. 15) with noncardiogenic pulmonary edema, hypoxemia, and diffuse pulmonary infiltrates.
APPROACH TO THE PATIENT Shock
Obtain history for underlying causes, including cardiac disease (coronary disease, heart failure, pericardial disease), recent fever or infection leading to sepsis, drug effects (e.g., excess diuretics or antihypertensives), conditions leading to pulmonary embolism (Chap. 142), potential sources of bleeding.
Jugular veins are flat in oligemic or distributive (septic) shock; jugular venous distention (JVD) suggests cardiogenic shock; JVD in presence of paradoxical pulse (Chap. 119) may reflect cardiac tamponade (Chap. 125). Check for asymmetry of pulses (aortic dissection—Chap. 134). Assess for evidence of heart failure (Chap. 133), murmurs of aortic stenosis, acute mitral or aortic regurgitation, ventricular septal defect. 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 typically accompany septic shock. Sepsis may not cause fever in elderly, uremic, or alcoholic pts. Skin lesions may suggest specific pathogens in septic shock: petechiae or purpura (Neisseria meningitidis or Haemophilus influenzae), ecthyma gangrenosum (Pseudomonas aeruginosa), generalized erythroderma (toxic shock due to Staphylococcus aureus or Streptococcus pyogenes).
Obtain hematocrit, WBC, electrolytes, platelet count, PT, PTT, DIC screen, electrolytes. 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 (heart failure, tension pneumothorax, pneumonia). Echocardiogram is often helpful (cardiac tamponade, left/right ventricular dysfunction, aortic dissection).
Central venous pressure or pulmonary capillary wedge (PCW) pressure measurements may be necessary to distinguish between different categories of shock (Table 12-2): 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.
TABLE 12-2 PHYSIOLOGIC CHARACTERISTICS OF FORMS OF SHOCK
TREATMENT Shock (See Fig. 12-1).
FIGURE 12-1 An algorithm for the resuscitation of the pt in shock. *Monitor SVO2, SVRI, and RVEDVI as additional markers of correction for perfusion and hypovolemia. Consider age-adjusted CI. SVO2, saturation of hemoglobin with O2 in venous blood; SVRI, systemic vascular resistance index; RVEDVI, right-ventricular end-diastolic volume index. CI, cardiac index in (L/min) per m2; CVP, central venous pressure; ECHO, echocardiogram; Hct, hematocrit; HR, heart rate; PAC, pulmonary artery catheter; PCWP, pulmonary capillary wedge pressure in mmHg; SBP, systolic blood pressure; VS, vital signs; W/U, work up.
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, pH, calcium, phosphate, lac-tate, urine Na concentration (<20 mmol/L suggests volume depletion). Consider monitoring of CVP and/or pulmonary artery pressure/PCW pressures in pts with ongoing blood loss or suspected cardiac dysfunction.
• 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 or Ringer’s lactate, then whole blood, 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 12-3) if systemic vascular resistance (SVR) is decreased (begin with norepinephrine [preferred] or dopa-mine; for persistent hypotension add phenylephrine or vasopressin).
TABLE 12-3 VASOPRESSORS USED IN SHOCK STATESa
• If CHF present, add inotropic agents (usually dobutamine) (Table 12-3); aim to maintain cardiac index >2.2(L/m2)/min [>4.0(L/m2)/min in septic shock].
• Administer 100% O2; intubate with mechanical ventilation if <70 mmHg.
• If severe metabolic acidosis present , administer NaHCO3.
• Identify and treat underlying cause of shock. Cardiogenic shock in acute MI is discussed in Chap. 128. Emergent coronary revascularization may be lifesaving if persistent ischemia is present.
SEPTIC SHOCK (SEE CHAP. 13)
For a more detailed discussion, see Maier RV: Approach to the Patient With Shock, Chap. 270, p. 2215, and Hochman JS, Ingbar DH: Cardiogenic Shock and Pulmonary Edema, Chap. 272, p. 2232, in HPIM-18.