WHAT IS SHOCK- A Simplified approach, iSHOCK

iSHOCK

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

Oligemic shock

Hemorrhage

Volume depletion (e.g., vomiting, diarrhea, diuretic overusage, 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)

CLINICAL FEATURES:

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 with noncardiogenic pulmonary edema, hypoxemia, and diffuse pulmonary infiltrates.

EXAMINATION:

Jugular veins are flat in oligemic or distributive (septic) shock; jugular venous distention (JVD) suggests cardiogenic shock; JVD in presence of paradoxical pulse may reflect cardiac tamponade. Check for asymmetry of pulses. Assess for evidence of heart failure, 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 aureusor Streptococcus pyogenes ).

LABORATORY Findings:

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: 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 OPTIONS:

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, lactate, 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 if systemic vascular resistance (SVR) is decreased (begin with norepinephrine [preferred] or dopamine; for persistent hypotension add phenylephrine or vasopressin).

If CHF present, add inotropic agents (usually dobutamine); 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 PO₂ <70 mmHg.

If severe metabolic acidosis present (pH <7.15), administer NaHCO₃.

Identify and treat underlying cause of shock. Cardiogenic shock. Emergent coronary revascularization may be lifesaving if persistent ischemia is present.