Introduction

Essentials of Diagnosis

• Hypotension, tachycardia, oliguria, altered mental status.
• Peripheral hypoperfusion and hypoxia.

General Considerations
Shock occurs when the rate of arterial blood flow is inadequate to meet tissue metabolic needs. Tissue oxygen delivery is dependent on cardiac output, hemoglobin saturation, and peripheral microcirculation -  some or all of these factors are altered in the shock state. The physiologic response to shock is mediated by the neuroendocrine system through release of catecholamines, renin, antidiuretic hormone, glucagon, cortisol, and growth hormone. These hormones are responsible for many of the clinical manifestations of shock: tachycardia, oliguria, delayed capillary refill, increasing agitation, and insulin resistance. Treatment must be directed both at the manifestations of shock and at its cause.

Classification (Table 12-1)

A. Hypovolemic Shock
Decreased intravascular volume resulting from loss of blood, plasma, or fluids and electrolytes may be obvious (eg, external hemorrhage) or subtle (eg, sequestration in a “third space”). Compensatory vasoconstriction temporarily reduces the size of the vascular bed and may transiently maintain the blood pressure, but unreplaced ongoing losses of over 15% of the blood volume result in hypotension, increased peripheral resistance, collapse of capillary and venous beds, and progressive tissue hypoxia. Even a moderate sudden loss of circulating fluids can result in severe damage to vital organs.

B. Cardiogenic Shock
Pump failure can be related to myocardial infarction, cardiomyopathy, myocardial contusion, valvular incompetence or stenosis, or arrhythmias. See discussion in Heart Diseases Section.

C. Obstructive Shock
Cardiac tamponade, tension pneumothorax, and massive Pulmonary embolism can cause acute decrease in cardiac output resulting in shock. These are medical emergencies requiring prompt diagnosis and treatment. Pericardiocentesis or pericardial window, chest tube placement, or catheter-directed thrombolytic therapy can be lifesaving.

D. Distributive Shock
Reduction in systemic vascular resistance from sepsis, anaphylaxis, systemic inflammatory response syndrome (SIRS) produced by severe pancreatitis or burns, or acute adrenal insufficiency may result in inadequate cardiac output despite normal circulatory volume. Elevated nitric oxide levels may explain many of the physiologic aspects of the disease.

1. Septic shock
Sepsis is the most common cause of distributive shock and carries a mortality of 40-80%. Typically, patients present with fever, chills, hypotension, hyperglycemia, and altered mental status due to gram-negative bacteremia (Escherichia coli, Klebsiella, Proteus, and Pseudomonas). Gram-positive cocci and gram-negative anaerobes (bacteroides) are less often implicated. Risk factors include extremes of age, diabetes, immunosuppression, and recent urinary, biliary, or gynecologic manipulation, such as placement of a percutaneous nephrostomy or biliary drain in an obstructed system.

2. Neurogenic shock
Neurogenic shock is caused by traumatic spinal cord injury or effects of an epidural or spinal anesthetic. Reflex vagal parasympathetic stimulation evoked by pain, gastric dilation, or fright may simulate neurogenic shock, producing hypotension, bradycardia, and syncope.