1. Shock is a defined as inadequate end-organ perfusion that, left to itself, will result in anaerobic metabolism and ultimately end-organ failure and death.

2. A momentary pause in the act of death. R Adams Cowley.

1. Perfusion may be decreased systemically with obvious signs such as hypotension and tachycardia.

2. Perfusion may be decreased because of maldistribution as in septic shock, where systemic perfusion may appear elevated but ineffective.

3. Malperfusion may be isolated, leading to single-system failure such as in thrombotic or occlusive disease of the gastrointestinal (GI) tract or extremity.

4. Prognosis is determined by age, degree of shock, duration of shock, number of organs affected, previous organ dysfunction, precipitating factors, and genetic predisposition.

1. Initial loss of circulating intravascular volume results in decrease in cardiac preload, increase in afterload (vasoconstriction).

2. Causes.

a. Hemorrhage: trauma, GI bleeding, nontraumatic internal bleeding (such as aneurysm, ectopic rupture), liver adenoma, or vaginal bleeding (OB: abruption placenta).

b. Nonhemorrhagic: fluid loss from the GI tract (vomiting, diarrhea, fistula), urinary losses (hyperglycemia with glycosuria, DI), prolonged evaporative loss (fever, hyperthermia), and internal fluid shifts (third spacing as with a bowel obstruction or pancreatitis).

3. Most common form of shock (fluid/blood loss).

4. All forms of shock have some component of decreased preload and benefit from intravascular infusion.

5. Clinical signs depend on the volume lost and patient response (Table 107-1). Usual symptoms include tachycardia, hypotension, decreased urine output, mental status changes, and tachypnea.

6. Initial treatment is with volume resuscitation with isotonic crystalloid solution, and, in addition, blood if from hemorrhage. In those patients requiring massive transfusion (>10 units packed red blood cells [PRBCs] in 24 hours), transfusing fresh frozen plasma (FFP) and blood in a 1:1 ratio while minimizing the use of crystalloids has been shown to have a clear survival benefit in trauma. Concomitant hemorrhage control is key to a successful resuscitation. Colloid infusion (albumin) has no value in the initial resuscitation of hypovolemic shock.

1. Caused by a mechanical obstruction to normal cardiac output (CO) with a decrease in systemic perfusion.

2. Frequent causes: cardiac tamponade and tension pneumothorax.

a. Clinical signs.

i. Jugular venous distension.

ii. Tachycardia.

iii. Hypotension.

b. Ultrasound exam can quickly confirm pericardial fluid (tamponade) or pneumothorax (tension pneumothorax).

3. Other causes are massive venous thromboembolism and air embolism.

4. Treatment is maximizing preload (isotonic crystalloids) and relief of the obstruction.

1. Caused by myocardial (pump) failure.

2. Most common cause is extensive myocardial infarction.

3. Other causes are reduced contractility (cardiomyopathy, sepsis induced), aortic stenosis, mitral stenosis, atrial myxoma, acute valvular failure, and cardiac dysrhythmias.

4. Treatment is maximizing preload, cardiac performance, and reducing afterload.

1. Caused by systemic vasodilatation from an inciting cause (infection, anaphylaxis, neurologic injury) resulting in systemic hypotension, and increased or decreased CO.

2. Sepsis is the most common precipitant of distributive shock. The endothelial toxicity and diffuse vasodilation are enhanced by messengers of the inflammatory response such as tissue necrosis factor-α (TNF-α) and interleukins 1 and 6.

3. Septic shock is associated with a brisk and often extensive inflammatory response. Despite a high CO, there is cellular hypoxia likely associated with disruption of mitochondrial function manifest as poor oxygen extraction/utilization.

4. In addition to sepsis, other causes of the systemic inflammatory response syndrome (SIRS) include posttraumatic shock and pancreatitis.

5. Treatment of septic shock is with massive volume to supplement preload, augmentation of blood pressure (BP) with vasoconstrictors as necessary, and treatment of the underlying cause.

6. Other causes of distributive shock are anaphylaxis, severe liver dysfunction, and neurogenic shock.

7. Neurogenic shock is due to cervical spinal cord injury with loss of sympathetic vascular tone. There is little inflammatory response. The patient has hypotension, bradycardia, and warm extremities. Treatment is with judicious volume expansion and a vasoconstrictor (low-dose dopamine or phenylephrine).

1. Caused by hypothyroidism, hyperthyroidism with cardiac collapse, or adrenal insufficiency. Treatment is focused on the underlying disease.

2. Adrenal insufficiency may be a contributor to shock in critically ill patients. Patients unresponsive to treatment should be tested for adrenal insufficiency.

A. The result of shock is tissue anaerobic metabolism, systemic acidosis with elevated lactate.

B. Cellular hypoxia leads to cellular ischemia. Ischemic cells are primed by alterations of calcium and adenosine 3′,5′-cyclic monophosphate (cAMP) and creation of superoxide radicals.

C. Endothelial cells under hypoxic conditions will have enhanced vascular permeability and less control over membrane transport functions.

D. Reperfusion can result in release of oxygen radicals that may cause further cell damage.

E. These processes activate neutrophils and the release of enzymes, oxidants, and proinflammatory cytokines.

F.

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