Cardiovascular Dysfunction Chapter 48 1483

Table 48-6 Types of Shock

CHARACTERISTICS
Hypovolemic
Reduction in size of vascular
compartment
Falling blood pressure
Poor capillary filling
Low central venous pressure

Distributive
Reduction in peripheral vascular
resistance
Profound inadequacies in tissue
perfusion
Increased venous capacity and
pooling
Acute reduction in return blood
flow to the heart
Diminished cardiac output

Cardiogenic
Decreased cardiac output

BOX 48-12 Clinical Manifestations of Shock

MOST FREQUENT CAUSES
Blood loss (hemorrhagic
shock)Trauma, gastrointestinal
bleeding, intracranial
hemorrhage
Plasma lossIncreased capillary
permeability associated with
sepsis and acidosis,
hypoproteinemia, burns,
peritonitis
Extracellular fluid lossVomiting,
diarrhea, glycosuric diuresis,
sunstroke
Anaphylaxis (anaphylactic
shock)Extreme allergy or
hypersensitivity to a foreign
substance
Sepsis (septic shock, bacteremic
shock, endotoxic shock)
Overwhelming sepsis and
circulating bacterial toxins
Loss of neuronal control
(neurogenic shock)Interruption
of neuronal transmission (spinal
cord injury)
Myocardial depression and
peripheral dilationExposure to
anesthesia or ingestion of
barbiturates, tranquilizers,
opioids, antihypertensive
agents, or ganglionic blocking
agents
After surgery for congenital heart
disease
Primary pump failureMyocarditis,
myocardial trauma, biochemical
derangements, congestive heart
failure
DysrhythmiasSupraventricular
tachycardia, atrioventricular
block, and ventricular
dysrhythmias; secondary to
myocarditis or biochemical
abnormalities (occasionally)

rate of cardiac contraction and constriction of arterioles and

veins, thereby increasing peripheral vascular resistance.
Simultaneously the lowered blood volume leads to the release
of large amounts of catecholamines, antidiuretic hormone,
adrenocorticosteroids, and aldosterone in an effort to conserve body fluids. This causes reduced blood flow to the skin,
kidneys, muscles, and viscera to shunt the available blood to
the brain and heart. Consequently, the skin feels cold and
clammy, there is poor capillary filling, and glomerular filtration rate and urinary output are significantly reduced.
As a result of impaired perfusion, oxygen is depleted in the
tissue cells, causing them to revert to anaerobic metabolism,
producing lactic acidosis. The acidosis places an extra burden

Compensated
Apprehensiveness
Irritability
Unexplained tachycardia
Normal blood pressure
Narrowing pulse pressure
Thirst
Pallor
Diminished urinary output
Reduced perfusion of extremities

Decompensated
Confusion and somnolence
Tachypnea
Moderate metabolic acidosis
Oliguria
Cool, pale extremities
Decreased skin turgor
Poor capillary filling

Irreversible
Thready, weak pulse
Hypotension
Periodic breathing or apnea
Anuria
Stupor or coma

on the lungs as they attempt to compensate for the metabolic

acidosis by increasing respiratory rate to remove excess carbon
dioxide. Prolonged vasoconstriction results in fatigue and
atony of the peripheral arterioles, which leads to vessel dilation. Venules, less sensitive to vasodilator substances, remain
constricted for a time, causing massive pooling in the capillary
and venular beds, which further depletes blood volume.
Complications of shock create further hazards. Central
nervous system hypoperfusion may eventually lead to cerebral
edema, cortical infarction, or intraventricular hemorrhage.
Renal hypoperfusion causes renal ischemia with possible
tubular or glomerular necrosis and renal vein thrombosis.
Reduced blood flow to the lungs can interfere with surfactant
secretion and result in acute respiratory distress syndrome
(ARDS), characterized by sudden pulmonary congestion and
atelectasis with formation of a hyaline membrane. Gastrointestinal tract bleeding and perforation are always a possibility
after splanchnic ischemia and necrosis of intestinal mucosa.
Metabolic complications of shock may include hypoglycemia,
hypocalcemia, and other electrolyte disturbances.

Diagnostic Evaluation

The etiology of shock can be discerned from the history and

physical examination. The severity of the shock is determined
by measurements of vital signs, including CVP and capillary
filling (Box 48-12). Shock can be regarded as a form of compensation for circulatory failure. Because of its progressive nature,
it can be divided into the following three stages or phases:
1. Compensated shockVital organ function is
maintained by intrinsic compensatory mechanisms;