Page 240 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Circulatory Shock
(Circulatory) shock is the term given to acute ! Metabolic–toxic causes are decompensated
or subacute progressive generalized circula- liver cirrhosis, acute liver failure, uremia, var-
tory failure with an abnormal microcirculation ious forms of poisoning, etc.
and underperfusion of vital organs. In a wider ! Reduced cardiac output may also be caused
sense shock also includes disorders of O 2 supply by peripheral vascular distension (no pallor)
and utilization with (initially) undiminished with venous pooling of blood (decreased ve-
perfusion. nous return), as may happen in anaphylactic
The cause of shock is usually reduced cardi- shock (food or drug allergy), in which vasoac-
ac output, with the following possible causes: tive substances are released (histamine etc).
! In hypovolemia (hypovolemic shock) the ! In septic–toxic shock the cardiac output is
central venous pressure is reduced, and thus Gram-negative bacteria (tachycardia and re-
at first raised by the action of toxins of, usually
the venous return decreased. As a result stroke
Heart and Circulation cause of the hypovolemia can be bleeding normal blood pressure then falls, respiratory
duced total peripheral resistance). The initially
volume falls (Frank–Starling mechanism). The
failure occurs, and finally a late stage develops
(hemorrhagic shock) or some other loss of fluid
with reduced cardiac output and high total
to the outside, such as via the gastrointestinal
peripheral resistance, disseminated intravas-
tract (severe bleeding, massive vomiting, per-
cular coagulation (DIC), etc. (see below).
sistent diarrhea), via the kidneys (e.g., diabetes
when, for example, brain stem or spinal cord
polyuria after acute renal failure), or via the
trauma or intoxication (barbiturates, narcot-
skin (extensive burns, profuse sweating with-
7 mellitus or insipidus, high-dosage diuretics, ! Neurogenic shock is rare, but it may occur
out fluid intake). Loss of blood internally can ics) disturb autonomic nervous system regula-
also be a reason for hypovolemic shock, such tion of the heart and circulation and the ve-
as hemorrhage into the soft tissues (e.g., in nous return is markedly reduced.
fractures, especially of the thigh and pelvis, or Symptoms (→ B, left). Hypovolemic and
in the region of the retroperitoneum), into the hemorrhagic shock is often associated with a
thorax (e.g., rupture of an aortic aneurysm), or reduced blood pressure (narrow pulse ampli-
into the abdomen (e.g., rupture of the spleen) tude), increased heart rate, pallor with cold
as well as sequestration of large amounts of sweat (not in shock that is due to vascular dis-
fluid in ileus, peritonitis, liver cirrhosis (as- tension), diminished urine output (oliguria),
cites), or acute pancreatitis. and marked thirst. The resulting (blood) vol-
! Cardiogenic shock. Primary or secondary ume deficit can be estimated by means of the
heart failure can be caused by acute myocardial shock index (heart rate per minute/systolic
infarction, acute decompensating heart failure, blood pressure in mmHg):
malignant arrhythmias, cardiomyopathy, • 0.5 = normal or blood loss < 10%;
acute valvar regurgitation, obstruction of the • 1.0 = blood loss < 20–30% (incipient shock);
large vessels (e.g., pulmonary embolism) or by • 1.5 = blood loss > 30–50% (manifest shock).
impairment of cardiac filling (mitral stenosis, Most of the above symptoms are expressions
pericardial tamponade, constrictive pericardi- of counterregulatory mechanisms of the or-
tis). In these conditions, in contrast to hypovo- ganism against incipient shock: compensated
lemic shock, the central venous pressure is shock (→ A). Rapidly active mechanisms sup-
raised (congestive shock). plement each other to raise the reduced blood
! Hormonal causes of shock include adrenal pressure, slower ones to counteract the volume
hypofunction (Addisonian crisis; → p. 270), deficit.
diabetic coma (→ p. 288ff.), hypoglycemic ! Blood pressure compensation (→ A, left). A
shock (insulin overdosage, insulinoma; → drop in blood pressure leads to a decrease in
p. 292), hypothyroid or hyperthyroid coma, the afferent signals of the arterial pressorecep-
and coma in hypoparathyroidism or hyper- tors. This results in activation of the pressor
230 parathyroidism (→ p.128). areas in the central nervous system and to an
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Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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