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Lecture 10

BIOC63H3 Lecture Notes - Lecture 10: Cardiogenic Shock, Hypovolemia, Vasodilation


Department
Biological Sciences
Course Code
BIOC63H3
Professor
Ivana Stehlik
Lecture
10

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Shock and Hemorrhage
Figure 1
Although the term shock is used by the layman to describe a psychological state, clinically it
refers to an acute condition where cardiac output is insufficient for adequate perfusion of the
tissues. The patient appears pale with cold skin, a weak pulse, and rapid shallow breathing. Urine
output is reduced, and the blood pressure is generally low.
Circulatory shock may be caused by a reduced blood volume (hypovolemic shock), profound
vasodilatation (vasogenic shock), failure of the heart to maintain output due to cardiac disease
(cardiogenic shock), or loss of vascular tone (neurogenic shock)
(Figure 1).
Hemorrhagic shock (Hypovolemic Shock)
Blood loss (hemorrhage) is a common cause of hypovolemic shock, and will be used to
demonstrate compensatory mechanisms. Loss of up to ~10% of total blood volume does not
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elicit shock, as adequate perfusion can be maintained. If 20-30% of blood volume is lost, shock
is normally induced and blood pressure may be depressed, although death is not common. Loss
of 30-40% of volume, however, causes a profound reduction in blood pressure, with sever shock
which may lead to irreversible shock, or other serious complications. Above 50% death is
generally inevitable.
Immediate compensation (Figure 2)
The baroreceptors detect the fall in blood pressure, sympathetic drive is increased, and
parasympathetic drive is decreased. Heart rate rises, and vasoconstriction increases the resistance
of the splanchic, cutaneous, renal and skeletal muscle circulations, increasing total peripheral
resistance and supporting blood pressure. Perfusion in these tissues is reduced, leading to pallor,
reduced urine production, and lactic acidosis. The increased sympathetic discharge also results in
sweating, and the characteristic clammy skin. Sympathetic activity in the kidneys, coupled with
reduced renal artery pressure, stimulates the rennin-angiotensin system, which results in the
production of angiotensin II, a powerful vasoconstrictor. This plays an important additional role
in the initial recovery of blood pressure, and stimulates the feeling of intense thirst. In more
severe blood loss the reduction in cardiac stretch receptor output stimulates the production of
vasopressin (antidiuretic hormone), and epinephrine production by the adrenal gland is
increased both which contribute to the vasoconstriction. In combination these initial mechanisms
may prevent any significant fall in blood pressure following moderate blood loss, even though
the degree of shock may be serious.
Medium-term mechanisms (Figure2)
The sympathetic-mediated vasoconstriction leads to a decrease in capillary hydrostatic pressure.
The oncotic pressure exerted by plasma proteins is however maintained, resulting in movement
of fluid from the interstitial space back into the vasculature. This „internal transfusion‟ may
increase blood volume by ~0.51 L. Increased glucose production by the liver may contribute to
this process by raising the osmolarity of plasma and interstitial fluid, and drawing water from the
intracellular compartment. However this process results in hemodilution, and so reduces O2
delivery. Patients with severe shock often present with a reduced hematocrit.
Long-term recovery (Figure 2)
Fluid volume is brought back to normal over a day or two by increased fluid intake and
decreased fluid loss in the urine. Urine production is decreased by sympathetic renal
vasoconstriction and stimulation of aldosterone production by angiotensin II causes increased
reabsorption of Na+ in the kidneys, elevating the blood volume. Water reabsorption is also
increased by vasopressin. The liver replaces plasma proteins within a week, and haematocrit
returns to normal within a few weeks as a result of stimulation of erythropoiesis.
Decompensated or irreversible is used to describe the condition of those patients where, after a
period of time, cardiac output remains depressed or may decline, even in the face of a
replenished blood volume and vasoconstrictor drugs. Irreversible shock commonly occurs when
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