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U N I T 5
Circulatory Function
Circulatory Failure (Shock)
Circulatory shock can be described as an acute failure
of the circulatory system to supply the peripheral tissues
and organs of the body with an adequate blood supply,
resulting in cellular hypoxia.
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Most often hypotension
and hypoperfusion are present, but shock may occur in
the presence of normal vital signs. Shock is not a specific
disease but a syndrome that can occur in the course of
many life-threatening traumatic conditions or disease
states. Moreover, no single classification system exists;
rather, shock can be classified by the cause, primary
pathophysiological derangement, or clinical manifesta-
tions. Generally each type of shock has certain distin-
guishing features; nonetheless, all types of shock reflect
an imbalance between oxygen supply and demand. As
a result, all shock states share common derangements,
such as inadequate peripheral tissue perfusion, altera-
tions in cellular metabolism and function, and impaired
organ perfusion, and all share common compensatory
mechanisms in response to these derangements.
Pathophysiology of Shock
Circulatory failure results in hypoperfusion of organs
and tissues, which in turn results in an insufficient sup-
ply of oxygen and nutrients for cellular function and the
accumulation of waste products.
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The cellular injury cre-
ated by an inadequate delivery of oxygen and substrates
also induces the production and release of inflammatory
mediators that further compromise perfusion through
functional and structural changes within the microvas-
cular circulation. This leads to a vicious cycle in which
impaired perfusion is responsible for cellular injury,
which causes maldistribution of blood flow, further
compromising cellular perfusion, and can culminate in
irreversible end-organ damage.
Cellular Responses
Shock ultimately exerts its effect at the cellular level, with
failure of the circulation to supply body cells with the
oxygen and nutrients needed for production of ATP. Cells
require ATP for a number of functions, including opera-
tion of the Na
+
/K
+
−ATPase membrane pump that moves
sodium out of the cell and returns potassium to the inside
of the cell. The cell uses two pathways to convert nutri-
ents to ATP (see Chapter 1). The first is the anaerobic
(non–oxygen-dependent) glycolytic pathway, located in
the cytoplasm, which converts glucose to ATP and pyru-
vate. The second is the aerobic (oxygen-dependent) path-
way, which is located in the mitochondria. When oxygen
is available, pyruvate from the anaerobic pathway moves
into the mitochondria and enters the aerobic pathway,
where it is transformed into ATP and the metabolic by-
products carbon dioxide and water. When oxygen is
lacking, pyruvate is converted to lactic acid.
As a shock state progresses, cellular metabolism
becomes anaerobic because of the decreased availability
of oxygen. Excess amounts of lactic acid accumulate in
there is impaired ejection of blood from the heart
during systole; with diastolic dysfunction, there
is impaired filling of the heart during diastole.
Left ventricular dysfunction is characterized by
congestion in the pulmonary circulation and
impaired blood flow in the peripheral circulation,
and right ventricular dysfunction by congestion in
the peripheral circulation.
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The manifestations of heart failure include
fluid retention and edema, shortness of breath,
fatigue and impaired exercise tolerance, impaired
gastrointestinal function and malnutrition, and
cyanosis. When performance of the right ventricle
is impaired, there is dependent edema of the
lower parts of the body, engorgement of the
liver, and ascites. With failure of the left ventricle,
pulmonary congestion with shortness of breath
and chronic, nonproductive cough are common.
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The acute heart failure syndromes represent a
gradual or rapid change in heart failure signs
and symptoms, indicating the need for urgent
therapy.These symptoms are primarily the result
of pulmonary congestion due to elevated left
ventricular filling pressures with or without a low
cardiac output.
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The diagnostic methods in heart failure are directed
toward establishing the cause and extent of the
syndrome.Treatment is directed toward correcting
the cause whenever possible, improving cardiac
function, maintaining the fluid volume within a
compensatory range, and developing an activity
pattern consistent with individual limitations
in cardiac reserve. Among the medications used
in the treatment of heart failure are diuretics,
digitalis, ACE inhibitors and angiotensin receptor
blocking agents,
β
-adrenergic receptor blockers,
vasodilators, and aldosterone blockers.
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Among the devices used to treat heart failure
patients with a reduced ejection fraction are an
implantable cardiac defibrillator and ventricular
assist devices. Heart transplantation remains the
treatment of choice for many persons with end-
stage heart failure.
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The manifestations of heart failure in the elderly
often are different and superimposed on other
disease conditions; therefore, heart failure often
is more difficult to diagnose in the elderly than in
younger persons. Because the elderly are more
susceptible to adverse and toxic medication
reactions, medication doses need to be adapted
and more closely monitored.
SUMMARY CONCEPTS
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