Chapter 19
monitored because it is a good index of venous return and the
volume of fl
uid within the cardiovascular system (see Figure
12–57). The oxygen content of the blood is maintained by
ventilating the lungs with supplemental oxygen to make sure
that hemoglobin is saturated with oxygen (see Figure 13–26).
It is also helpful to reduce the patient’s demand for oxygen
by paralyzing the respiratory muscles with drugs and provid-
ing mechanical ventilation, usually through a tube placed in
the trachea attached to a positive-pressure pump. Otherwise,
the increase in rate and depth of breathing that is typical of a
patient in septic shock causes a marked increase in oxygen use
by the respiratory muscles, and directs blood fl ow away from
other organs already suffering from lack of oxygen.
The infection must be treated while also restoring cardio-
vascular function. Antibiotics that act on a wide variety of types
of bacteria are administered as soon as possible after sepsis is
diagnosed. The source of the infection is then located, accumu-
lated pus and dead tissue are removed, and the surrounding tis-
sue is thoroughly cleaned. Ideally, samples of blood and/or pus
from the site of infection can be grown in culture, and within
48 h the specifi c bacterial species involved in the infection can be
identifi ed. The intravenous antibiotic therapy can then be altered
to use drugs known to specifi cally target the invading species.
Recent clinical studies have suggested other therapeutic
measures that can increase the survival rate of patients with sep-
tic shock. Pharmacological doses of glucocorticoid injections
have also shown promise in some patients with septic shock.
These hormones activate mechanisms throughout many tissues
of the body that help the body cope with stress (see Table 11–3).
Important among those effects are the inhibition of the infl am-
matory response and the enhancement of the sensitivity of vas-
cular smooth muscle to adrenergic agents like norepinephrine.
Over a six-day period, the condition of our patient grad-
ually improved. His blood pressure increased and stabilized,
and the intravenous fl uid and norepinephrine infusions were
gradually reduced and then stopped. The edema in his lungs
and tissues slowly subsided, he regained consciousness, and he
was eventually able to maintain oxygen saturation in his arteri-
al blood without mechanical ventilation. During his two-week
hospital stay, the brain, liver, and kidney function returned
to normal, and he had no apparent long-term organ damage
from his ordeal. He has been extremely fortunate; approxi-
mately 500,000 cases of severe septic shock occur in the Unit-
ed States each year and less than half of those patients survive.
His youth and relatively good initial physical condition were
most likely instrumental in helping him beat the odds.
Case 19–1: A Woman with Palpitations and Heat
I. Case Presentation
a. Her symptoms are nervousness, palpitations, feelings of
warmth in a cool room, and signifi cant weight loss despite
eating a lot.
II. Physical Examination
a. Her systolic blood pressure is increased and her diastolic
pressure is decreased. Her resting heart rate is 100 beats per
b. She has an enlarged thyroid gland (goiter) and her eyes
bulge out (proptosis).
c. She has increased knee jerk refl exes and her hands are
III. Laboratory Tests
a. She has increased thyroid hormone and decreased thyroid-
stimulating hormone in the blood.
IV. Diagnosis
a. She is diagnosed with hyperthyroidism (excess thyroid
hormone activity).
b. Hyperthyroidism is usually caused by Graves’ disease—an
autoimmune disease.
V. Physiological Integration
a. Autoimmune production of thyroid-stimulating
immunoglobulins (TSIs) stimulates the thyroid gland to
produce too much thyroid hormone and to enlarge. The
excess thyroid hormone suppresses the release of thyroid-
stimulating hormone from the anterior pituitary gland.
b. Infi ltration of the muscles controlling eye movement by
white blood cells leads to infl ammation and proptosis.
c. Increased thyroid hormone in the blood leads to an
increase in sensitivity to catecholamines, resulting in an
increase in systolic blood pressure and heart rate.
d. Increased thyroid hormone leads to increased metabolic
rate in a variety of tissues. This causes heat intolerance,
hyperactive refl exes, and a small decrease in diastolic
VI. Therapy
a. Three possible therapies include radioactive iodide
administration to destroy much of the thyroid gland,
drugs that block the synthesis of thyroid hormone, or
surgical removal of the thyroid gland.
Case 19–2: A Man with Chest Pain After a Long
Airplane Flight
I. Case Presentation
a. A man has chest pain and shortness of breath after an 8-h
fl ight.
II. Physical Examination
a. He has an increased heart rate but his ECG does not show
evidence of a heart attack.
b. His chest x-ray is essentially normal.
III. Laboratory Tests
a. He is hypoxemic and has an acute respiratory alkalosis.
IV. Diagnosis
a. His ventilation-perfusion scan shows evidence of a
pulmonary embolism (blockage of pulmonary blood fl ow).
b. An ultrasound of his legs shows a deep vein thrombosis.
c. A clot formed in his leg veins because he sat for a long
period of time. In addition, there is evidence that he has a
genetic disorder of coagulation. The clot migrated to the
lung, causing a pulmonary embolus.
V. Physiological Integration
a. Hypoxemia is caused by a dramatic disruption of the
regional balance between ventilation and perfusion
throughout the lung.
b. Hyperventilation due to anxiety and pain, as well as
hypoxemia, caused an acute respiratory alkalosis.
VI. Therapy
a. Treatment focuses on anticoagulation with heparin (to
prevent clotting) and recombinant tissue plasminogen
activator (to dissolve the clots).
b. Long-term anticoagulation therapy is recommended.
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