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Physiology II
Cardiovascular Case G

secondary hypertension 

the patient: a 38-year-old black male 

chief complaint: persistent headache

history: The patient presented to the University Health Center complaining of persistent occipital morning headaches of six weeks duration. The pain was not relieved by frequent use of acetaminophen. Further questioning by the family practice resident revealed that the patient had also been experiencing episodes of dizziness and epistaxis. A dietary history revealed that the patient regularly sprinkled salt on his food before tasting it, and frequently ate bacon, french fries, Kentucky Fried Chicken, salty popcorn, and canned black-eyed peas. The patient indicated that he had no regular exercise regimen and that his desk job required no physical exertion but was a significant source of daily stress. His family history revealed that "almost everybody in my family has high blood pressure". His father was on dialysis and died of a stroke at age 55.

physical examination: The patient was 170 cm tall and weighed 95.5 kg. Respirations were quiet and regular at 12 breaths/min, heart rate was 82 beats/min, and arterial blood pressure was 190/110 mm Hg sitting and standing. His fundi showed A-V nicking and arteriolar narrowing. The remainder of the physical examination was unremarkable. His initial screening laboratory tests were also unremarkable, but his EKG showed evidence of left ventricular hypertrophy.

clinical course: One month later, after having been counseled on the importance of a low-salt, low-fat, weight-loss diet and the value of regular exercise, the patient's blood pressure was still 180/105 mm Hg. Anti-hypertensive medication was initiated, in the form of an ACE inhibitor, Enalapril, 2.5 mg q.i.d. The patient's blood pressure did not respond, and the dosage was increased to 20 mg, b.i.d. His blood pressure stabilized at 175/100 mm Hg.


1. Discuss this patient in terms of the risk factors most commonly associated with the development of hypertension:  The patient's dietary history shows a diet high in fat & cholesterol which leads to atherosclerosis. Plaques lead to hardening of arterial walls and loss of elasticity and responsiveness to changes in blood pressure, hence this patient's HTN. His other risk factors include a diet high in sodium. As the sodium accumulates in the body it increases the ECF volume by 1. increasing the osmolality of the body fluids, which stimulates thirst, making the person drink extra amounts of water to dilute the ECF salt to a normal concentration (this increases the ECF volume) and 2. causing increased amounts of ADH to be secreted. Other risk factors include the patient's lack of physical activity and increased body weight (no regular exercise regimen and a "desk job"). This can lead to HTN through ? a decrease in compliance of blood vessels. The patient's job being a "significant source of stress" is a risk factor for HTN because prolonged nervous tension can maintain prolonged increase in sympathetic stimulation of the blood vessels and kidneys and therefore lead to chronic elevation of arterial pressure. Examining this patient's family history shows a strong risk factor for HTN. Hereditary factors can play a very important role.

2. What are the normal responses of the renal/body fluid mechanism to a HIGH LEVEL OF SODIUM INTAKE such as that seen in this patient?  This patient's high level of sodium intake can increase the arterial pressure through the renal-body fluid mechanism. The arterial pressure will be regulated at a new higher pressure level corresponding to the level of sodium intake. (See Graph B pg. 223, Guyton)

Remember, the two primary determinants of long-term arterial pressure are 1. The degree of shift of the renal output curve for water and salt and 2. The level of the water and salt intake line (which would apply here).

Increase in Na+ intake will cause increased ECF volume, which increases the blood volume, which increases the mean circulatory filling pressure, which increases venous return of blood to the heart which increases cardiac output--which leads to increased arterial pressure (increased C.O. also has an indirect effect of increasing SVR).

3. Discuss this patient's response to his hypertension in terms of PRELOAD, AFTERLOAD, and PATTERNS OF HYPERTROPHY:  
PRELOAD-- The patient's preload remains high (from increased Na+ intake & increased ECF volume)--his BP did not respond to anti-hypertensive medication and stabilized @ 175/100 mmHg.
AFTERLOAD-- The patient has arteriolar narrowing in response to chronic increased MSAP. His afterload is high, and as a result he shows evidence of left ventricular hypertrophy.
PATTERNS OF HYPERTROPHY-- The pt's EKG showed evidence of left ventricular hypertrophy. This is the ventricular response to a chronic increase in afterload. This structural remodeling occurs from the high pressure which the ventricle must pump against. The ventricular wall thickness is increased or hypertrophied.

4. What would be the PHYSIOLOGICAL GOALS of treating a patient such as this with an ACE inhibitor? With a diuretic? With a vasodilator?  
ACE Inhibitor--suppresses the renin-angiotensin-aldosterone system, prevents the conversion of angiotensin I to angiotensin II, leads to decreased BP & decrease in aldosterone secretion, blocks the remodeling that occurs in blood. vessels w/ HTN.
Diuretic--block active transport of sodium through the tubular wall; this blockage in turn prevents the reabsorption of water as well (would decrease ECF volume & lead to decreased BP).
Vasodilator--Drugs that increase renal blood flow. Different ones act in one of the following ways; inhibiting sympathetic nervous signals to the kidneys or by blocking the action of the sympathetic transmitter substance on the renal vasculature 2. by directly paralyzing the smooth muscle of the renal vasculature or 3. by blocking the action of the renin-angiotensin system on the renal vasculature of renal tubules. (Guyton, pg. 234)


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