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Congestive Heart Failure from Hypertension
Dr. Gary Mumaugh – UNW St. Paul
CASE HISTORY
Mrs. B is a 66-year-old African-American admitted to the critical care unit with a complaint
of shortness of breath and palpitations. The physician’s admitting diagnosis was
uncontrolled hypertension complicated by atrial fibrillation and congestive heart failure.
Past History
Mrs. B past history includes pertussis, as well as the usual childhood diseases with no
sequela. Her mother died of cardiac issues when Mrs. B was in her early twenties. Mrs.
B was married at the age of 24 and she described her health as being very good until the
past year, although at each one of her six births the nurse midwife told her that her blood
pressure was “up”. Her husband died 1 year ago from a “stroke”, and since his death Mrs.
B has been troubled with periods when she “couldn’t get enough air.”
Current Status
Mrs. B has noticed that she is most short of breath when she is laying down flat. She is
able to sleep with three or four pillows but she prefers to sleep in her recliner chair. She
enjoys walking about the neighborhood and talking to friends, but lately she does this
much less because she comes home very tired and short of breath. When visiting her
daughter on a cold December day, she climbed the stairs to the second floor when she
began to experience chest discomfort. At first she attributed her discomfort to her usual
exertional dyspnea. She sat at the stairs for several minutes, but she still could not catch
her breath and she felt a “pounding with a funny rhythm” in her chest. Mrs. B’s daughter
took her to the emergency room.
On arrival at the emergency room, Mrs. B was alert and oriented to person, place, and
time. Her pupils were constricted, equal and reactive to light. Her skin was cool and dry,
and her mucous membranes and nail beds were pink. Her blood pressure was 200/140,
pulse rate was 110 and respiration was 30 and labored. Her ECG revealed atrial fibrillation
and rapid ventricular response and frequent premature ventricular complexes. The
emergency room gave Oxygen by mask at 10 L/min. Her weight was estimated to be 110
pounds. She was given IV lidocaine to suppress the ventricular ectopic beats. To control
her blood pressure, a nitroprusside drip was started IV. Five minutes latter, her blood
pressure was 160/95. A 12-lead ECG showed no evidence of acute MI. Blood was drawn
to determine cardiac enzymes and electrolytes. A lidocaine drip was started IV and a
loading dose of IV digoxin was given to control the ventricular response to the atrial
fibrillation. She was transferred from the emergency room to the critical care unit.
The critical care nurse recorded vital signs of blood pressure 160/90, cardiac rhythm
revealed atrial fibrillation with ventricular response of 108, occasional premature
ventricular complexes were noted, respirations were 28 with oxygen mask at 10 L/min.
She was alert and oriented and able to follow orders. She moved all her extremities with
equal strength. When listening to Mrs. B’s chest, the nurse noted fine rales in the posterior
base of both lungs. A soft systolic ejection murmur was heard over the aortic valve area.
No friction rubs were heard. On palpation, Mrs. B’s abdomen was soft and without masses
or organomegaly. She complained of tenderness with deep palpation of the hepatic area.
Her skin was cool and dry and pitting edema was noted in her lower legs. And over the
sacrum. The nurse assisted Mrs. B to a bedside commode, where she voided 100 ml of
dark amber urine that had a specific gravity of 1.025.
Mrs. B’s cardiac enzyme levels did not elevate in patterns seen in myocardial infarction.
Her (SGOT) serum glutamic oxaloacetic transaminase and (LDH) lactic dehydrogenase
levels were elevated. The cardiologist attributed this to venous congestion in her liver.
The serum electrolyte levels drawn on admission showed low serum potassium and high
serum sodium. Other values were within normal limits.
Mrs. B’s cardiac rhythm converted to sinus rhythm with a rate of 80 beats/min after she
had a second dose of digoxin. She was successfully weaned from the lidocaine drip.
About 15 minutes after Mrs. B converted to sinus rhythm, she stated to the nurse that she
was breathing better and did not feel her heart “pounding.” The nurse assessed Mrs. B
carefully to be certain that no arterial emboli were release from the atria now that there
were contracting again. Mrs. B was placed on oral antihypertensive therapy and
successfully weaned from the nitroprusside drip.
Name __________________________________________________ Mailbox _______
Congestive Heart Failure from Hypertension
1. Which of the following is NOT likely to offer an explanation for the etiology of Mrs.
B’s essential hypertension?
A. High potassium intake
B. High sodium intake
C. Genetic factors
D. Sympathetic nervous system activity
2. Which of the following explains why some individuals with hypertension, such as
Mrs. B, develop congestive heat failure?
A. Preload becomes so low that efficient ventricular contraction is lost
B. Afterload becomes so low that myocardial ischemia occurs
C. Structural changes in the cardiac valves produce abnormal hemodynamics.
D. Afterload becomes so high that the ventricles cannot maintain adequate
forward flow.
3. Explain why long-term hypertension is one of the main contributing factors of
congestive heart failure.
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4. How did atrial fibrillation contribute to Mrs. B’s shortness of breath?
A. Loss of synchronized atrial and ventricular contraction resulted in mild
pulmonary edema.
B. Her sympathetic response to stress caused her to be more anxious.
C. The dilated atria pressed on her bronchi and esophagus.
D. They are not related.
5. What would explain Mrs. B’s pitting edema?
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6. Does Mrs. B have left-sided or right-sided heart failure? ____________________
7. Explain your rationale for your left or right diagnosis.
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