[Expert Solution]: Mrs

Mrs. B. is a 66 year-old female admitted to the critical care unit with a chief complaint of shortness of breath and palpitations. The physician’s preliminary diagnosis was uncontrolled hypertension complicated by atrial fibrillation and congestive heart failure. Mrs. B.’s past health history includes pertussis, as well as the usual childhood illnesses without sequelae. Her mother died when Mrs. B. was in her early twenties. Mrs. B. noticed that she is particularly short of breath when lying flat. She is able to sleep with three or four pillows but prefers to sleep in a recliner chair. Although she enjoys walking about the neighborhood, she is going out less often and coming home very tired. When Mrs. B. was visiting her daughter on a cold December day, she climbed the stairs to the second floor and began to experience chest discomfort. At first she attributed her discomfort to her usual shortness of breath with exertion. She sat down on the top of the stairs to rest and “catch her breath”. After 5 minutes, she was still very short of breath and noticed that she could feel her heart pounding in her chest. Mrs. B.’s daughter drove 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 mucus membranes and nail beds were pink. Mrs. B’s blood pressure was 200 mmHg. Korotkoff sounds were first heard at 198 mmHg, then there was silence until the sounds were heard again between 140 mmHg and 100 mmHg. Her heart rate was 110, strong and irregular; respirations were 30 and labored. The cardiac monitor displayed atrial fibrillation with frequent premature ventricular complexes. Mrs. B. was given an intravenous bolus of 50mg of lidocaine to suppress the ventricular ectopic beats. To control her blood pressure, a nitroprusside drip was started intravenously. Five minutes later, Mrs. B.’s systolic blood pressure was 160 mmHg and diastolic pressure was 95 mmHg. No ventricular ectopic complexes were seen. A 12-lead electrocardiogram showed no evidence of acute myocardial injury. The emergency room team judged Mrs. B. stable enough to be transferred to the critical care unit. The critical care nurse receiving Mrs. B. recorded her vital signs. Her respirations were 28 with oxygen by mask at 10L/min. The nurse positioned Mrs. B. is a semi-Fowler position. While listening to Mrs. B.’s chest, the nurse noted fine rales in the posterior base of both lungs. A summation S3, S4 gallop was present. A soft, systolic ejection murmur was heard over the aortic valve area. Pitting edema was noted in her lower legs. Mrs. B.’s cardiac enzyme levels did not elevate in a pattern of myocardial infarction. Her serum SGOT and LDH (lactic dehydrogenase) levels were elevated. Her 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 received a dose of digoxin. She was successfully weaned from the lidocaine drip. About 15 minutes after Mrs. B. converted to sinus rhythm, she commented to the nurse that she was much less short of breath and did not feel her heart pounding. 1. Which of the following explains why some individuals with hypertension, such as Mrs. B., develop congestive heart 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 flow 2. 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 3. Why did the nurses not hear the Korotkoff sounds between 198 mmHg and 140 mmHg when Mrs. B.’s blood pressure was measured by cuff on admission to the emergency room? a. There was increased systemic resistance b. There was decreased left ventricular afterload c. The cardiac output was too low d. Blood flow was not turbulent enough to make sounds