Mrs. M, a 72-year-old African American, arrived at the ER in moderate distress. Her legs were swollen, and she had experienced shortness of breath that had been getting more severe over the past several days. Mrs. M coughed when recumbent and therefore had trouble sleeping at night. She had poor exercise tolerance at baseline and said she had recently been having difficulty walking from her bedroom to the bathroom.
Mrs. M’s medical history was positive for adult-onset diabetes, hypertension, hyperlipidemia, congestive heart failure (CHF), transient ischemic attack, chronic renal insufficiency, and arthritis. She was 64-in tall and obese (196 lb). Her mother had died from a stroke; her father’s cause of death was unknown.
Mrs. M’s 68-year-old sister suffered from hypertension and high cholesterol. Although she was taking multiple medications, Mrs. M admitted that she was not always compliant with her medications or a low-fat, low-salt diet.
When Mrs. M was first diagnosed with CHF three years earlier, cardiac catheterization revealed nonobstructed coronary arteries with decreased left ventricular function and an ejection fraction (EF) of 35%. Two years later, an echocardiogram showed improvement in her EF to 50%.
Although there was no evidence of wall-motion abnormalities, mild-to-moderate mitral-valve regurgitation, moderate left atrial dilatation, and left ventricular hypertrophy (LVH) were observed.
Mrs. M also suffered from chronic renal insufficiency, likely a result of her CHF and diabetes. Her renal disease was slowly worsening, and she was referred to a specialist to evaluate her kidney disease.
2. Examination and Labs
Mrs. M’s vital signs were BP 200/90 mm Hg, heart rate 100 beats per minute, and respiration rate 20 breaths per minute. On physical exam, her heart rate was regular; a 2/6 systolic murmur without radiation was heard. Carotid pulses were 2+ bilaterally without bruits; there was no evidence of jugular venous distension.
On abdominal exam, the liver edge was palpable, and there was no ascites. Extremities demonstrated 2+ pedal edema above the ankle bilaterally. An ECG showed normal sinus rhythm with left-axis deviation, left atrial enlargement, and LVH with a strain pattern. A chest x-ray was positive for cardiomegaly and vascular prominence consistent with moderate CHF.
Mrs. M’s laboratory findings included potassium 5.4 mEq/L, blood urea nitrogen 68 mg/dL, creatinine 2.4 mg/dL, sodium 134 mEq/L, glucose 200 mg/dL, alkaline phosphatase 297 units/L, aspartate aminotransferase 60 units/L, alanine aminotransferase 54 units/L, WBCs 5,200/µL, and hematocrit 32%. Thyroid function tests were normal.
Urinalysis was positive for glucose (100 mg/dL) and protein (30 mg). Hemoglobin A1c was 10 g/dL. Fasting lipids revealed a total cholesterol of 175 mg/dL, LDL 120 mg/dL, HDL 60 mg/dL, and triglycerides 180 mg/dL. Serial cardiac enzymes were negative.
Mrs. M was admitted to the cardiac unit with a diagnosis of acute exacerbation of CHF and acute hypertension.
When Mrs. M was treated with high-dose IV furosemide, she voided a large amount of urine, which led to her losing 4 kg over four days. Her hypertension was controlled with the addition of hydralazine 10 mg b.i.d. and maximization of clonidine to 0.2 mg t.i.d.
A healthier diet and adherence to medication helped stabilize Mrs. M’s BP at 125/80. Her lipid profile, with still moderately high LDL and triglycerides, called for an increase of atorvastatin to 20 mg. Her insulin was increased to 50 units at night.
On discharge, Mrs. M was urged to choose her foods carefully and to maintain a diet low in sodium and saturated fat. She was told to log her glucose and weigh herself daily, watching for signs of water retention. The importance of staying active was also stressed. Mrs. M agreed to improve her adherence. She was scheduled for a follow-up visit with her primary-care physician and cardiologist in two weeks.
CHF is usually described as a clinical syndrome in which left ventricular function and neurohormonal regulation lead to functional limitations, fluid retention, and risk of sudden death from arrhythmia.1 Hypertension and congential heart disease (CHD) are leading triggers in the development of CHF.
Mrs. M, at initial diagnosis, was found to have left ventricular systolic dysfunction with moderately low EF and normal coronary arteries and was classified as New York Heart Association stage II-III.
During acute exacerbation of CHF, treatment with a diuretic is first-line therapy to reduce volume overload. Once the patient is euvolemic, ACE inhibitors and beta blockers are the cornerstone of treatment.1,2 However, Mrs. M could not be prescribed an ACE inhibitor because of persistent hyperkalemia.
In addition to treating Mrs. M’s heart failure, lifestyle modifications and CHD risk factors still needed to be addressed. Her BP was not well controlled and was probably the cause of her current CHF exacerbation. Therefore, maximizing BP medication was essential. Her clonidine dose was increased to 0.2 mg t.i.d., and hydralazine 10 mg t.i.d. was initiated. Hydralazine is often recommended for patients who cannot tolerate ACE inhibitors and need further BP control.3
Mrs. M had gained weight, and her blood glucose was elevated. She needed to avoid sugars and to eliminate empty carbohydrates from her diet. According to the new National Cholesterol Education Program Adult Treatment Panel III guidelines, regular physical activity and weight loss reduce insulin resistance, BP, and lipids in CHD patients.4
Despite having arthritis, Mrs. M struggled to stay active. As nonsteroidal anti-inflammatory agents are known to block the effects of diuretics and ACE inhibitors, Mrs. M was advised to take acetaminophen to manage pain.
Mrs. M’s LDL and triglyceride levels were still not at goal. In high-risk patients with heart disease and diabetes, the recommended LDL level is <100 and triglycerides <150.5 Her atorvastatin dose was increased to 20 mg in the hospital. Since she was also taking amlodipine for hypertension, a combination of amlodipine/atorvastatin was prescribed at discharge.
To avoid rehospitalization, a visiting nurse will help Mrs. M administer medication and evaluate for early warning signs of CHF exacerbation. Her family has also been educated about the importance of her adopting lifestyle changes to decrease the likelihood of hospital readmission. Mrs M will follow with up with her cardiologist.
Catherine Lange, MS, PA-C, is a certified physician assistant in the department of cardiology at Montefiore Medical Center, Bronx, N.Y.
- Sackner-Bernstein J, Hart D. Neurohormonal antagonism in heart failure: what is the optimal strategy? Mt Sinai J Med. 2004;71:115-126.
- Hunt SA, Baker DW, Chin MH, et al. ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult: Executive Summary. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1995 Guidelines for the Evaluation and Management of Heart Failure): Developed in Collaboration with the International Society for Heart and Lung Transplantation; Endorsed by the Heart Failure Society of America. Circulation. 2001;104:2996-3007.
- Cohn JN, Johnson G, Ziesche S, et al. A comparison of enalapril with hydralazin-isosorbide dinitrate in the treatment of chronic congestive heart failure. N Engl J Med. 1991;325:303-310.
- Grundy S, Cleeman J, Merz C, et al. Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III guidelines. Circulation. 2004;110:227-239.
- Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults. Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA. 2001;285:2486-2497.