2) What are the most common causes of CHF in an adult? Given the information in this case, which cause seems to be the most likely?
3) It is sometimes useful to make the distinction between systolic and diastolic dysfunction in patients with heart disease. Which appears to be operating in this patient?
4) Explain the probable mechanism and significance of her abnormal findings on physical examination.
5) You are curious as to the usefulness of the S3 in making a diagnosis of CHF. You go to the literature and find two studies. The first study started with 100 patients with Echocardiographically proven LV systolic dysfunction and an ejection fraction estimated at less than 35%. Of that group, 80 patients had an S3. The other study took 100 normal volunteers and performed auscultation and Echocardiography. Of that group, 10 patients with normal Echocardiograms had an S3. You then see a patient in your office with a history of exertional dyspnea. You estimate before examining him that he has a "50-50 chance" of having congestive heart failure. If you hear an S3, what do you then think are his chances of having CHF?
6) What important physiologic adaptations have probably occurred in this patient?
7) What (qualitative) predictions would you make about the following measurements? a) LVEDP b) Cardiac output c) Ejection fraction d) Myocardial oxygen consumption
8) What diagnostic tests would you consider in this case?
9) In a patient with previously stable CHF who presents with an exacerbation, what underlying causes of the deterioration should one consider?
10) How would you treat this patient's pulmonary edema in the acute setting?
11) You obtain the following studies: An ECHOCARDIOGRAM shows a thin LV wall, an enlarged LV, and severe hypokinesis of the septum and lateral wall of the LV. The visually estimated EF is 35%. There is mild mitral regurgitation and no other significant valvular abnormalities. There is a small, hemodynamically insignificant pericardial effusion. There is enlargement of the RV as well. There is no evidence of intracardiac shunting. A cardiac catheterization shows complete occlusion of the proximal Left Anterior Descending coronary artery. There is diffuse disease in the Circumflex Coronary Artery. The Left Main coronary artery has a 20% stenosis. There is diffuse, mild disease in the Right Coronary Artery. There is no intraventricluar thrombus identified on either study. EF measured on the LV-gram is 30%. a) Will this patient benefit from surgical intervention? b) What medical therapy is available for this patient?
12) An article in JAMA (1995. May 10; 273:1450-6) describes a meta-analysis of ACE inhibitors in the treatment of CHF. Combining the results of 32 trials, they compared 3870 patients receiving ACE inhibitors to 3235 patients receiving placebo. The results were as follows: Mortality in ACE inhibitor-treated group 15.8% Mortality in placebo (standard Rx.) group 21.9% Absolute risk reduction (with confidence interval) 6.1% (4.3% to 8.0%) P value for risk reduction < .001 Number needed to treat -NNT- with CI 16 (12 to 23) Mortality from progressive CHF in ACE treated group 6.5% Mortality from progressive CHF in ACE control group 10.5% Absolute risk reduction (with confidence interval) 4% (2.7% to 5.3% Number needed to treat -NNT- with CI 25 (19 to 38)
Consider the following questions about the results of this study.
a) Is there a physiologic reason to expect that ACE inhibition would improve prognosis in CHF? b) Were the numbers of patients studies enough to achieve results that are believable? c) What does this analysis say about the possibility that the mortality benefit is through some mechanism other than treating the underlying heart failure? d) Does it seem reasonable to treat all patients with CHF with ACE inhibitors, even though many do not seem to benefit from the intervention? What additional information would you like to have before answering that question?
13) Given the high mortality of CHF, what should a responsible physician tell the patient about the disease? What additional discussion should take place? When and where is it most appropriate to have those discussions?
14) Should this patient take ASA?
15) Should this patient be anticoagulated?
16) What is the most likely cause of her cough?
17) You manage this patient medically for 4 years. On her 68th birthday she is admitted to the ICU in acute pulmonary edema. She requires intubation and vigorous therapy, and suffers one "Dr. Cart" during her stay. She is extubated after one week and transferred out of the ICU, only to decompensate on the ward and require readmission to the ICU. She does well on intravenous inotropes in the CCU, but you have difficulty keeping her out of pulmonary edema in any other setting. Is this patient a candidate for heart transplantation? What other options do we have for treatment?