For Student

History
An 85-year-old woman is brought to the emergency department by her home health aide because
of shortness of breath and worsening cough for 1 week. She has a long history of hypertension,
diabetes, chronic obstructive pulmonary disease (COPD), bronchiectasis, osteoporosis, and
osteoarthritis. She had smoked heavily all her adult life but quit 20 years ago. Over the last 2
years, she has had several admissions for COPD exacerbation, which responded to antibiotics
and corticosteroids.
The patient adheres carefully to her regimen of medications, which include inhaled
corticosteroids and bronchodilators, lisinopril, rosiglitazone, calcium and vitamin D, and
acetaminophen. Her blood pressure and blood sugar have been under good control. She lives by
herself and is assisted by a home health aide 8 hours a day.
In the emergency room, her blood pressure is 170/90, pulse is 88 and regular, respiratory rate is
28 per minute, and temperature is 98 ◦F. Lung examination reveals basilar crackles (unchanged
from previous examinations), diffuse rhonchi, and wheezing. No peripheral edema is noted. The
electrocardiogram (EKG) reveals left ventricular hypertrophy (LVH). Chest X-ray shows poor
inspiration, increased vascular markings, and a retrocardiac infiltrate. She is admitted and treated
with intravenous methylprednisone, antibiotics, and nebulized bronchodilators. She feels better
in a few hours.
The next morning, to your surprise, you find the patient’s respiratory status has worsened. She is
sitting upright in bed, has labored breathing, and wheezing can be heard without the stethoscope.
A repeat chest X-ray is performed.A repeat chest X-ray showed small bilateral pleural effusions
and pulmonary vascular congestion, in addition to the previous finding of a retrocardiac infiltrate

Tasks:
1. What is the cause of the patient’s worsening condition?
2. What is the pathophysiology? How can the diagnosis be confirmed?
3. What factors could have contributed to this patient’s problem?
4. How should this condition be treated?
Student’s name
For examiner
Task 1 (3.0)When an elderly patient presents with cough, dyspnea, or wheezing, congestive
heart failure (CHF) should always be in the differential diagnosis, even when there is a history of
COPD. This is especially important when the patient has a history of hypertension, diabetes, or
ischemic heart disease. This patient’s medical history made COPD exacerbation the major
consideration on admission. However, despite aggressive treatment, her wheezing and dyspnea
eventually worsened. Wheezing is a common finding in elderly patients with CHF, even in those
without a known history of bronchospastic disease. Patients with this “cardiac asthma” have a
bronchospastic response to methacholine, compared with heart failure patients who do not have
wheezing. A repeat chest X-ray showed small bilateral pleural effusions and pulmonary vascular
congestion, in addition to the previous finding of a retrocardiac infiltrate. Intravenous furosemide
and morphine were given and the patient improved. The dose of lisinopril was increased to 10
mg daily, with a plan to increase further, as tolerated. Repeat EKG showed no changes and
cardiac enzymes were normal. Thyroid function tests and repeat complete blood count (CBC)
were ordered, and an echocardiogram was performed.
Task 2 (3.0) The patient’s echocardiogram revealed LVH, normal left ventricular (LV) function
with an ejection fraction (EF) of 65%, and mild pulmonary hypertension. CHF with preserved
left ventricular function suggests the patient has diastolic dysfunction – an important cause of
CHF in the elderly. Heart failure can be associated with either reduced cardiac output (LV
systolic dysfunction) or with normal cardiac output. If the maintenance of adequate cardiac
output requires a higher than normal LV filling pressure, it is referred to as diastolic dysfunction.
The patient may be asymptomatic or may experience only reduced exercise tolerance, or may
have overt heart failure that is clinically identical to LV failure. Among patients with CHF,
diastolic dysfunction accounts for fewer than 103 Wheezing 10% of cases under the age of 65,
but the proportion increases with advancing age, accounting for more than 50% of cases after age
75. Many factors may affect diastolic function, the most important being LV relaxation, LV
stiffness, and left atrial function. LV relaxation, which occurs during early diastole, is an energy-
dependent process and can be readily affected by ischemia. LV diastolic stiffness or compliance
is affected by myocardial fiber distensibility, connective tissue elasticity, chamber size, wall
thickness, and the condition of the pericardium. Left atrial contraction, which occurs in late
diastole, accounts for less than 20% of filling volume in young, healthy persons, whereas, in
patients with early diastolic dysfunction, the left atrium increases contractility to compensate for
LV diastolic dysfunction and can contribute up to 50% of the filling volume. Diastolic
dysfunction can be caused by impaired energy-dependent ventricular relaxation, which occurs in
ischemic heart disease, hypertrophy, tachycardia, and increased afterload such as in aortic
stenosis, or it can be due to reduced passive elastic properties, which occur in hypertension with
LVH or if there are increased myocardial connective tissue components, such as fibrosis,
diabetes, or infiltrative diseases such as amyloidosis. Both mechanisms exist to a limited degree
in normal aging. Diastolic dysfunction is more common in women than in men and is the cause
of nearly two-thirds of all CHF cases in women over the age of 80. The reason for the gender
difference is not clear, but it may be related to the greater frequency of systolic heart failure in
the male cohort. Accurate diagnosis of diastolic dysfunction requires simultaneous
measurements of LV pressures and volumes to create pressure–volume curves, using cardiac
catheterization. This is invasive and unpractical. Clinically, the diagnosis of diastolic heart
failure relies on clinical criteria for CHF with documentation of preserved LV function by
Doppler echocardiogram (i.e. EF >45%), and absence of other conditions that also cause CHF
with normal LV systolic function, such as anemia and thyrotoxicosis. This patient’s thyroid
function tests and CBC were normal.
Task 3 (2.0) Long-standing hypertension, diabetes, and possible coronary artery disease, as well
as aging, probably all contributed to this patient’s diastolic dysfunction. Thiazolidinediones, such
as rosiglitazone, may cause fluid retention and precipitate overt CHF in patients with underlying
cardiac dysfunction. These drugs are believed to produce peripheral vasodilatation, which leads
to decreased mean arterial pressure and consequent renal retention of sodium and water.
Recently, in vitro evidence of pulmonary endothelial cell permeability has been reported (see
Idris et al., 2003), but more research is needed to confirm a cellular mechanism. The
exacerbation of COPD and the overnight intravenous fluid infusion might also have contributed
to the rapid worsening of this patient’s CHF. After alleviation of pulmonary congestion with
diuretics, the dose of lisinopril was further increased to 20 mg and the patient tolerated it well.
Her weight decreased by 104 Case studies in geriatric medicine 6 pounds over 4 days. Her
pneumonia and COPD improved and corticosteroids were tapered. Rosiglitazone was
discontinued, glipizide was instituted, and the patient was discharged home.
Task 4 (2.0) Treatment of underlying or exacerbating conditions, such as hypertension,
myocardial ischemia, and tachyarrhythmias, is important. In contrast to systolic heart failure,
virtually no randomized controlled trials have been conducted of the treatment of diastolic heart
failure. Clinical experience and limited evidence indicate that most treatments for systolic heart
failure can also benefit patients with diastolic heart failure. Diuretics are useful for acute
exacerbation of pulmonary congestion and fluid retention, such as in this case. However, since
patients with diastolic dysfunction depend on an adequate preload to maintain normal cardiac
output, overuse of diuretics should be avoided. There is some evidence that angiotensin-
converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) improve diastolic
function. A possible mechanism might be their ability to affect beneficially the myocardial
remodeling process in CHF. Beta-blockers may also be beneficial for patients with diastolic
dysfunction. In addition to their antihypertensive and anti-ischemic properties, they improve
diastolic filling by reducing heart rate in patients with tachycardia. Digoxin is not usually
recommended in patients with CHF associated with diastolic dysfunction, but it has been used
successfully and safely to control heart rate in patients with atrial fibrillation coexisting with
diastolic dysfunction.