Ambulatory Care Curriculum
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OUTPATIENT MANAGEMENT OF HEART FAILURE
Objectives
I. To know that heart failure (HF) is largely preventable primarily through control of blood pressure and coronary artery
disease
2. Understand the classification of heart failure that emphasizes its evolution and progression (stages A, B, C, D)
3. Recognize patients with diastolic heart failure by knowing the clinical characteristics of patients with diastolic (HFpEF)
versus systolic (HFrEF) heart failure.
4. Know what medications all patients with left ventricular dysfunction should receive
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
The mortality from HF is increasing because of the longer survival of patients with cardiovascular
disease, the growing aging population and worsening risk profile (obesity & diabetes). The median
survival is 1.7-2.1 years following onset in men (50% from sudden death) with 50-75% dying within 5
years of diagnosis.

HTN and CAD are the 2 conditions which represent the highest population attributable risk for the
development of HF with DM and obesity following close behind.

The way we think about HF has changed radically in the past 20 years. Formerly it was thought of as a
hemodynamic problem, with filling pressures rising as cardiac output fell. This paradigm was
superseded by the neurohormonal model which posited a maladaptive activation of the sympathetic
nervous system and the RAAS in response the decrease in forward flow and increase in filling pressure.
The circulation is in effect trying to protect itself with mechanisms which are adaptive in the short run
but highly maladaptive in the long run, leading to progressive remodeling of the heart (cell dropout,
elongation & hypertrophy progressing toward hypoxia and death)

There is increasing knowledge about the usefulness of biomarkers (NT-pro-BNP, STZ, galectin-3,
NGAL) in elucidating the pathogenesis, predicting outcomes in patients with HF and in directing
therapy. More recent studies (STOP-HF) have shown promise in identifying patients at increased risk
for developing HF.

Most evidence-based guidelines on the management of HF are not being followed despite the evidence
that pharmacotherapy reduces both morbidity and mortality with systolic dysfunction.

There are some new drug therapies on the horizon but none hold much promise. The focus should
remain on those drugs that have been shown to improve outcome (ACEI,betablockers, aldosterone
inhibitors) and lament the lack of effective therapy for diastolic dysfunction (control blood pressure and
central blood volume).

“Early” consideration of advanced therapies (mechanical circulatory support, transplant) may preserve
other organ function and give the patient more options.
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Management is more than ever a team effort and should start with patient education.
Clinical Problem 1
A 62-year old retired CTA bus driver has been under your care for hypertension and DM for the past 12 years. She
presents to your office for a routine visit and complains of leg swelling, mild exertional dyspnea and 10-pound weight
gain over the past 10 days. She denies chest pain, orthopnea, PND, or nocturia. She does not smoke or use alcohol. Her
current medications include Metformin 2000 mg/day, Atenolol 100 mg/day, HCTZ 25 mg/day, ECASA 325mg/day,
ibuprofen 600 mg TID and Lisinopril 20 mg/day.
On exam:
BP 170/100, RR20, HR66, T 980 F
Gen: Overweight AA female in no apparent respiratory distress
Neck: JVP midway to angle of jaw, positive hepatojugular reflux
Lungs: Dull at bases
CV: S4 audible, PMI diffuse in the MCL, 2/6 HSM at apex
Abd: obese, without hepatomegaly
Ext: Bilateral ankle edema present
1.
What are the likely pathophysiologic mechanisms at work in this patient’s heart failure?
2.
There are several published guidelines for the diagnosis of diastolic heart failure but no consensus on the
criteria. How would you define it?
3.
What ACC/AHA stage heart failure does this patient represent? Functional class? What role does this
information play in the management of patients with HF?
4.
What is the significance of the patient's blood pressure and how will it affect your management?
5.
Lab tests are done. Hg is 9. BNP is 500 pg/ml. The uric acid is borderline high.
Which of the following is FALSE?
a. BNP and NTproBNP are equally affected by renal function and age
b. Normal levels of BNP have high negative predictive value
c. CRP albeit not very specific has been associated with worse risk
d. Galectin-3 reflects fibroblastic activity
e. Correcting the anemia has been shown to not improve outcomes in the RED-HF trial
f. Troponins can be elevated in decompensated HF without an ischemic event and is associated with a
worse outcome in non-ischemic patients.
6.
The single most useful diagnostic test in the evaluation of heart failure is?
a. ECG
b. Echo/Doppler
c. CXR
d. Exercise stress test
e. Sleep study
7.
The goals of therapy of patients with HF with preserved LVF (HFpEF) include which of the following:
a. Control the heart rate to allow for adequate ventricular filling and maintain NSR if possible
b. Control volume status to decrease diastolic pressures
c. Control BP or other stimuli to LVH (minimize symptoms and even regression of LVH)
d. All of the above
8.
Regarding the pharmacologic management of diastolic HF which of the following is FALSE:
a. Vasodilators are first line therapy in decompensated diastolic HF and alleviate symptoms and improve
exercise capacity
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b.
c.
d.
e.
Diuretics are useful to control symptoms and improve exercise capacity
Beta blockers are useful to control heart rate and BP and may play a role in regression of LVH.
ACEI may improve diastolic dysfunction by leading to regression of LVH and by direct improvements
via a bradykinin-mediated mechanism.
None of the above
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Clinical Problem 2
A 74-year old retired elementary school principal is referred to you for general care after a change in his HMO provider.
He has a history of CAD and suffered a large anterior wall infarction eight months ago complicated by acute pulmonary
edema requiring mechanical ventilation. He subsequently underwent a PTCA and stenting of the LAD and has had no
ischemic symptoms since. The LV ejection fraction was last measured at 25% by echocardiogram done three months ago.
There was mild mitral regurgitation noted.
For the past two months he has noted increasing dyspnea on exertion and an eight-pound weight gain. He never complains
of chest discomfort, but is only able to walk up one flight of stairs before having to rest. He uses 3 pillows to prop his
head up at night and will occasionally wake up in the middle of the night with a dry cough.
His medications include Lisinopril 20mg/day, ASA 325 mg/day and furosemide 20 mg/day. He has no drug allergies.
Exam:
BP 110/70 HR 110 RR20 T970 F
General: Appears older than stated age, able to complete sentences, comfortable while sitting.
Neck: JVD = 10 cm at 45 degrees
Lungs: Few crackles at bases
CV: PMI laterally displaced. Sl S2 regular, soft S3 and 3/6 HSM at apex radiating to axilla. No rub.
Abd: Normal
Ext: Bilateral ankle edema 1 +
1.
What factors may be contributing to this patient’s apparent exacerbation of heart failure?
2.
What further diagnostic testing is indicated at this time?
3.
Is there an indication to admit this patient to the hospital for treatment at this time?
4.
How would you treat this patient’s symptoms? Is there a need for an adjustment in his present medication
regimen? What medications would you add or remove and why?
5.
List those mediations that improve mortality in patients with LV dysfunction and CHF. If you were forced to
pick one medication to treat chronic heart failure based on evidence, which one would provide tile greatest
survival advantage?
6.
7.
In this patient with volume overload which of the following is FALSE about the use of diuretics in treating
decompensated systolic HF?:
a. They relieve symptoms of dyspnea and edema in most patients
b. They are associated with deactivation of the RAAS and sympathetic NS
c. They have been shown to increase overall mortality
d. The DOSE study showed that there was no advantage of continuous infusion over bolus dosing
Would you anticoagulate this patient?
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REQUIRED READING
1.
2.
McMurray J. Systolic Heart Failure. NEJM 2010;362:228-38
Meyer T et al. Heart failure with preserved ejection fraction (diastolic dysfunction). Ann Int Med 2013;158(1)
References
2009 Focused Update: ACCF/AHA Guidelines for the Diagnosis and Management of Heart Failure in Adults
A
Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice
Guidelines
Mariell Jessup, MD, FACC, FAHA et al International Society for Heart and Lung Transplantation Representative
J Am Coll Cardiol. 2009;53(15):1343-1382. doi:10.1016/j.jacc.2008.11.009
ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult. J Am Coll
Cardiol 2005;46:1116-1143
The effect of cardiac resynchronization on morbidity and mortality in heart failure. NEJM 2005;352:1539-49
Huynh. Long-term survival in elderly patients hospitalized for heart failure: 14-year follow-up from a prospective
randomized trial. Arch Int Med 2006;166:1892-8
Owan. Trends in prevalence and outcome of heart failure with preserved ejection fraction. NEJM 2006;355:251-9
Braunwald E. Biomarkers in Heart Failure. NEJM 2008;358:2148
Felker G, et al. Diuretic Strategies in patients with acute decompensated heart failure. NEJM 2011;364
Eikelboom J & Connolly S. Warfarin in heart failure (Ed). NEJM 2012;366:1936
How to diagnose diastolic heart failure. European Study Group on Diastolic Heart Failure. Eur Heart J. 1998;19:990-1003
Saxon LA, Stevenson WG, Middlekauff HR, Fonarow G, Woo M, Moser D, et al. Predicting death from progressive heart
failure secondary to ischemic or idiopathic dilated cardiomyopathy. Am J Cardiol. 1993;72:62Ezekowitz JA, McAlister FA, Armstrong PW. Anemia is common in heart failure and is associated with poor outcomes:
insights from a cohort of 12 065 patients with new-onset heart failure. Circulation. 2003;107:223-5
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