Resident Version
Congestive Heart Failure Module
Created by Dr. Cody S. Deen
Objectives:
1. Identify history and physical exam findings consistent with Congestive Heart
Failure.
2. Understand the utility of BNP for the internist.
3. Understand the different classification schemes of congestive heart failure.
3. Identify the workup and differential diagnosis of Congestive Heart Failure.
4. Identify potential complications from Congestive Heart Failure.
5. Identify medical treatments for the patient with Congestive Heart Failure.
6. Identify non-medical treatments for the patient with Congestive Heart Failure.
References:
1. Crawford, Peter A. The Washington Manual Subspecialty Consult Series
Cardiology Subspecialty Consult. 2004.
2. Jessup, Merriel and Susan Brozena. “Congestive Heart Failure.” NEJM (May
15, 2003. 248:2007-18.)
3. www.uptodate.com “Overview of the therapy of heart failure due to systolic
dysfunction”. Wilson S Colucci, MD. Accessed on December 2007.
CASE
49 year old male presents to the Emergency Department with a complaint of SOB.
Patient reports that his breathing has gotten progressively worse over the last 2
months and is especially difficult when he is trying to sleep at night. He has several
episodes of waking up gasping for air and is only able to fall asleep when he is sitting
upright. The patient reports that he currently has SOB after walking 20 feet.
Patient has only minimal white sputum. He denies fever, chills, green sputum, and
sick contacts but does affirm bilateral lower extremity swelling. Social history is
significant for a 60 pack year tobacco history, rare alcohol use and currently living
in his van. Patient reports that his father had heart bypass surgery in his 60s.
Currently, the patient has not seen a doctor in 30 years and takes no medications.
Physical Exam is significant for HR=98, BP= 165/100, afebrile, RR=22 and sat=
85%RA, wt =198#.
Lung exam reveals decreased breath sounds throughout and bilateral crackles at
the bases, CV exam reveal an enlarged laterally displaced PMI, with a normal S1
and S2, +S3 and no murmurs. Extremities show 2-3+ pitting edema to mid-thigh
bilaterally.
CXR reveals bilateral small pleural effusion, and prominent pulmonary
vasculature.
1. What is the likely diagnosis and what additional testing and labs would you
want?
2. What class of congestive heart failure is this patient demonstrating?
3. What is the utility of BNP for diagnosing heart failure in this patient?
4. Are there other utilities of BNP in patients with congestive heart failure?
Further Patient Information
The patient undergoes ECG, as well as recommended screening labs. ECG reveals
sinus tachycardia, LVH and q waves in V1-V4. Labs are significant for sodium of
128, a BUN of 45 a creatinine of 1.9, and a random glucose of 245. UA, LFTs, and
TSH are all within normal limits. Lipid Panel reveals total cholesterol of 250, HDL
of 24, and LDL of 169. Urine electrolytes ordered for elevated creatinine suggest
pre-renal azotemia (FENa <1%). Echocardiogram reveals an Ejection Fraction
(EF) of 35-40%, left ventricular hypertrophy, septal and anterior wall hypokinesis,
normal valves, and elevated pulmonary artery and right atrial pressures.
5. What is the most likely etiology of his congestive heart failure based on this
information?
6. What are additional potential causes of Congestive Heart Failure?
7. What is the next diagnostic step in evaluating this patient?
The patient however is unable to lay flat and thus you must improve his symptoms
before he can undergo cardiac catherization. You want to treat his heart failure but
are unsure about giving a patient lasix with pre-renal azotemia.
8. What are the common physiological derangements of congestive heart failure?
9. What is the initial management of heart failure?
You fluid and salt restrict the patient, requesting daily weights and strict ins and
outs. You decide that by reducing the preload of the patient (with diuretics) you
may effectively shorten the sarcomere length back to an ideal relationship which
will allow more force to be generated during contraction thus increasing cardiac
contractility and cardiac output. You give the patient 40mg of IV lasix and are
pleased with his 24 hour net loss of ~2L. Repeat creatinine is 1.6 and the patient
feels much better.
10. You also decide to improve his afterload by treating his blood pressure what
antihypertensive would you use?
11. Which other medications have been shown to have a mortality benefit in
congestive heart failure and in what setting should they be considered?
After 6 days of diuresis and afterload reduction with ACE-I your patient has lost 15
pounds and is able to walk the hallway of 7 South without oxygen or SOB. You add
a beta blocker to his ACE-I, ASA, and statin. The patient undergoes catherization
which shows severe 3 vessel disease and he is scheduled for 3-vessel CABG later that
week. He does well and you don’t see him for several years.
He presents to the ED ten years later and is on maximal medical therapy (maximum
ACE-I, maximum Beta blocker, aldactone 40 mg, lasix 200 mg daily, asa, statin. He
has undergone an additional CABG three years prior). Currently he has SOB at all
times including while resting in an upright position. His EF now is 15-20%.
12. What additional non-medical therapies should be considered at this time?
Discussion Outline:
Heart failure work up:
American College of Cardiology class I indications for the workup of heart failure
include a basic metabolic panel, urinalysis, fasting glucose, lipid panel, TSH, liver
function tests, and a CBC. Additionally a twelve lead ECG along with Chest x-ray and
Echocardiogram should also be performed. Cardiac Catherization should be performed
in any patient who has history of angina or evidence of ischemia. ?BNP.
New York Heart Classification of Congestive Heart Failure Classes
Class I - symptoms of HF only at activity levels that would limit normal
individuals
Class II - symptoms of HF with ordinary exertion
Class III - symptoms of HF with less than ordinary exertion
Class IV - symptoms of HF at rest
Utility of BNP for diagnosing heart failure:
Brain Natriuretic Peptide’s utility to diagnose congestive heart failure has been evaluated
in the Breathing Not Properly Study. This study examined 1586 patients with a
complaint of acute dyspnea Approximately 47% of patients enrolled had congestive
heart failure and were found to have a mean BNP of 675 pg/ml compared to the group
without congestive heart failure who had a mean of 110 pg/ml.
Setting a normal value at 100pg/ml, the BNP had a sensitivity of 90%, a specificity of
76%, and a positive predictive value of 83%. The negative predictive value of BNP has
been shown to be between 90 and 97% in multiple studies. This finding suggests that the
greatest utility of a BNP may be in its ability to exclude congestive heart failure as a
cause of acute dyspnea.
Mortality rates associated with BNP levels suggest that patient’s with extremely high
elevations in BNP may have higher risk of death during hospitalization than those with
only moderately elevated BNP. Patients with BNP levels of 480- 839 pg/ml have been
reported to have a 2.8% in hospital mortality compared to a 6% hospital mortality in
patients with a value > 1739pg/ml
Causes of Congestive Heart Failure:
Causes of CHF can be divided into Diastolic Dysfunction and Systolic Dysfunction.
Common causes of Systolic Dysfunction include CAD, HTN, Diabetes/ small vessel
disease, valvular heart disease, toxins (ethanol, methamphetamine, cocaine, doxorubicin),
infectious (coxsackie virus) and thyroid abnormalities.
Common causes of Diastolic Dysfunction include HTN, hypertrophic cardiomyopathy,
restrictive cardiomyopathy (amyloidosis, sarcoidosis, hemachromatosis), and constrictive
pericarditis.
Common physiological derangements of congestive heart failure:
- Pre-renal azotemia- due to poor cardiac output and compensatory elevation in
systemic vascular resistance.
- Confusion and lethargy- due to poor cardiac output and compensatory elevation
in systemic vascular resistance producing decreased cerebral perfusion
- Exercise intolerance.
- Hepatic Congestion with mild transaminitis, mild derangements in clotting, and
elevated bilirubin- due to hepatic congestion from elevated right sided heart
pressure.
-Lower extremity edema and elevated jugular venous distention- from elevated
right sided heart pressure
-Pulmonary edema- due to elevated left ventricular end diastolic pressures
(LVEDP)
-Orthopnea, PND, pleural effusion, lower extremity edema, elevated neck veinsfrom pulmonary edema and elevated LVEDP.
Management of heart failure:
Initial management includes fluid restriction at 1.5cc/day, sodium restriction at 2 grams
of salt per day, appropriate treatment of blood pressure (afterload reduction) with a goal
<130/80, oxygen to improve oxygen delivery, and diuresis (preload reduction).
Medications used in CHF and its benefits:
Beta blockers- carvedilol and metoprolol have both been shown to have improvement in
mortality for congestive heart failure patients. There may be some evidence that
carvedilol is superior to metoprolol in severe heart failure patients (COMET trial).
Usually initiated and up titrated after patient has improved to class II symptoms.
Angiotensin receptor blockers/ ACE-I- Have been shown to improve mortality. Does
not tend to worsen azotemia if started at low dose and slowly titrated. Usually initiated
after diuretic therapy in acute heart failure.
Aldactone- for patients with class III or class IV CHF and already on loop diuretics and
ACE-I therapy, the RALES trial showed 30% mortality reduction at 24 months for
spironolactone treated group.
Hydralazine and Nitrates- A-HEFT demonstrated a mortality benefit in AfricanAmerican patients put on a combination of hydralazine plus nitrates. Previous studies
had shown reduced benefit of ACE-I in African-American CHF patients. Data has been
extrapolated to patients unable to tolerate ACE-I or ARB for CKD.
ASA- only beneficial in patient with CAD
Statins- observational and retrospective studies indicate there may be a benefit for nonischemic heart failure for lowering admission rates due to CHF exacerbations. One post
hoc analysis showed decreased rate of arrhythmic deaths and overall mortality with
stating therapy in non-ischemic cardiomyopathy.
Digoxin- no mortality benefit, but it does improve symptoms and decreases admissions
for CHF exacerbations
Additional therapies to be considered:
Biventricular Pacemaker- CARE-HF trial showed a modest mortality benefit and
symptomatic improvement in patients with EF<35%, Class III or IV CHF and
QRS>120ms.
Cardiac Transplant
Hospice
Post Module Evaluation
Please place completed evaluation in an interdepartmental mail envelope and address to
Dr. Wendy Gerstein, Department of Medicine, VAMC (111).
1) Topic of module:__________________________
2) On a scale of 1-5, how effective was this module for learning this topic? _________
(1= not effective at all, 5 = extremely effective)
3) Were there any obvious errors, confusing data, or omissions? Please list/comment
below:
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
4) Was the attending involved in the teaching of this module? Yes/no (please circle).
5) Please provide any further comments/feedback about this module, or the inpatient
curriculum in general:
6) Please circle one:
Attending
Resident (R2/R3)
Intern
Medical student