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Case 4
67-year-old woman with shortness of breath and leg
swelling - Ms. Rivers
Author: Parekha Yedla, M.D., University of Alabama at Birmingham
Learning Objectives:

1. Interpret neck vein findings for jugular venous distention (JVD) and abdominal
jugular reflux.

2. Identify and translate auscultatory findings of the heart including rate, rhythm,
S3/S4, and murmurs.

3.
4.
5.
6.

List the major pathologic states that cause dyspnea.

Compare the differing etiologies and signs of left-sided vs. right-sided heart failure.
Utilize the staging system for heart failure.
Discuss the factors leading to symptomatic exacerbation of HF, including ischemia,
arrhythmias, anemia, hypertension, thyroid disorders, non-compliance with
medications and dietary restrictions, and use of nonsteroidal anti-inflammatory
drugs (NSAIDS).

7. Interpret B-type natriuretic peptide (BNP) results.

8. Recommend pharmacologic management of heart failure.

Dyspnea
Key Findings from

Bilateral lower extremity edema

History

Orthopnea
Cough

Elevated jugular venous pressure (JVP)

Crackles
Key Findings from

S3

Physical Exam

Bilateral pitting edema

Murmur
Tachypnea/tachycardia

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Congestive heart failure

Angina
Differential
Diagnosis

Pulmonary hypertension
Pulmonary embolism
Interstitial lung disease
Chronic kidney disease
Valvular disorder

Elevated BNP
EKG: Leftward axis, left ventricular
Key findings from

hypertrophy

Testing

Chest x-ray: Cardiomegaly and increased

pulmonary vasculature
Echo: Ejection fraction 30-35%

Final Diagnosis

Congestive heart failure

Summary of clinical scenario: A 67-year-old woman who comes to the

emergency department with shortness of breath on exertion and bilateral lower
leg swelling. Found to have orthopnea and cough. Exam is remarkable for
elevated JVP, crackles, S3 and murmur, all suggestive of congestive heart failure.
After diagnosis and appropriate treatment, the patient returns to the emergency
department with acute decompensated heart failure.
Case highlights: Students learn major causes of dyspnea, including
pathophysiology, symptoms, and signs. Types of processes and most common
disease etiologies for heart failure are discussed, including importance of age,
gender, ethnicity, and genetics. The physiological basis and scientific evidence
supporting treatment are demonstrated.

Key Teaching Points

Knowledge:
Heart failure:
Definition: Syndrome caused by cardiac dysfunction, generally resulting from
myocardial muscle dysfunction or loss and characterized by either left ventricle
(LV) dilatation or hypertrophy or both.
Etiology

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In U.S. and Europe hypertension and coronary artery disease are the
primary risk factors for developing heart failure.
CAD should be considered especially in patients with symptoms or risk
factors.
Less common etiologies:
Amyloid infiltration classically results in a restrictive cardiomyopathy
which is characterized by abnormal diastolic function
Often presentsas other restrictive diseaseswith relatively
more right-sided symptoms (e.g., edema, abdominal discomfort,
and ascites), although filling pressures are elevated in both
ventricles
Constrictive pericarditis and tamponade may present with dyspnea
and signs of right heart failure resulting from impaired ventricular
filling
Hemochromatosis, an infiltrative disease resulting in abnormal iron
deposition in multiple organs is a rare cause of CHF
Hyperthyroidism can cause CHF by the mechanism of high output
heart failure if untreated for some time
Hypertrophic obstructive cardiomyopathy can be inherited in an
autosomal dominant fashion or acquired due to disproportionate
hypertrophy of the interventricular septum
Findings include systolic murmur at the left lower sternal border
and hypertrophy on echo
Viral cardiomyopathy (caused by various viruses that cause
myocarditis) can lead to an enlarged left ventricle with decreased
systolic function and is one of many causes of dilated cardiomyopathy
Neurohumoral hypothesis
Decreases in blood pressure, stroke volume (pulse pressure), and perfusion
(flow) are sensed by mechanoreceptors in the LV, carotid sinus, aortic arch,
and renal afferent arterioles
Diminished activation of these receptors leads to:
Augmentation of sympathetic outflow, resulting in tachycardia and
arrhythmias;
Activation of the renin-angiotensin-aldosterone system (RAAS),
causing myocyte hypertrophy and collagen synthesis, and
Nonosmotic release of arginine vasopressin (AVP), which can lead to
hyponatremia
Heightened peripheral vasoconstriction (which causes edema) occurs, along
with increased blood volume
Classification
Systolic heart failure: Clinical syndrome characterized by signs and
symptoms of HF and reduced left ventricular ejection fraction (LVEF).
Most commonly associated with LV chamber dilation.
Diastolic heart failure: Clinical syndrome characterized by signs and

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symptoms of HF with preserved LVEF.

Comprises about a third of heart failure cases
Most commonly associated with a nondilated LV chamber
Patients with diastolic heart failure have impaired ventricular
relaxation and elevated filling pressures
Prevalence of diastolic heart failure increases with age, if patient is
female, and with hypertension
Left-sided heart failure: Refers to symptoms and signs of elevated pressure and
congestion in pulmonary veins and capillaries
Non-ischemic causes:
Valvular disorders
Arrhythmias
Alcohol
Chemotherapy
Myocarditis (viral, bacterial, parasitic, autoimmune)
Illicit drugs: cocaine
Idiopathic causes
Right-sided heart failure: Refers to symptoms and signs of elevated pressure and
congestion in systemic veins and capillaries, characterized by jugular vein
engorgement and hepatic congestion.
Most common cause of right heart failure is left heart failure
Staging: After heart failure is diagnosed, assess functional capacity and volume
status.
After heart failure is diagnosed, use the New York Heart Association (NYHA)
functional classification tool:
Class I

No symptoms

Class II

Symptoms with ordinary activity

Class III

Symptoms with less than ordinary activity

Class IV

Symptoms at rest or with any minimal activity

Assess volume status clinically, using:

Orthostatic blood pressure changes
Weight
Jugular venous pressure
Presence of edema in dependent areas
Complications:
Acute heart failure
40-50%: No precipitant
Acute coronary syndrome

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rule out with ECG and cardiac biomarkers.

Arrythmias
Atrial arrhythmias, especially atrial fibrillation more common
than ventricular arrhythmias
Infections
Pneumonia, UTI, sepsis syndromes
NSAID
10x increased risk of hospitalization
Acute valvular regurgitation
Post MI, endocarditis
Severe anemia, thyrotoxicosis
Can cause high output failure
Non-adherence to diet/medications
Uncontrolled hypertension
Acute renal failure
Pulmonary embolus

Skills:
History:
Dyspnea:
Subjective experience of breathing discomfort consisting of qualitatively distinct
sensations varying in intensity.
Etiology: Multiple physiological, psychological, social, and environmental factors.
85% accounted for by:
Congestive heart failure (CHF)
Asthma
Chronic obstructive pulmonary disease (COPD)
Pneumonia
Cardiac ischemia
Interstitial lung diseases
Psychogenic causes
Other important causes:
Anemia
Pulmonary embolus
Pneumothorax
Malignancy
Valvular disorders
Metabloic acidosis
Arrhythmias
Neuromuscular disorders
Orthopnea: Shortness of breath that begins or increases when patient lies down
(often accompanied by nocturnal cough; ask if patient has had to sleep on more
than one pillow recently and if this has helped his/her breathing)

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Etiology: Redistribution of fluid from the splanchnic circulation and lower

extremities into the central circulation during recumbency, with a resultant
increase in pulmonary capillary pressures
Paroxysmal nocturnal dyspnea (PND): Acute episodes of shortness of breath
at night that awakens the patient from sleep usually one to three hours after the
patient retires.
Sitting upright helps in orthopnea but not in PND.
Patients usually open a window to get some fresh air and feel better.
PND is a less common symptom, but specific for heart failure.
Physical exam:
First, observe patient for signs of breathlessness
Listen for audible stridor or wheezing
Volume status can be assessed clinically using orthostatic blood pressure
changes, weight, JVP, and presence of edema in dependent areas with or
without crackles.
Vitals
Look for increased pulse, respiratory rate, and decreased oxygen saturation
Cardiac
Elevated jugular venous pressure (JVP): Increased pressure or volume
overload
Measure elevation of neck veins above the sternal angle and add 5 cm
for distance of right atrium below the sternal angle. (Normal CVP 8
cm H2O.)
Jugular venous distention has 55-65% sensitivity and 74-80%
specificity for increased filling pressure
Tachycardia occurs in 81% of patients with pulmonary embolism
Murmurs
Presence of S3
Specific, but not sensitive, for left ventricular dysfunction
Results from increased atrial pressure leading to increased flow
rates, as seen in CHF
CHF most common cause of a S3
Associated dilated cardiomyopathy with dilated ventricles also
contribute to the sound
Less commonly, valvular regurgitation and left to right shunts
may also result in a S3 due to increased flow (may be a normal
physiological finding in patients less than age 40)
Presence of S4
Lung
Accessory muscle use indicates increased work of breathing

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Wheezes or rhonchi found in

Chronic obstructive pulmonary disease
Crackles found in
Pulmonary edema
Interstitial lung disease (common in patients with interstitial
pulmonary fibrosis to have late inspiratory, fine crackles)
CHF (coarse or fine and mostly occur in the early inspiratory phase of
the cycle)
Abdomen
Hepatomegaly and exaggerated hepatojugular reflux are suggestive of right
heart failure
Extremities
Look for edema or clubbing of the digits
Bilateral lower extremity edema: consider volume overload
Unilateral lower extremity edema: consider deep vein thrombosis with
subsequent pulmonary embolism
Cardiac murmurs:
Systolic: Heard best in right upper sternal border. Most mid-systolic murmurs are
benign.
Aortic stenosis: Systolic ejection murmur radiating to carotids arteries
Aortic sclerosis: Valve thickening without outflow obstruction.
High output states: Anemia, fever, thyrotoxicosis, and pregnancy.
Also, pulmonic stenosis, and hypertrophic cardiomyopathy (consider in
younger patients).
Mitral regurgitation: Pan-systolic murmur heard well in the mitral area.
Diastolic:
Aortic regurgitation - Early diastolic murmur (second left-upper sternal
border).
Differential diagnosis:
1. Congestive heart failure (CHF): Clinical syndrome with many possible
causes. Signs and symptoms include dyspnea, orthopnea, leg edema (from
increased hydrostatic pressure), crackles, S3, elevated JVP, hepatomegaly.
2. Interstitial lung disease: Symptoms and signs are cough, dyspnea, bilateral
crackles.
3. Angina: Can present as dyspnea, an angina equivalent. Can lead to CHF in
the setting of ischemic heart disease and prior myocardial infarction.
4. Chronic kidney disease: Long-standing hypertension can cause renal failure,
which leads to volume overload. In nephrotic syndrome, see edema due to
decreased oncotic pressure from hypoproteinemia. Would expect other

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uremic symptoms (pericardial rub, lethargy, nausea, pruritis).

5. Valvular disease with secondary heart failure: Presentation includes
dyspnea, murmur, and signs of heart failure.
Less likely diagnoses
Pneumonia: Usually accompanied by fever
Pneumothorax: Would expect acute chest pain
Pulmonary hypertension: May be primary or secondary. The most potent stimulus
for causing pulmonary artery vasoconstrictionresulting in pulmonary
hypertensionis hypoxia. Examples of secondary causes are chronic obstructive
pulmonary disease, obstructive sleep apnea, and pulmonary embolus. Pulmonary
hypertension causes right ventricular hypertrophy and cardiac failure. Dyspnea
and edema are symptoms of right heart failure.
Pulmonary embolism: Unlikely if no risk factors and no history of prior deep
venous thrombosis or pulmonary embolism.
Studies:
CBC: Useful to check for anemia.
Basic metabolic panel: Check for electrolyte abnormalities, renal function, and
signs of volume depletion.
B-type natriuretic peptide (BNP) assay: Improves accuracy of diagnosis of
acute heart failure in patients presenting with dyspnea. Most useful when pretest
probability is intermediate for heart failure (high negative predictive value for
diagnosis of heart failure).
BNP is a 32-amino-acid polypeptide secreted by the cardiac ventricles in
response to ventricular volume expansion and pressure overload
Prohormone is cleaved to generate active hormone (BNP) and an N-terminal
biologically inactive fragment (NTproBNP)
Both are then released into bloodstream in 1:1 ratio
Both may be used in diagnosing CHF
BNP <100
BNP 100-500 pg/mL
pg/mL
Heart
failure
unlikely

Clinical judgment and further testing to rule

out stable base-line LV dysfunction and other
conditions as cause of acute dyspnea is
recommended.

BNP >500
pg/mL
Heart
failure
more
likely

BNP can be elevated in:

Women
Renal failure,
Acute coronary syndrome,

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Myocardial infarction,
Right heart strain (due either to pulmonary embolism, COPD, or other
causes of right heart failure)
Levels of BNP correlate with severity of heart failure symptoms and
prognosis, including risk for re-hospitalization and mortality
TSH:
Hyperthyroidism can cause high output heart failure
Severe hypothyroidism can cause congestive heart failure
Echocardiogram: Perform if murmur is:
1.
2.
3.
4.

Symptomatic
Continuous
Diastolic
Intensity > 3/6

Electrocardiogram (ECG): Evaluates for:

Ischemic changes
Ventricular hypertrophy
Signs of old infarction
Arrhythmias
Conduction abnormalities
Chest x-ray: Will show:
Cardiomegaly
Pulmonary vascular congestion (CHF)
Interstitial edema or fibrosis (interstitial lung disease)
Hyperinflation (COPD)
Hampton's hump or Westermark's sign (pulmonary embolism)
Consolidation (pneumonia)
Pneumothorax
Pleural effusions.
Signs of heart failure on chest x-ray ("ChECK"):
Cephalization (Ch): dilation of the pulmonary vessels radiating upward
from the hilum due to fluid overload.
Effusions (look for blunting of the costophrenic angles).
Cardiomegaly (heart shadows occupying >50% of the thoracic
diameter).
Kerley B lines (horizontal, peripheral white markings, especially at the
bases).
Urinalysis: Assess for proteinuria
Liver panel:Assess for hypoalbuminemia
Perform later if initial workup inconclusive:

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Pulmonary function tests: Will identify obstructive or restrictive lung

disease
D-dimer with venous ultrasound: To rule out deep vein thrombosis and
pulmonary embolism

Management:
Hospitalization not necessary if no acute distress, blood pressure stable, and
no hypoxia
Regular physical activity and a moderate-intensity exercise program are
recommended for patients with less severe heart failure after their
symptoms have stabilized and they are euvolemic
Consider referral to a cardiac rehabilitation program can also be considered
Advise patient to restrict salt intake to 2 grams/day and fluid intake to 1.5
to 2.0 L/day. Recommend patients with fluid retention or renal dysfunction
to check their weight each morning
Encourage patients to adhere to medication regimens to optimize risk-factor
control
Keep immunizations up to date, especially influenza and pneumococcal
vaccines
Medications:

Drug class

Morbidity
Mechanism
and
mortality

Comments

ACE inhibitor
Captopril,
Enalapril,
Lisinopril,
Ramipril

Reduces:
Afterload
Sympathetic
activation
Ventricular
remodeling.

ARBs
Candesartan,
Valsartan

For patients
intolerant to
Same as ACE
ACE-I or as
Decreased
inhibitors.
adjunct to
ACE-I and
beta blockers

Decreased

Control blood
pressure
Beta Blockers Decrease
heart rate
Carvedilol,
Effect is dose
Decreased
Reduces
Metoprolol XL,
dependent
effects of
Bisoprolol
sympathetic
activity

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Drug class

Mechanism

Morbidity
and
mortality

Comments

Decreased
morbidity
No effect
on
mortality

Lower digoxin
levels are as
effective as
high levels

Decreases
incidents of
sudden death

Digoxin

In patients
with
sinus rhythm,
improves
myocardial
contractility.

Counteracts
the effects of
aldosterone
(sodium
Aldosterone
retention,
antagonist
potassium
Decreased
Spironolactone, wasting,
Eplerenone
myocardial
hypertrophy,
fibrosis, and
endothelial
dysfunction)

Hydralazine
and
Isosorbide
dinitrate

Hydralazine
reduces
Afterload.
Isosorbide
dinitrate
reduces both
preload and
afterload.

Decreased
morbidity
Decreased
mortality
in
African
Americans

Diuretics
Loop and
Thiazide

Enhance
excretion of
sodium and
water
Block sodium
reabsorption
at specific
sites in renal
tubule.

Decreased
morbidity
No effect
on
mortality

Anticoagulant

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In patients
intolerant to
ACE-I or in
addition to
standard
heart failure
therapy in
AfricanAmericans

Indicated in
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Drug class

Mechanism

Morbidity
and
mortality

Comments
fibrillation,
with LV
thrombus, or
history of
stroke or
pulmonary
embolism

Adverse effects and contraindications of medications used in systolic heart failure:

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Drug class

Adverse effects

Contraindications

ACE inhibitors

Hypotension
Azotemia
Hyperkalemia
Patients with
Angioedema
hypotension,
Non-productive
volume depletion
cough
(due to bradykinins)

ARBs

Hypotension
Azotemia
Hyperkalemia

Beta blockers

Bradycardia
Heart block
Symptomatic
hypotension

Patients with
asthma who
have active
bronchospasm

Aldosterone
antagonists

Severe
hyperkalemia
Spironolactone
Can cause painful
gynecomastia

Patients with
creatinine >
2.5 mg/dL

Diuretics

Electrolyte and
volume depletion
Hypotension
Azotemia

Digoxin

Nausea
Diarrhea
Vision changes
Arrhythmias

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Medications by NYHA Class:

ACE inhibitor, ARB if needed (if cant tolerate ACE inhibitor or

ARB, add nitrate/hydralazine)
Add beta-blocker, as it decreases mortality by 30% (start at
Class I
& II

a low dose after patient is euvolemic and titrate dose up

every 2 weeks until the maximal effective dose is reached.
Add digoxin if patient continues to have symptoms and
recurring hospitalizations
Begin loop diuretic if evidence of fluid overload
Oxygen, if indicated

Class
III or
IV

Spironolactone
Oxygen, if indicated

Neuroendocrine-blocking agents: New, more innovative neuroendocrineblocking agents are being developed, adding strong support to the neurohumoral
hypothesis.
Device therapies: Both devices are expensive; cost varies across the world, but
is generally from $50,000 to $90,000 each.
Implantable cardioverter defibrillator (ICDs)
Prophylactic implantation of an ICD demonstrated a survival benefit in
patients with ischemic cardiomyopathy (with asymptomatic nonsustained
ventricular tachycardia, prior MI, and LVEF 30%) and nonischemic
cardiomyopathy (LVEF 5%)
Biventricular pacemaker
Shown to benefit patients with severe symptoms (NYHA class III or IV) of
heart failure and evidence of ventricular dyssynchrony (left ventricular
enlargement and QRS prolongation >120ms)
Randomized trials showed that cardiac-resynchronization therapy resulted
in:
Reduction in symptoms
Improved functional capacity
Reduction in the number of hospitalizations for worsening heart failure
Increased survival
Discharge criteria: The HFSA (Heart Failure Society of America) guidelines
suggest the following discharge criteria for all patients:

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Exacerbating factors are addressed

At least near-optimal volume status is achieved
Transition from intravenous to oral diuretic is completed
Patient and family education has been completed
Near optimal pharmacological therapy is achieved
A follow-up clinic visit scheduled, usually within 7-10 days
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