CONGESTIVE HEART FAILURE

Alda Olvia 17310021

Lulu Rif’atunnissa 17310055
Intan Utami Putri 17310132
Richard E. Langingi 17310239
 A 66-year-old woman presents to your office complaining of
shortness of breath and bilateral leg edema that have
been worsening for 3 months. She emphatically tells you, “I
get out of breath when I do housework and I can’t even walk to
the corner.” She has also noticed difficulty sleeping
secondary to a dry cough thatwakes her up at night and
further exacerbation of her shortness of breath while lying
flat. This has forced her to use three pillows for a good night’s
sleep. She denies any chest pain, wheezing, or febrile illness.
She has no past illnesses and takes no medications. She’s never
smoked and drinks socially. On examination, her blood
pressure is 187/90 mm Hg, her pulse is 97 bpm, her
respiratory rate is 16 breaths per minute, her
temperature is 98°F (36.6°C), and her oxygen saturation
is 93% on room air by pulse oximetry. She has a pronounced
jugular vein. Cardiac examination reveals a pansystolic
murmur. Examination of her lung bases produces dullness
bilaterally. You find 2+ pitting edema of both ankles. An
ECG shows a normal sinus rhythm and a chest x-ray
demonstrates mild cardiomegaly with bilateral pleural
effusions. You decide she needs further workup, so you call
the hospital where you have admitting privileges and arrange
for a telemetry bed.
 1. What is the most likely diagnosis?
 2. What is the next diagnostic step?

 3. What is the initial step in therapy?

KEYWORD
 A 66 year-old woman
 Shortness of breath and bilateral leg the have been
worsening for 3 months
 Get out of breath when l do housework and l can’t even
walk to the corner
 Noticed difficulty sleeping secondary to a dry cough
 Blood pressure is 187/90 mm Hg, her pulse is 97 bpm, her
respiratory rate is 16 breaths per minute
 Oxygen saturation is 93% on room air by pulse oximetry
 She has a pronounced jugular vein
 Cardiac examination reveals a pansystolic murmur
 Examination of her lung bases produces dullness
bilaterally
 An ECG shows a normal sinus rhythm and a chest x-ray
demonstrates mild cardiomegaly with bilateral pleural
effusions
PROBLEM

A 66 years old woman presents to your office

complaining of a shortness of breath and bilateral
leg edema that have been worsening for 3 months
DD
 Pulmonary edema
 Pleura effusion

 Coronary thrombosis

 Congestive heart failure

HIPOTESIS
 A 66 years old woman presents to your office
complaining of a shortness of breath and bilateral
leg edema that have been worsening for 3 months
because of Congestive heart failure
LEARNING ISSUE
1. DEFINITION
Chronic heart failure (CHF) is a progressive
syndromethat results in a poor quality of life for
the patient andplaces an economic burden on the
health care system. Despiteadvances in the control
of cardiovascular diseases suchas myocardial
infarction (MI), the incidence and prevalenceof
CHF continue to increase.
2. CLASSIFICATION
The New York Heart Association (NYHA) functional
classification defines four functional classes as:
 Class I: HF does not cause limitations to physical
activity; ordinary physical activity does not cause
symptoms.
 Class II: HF causes slight limitations to physical
activity; the patients are comfortable at rest, but
ordinary physical activity results in HF symptoms.
 Class III: HF causes marked limitations of physical
activity; the patients are comfortable at rest, but less
than ordinary activity causes symptoms of HF.
 Class IV: HF patients are unable to carry on any
physical activity without HF symptoms or have
symptoms when at rest.
3. ETIOLOGY
Heart failure is caused by several disorders,
including diseases affecting the pericardium,
myocardium, endocardium, cardiac valves,
vasculature, or metabolism. The most common
causes of systolic dysfunction (HFrEF) are
idiopathic dilated cardiomyopathy (DCM), coronary
heart disease (ischemic), hypertension, and
valvular disease. For diastolic dysfunction
(HFpEF), similar conditions have been described as
common causes, adding hypertrophic obstructive
cardiomyopathy, and restrictive cardiomyopathy.
4. EPIDEMIOLOGY
Approximately 5.1 million people in the United
States have clinically manifest heart failure, and
the prevalence continues to increase. Heart
failure incidence has remained stable over the past
decades, with more than 650,000 new cases heart
failure cases diagnosed annually, especially for
individuals greater than 65 years of age. Because
prevalence is greater in this age group, heart
failure is expected to worsen in the future.
5. PATOFISIOLOGY
The adaptive mechanisms that may be adequate to
maintain the overall contractile performance of the heart at
relatively normal levels become maladaptive when trying to
sustain adequate cardiac performance. The primary myocardial
response to chronically increased wall stress is myocyte
hypertrophy, death due to apoptosis, and regeneration. This
process eventually leads to remodeling, usually the eccentric
type, and reduced cardiac output, causing a cascade of the
neurohumoral and vascular mechanism.
Decreased carotid baroreceptor stimulation and renal
perfusion will activate the sympathetic nervous system and
Renin-Angiotensin-Aldosterone system. Sympathetic nervous
system activation will cause increased heart rate and inotropy,
leading to myocardial toxicity. Renin-Angiotensin-Aldosterone
system activation leads to vasoconstriction, increasing afterload
(angiotensin II) and hemodynamic alterations, increasing
preload (aldosterone). All of these mechanisms will cause
6. SYMPTOMPS
Symptoms of heart failure include those due
to excess fluid accumulation (dyspnea, orthopnea,
edema, pain from hepatic congestion, and
abdominal distention from ascites) and those due to
a reduction in cardiac output (fatigue, weakness)
that is most pronounced with physical exertion.
Acute and subacute presentations (days to
weeks) are characterized by shortness of breath at
rest and/or with exertion, orthopnea, paroxysmal
nocturnal dyspnea, and right upper quadrant
discomfort due to acute hepatic congestion
(right heart failure). Palpitations, with or without
lightheadedness can occur if patient develops atrial
or ventricular tachyarrhythmias.
7. EVALUATION
 Tests include:
 Electrocardiogram (ECG): important for identifying
evidence of acute or prior myocardial infarction or acute
ischemia, also rhythm abnormalities, such as atrial
fibrillation.
 Chest x-ray: characteristic findings are cardiac-to-thoracic
width ratio above 50%, cephalization of the pulmonary
vessels, Kerley B-lines, and pleural effusions.
 Blood test: Cardiac troponin (T or I), complete blood count,
serum electrolytes, blood urea nitrogen, creatinine, liver
function test and brain natriuretic peptide (BNP). BNP (or
NT-proBNP) level adds greater diagnostic value to the
history and physical examination than other initial tests
mentioned above.
 Transthoracic Echocardiogram: to determine ventricular
function and hemodynamics.
8. DIAGNOSIS
Framingham criteria, widely used in clinical
research, comprise a series of major and minor cri teria
that aid in the diagnosis of heart failure and emphasize
the importance of jugular venous pressure elevation, an
S3 gallop, and a positive hepatojugular reflex in
establishing a diagnosis, while minimizing the
importance of lower extremity edema.The use of brain-
type natriuretic peptides, intheir active or inactive
circulating forms, has evolved during the past decade,
but the most well-established use remains in
discriminating between causes of dyspnea when the
diagnosis is in doubt. Comorbid conditions must be
taken into account because renal insufficiency increases
these levels and obesity lowers them.
9. MANAGEMENT
 a. Diuretics(thiazides,loop diureticsand potassium
sparing)(toreducetheedemabythe reductionof blood
volumeand venouspressure)and salt restriction(to
reducefluid retention)inpatientswith
currentorpreviousheartfailuresymptomsand
reducedleft ven tricularejectionfraction (LVEF)for
symptomaticrelief.
 b. Angiotensin-convertingenzymeinhibitors(ACEIs)or
angiotensinreceptorblockers(ARBs) forneuro-
hormonalmodification,vasodilatationandimprovement
inLVEF (substitutethem withhydralazineand/or
nitratesinpatients unresponsivetoACEIsandARBs).
 c. Beta-adrenergicblockersforneuro-hormonal
modification,improvementinsymptomsandLVEF,
survivalbenefit,arrhythmiapreventionandcontrol of
ventricularrate.
THANK YOU