Heart Failure

Clinical Manifestation
Diagnosis
Management
Presenter
Edry Joseph
Outline
1. Definition
2. Etiology
3. Pathophysiology
4. Clinical Manifestation
5. History and Exam
6. Work up and Diagnosis
7. Management
 ➢ Pathophysiologic state in which the
heart, via an abnormality of cardiac
function (detectable or not), fails to

What is Heart
pump blood at a rate
commensurate with the

Failure ?
requirements of the metabolizing
tissues

➢ Able to do so only with an elevated

diastolic filling pressure.
Etiology of
Heart Failure
Eccentric
Hypertrophy
Volume overload-induced
cardiac hypertrophy is known as
eccentric
Clinical Manifestation
Acute & Subacute Setting

Pulmonary congestion
Fluid
Retention Hepatic Congestion

Constitutional/ Other
Symptoms
Pulmonary Congestion
Extertional ● Degree of activity necessary
to induce the symptom.
Dyspnea
● Early symptoms of Heart failure
Specificity and sensitivity of 89
Orthopnea ●

and 44 percent

Paroxysmal ● Sensation of shortness of breath

that awakens the patient, often after
Nocturnal 1 or 2 hours of sleep, and is usually
relieved in the upright position.
Dyspnea
 ● Decreased pulmonary function
Dyspnea at secondary to decreased
compliance and increased airway
rest
resistance

Acute
Pulmonary
Edema
Acute Pulmonary edema
➢ It is a medical emergency and has a very dramatic clinical presentation.

➢ Sudden increase in PCWP (usually >25 mm Hg) as a result of acute and fulminant
LV failure

➢ The patient appears extremely ill, poorly perfused, restless, sweaty, tachypneic,
tachycardic, hypoxic, and coughing, with an increased work of breathing and using
respiratory accessory muscles and with frothy sputum that on occasion is blood
tinged.
Hepatic Congestion
Diffuse venous congestion within the liver that results from right-sided heart failure

There can be associated right upper quadrant pain secondary to stretching of the liver
capsule.

Congestive hepatopathy is suspected in patients who have right-sided heart failure,

jaundice, and tender hepatomegaly.
Constitutional/ Other Symptoms
● Anorexia/nausea

● Weight loss/bloating

● Fatigue/weakness

● Oliguria/ nocturia

● Cerebral symptoms of varying severity, ranging from anxiety to memory impairment and

confusion
Chronic Setting
Over time, pulmonary venous capacitance and lymphatic drainage accommodates to the
chronic state of volume overload

Patients in this setting present with excessive fatigue and low-output symptoms, and some
report dyspnea predominantly with exertion rather than at rest or in the supine position

Anorexia is secondary to several factors including poor perfusion of the splanchnic

circulation, bowel edema, and nausea induced by hepatic congestion.
Predominant Right Sided Heart Failure
➢ Right-sided failure may be manifested as peripheral edema with swelling of the legs

(gravity dependent), and ascites, scrotal edema, hepatomegaly, and splenomegaly

History
➢ History alone is insufficient to make the diagnosis of HF

➢ Detailed history remains the single best discriminator to determine

★ Acuity

★ Etiology (Initial +/- precipitating)

★ Rate of progression of HF
Physical Examination
Vital Signs:

Mild or moderate HF: Normal Vital signs

Advanced HF :

★ Resting sinus tachycardia

★ Narrow pulse pressure

★ Diaphoresis

★ Peripheral vasoconstriction
Cardiovascular Exam
Apex beat :

Displaced- indicative of LV enlargement

Cardiovascular Exam
Jugular Venous Pressure

Elevated jugular venous pressure -Manifestation of abnormal right heart dynamics, mostly
commonly reflecting elevated pulmonary capillary wedge pressure from left heart failure

Estimated from the height above the right atrium of venous pulsations in the internal jugular
vein
Jugular Venous Pressure
Cardiovascular Exam
Heart Sounds

S1 and S2 - Normal

S3- left atrial pressures exceeding 20 mmHg and increased LV end-diastolic pressures (>15
mmHg).

S3 has a low sensitivity (eg, 4 to 11 percent) but high specificity (eg, 99 percent) for clinical
diagnosis of HF

Systematic review and individual patient data meta-analysis of diagnosis of heart failure, with modelling of implications of different diagnostic strategies in
primary care.

Health Technol Assess. 2009 Jul;13(32):1-207, iii

Cardiovascular Examination
Pulsus alternans; pulse alternates between a larger and smaller volume on a beat-to-beat
basis and is seen in severe cardiac failure.

Pedal edema; Right sided Heart Failure

Distal pedal pulse ;

May not be present in patients with advanced diseases not being treated with vasodilators
Respiratory Exam
Tachypnea or an increase in respiratory rate above 18 per minute indicates respiratory
distress in heart failure and suggests pulmonary congestion.

Cheyne-Stokes breathing is an ominous sign and is associated with poor outcomes in heart
failure.

Rales/crackles and wheezing; signs of pulmonary edema secondary to elevated left-sided

filling pressure.
Work Up
Electrocardiogram

The presence of left atrial enlargement and left ventricular (LV) hypertrophy (LVH) is
sensitive (although nonspecific) for chronic LV dysfunction

Suggest an acute tachyarrhythmia or bradyarrhythmia as the cause of heart failure.

Diagnosis of acute myocardial ischemia or infarction as the cause of heart failure, or it may
suggest the likelihood of a prior myocardial infarction or the presence of coronary artery
disease as the cause of heart failure.
Laboratory Test
Complete Blood Count

Aids in the assessment of severe anemia, which may cause or aggravate heart failure.

Leukocytosis may signal underlying infection

Laboratory Test
Renal Function

Blood urea nitrogen (BUN) and creatinine levels can be within reference ranges in
patients with mild to moderate heart failure and normal renal function, although
BUN levels and BUN/creatinine ratios may be elevated.
Laboratory Test
Severe heart failure, particularly those on large doses of diuretics for long periods,
may have elevated BUN and creatinine levels indicative of renal insufficiency
owing to chronic reductions of renal blood flow from reduced cardiac output.

Diuresing this group of patients is complex. In some individuals, diuretics will

improve renal congestion and renal function, whereas in others, overaggressive
diuresis may aggravate renal insufficiency due to volume depletion.

Hyponatremia generally indicates severe HF, though other causes should be

considered
Laboratory Test
Liver function test

May be affected by hepatic congestion.

In one study, gamma-glutamyltransferase level >2 times the upper limit of normal
was the only standard initial blood test that added diagnostic value to the history
and physical examination
Laboratory Test
Natriuretic peptide (NP [BNP or NT-proBNP]) levels provide evidence as to
whether HF is present

NP levels are often (but not exclusively) elevated in patients with HFrEF, but may
be normal in a substantial number of patients with HFpEF. Thus, the presence of
an elevated NP level increases the likelihood that HF is present, but a normal level
does not exclude it, particularly in patients with a normal LVEF or obesity.
Chest radiography
Findings suggestive of HF include:

1. Cardiomegaly (cardiac to thoracic width ratio above 50 percent),

2. Cephalization of the pulmonary vessels
3. Kerley B-lines
4. Pleural effusions
Echocardiogram
Two-dimensional (2-D) echocardiography is recommended in the initial evaluation
of patients with known or suspected heart failure.

An echocardiogram alone does not establish or exclude the diagnosis of HF but is

helpful to identify findings consistent with HF and to identify potential causes of HF

Doppler and 2-D echocardiography may also be used to determine both systolic
and diastolic left ventricular (LV) performance, cardiac output (ejection fraction),
and pulmonary artery and ventricular filling pressures. In addition,
echocardiography may be used to identify clinically important valvular disease
Approach to Diagnosis
Management
NON PHARMACOLOGICAL

Physical activity

-2012 meta-analysis showed that aerobic exercise training, particularly over

the long term, can reverse left ventricular remodelling in clinically stable heart
failure patients

Whereas strength training had no effect on remodelling.

Management
Dietary Modification

➢ Dietary sodium restriction to 2-3 g/day

➢ Fluid restriction to 2 L/day is recommended for patients with evidence of

hyponatremia (Na < 130 mEq/dL) and for those whose fluid status is difficult

to control despite sodium restriction and the use of high-dose diuretics.

➢ Caloric supplementation is recommended for patients with evidence of

cardiac cachexia.
Pharmacological management
Pharmacologic therapy of HFrEF

➢ Improve symptoms

➢ Slow or reverse deterioration in myocardial function

➢ Reduce mortality
Initial Therapy
A combination of:

Diuretic therapy + a renin-angiotensin system inhibitor (ARNI,

ACE inhibitor, or single agent ARB) + a beta blocker.

Alternative;

Hydralazine + nitrate if angiotensin system blocker is not tolerated. T

Secondary therapy
Selected patients with HFrEF

➢ Mineralocorticoid receptor antagonist

➢ Ivabradine
➢ Dapagliflozin
➢ Hydralazine plus nitrate (in addition to initial therapy with an
angiotensin system blocker or hydralazine plus nitrate)
➢ Digoxin.
Device Therapy
Devices recommended in selected patients with HF include the
following:

➢ An implantable cardioverter-defibrillator (ICD) for primary or

secondary prevention of sudden cardiac death ●
➢ Cardiac resynchronization therapy (CRT) with biventricular pacing
is indicated in selected patients with HFrEF with a prolonged QRS
duration. Most patients who satisfy criteria for CRT implantation
are also candidates for an ICD and receive a combined device.
Ventricular assist device
To support the acutely or chronically decompensated heart (ie,
American College of Cardiology/American Heart Association
[ACC/AHA] stage D)

Depending on the particular device used, the right ventricle (RV) and
left ventricle (LV) can be assisted with a LV assist device (LVAD), a
RVAD, or a biventricular assist device (BiVAD
Summary
➢ Heart failure is a very complex and multifactorial disorder

➢ In acute settings patients experience fluid retention and may

present in a number of ways

➢ Management is focused on symptomatic relief, improving mortality

rate and slowing myocardial deteriorating .