0% found this document useful (0 votes)
36 views

Congestive Heart Failure: Dr. Asif Wazir

Uploaded by

Hillary Bushnell
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
0% found this document useful (0 votes)
36 views

Congestive Heart Failure: Dr. Asif Wazir

Uploaded by

Hillary Bushnell
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
You are on page 1/ 21

Congestive Heart Failure

Dr. Asif Wazir


General Characteristics
1.CHF is a clinical syndrome resulting from the heart’s inability to
meet the body’s circulatory demands under normal physiologic
conditions. It is the final common pathway for a wide variety of
cardiac diseases (see also
2.Pathophysiology
a.Frank–Starling relationship
• In a normal heart, increasing preload results in greater
contractility.
• When preload is low (at rest), there is little difference in
performance between a normal and a failing heart. However,
with exertion a failing heart produces relatively less contractility
and symptoms occur
Frank–Starling relationship
3.Heart Failure with reduced Ejection Fraction (HFrEF) or
systolic dysfunction
a.Owing to impaired contractility (reduced EF <40%)
b.Causes include:
• Ischemic heart disease or after a recent MI—infarcted
cardiac muscle does not pump blood (decreased EF)
• idiopathic
• HTN
• Myocarditis (postviral, giant cell, autoimmune)
• Drugs: Alcohol, cocaine, methamphetamines, chemotherapy
(anthracyclines and trastuzumab)
• Infiltrative disease (amyloidosis, sarcoidosis,
hemochromatosis, Wilson
• disease) Radiation therapy
Thyroid disease
• Peripartum cardiomyopathy
4.Heart Failure with preserved Ejection Fraction (HFpEF) or diastolic
dysfunction
a.Owing to impaired ventricular filling during diastole (either impaired
relaxation or increased stiffness of ventricle or both).
b.Echocardiogram shows impaired relaxation of left ventricle.
c.Causes include:
• HTN leading to myocardial hypertrophy—most common cause
of diastolic dysfunction
• Valvular diseases such as aortic stenosis (AS), mitral stenosis,
and aortic
• regurgitation
• Restrictive cardiomyopathy (e.g., amyloidosis, sarcoidosis,
hemochromatosis in their early phases)
Clinical Features
1.Symptoms of left-sided heart failure
a.Dyspnea—difficulty breathing secondary to pulmonary congestion/edema
b.Orthopnea—difficulty breathing in the recumbent position; relieved by
elevation of the head with pillows
c.Paroxysmal nocturnal dyspnea (PND)—awakening after 1 to 2 hours of
sleep
due to acute shortness of breath (SOB)
d.Nocturnal cough (nonproductive)—worse in recumbent position (same
pathophysiology as orthopnea)
e.Confusion and memory impairment occur in advanced CHF as a result
of
inadequate brain perfusion
f.Diaphoresis and cool extremities at rest—occur in desperately ill
patients (NYHA class IV)
2.Signs of left-sided heart failure
a.Displaced PMI (usually to the left) due to cardiomegaly
b.Pathologic S3 (ventricular gallop)
• Rapid filling phase “into” a noncompliant left ventricular chamber
• May be normal finding in children; in adults, usually associated
with CHF May be difficult to hear, but is among the most
specific signs of CHF Heard best at apex with bell of
stethoscope
• The sequence in the cardiac cycle for S3: S3 follows S2 (ken-tuck-
Y)
c.S4 gallop
• Sound of atrial systole as blood is ejected into a noncompliant, or stiff,
left ventricular chamber
• Heard best at left sternal border with bell of stethoscope
• The sequence in the cardiac cycle for S4: S4 precedes S1 (TEN-nes-see)
d.Crackles/rales at lung bases
• Caused by fluid spilling into alveoli; indicates pulmonary edema
• Rales heard over lung bases suggest at least moderate severity of left
ventricular heart failure
e.Dullness to percussion and decreased tactile fremitus of lower lung fields
caused by pleural effusion
f.Increased intensity of pulmonic component of second heart sound suggests
pulmonary HTN (heard over left upper sternal border)
3.Symptoms/signs of right-sided heart failure
a.Peripheral pitting edema—pedal edema lacks specificity as an isolated
finding.
In the elderly, it is more likely to be secondary to venous insufficiency
b.Nocturia—due to increased venous return with elevation of legs
c.Jugular venous distention (JVD)
d.Hepatomegaly/hepatojugular reflux
e.Ascites
f.Right ventricular heave (found with pulmonary HTN)
4.Given enough time, left-sided heart failure can lead to right-sided heart
failure (most common cause right-sided heart failure)
a.Patients may present with sign/symptoms of both right- and left-sided HF
Diagnosis
1.Chest x-ray (CXR)
a.Cardiomegaly
b.Kerley B lines are short horizontal lines near periphery of the lung near the costophrenic
angles, and indicate pulmonary congestion secondary to dilation of pulmonary lymphatic
vessels
c.Prominent interstitial markings
d.Pleural effusion
2.Echocardiogram (transthoracic)
a.Initial test of choice—should be performed whenever CHF is suspected based on history,
examination, or CXR.
b.Useful in determining whether systolic or diastolic dysfunction predominates,
and determines whether the cause of CHF is due to a myocardial, valvular, or pericardial
process.
c.Estimates EF (very important): Patients with systolic dysfunction (EF <40%) should be
distinguished from patients with preserved left ventricular function (EF >40%).
d.Shows chamber dilation and/or hypertrophy.
3.B-type natriuretic peptide (BNP) is released from the ventricles in
response to ventricular volume expansion and pressure overload.
a.BNP levels >100 pg/mL correlate strongly with the presence of
decompensated CHF. (Unit of measurement varies.)
b.BNP may be useful in differentiating between dyspnea caused by CHF
and
COPD.
c.N-terminal pro-BNP (NT-proBNP) is a newer assay with similar predictive
value as BNP. The normal range for this value depends on the age of the
patient, but an NT-proBNP <300 virtually excludes the diagnosis of HF.
d.BNP may be falsely low in obese patients.

4. ECG is usually nonspecific but can be useful for detecting chamber


enlargement and presence of ischemic heart disease or prior MI.
5.Radionuclide ventriculography using technetium-99m (“nuclear
ventriculography”). Also called multigated acquisition (MUGA)
scan.
6.Cardiac catheterization can provide valuable quantitative
information regarding
diastolic and systolic dysfunction, and can clarify the cause of CHF if
noninvasive test results are equivocal. Consider coronary angiography to
exclude CAD as an underlying cause of CHF.
7.Stress testing
a.Identifies ischemia and/or infarction
b.Quantifies level of conditioning
c.Can differentiate cardiac versus pulmonary etiology of dyspnea
d.Assesses dynamic responses of HR, heart rhythm, and BP
Treatment
1.Systolic dysfunction
a.General lifestyle modification
• Sodium restriction (less than 4 g/day)
• Fluid restriction (1.5 to 2.0 L daily)
• Weight loss
• Smoking cessation
• Restrict alcohol use
• Exercise program
• All patients should monitor weight daily
to detect fluid accumulation
• Annual influenza vaccine and
pneumococcal vaccine recommended
b.Diuretics
• Most effective means of providing symptomatic relief to patients
with moderate to severe CHF
• Recommended for patients with systolic failure and volume
overload
Have not been shown to reduce mortality or improve prognosis,
just for symptom control. Goal is relief of signs and symptoms of
volume overload (dyspnea, peripheral edema)
• Loop diuretics: Furosemide (Lasix)—usually used. Other options
include bumetanide (Bumex) and torsemide
• Thiazide-like diuretics: Metolazone and chlorothiazide. Used to
augment diuresis with loop diuretics
Therapies to improve outcomes: Standard therapy includes the following
(medications in parentheses have been shown to improve mortality in
HFrEF):
• ACE inhibitor (enalapril, lisinopril, captopril) or ARB (valsartan,
losartan, candesartan)
• β-Blockers (metoprolol succinate, carvedilol, bisoprolol)
• Aldosterone antagonists (spironolactone, eplerenone)
• Primary prevention of sudden cardiac death with ICD implantation if
EF <35% on optimal medical therapy
• Hydralazine and nitrates (isosorbide dinitrate)
• Ivabradine is a funny channel inhibitor that has been shown to reduce
hospitalizations in patients with reduced EF and HR >70
• Digoxin was once regularly used for HFrEF, but has not been
shown to improve mortality
2.HFpEF: Few therapeutic options available; patients are treated
symptomatically
(NO medications have proven mortality benefit)
• Diuretics are used for symptom control (volume overload)
• Patients should continue salt and fluid restriction, take daily
weights
• No other drug classes have been shown to produce significant
mortality benefit in randomized controlled trials
Acute Decompensated Heart Failure
Findings:
A.Acute dyspnea associated with elevated left-sided filling pressures, with or
without pulmonary edema.
B.Most commonly due to LV systolic or diastolic dysfunction.
C.Flash pulmonary edema refers to a severe form of heart failure with
rapid accumulation of fluid in the lungs.
Diagnosis
D.Differential includes pulmonary embolism, asthma, and pneumonia, all of
which can cause rapid respiratory distress.
E.Diagnostic tests include ECG, CXR, ABG, B-type natriuretic peptide
(BNP),
echocardiogram, and possible coronary angiogram if indicated.
Treatment
A.Oxygenation and ventilatory assistance with nonrebreather face mask,
noninvasive positive pressure ventilation, or even intubation as indicated.
B.Diuretics to treat volume overload and congestive symptoms—this is the
most
important intervention. Decreases preload.
C.Nitrates—IV nitroglycerin (venodilator) in patients without
hypotension. Decreases preload.
D.Patients who have pulmonary edema despite use of oxygen,
diuretics, and nitrates
may benefit from use of inotropic agents (dobutamine). Digoxin takes
several weeks to work and is not indicated in an acute setting.
E.Dietary sodium and fluid restriction.
THANK YOU

You might also like