Congestive Heart Failure
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Transcript Congestive Heart Failure
Heart Failure
Heart Failure
Clinical syndrome that develops when the
heart cannot maintain adequate output, or
can do so only at the expense of elevated
ventricular filling pressure.
Heart Failure
Results from any structural or
functional abnormality that impairs
the ability of the ventricle to eject
blood (Systolic Heart Failure) or
to fill with blood (Diastolic Heart
Failure).
The prevalence of heart failure rises with age
Almost all forms of heart disease can lead to
heart failure.
Mechanisms of heart failure
Reduced ventricular contractility
CAD (segmental dysfunction) ‘cardiomyopathy(global dysfunction)
o
Ventricular outflow obstruction
Hypertension, aortic stenosis
(left heart failure)
Pulmonary hypertension, pulmonary stenosis (right heart failure).
Ventricular inflow obstruction Mitral stenosis,tricuspid
stenosis
Ventricular volume overload Ventricular septal defect.
Arrhythmia Atrial fibrillation ,Tachycardia cardiomyopathy
Complete heart block Bradycardia.
Diastolic dysfunction
Constrictive pericarditis, Restrictive cardiomyopathy
Cardiac tamponade.
Pathophysiology
Cardiac output is determined by preload (the volume
and pressure of blood in the ventricles at the end of
diastole) afterload (the volume and pressure of blood
in the ventricles during systole) and myocardial
contractility.
Fall in cardiac output. activates counterregulatory neurohumoral
mechanisms , renin–angiotensin–aldosterone system leads to
vasoconstriction, sodium and water retention, and sympathetic
nervous system activation. Activation of the sympathetic nervous
system may initially sustain cardiac output through increased
myocardial contractility (inotropy)and heart rate (chronotropy).
Prolonged sympathetic stimulation also causes negative effects,
including cardiac myocyte apoptosis,hypertrophy and focal
myocardial necrosis. Sympathetic stimulation also causes
peripheral vasoconstriction and arrhythmias.
The Vicious Cycle of Congestive Heart
Failure
LV Dysfunction causes
Decreased cardiac output
Decreased Blood Pressure and
Decreased Renal perfusion
Stimulates the Release
of renin, Which allows
conversion of
Angiotensin
to Angiotensin II.
Angiotensin II stimulates
Aldosterone secretion which
causes retention of
Na+ and Water,
increasing filling pressure
Types of Heart Failure
-Left, right and biventricular heart failure.
-Diastolic and systolic dysfunction.
-High-output failure.
-Acute and chronic heart failure.
Causes of Low-Output Heart Failure
chronic
Systolic Dysfunction
Coronary Artery Disease
Idiopathic dilated cardiomyopathy (DCM)
Hypertension
Valvular Heart Disease
Diastolic Dysfunction
Hypertension
Coronary artery disease
Hypertrophic obstructive cardiomyopathy (HCM)
Restrictive cardiomyopathy
Acute Decompensaated Heart Failure
Causes:
Acute MI
Rupture of chordae tendinae/acute mitral
valve insufficiency
Volume Overload
Transfusions, IV fluids
Worsening valvular defect
Pulm.embolism
Myocarditis
Factors that may precipitate or aggravate
heart failure in pre-existing heart disease
Myocardial ischaemia or infarction
Intercurrent illness, e.g. infection
Arrhythmia, e.g. atrial fibrillation
Inappropriate reduction of therapy
Administration of a drug with negative inotropic (βblocker)or fluid-retaining properties (NSAIDs,
corticosteroids)
Pulmonary embolism
Conditions associated with increased metabolic
demand, e.g. pregnancy, thyrotoxicosis, anaemia
IV fluid overload, e.g. post-operative IV infusion
Clinical Presentation of HeartFailure(Acute)
Sudden onset of dyspnoea that rapidly progresses to
acute respiratory distress, orthopnoea and cough.
The patient appears agitated, pale and clammy. The
peripheries are cool to the touch and the pulse is
rapid.The BP is usually high, The jugular venous
pressure (JVP) is usually elevated.
Auscultation A ‘gallop’rhythm, with a third heart
sound,is heard. A new systolic murmur may signify
acute mitral regurgitation or ventricular septal rupture.
crepitations at the lung bases, or throughout the
lungs if pulmonary oedema is severe.
Clinical Presentation of Heart Failure(Chronic)
Due to excess fluid accumulation:
Dyspnea (most sensitive symptom
Orthopnea, Paroxysmal Nocturnal Dyspnea (PND)
Edema
Hepatic congestion
Ascites
Due to reduction in cardiac ouput:
Fatigue (especially with exertion)
Weakness
Poor renal perfusion leads to oliguria and uraemia
Chronic heart failure is sometimes associated with
marked weight loss (cardiac cachexia).
Physical Examination in Heart Failure
Dyspniac
Cool, pale, cyanotic extremities
Have sinus tachycardia, diaphoresis and peripheral vasoconstriction
Displaced Apex
S3 gallop Low sensitivity, but highly specific
Crackles or decreased breath sounds at bases (effusions) on
lung exam
Elevated jugular venous pressure
Lower extremity edema
Ascites
Hepatomegaly
Splenomegaly
Measuring Jugular Venous Pressure
Complications
Renal failure
Hypokalaemia
Hyperkalaemia
Hyponatraemia
Impaired liver function
Thromboembolism
Atrial and ventricular arrhythmias
Impaired liver function
Lab Analysis in Heart Failure
CBC
Serum electrolytes and creatinine
To evaluate for possible diabetes mellitus
Thyroid function tests
before starting high dose diuretics
Fasting Blood glucose
Since anemia can exacerbate heart failure
Since thyrotoxicosis can result in A. Fib,
and hypothyroidism can results in HF.
Iron studies
To screen for hereditary hemochromatosis as cause of heart failure.
To evaluate for possible lupus
ANA
Viral studies
BNP
If viral mycocarditis suspected
brain natriuretic pepetide
Chest X-ray in Heart Failure
Cardiomegaly
Cephalization of the pulmonary
vessels
Kerley B-lines
Pleural effusions
Cardiomegaly
Pulmonary vessel congestion
Pulmonary Edema due to Heart Failure
Kerley B lines
Further Cardiac Testing in Heart
Failure
Exercise Testing
Should be part of initial evaluation of all patients
with CHF.
Coronary arteriography
Should be performed in patients presenting with
heart failure who have angina or significant
ischemia.
Endomyocardial biopsy
Not frequently used
Really only useful in cases such as viral-induced
cardiomyopathy
.
Cardiac Testing in Heart Failure
Electrocardiogram:
May show specific cause of heart
failure:
Ischemic heart disease
Dilated cardiomyopathy: first degree AV
block, LBBB, Left anterior fascicular block
Echocardiogram:
Left ventricular ejection fraction
Structural/valvular abnormalities
Management of acute HF
acute medical emergency:
Sit the patient up to reduce pulmonary Congestion.
Give oxygen (high-flow, high-concentration).
IV frusemide 50-100 mg
Administer nitrates, such as IV glyceryl trinitrate
until clinical improvement occurs or systolic BP falls.
Continuous monitoring of cardiac rhythm, BP .
Intravenous opiates must be used sparingly in
distressed patients.
If these measures prove ineffective, inotropic agents
may be required to augment cardiac output,
particularly in hypotensive patients ( Dopamine).
Management of chronic heart failure
General measures
Drug therapy
Device therapy
Cardiac transplant
General measures
Education
Diet
•Good general nutrition and weight reduction for the obese
•Avoidance of high-salt foods and added salt.
Alcohol
Smoking
Exercise
•Regular moderate aerobic exercise within limits of symptoms
Vaccination
•Consider influenza and pneumococcal vaccination
Treatment of the underlying cause of heart failure (CAD)
Drug therapy
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Loop diuretics
ACE inhibitor (or ARB if not
tolerated)
Beta blockers
Digoxin
Hydralazine, Nitrate
Potassium sparing diuretcs
Ivabradine
Diuretics
Loop diuretics
Furosemide, buteminide
diuretics produce an increase in urinary
sodium and water excretion, leading to
reduction in blood and plasma volume
Potassium-sparing diuretics
Spironolactone, eplerenone
Help enhance diuresis
Maintain potassium
Shown to improve survival in CHF
ACE Inhibitor
Improve survival in patients with all
severities of heart failure.
Begin therapy low and titrate up as
possible:
Enalapril – 2.5 mg po BID
Captopril – 6.25 mg po TID
Lisinopril – 5 mg po QDaily
If cannot tolerate, may try ARB
Beta Blocker therapy
Certain Beta blockers (carvedilol,
metoprolol, bisoprolol) can increase
ejection fraction, improve symptoms,
reduce the frequency of hospitalisation and
reduce mortality.
Contraindicated:
Heart rate <60 bpm
Symptomatic bradycardia
Signs of peripheral hypoperfusion
COPD, asthma
PR interval > 0.24 sec, 2nd or 3rd degree block
Hydralazine plus Nitrates
Dosing:
Hydralazine
Isosorbide dinitrate
Started at 25 mg po TID, titrated up to 100
mg po TID
Started at 40 mg po TID/QID
Decreased mortality, lower rates of
hospitalization, and improvement in
quality of life.
Ivabradine
It reduces hospital admission and
mortality rates in patients with heart
failure due to moderate or severe left
ventricular systolic impairment.
Other medication in Heart Failure
Digoxin can be used to provide rate control in
patients with heart failure and atrial fibrillation. In
patients with severe heart failure, digoxin reduces
the likelihood of hospitalisation for heart failure,
Statin therapy is recommended in CHF for
the secondary prevention of cardiovascular
disease.
Some studies have shown a possible benefit
specifically in HF with statin therapy
Meds to AVOID in heart failure
NSAIDS
Thiazolidinediones
Can cause worsening of preexisting HF
Include rosiglitazone (Avandia), and
pioglitazone (Actos)
Cause fluid retention that can exacerbate HF
Metformin
People with HF who take it are at increased
risk of potentially lethic lactic acidosis
Implantable Cardioverter-Defibrillators
for HF( ICD) -CRT
Sustained ventricular
tachycardia is associated with
sudden cardiac death in HF.
About one-third of mortality in
HF is due to sudden cardiac
death.
Patients with ischemic or
nonischemic cardiomyopathy,
NYHA class II to III HF, and
LVEF ≤ 35% have a significant
survival benefit from an
implantable cardioverterdefibrillator (ICD) for the
primary prevention of SCD.
Cardiac-Resynchronization-Therapy
Management of Refractory Heart
Failure
Inotropic drugs:
Mechanical circulatory support:
Dobutamine, dopamine, milrinone,
nitroprusside, nitroglycerin
Intraaortic balloon pump
Left ventricular assist device (LVAD)
Cardiac Transplantation