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Transcript
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 counter regulatory 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
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 output:
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
Complications







Renal failure
Hypokalaemia
Hyperkalaemia
Hyponatraemia
Impaired liver function
Thromboembolism
Atrial and ventricular arrhythmias
Lab Analysis in Heart Failure

CBC
Since anemia can exacerbate heart failure
Serum electrolytes and creatinine
 before starting high dose diuretics
Fasting Blood glucose
 To evaluate for possible diabetes mellitus
Thyroid function tests
 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.
ANA
 To evaluate for possible lupus
Viral studies If viral mycocarditis suspected








BNP
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
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
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

Management of acute HF








acute medical emergency:
Sit the patient up to reduce pulmonary Congestion.
Give oxygen (high-flow, high-concentration).
IV diuretics (lasix)
Continuous monitoring of cardiac rhythm, BP .
Administer nitrates, such as IV glyceryl trinitrate until
clinical improvement occurs or systolic BP falls.
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 cessation
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
1.
2.
3.
4.
5.
6.
ACE inhibitor (or ARB if not tolerated)
Beta blockers
Potassium sparing diuretics
Hydralazine, Nitrate
Loop diuretics
Digoxin
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 Q Daily


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.
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 lethal 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