Heart Failure Dz

HEART FAILURE

Dr. Dian Zamroni, Sp.JP, FIHA

Definition of heart failure

• Clinical syndrome that can result from any structural or

functional cardiac disorder that impairs the ability of the

ventricle to fill with or eject blood

• A syndrome caused by cardiac dysfunction

- Generally resulting from myocardial muscle dysfunction or loss

- Characteristic by left ventricular dilatation or hypertrophy

- Leading to neurohormonal and circulatory abnormalities and

characteristic symptoms :

- fluid retention

- shortness of breath

- fatique, especially on exertion

AHA / ACC HF guidelines 2001

HFSA guideline 2006

EPIDEMIOLOGY

Definition of heart failureCriteria 1 and 2 should be fulfilled in all cases

1. Symptoms of heart failure(at rest or during exercise)

And

2. Objective evidence of cardiac

dysfunction(at rest)

And

(in case where the diagnosis is in doubt)

3. Response to treatment directed

towards heart failure

SYMPTOM & SIGN HEART FAILURE

Framingham Criteria for Dx of

Heart Failure• Major Criteria:

– PND

– JVD

– Rales

– Cardiomegaly

– Acute Pulmonary Edema

– S3 Gallop

– Positive hepatic Jugular reflex

– ↑ venous pressure > 16 cm H2O

Dx of Heart Failure (cont.)

• Minor Criteria

LL edema,

Night cough

Dyspnea on exertion

Hepatomegaly

Pleural effusion

↓ vital capacity by 1/3 of normal

Tachycardia 120 bpm

Weight loss 4.5 kg over 5 days management

DIAGNOSTIC• Suspected Heart Failure because of

SYMPTOMS and/or SIGNS

Assess presence of CARDIAC DISEASE

by ECG, X-Ray or BNP (if available)

VENTRICULAR FUNCTION Imaging by ECHO-Doppler,

Nuclear angiography or MRI if available

Heart Failure: Systolic / DiastolicIdentify etiology, evaluate severity, choose therapy

ESC HF guidelines 2001

Tests abnormal

Tests abnormal

NORMAL

No Heart Failure

NORMAL

No Heart Failure

Heart Failure

• What Causes Heart Failure?

– Coronary artery disease

• Cholesterol and fatty deposits build up in

the heart’s arteries

• Less blood and oxygen reach the heart

muscle

• This causes the heart to work harder and

occasionally damages the heart muscle

Heart Failure

• What Causes Heart Failure?

– Heart attack

• An artery supplying blood to the heart

becomes blocked

• Loss of oxygen and nutrients damages

heart muscle tissue causing it to die

• Remaining healthy heart muscle must pump

harder to keep up

Heart Failure

• What Causes Heart Failure?– High blood pressure

• Uncontrolled high blood pressure doubles a

persons risk of developing heart failure

• Heart must pump harder to keep blood

circulating

• Over time, chamber first thickens, then gets

larger and weaker

Heart Failure

• What Causes Heart Failure?– Abnormal heart valves

– Heart muscle disease

• Damage to heart muscle due to drugs,

alcohol or infections

– Congenital heart disease

– Severe lung disease

Heart Failure

• What Causes Heart Failure?– Diabetes

• Tend to have other conditions that make the

heart work harder

• Obesity

• Hypertension

• High cholesterol

Heart Failure

• What Causes Heart Failure?– Severe anemia

• Not enough red blood cells to carry oxygen

• Heart beats faster and can become overtaxed with

the effort

– Hyperthyroidism

• Body metabolism is increased and overworks the

heart

– Abnormal Heart Rhythm

• If the heart beats too fast, too slow or irregular it may

not be able to pump enough blood to the body

Signs and Symptoms of

Heart Failure

Shortness of Breath (dyspnea)

• WHY?

– Blood “backs up” in the pulmonary

veins because the heart can’t keep up

with the supply an fluid leaks into the

lungs

• SYMPTOMS

– Dyspnea on exertion or at rest

– Difficulty breathing when lying flat

– Waking up short of breath

Persistent Cough or Wheezing

• WHY?

– Fluid “backs up” in the lungs

• SYMPTOMS

– Coughing that produces white or pink blood-tinged

sputum


Heart Failure

– Edema

• WHY?

– Decreased blood flow out of the weak heart

– Blood returning to the heart from the veins

“backs up” causing fluid to build up in tissues

• SYMPTOMS

– Swelling in feet, ankles, legs or abdomen

– Weight gain


Heart Failure

– Tiredness, fatigue

• WHY?

– Heart can’t pump enough blood to meet needs of

bodies tissues

– Body diverts blood away from less vital organs

(muscles in limbs) and sends it to the heart and

brain

• SYMPTOMS

– Constant tired feeling

– Difficulty with everyday activities


Heart Failure

– Lack of appetite/ Nausea

• WHY?

– The digestive system receives less blood

causing problems with digestion

• SYMPTOMS

– Feeling of being full or sick to your stomach


Heart Failure

– Increased heart rate

• WHY?

– The heart beats faster to “make up for” the loss

in pumping function

• SYMPTOMS

– Heart palpitations

– May feel like the heart is racing or throbbing


Heart Failure

Heart Failure

• New York Heart Association (NYHA)

Functional Classification

Class % of

patients

Symptoms

I 35% No symptoms or limitations in ordinary physical

activity

II 35% Mild symptoms and slight limitation during

ordinary activity

III 25% Marked limitation in activity even during minimal

activity. Comfortable only at rest

IV 5% Severe limitation. Experiences symptoms even at

rest

Treatment Objectives

Survival

Morbidity

Exercise capacity

Quality of life

Neurohormonal changes

Progression of CHF

Symptoms

Heart Failure

• Treatment Options

– The more common forms of heart failure

cannot be cured, but can be treated

• Lifestyle changes

• Medications

• Surgery

Heart Failure

Management


– Stop smoking

– Loose weight

– Avoid alcohol

– Avoid or limit caffeine

– Eat a low-fat, low-sodium diet

– Exercise

Heart Failure


– Reduce stress

– Keep track of symptoms and weight and

report any changes or concern to the

doctor

– Limit fluid intake

– See the doctor more frequently

Physiology - Treatment

Treatment

Pharmacologic Therapy

•ACE inhibitors

•Diuretics

•Beta Blockers• Digitalis

• Spironolactone

• Other

Heart Failure

• Medications used to treat Heart

Failure

– ACE Inhibitors

• Cornerstone of heart failure therapy

• Proven to slow the progression of heart

failure

• Vasodilator – cause blood vessels to

expand lowering blood pressure and the

hearts work load

VASOCONSTRICTION VASODILATATION

Kininogen

Kallikrein

Inactive Fragments

Angiotensinogen

Angiotensin I

RENIN

Kininase IIInhibitor

ALDOSTERONE

SYMPATHETIC

VASOPRESSIN

PROSTAGLANDINS

tPA

ANGIOTENSIN II

BRADYKININ

ACE-i. Mechanism of Action

A.C.E.

ACE-I. Clinical Effects

• Improve symptoms

• Reduce remodelling / progression

• Reduce hospitalization

• Improve survival

• Symptomatic heart failure

• Asymptomatic ventricular dysfunction

- LVEF < 35 - 40 %

• Selected high risk subgroups

ACE-i. Indications



ACE-i. Practical Use

•Start with very low dose

• Increase dose if well tolerated

•Renal function & serum K+ after 1-2 w

•Avoid fluid retention / hypovolemia (diuretic use)

•Dose NOT determined by symptoms

•Combine to overcome “resistance”

•Do not use alone

ACE-I. Adverse Effects

• Hypotension (1st dose effect)

• Worsening renal function

• Hyperkalemia

• Cough

• Angioedema

• Rash, ageusia, neutropenia, …

ACE-I. Contraindications

• Intolerance (angioedema, anuric renal fail.)

• Bilateral renal artery stenosis

• Pregnancy

• Renal insufficiency (creatinine > 3 mg/dl)

• Hyperkalemia (> 5,5 mmol/l)

• Severe hypotension

RENIN

Angiotensinogen Angiotensin I

ANGIOTENSIN II

ACE

Other pathways

Vasoconstriction Proliferative

Action

Vasodilatation Antiproliferative

Action

AT1 AT2

AT1

Receptor

BlockersRECEPTORS

Angiotensin II Receptor Blockers (ARB)

•Candesartan, Eprosartan, Irbesartan

Losartan, Telmisartan, Valsartan

•Efficacy not equal / superior to ACE-I

•Not indicated with beta blockers

• Indicated in patients intolerant to ACE-I

Angiotensin II Receptor Blockers (ARB)



Diuretics

• Essential to control symptomssecondary to fluid retention

• Prevent progression from HT to HF

• Spironolactone improves survival

• New research in progress

Cortex

Medulla

Thiazides

Inhibit active exchange of Cl-Na

in the cortical diluting segment of the

ascending loop of Henle

K-sparing

Inhibit reabsorption of Na in thedistal convoluted and collecting tubule

Loop diuretics

Inhibit exchange of Cl-Na-K inthe thick segment of the ascending

loop of Henle

Loop of HenleCollecting tubule

Diuretics

Diuretics. Indications

1.Symptomatic HF, with fluid retention

• Edema

• Dyspnea

• Lung Rales

• Jugular distension

• Hepatomegaly

• Pulmonary edema (Xray)



Loop Diuretics / Thiazides. Practical Use

•Start with variable dose. Titrate to achieve dry weight

•Monitor serum K+ at “frequent intervals”

•Reduce dose when fluid retention is controlled

•Teach the patient when, how to change dose

•Combine to overcome “resistance”

•Do not use alone

Loop diuretics. Dose (mg)

Initial Maximum

Bumetanide 0.5 to 1.0 / 12-24h 10 / day

Furosemide 20 to 40 / 12-24h 400 / day

Torsemide 10 to 20 / 12-24h 200 / day


Thiazides, Loop Diuretics. Adverse Effects

• K+, Mg+ (15 - 60%) (sudden death ???)

• Na+

• Stimulation of neurohormonal activity

• Hyperuricemia (15 - 40%)

• Hypotension. Ototoxicity. Gastrointestinal.

Alkalosis. Metabolic

Sharpe N. Heart failure. Martin Dunitz 2000;43

Kubo SH , et al. Am J Cardiol 1987;60:1322

MRFIT, JAMA 1982;248:1465

Pool Wilson. Heart failure. Churchill Livinston 1997;635

ß-Adrenergic BlockersMechanism of action

• Density of ß1 receptors

• Inhibit cardiotoxicity of catecholamines

• Neurohormonal activation

• HR

•Antiischemic

•Antihypertensive

•Antiarrhythmic

•Antioxidant, Antiproliferative

ß-Adrenergic BlockersClinical Effects

• Improve symptoms (only long term)

• Reduce remodelling / progression

• Reduce hospitalization

• Reduce sudden death

• Improve survival

• Symptomatic heart failure

• Asymptomatic ventricular dysfunction

- LVEF < 35 - 40 %

• After AMI



ß-Adrenergic BlockersIndications

•Patient stable

• No physical evidence of fluid retention

• No need for i.v. inotropic drugs

•Start ACE-I / diuretic first

•No contraindications

• In hospital or not

ß-Adrenergic BlockersWhen to start

Initial Target

Bisoprolol 1.25 / 24h 10 / 24h

Carvedilol 3.125 / 12h 25 / 12h

Metoprolol tartrate 6.25 / 12h 75 / 12h

Metoprolol succinnate 12,5-25 / 24h 200 / 24h

• Start Low, Increase Slowly• Increase the dose every 2 - 4 weeks

ß-Adrenergic BlockersDose (mg)

•Hypotension

•Fluid retention / worsening heart failure

•Fatigue

•Bradycardia / heart block

ß-Adrenergic BlockersAdverse Effects

•Review treatment (+/-diuretics, other drugs)

•Reduce dose

•Consider cardiac pacing

•Discontinue beta blocker only in severe cases

ß-Adrenergic Blockers

Contraindications

•Asthma (reactive airway disease)

•AV block (unless pacemaker)

•Symptomatic hypotension / Bradycardia

•Diabetes is NOT a contraindication

ALDOSTERONE

• Retention Na+

• Retention H2O

• Excretion K+

• Excretion Mg2+

• Collagen

deposition

Fibrosis- myocardium

- vessels

Spironolactone

Edema

Arrhythmias

Competitive antagonist of the

aldosterone receptor

(myocardium, arterial walls, kidney)

Aldosterone Inhibitors

-

Spironolactone. Indications

• Recent or current symptoms despite

ACE-i, diuretics, dig. and b-blockersAHA / ACC HF guidelines 2001

• Recommended in advanced heart failure

(III-IV), in addition to ACE-i and diuretics

• HypokalemiaESC HF guidelines 2001

Spironolactone. Practical use

• Do not use if hyperkalemia, renal insuf.

• Monitor serum K+ at “frequent intervals”

• Start ACE-i first

• Start with 25 mg / 24h

• If K+ >5.5 mmol/L, reduce to 25 mg / 48h

• If K+ is low or stable consider 50 mg / day

Digitalis. Mechanism of Action

Blocks Na+ / K+ ATPase => Ca+ +

• Inotropic effect

• Natriuresis

• Neurohormonal control- Plasma Noradrenaline

- Peripheral nervous system activity

- RAAS activity

- Vagal tone

- Normalizes arterial baroreceptors

NEJM 1988;318:358

Digitalis. Clinical Effects

• Improve symptoms

• Modest reduction in hospitalization

• Does not improve survival

Digitalis. Indications

• When no adequate response to

ACE-i + diuretics + beta-blockers

AHA / ACC Guidelines 2001

• In combination with ACE-i + diuretics

if persisting symptoms

ESC Guidelines 2001

• AF, to slow AV conduction

Dose 0.125 to 0.250 mg / day

• Digoxin toxicity

• Advanced A-V block without pacemaker

• Bradycardia or sick sinus without PM

• PVC’s and VT

• Marked hypokalemia

• W-P-W with atrial fibrillation

Digoxin. Contraindications

Other Drugs. (only in selected patients)

• Inotropics: refractory HF

• Nitrates: ischemia, angina, pulmonary congestion

• ARB: Contraindications to ACE-i

• Antiarrhythmics: (only amiodarone) H risk arrhyth.

• Anticoagulants: High risk of embolysm

• Ca channel blockers: (only amlodipine) ischemia

Heart Failure

• Treatment options– Surgery and other Medical Procedures

• Not often used in heart failure unless there

is a correctable problem

• Coronary artery bypass

• Angioplasty

• Valve replacement

• Defibrillator implantation

• Heart transplantation

• Left ventricular assist device (LVAD)

“The very essence of cardiovascular practice is

the early detection of heart failure”

Sir Thomas Lewis, 1933

Heart Failure Dz

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