Congestive Heart Failurebody System(3) - Copy

7/31/2019 Congestive Heart Failurebody System(3) - Copy

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TerminologyHeart Failure:The inability of the

heart to maintain an output adequate tomaintain the metabolic demands of the

body.Pulmonary Edema:An abnormal

accumulation of fluid in the lungs.

CHF with Acute PulmonaryEdema:Pulmonary Edema due to HeartFailure (Cardiogenic Pulmonary Edema)


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What is HFComplex syndrome that can result from any structural or

functional cardiac disorder that impairs the ability of the

heart to function as a pump to support a physiological

circulation.


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PathophysiologyMain Causes of Heart Failure: Ischemic Heart Disease (35-40%) Cardiomyopathy(dilated) (30-34%)

Hypertension (15-20%) Other Causes: Valvular Heart Disease. Congenital Heart Disease. Alcohol and Drugs.

Arrhythmias


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Pathophysiological

Changes in HFVentricular Dilatation.

Myocyte Hypertrophy.

Salt and Water Retention.Sympathetic Stimulation.

Peripheral Vasoconstriction.


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Signs & SymptomsSymptoms: Exertional Dyspnoea Orthopnia Paraxysmal Nocturnal Dyspnoea

Signs: Cardiomegaly Elevated Jugular Venous PressureTachycardia Hypotension

Bi-basal crackles Pleural effusion Ankle Edema AscitesTender hepatomegaly.


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Classification of heart

failureI. No limitation. Normal physical exercise

doesnt cause fatigue, dyspnea orpalpitations.

II. Mild limitation. Comfortable at rest butnormal physical activity produces fatigue,dyspnea or palpitations.

III. Marked limitation. Comfortable at rest butgentle physical activity produces markedsymptoms of HF.

IV. Symptoms of HF occur at rest and are

exacerbated by any physical activity.


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Kussmauls Sign

This is a rise in the JVP seen withinspiration. It is the opposite of what isseen in normal people and this reflectsthe inability of the heart tocompensate for a modest increase invenous return. This sign is classically

seen in constrictive pericarditis inassociation with a raised JVP. Thiscondition was originally described intuberculous pericarditis and is rarelyseen. Kussmauls sign is also seen inright ventricular infarction, right heart

failure, tricuspid stenosis, andrestrictive cardiomyopathy. It is notseen in acute cardiac tamponade-although it may be seen if tamponadeoccurs with a degree of constricivepericardiditis


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PMIThe apex beat, also called the point ofmaximum impulse (PMI), is the furthermost pointoutwards (laterally) and downwards (inferiorly)from the sternum at which the cardiac impulse canbe felt. The cardiac impulse is the result of theheart rotating, moving forward and striking againstthe chest wall during systole.

The normal apex beat can be palpated in theprecordiumleft 5th intercostal space, at the point

of intersection with the left midclavicular line. Inchildren the apex beat occurs in the fourth ribinterspace medial to the nipple. The apex beat mayalso be found at abnormal locations; in many casesofdextrocardia, the apex beat may be felt on the

right side. Lateral and/or inferior displacement ofthe apex beat usually indicates enlargement of the
http://en.wikipedia.org/wiki/Sternumhttp://en.wikipedia.org/wiki/Cardiachttp://en.wikipedia.org/wiki/Hearthttp://en.wikipedia.org/wiki/Systole_(medicine)http://en.wikipedia.org/wiki/Palpatehttp://en.wikipedia.org/wiki/Precordiumhttp://en.wikipedia.org/wiki/Dextrocardiahttp://en.wikipedia.org/wiki/Dextrocardiahttp://en.wikipedia.org/wiki/Precordiumhttp://en.wikipedia.org/wiki/Palpatehttp://en.wikipedia.org/wiki/Systole_(medicine)http://en.wikipedia.org/wiki/Hearthttp://en.wikipedia.org/wiki/Cardiachttp://en.wikipedia.org/wiki/Sternum


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S1The first heart sound - S1 - is in time with the pulse in your carotid artery in your

neck. The sound of the tricuspid valve closing may be louder in patients withpulmonary hypertension due to increased pressure beyond the valve. Non-heart-related factors such as obesity, muscularity, emphysema, and fluid around the heart

can reduce both S1 and S2.The position of the valves when the ventricles contract can have a big effect onthe first heart sound. If the valves are wide open when the ventricule contracts, a loudS1 is heard. This can occur with anemia, fever or hyperthyroid.

When the valves are partly closed when the ventricule contracts, S1 is faint.Beta-blockers produce a fainter S1. Structural changes in the heart valves can alsoaffect S1. Fibrosis and calcification of the mitral valve may reduce S1, while stenosisof the mitral valve may cause a louder S1.

S2

The second heart sound marks the beginning of diastole - the heart's relaxation phase- when the ventricles fill with blood. In children and teenagers, S2 may be morepronounced. Right ventricular ejection time is slightly longer than left ventricularejection time. As a result, the pulmonic valve closes a little later than the aortic valve.

Higher closing pressures occur in patients with chronic high blood pressure,pulmonary hypertension, or during exercise or excitement. This results in a louder A2(the closing sound of the aortic valve).

On the other hand, low blood pressure reduces the sound. The second heartsound may be "split" in patients with right bundle branch block, which results indelayed pulmonic valve closing. Left bundle branch blockmay cause aortic valve

closing (A2) to be slower than pulmonic valve closing (P2). S3 During diastole there are 2 sounds of ventricular filling: The first is from the atrial

walls and the second is from the contraction of the atriums. The third heart sound iscaused by vibration of the ventricular walls, resulting from the first rapid filling so it isheard just after S2. The third heart sound is low in frequency and intensity. An S3 iscommonly heard in children and young adults. In older adults and the elderly withheart disease, an S3 often means heart failure.

S4The fourth heart sound occurs during the second phase of ventricular filling: when theatriums contract just before S1. As with S3, the fourth heart sound is thought to be
http://www.chfpatients.com/text/pph.txthttp://www.chfpatients.com/coreg.htmhttp://www.chfpatients.com/text/bbb.txthttp://www.chfpatients.com/text/bbb.txthttp://www.chfpatients.com/coreg.htmhttp://www.chfpatients.com/text/pph.txt


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EdemaBilateral lower extremity

edema


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HypertensionHypertrophic Cardiomyopathy


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Mechanisms

Increased Heart RateSympathetic = Norepinephrine

DilationFrank Starling = Contractility

Neurohormonal

Redistribution of Blood to the Brain


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Low Output

Increased Preload Increased AfterloadNorepinephrine

Increased Salt Vasoconstriction Renal BloodFlow

Renin

Angiotension I

Angiotension II

Aldosterone


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q

q


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a true life-

threateningemergency


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TreatmentTreatment Prevention. Control of risk factorsPrevention. Control of risk factors Life styleLife style Treat etiologic cause / aggravating factorsTreat etiologic cause / aggravating factors

Drug therapyDrug therapy Personal care. Team workPersonal care. Team work

Revascularization if ischemia causes HFRevascularization if ischemia causes HF ICD (Implantable Cardiac Defibrillator)ICD (Implantable Cardiac Defibrillator)

Ventricular resyncronizationVentricular resyncronization Ventricular assist devicesVentricular assist devices Heart transplantHeart transplant Artificial heartArtificial heart Neoangiogenesis, Gene therapyNeoangiogenesis, Gene therapy

AllAll

Selected

patients

Selected

patients


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TreatmentPharmacologic Therapy

TreatmentPharmacologic Therapy

Diuretics

ACE inhibitors

Beta Blockers Digitalis

Spironolactone

Other

Diuretics

ACE inhibitors

Beta Blockers Digitalis

Spironolactone

Other


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DiureticsDiuretics

Essential to control symptomsEssential to control symptomssecondary to fluid retentionsecondary to fluid retention

Prevent progression from HT to HFPrevent progression from HT to HF

Spironolactone improves survivalSpironolactone improves survival

New research in progressNew research in progress


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CortexCortex

MedullaMedulla

Thiazides

Inhibit active exchange of Cl-Na

in the cortical diluting segment of the

ascending loop of Henle

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

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 diuretics

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

loop of Henle

Loop of HenleLoop of HenleCollecting tubuleCollecting tubule

DiureticsDiuretics


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Diuretics. IndicationsDiuretics. Indications

1.1.Symptomatic HF, with fluid retentionSymptomatic HF, with fluid retention

EdemaEdema

DyspneaDyspnea Lung RalesLung Rales

Jugular distensionJugular distension

HepatomegalyHepatomegaly Pulmonary edema (XrayPulmonary edema (Xray))

AHA / ACC HF guidelines 2001AHA / ACC HF guidelines 2001

ESC HF guidelines 2001ESC HF guidelines 2001


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Loop Diuretics / Thiazides. Practical UseLoop Diuretics / Thiazides. Practical Use

Start with variable dose. Titrate to achieveStart with variable dose. Titrate to achievedry weightdry weight

Monitor serum KMonitor serum K++ at frequent intervalsat frequent intervals

Reduce dose when fluid retention is controlledReduce dose when fluid retention is controlled

Teach the patient when, how to changeTeach the patient when, how to changedosedose

Combine to overcome resistanceCombine to overcome resistance

Do not use aloneDo not use alone


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Loop diuretics. Dose (mg)Loop diuretics. Dose (mg)

InitialInitial MaximumMaximum

BumetanideBumetanide 0.5 to 1.0 / 12-24h0.5 to 1.0 / 12-24h 10 /10 /

dayday

FurosemideFurosemide 20 to 40 / 12-24h20 to 40 / 12-24h 400 / day400 / day

TorsemideTorsemide 10 to 20 / 12-24h10 to 20 / 12-24h 200 / day200 / day



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Thiazides, Loop Diuretics. Adverse EffectsThiazides, Loop Diuretics. Adverse Effects

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

NaNa++

Stimulation of neurohormonal activityStimulation of neurohormonal activity

Hyperuricemia (15 - 40%)Hyperuricemia (15 - 40%)

Hypotension. Ototoxicity. Gastrointestinal.Hypotension. Ototoxicity. Gastrointestinal.

Alkalosis. MetabolicAlkalosis. MetabolicSharpe N. Heart failure. Martin Dunitz 2000;43Sharpe N. Heart failure. Martin Dunitz 2000;43

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

MRFIT, JAMA 1982;248:1465MRFIT, JAMA 1982;248:1465Pool Wilson. Heart failure. Churchill Livinston 1997;635Pool Wilson. Heart failure. Churchill Livinston 1997;635


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VASOCONSTRICTIONVASOCONSTRICTION VASODILATATIONVASODILATATION

KininogenKininogen

KallikreinKallikrein

Inactive FragmentsInactive Fragments

AngiotensinogenAngiotensinogen

Angiotensin IAngiotensin I

RENINRENIN

Kininase IIKininase IIInhibitorInhibitor

ALDOSTERONEALDOSTERONE

SYMPATHETICSYMPATHETIC

VASOPRESSINVASOPRESSIN

PROSTAGLANDINSPROSTAGLANDINS

tPAtPA

ANGIOTENSIN IIANGIOTENSIN II

BRADYKININBRADYKININ

ACE-i. Mechanism of ActionACE-i. Mechanism of Action

A.C.E.A.C.E.


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ACE-I. Clinical EffectsACE-I. Clinical Effects Improve symptoms

Reduce remodelling / progression Reduce hospitalization

Improve survival

Improve symptoms

Reduce remodelling / progression Reduce hospitalization

Improve survival


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Symptomatic heart failure

Asymptomatic ventricular dysfunction

- LVEF < 35 - 40 %

Selected high risk subgroups



- LVEF < 35 - 40 %

Selected high risk subgroups

ACE-i. IndicationsACE-i. Indications




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ACE-I. Adverse EffectsACE-I. Adverse Effects Hypotension (1st dose effect)Hypotension (1st dose effect)

Worsening renal functionWorsening renal function

HyperkalemiaHyperkalemia

CoughCough

AngioedemaAngioedema

Rash, ageusia, neutropenia, Rash, ageusia, neutropenia,


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ACE-I. ContraindicationsACE-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

ACE-I. ContraindicationsACE-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


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-Adrenergic Blockers

Mechanism of action

-Adrenergic Blockers

Mechanism of action Density of 1 receptors

Inhibit cardiotoxicity of catecholamines Neurohormonal activation

HR

Antiischemic

Antihypertensive

Antiarrhythmic

Density of 1 receptors

Inhibit cardiotoxicity of catecholamines

Neurohormonal activation

HR

Antiischemic

Antihypertensive

Antiarrhythmic


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-Adrenergic BlockersClinical Effects

-Adrenergic BlockersClinical Effects

Improve symptoms (only long term)

Reduce remodelling / progression

Reduce hospitalization

Reduce sudden death

Improve survival

Improve symptoms (only long term)

Reduce remodelling / progression

Reduce hospitalization

Reduce sudden death

Improve survival


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- LVEF < 35 - 40 %

After AMI



- LVEF < 35 - 40 %

After AMI



-Adrenergic Blockers-Adrenergic Blockers

IndicationsIndications


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HypotensionHypotensionFluid retention / worsening heart failureFluid retention / worsening heart failureFatigueFatigueBradycardia / heart blockBradycardia / heart block

-Adrenergic Blockers-Adrenergic Blockers

Adverse EffectsAdverse Effects

Review treatment (+/-diuretics, other drugs)Review treatment (+/-diuretics, other drugs) Reduce doseReduce dose Consider cardiac pacingConsider cardiac pacing Discontinue beta blocker only in severe casesDiscontinue beta blocker only in severe cases


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Na+Na+

K+K+

K+K+

Na+Na+

Na+Na+ Ca++Ca++

Ca++Ca++

Na-K ATPaseNa-K ATPase Na-Ca ExchangeNa-Ca Exchange

MyofilamentsMyofilaments

DigitalisDigitalis

CONTRACTILITYCONTRACTILITY

-


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Digitalis. Mechanism of ActionDigitalis. Mechanism of Action

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

Inotropic effectInotropic effect

NatriuresisNatriuresis

Neurohormonal controlNeurohormonal control-- Plasma NoradrenalinePlasma Noradrenaline

-- Peripheral nervous system activityPeripheral nervous system activity

-- RAAS activityRAAS activity

-- Vagal toneVagal tone

- Normalizes arterial baroreceptors- Normalizes arterial baroreceptors

NEJM 1988;318:358NEJM 1988;318:358


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Digitalis. Clinical EffectsDigitalis. Clinical Effects

Improve symptoms

Modest reduction in hospitalization

Does not improve survival

Improve symptoms

Modest reduction in hospitalization

Does not improve survival


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Digitalis. IndicationsDigitalis. Indications

When no adequate response toWhen no adequate response toACE-i + diuretics + beta-blockersACE-i + diuretics + beta-blockers

AHA / ACC Guidelines 2001AHA / ACC Guidelines 2001

In combination with ACE-i + diureticsIn combination with ACE-i + diuretics

if persisting symptomsif persisting symptoms

ESC Guidelines 2001ESC Guidelines 2001

AF, to slow AV conductionAF, to slow AV conduction

Dose 0.125 to 0.250 mg / dayDose 0.125 to 0.250 mg / day


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ALDOSTERONEALDOSTERONE

Retention Na+

Retention H2

O

Excretion K+

Excretion Mg2+

Retention Na+

Retention H2O

Excretion K+

Excretion Mg2+

CollagenCollagen

depositiondeposition

FibrosisFibrosis-- myocardiummyocardium

-- vesselsvessels

SpironolactoneSpironolactone

EdemaEdema

ArrhythmiasArrhythmias

Competitive antagonist of the

aldosterone receptor(myocardium, arterial walls, kidney)

Competitive antagonist of the

aldosterone receptor(myocardium, arterial walls, kidney)

Aldosterone InhibitorsAldosterone Inhibitors

-


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Spironolactone. Practical useSpironolactone. Practical use

Do not use if hyperkalemia, renal insuf.Do not use if hyperkalemia, renal insuf.

Monitor serum KMonitor serum K++ at frequent intervalsat frequent intervals

Start ACE-i firstStart ACE-i first

Start with 25 mg / 24hStart with 25 mg / 24h

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

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

New studies in progressNew studies in progress


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RENINRENIN

AngiotensinogenAngiotensinogen Angiotensin I

ANGIOTENSIN II

Angiotensin I

ANGIOTENSIN II

ACEACEOther pathwaysOther pathways

VasoconstrictionVasoconstriction Proliferative

Action

Proliferative

Action

VasodilatationVasodilatation Antiproliferative

Action

Antiproliferative

Action

AT1AT1 AT2AT2

AT1

Receptor

Blockers

AT1

Receptor

BlockersRECEPTORSRECEPTORS

Angiotensin II Receptor Blockers (ARB)Angiotensin II Receptor Blockers (ARB)


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1- VENOUS VASODILATATION

Preload

2- Coronary vasodilatation

Myocardialperfusion

3- Arterial vasodilatationAfterload

1- VENOUS VASODILATATION

Preload

2- Coronary vasodilatation

Myocardialperfusion

3- Arterial vasodilatationAfterload

Pulmonary congestion

Ventricular sizeVent. Wall stress

MVO2

Pulmonary congestion

Ventricular sizeVent. Wall stress

MVO2

NITRATES

HEMODYNAMIC EFFECTS

NITRATES

HEMODYNAMIC EFFECTS

Cardiac output

Blood pressure

Cardiac output

Blood pressure


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Nitrates. Clinical UseNitrates. Clinical Use

CHF with myocardial ischemia

Orthopnea and paroxysmal nocturnal dyspnea

In acute CHF and pulmonary edema:NTG sl / iv

Nitrates + Hydralazine in intolerance

to ACE-I (hypotension, renal insufficiency)

CHF with myocardial ischemia

Orthopnea and paroxysmal nocturnal dyspnea

In acute CHF and pulmonary edema:NTG sl / iv

Nitrates + Hydralazine in intolerance

to ACE-I (hypotension, renal insufficiency)


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Heart Transplant. IndicationsHeart Transplant. Indications

Refractory cardiogenic shockRefractory cardiogenic shock

Peak VO2 < 10 ml / kg / minPeak VO2 < 10 ml / kg / min

Severe symptoms of ischemia not amenable toSevere symptoms of ischemia not amenable torevascularizationrevascularization

Recurrent symptomatic ventricular arrhythmiasRecurrent symptomatic ventricular arrhythmiasrefractory to all therapeutic modalitiesrefractory to all therapeutic modalities

Contraindications: age, severe comorbidityContraindications: age, severe comorbidity


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Heart Failure and Myocardial IschemiaHeart Failure and Myocardial Ischemia

Coronary HD is the cause of 2/3 of HFCoronary HD is the cause of 2/3 of HF

Segmental wall motion abnormalities are notSegmental wall motion abnormalities are not

specific if ischemiaspecific if ischemia

Angina coronary angio and revascularizationAngina coronary angio and revascularization

No anginaNo angina Search for ischemia and viability in all ?Search for ischemia and viability in all ?

Coronary angiography in all ?Coronary angiography in all ?


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HEART FAILURE MODELSHEART FAILURE MODELS

CONGESTIVECONGESTIVE- Digoxin, Diurtics- Digoxin, Diurtics

HEMODYNAMIC - VasodilatorsHEMODYNAMIC - Vasodilators

NEUROHUMORAL - ACE inhibitors,NEUROHUMORAL - ACE inhibitors,

- Blockers, Spironolactone- Blockers, Spironolactone

IMMUNOLOGICAL -IMMUNOLOGICAL - Cytokine inhibitorsCytokine inhibitors


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THANK YOU

Congestive Heart Failurebody System(3) - Copy

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