gagal jantung 2013

7/30/2019 gagal jantung 2013

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Heart Failure


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CO = SV x HR-becomes insufficient to meetmetabolic needs of body

SV- determined by preload, afterload andmyocardial contractility

Classifications HF Systolic failure- dec. contractility

Diastolic failure- dec. filling

Mixed


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90/140= 64% EF- 55-65 (75) normal


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Volume of blood in ventricles at enddiastole

Depends on venous return Depends on compliance

Afterload

Force needed to eject blood into circulationArterial B/P, pulmonary artery pressureValvular disease increases afterload

Factors effecting

heart pump

effectiveness


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HF affects 5.7 Million: 3.1 M men, 2.6 Mwomen (self-report, age 20yo, NHANES-2008)

Lifetime risk 20% (40yo,Framingham[FHS])

Hospitalizations > 1 M / year Prevalence and Incidence of HF increases

with age 670,000 new cases age 45yo (FHS)

56,000 deaths; 1 in 9 deaths (NCHS) 50% diagnosed w/ HF die within 5 yrs

(Olmsted)

Roger V et al. Heart Disease and Stroke Statistics2011 Update. Circulation 2011;123(4):e18-


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The heart is not pumping as well as it should Usually, the heart has been weakened by an

underlying condition

Blocked arteries MI High blood pressure Infections

Heart valve abnormalities


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Heart failure can involve the left or right side ofthe heart or both

Usually the left side is affected first

Heart failure occurs when either side of the heartcannot keep up with the flow of blood


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What is Heart Failure?


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Involves the left ventricle (lower chamber) of theheart

Systolic failure

The heart looses its ability to contract or pumpblood into the circulation

Diastolic failure The heart looses its ability to relax because it

becomes stiff

Heart cannot fill properly between each beat


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Systolic failure- most common cause Hallmark finding: Dec. in *left ventricular

ejection fraction (EF) Due to

Impaired contractile function (e.g., MI) Increased afterload (e.g., hypertension) Cardiomyopathy

Mechanical abnormalities (e.g., valvedisease)
http://www.nlm.nih.gov/medlineplus/ency/article/001105.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/001105.htm


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Diastolic failure

Impaired ability of ventricles to relax and fill

during diastole > dec. stroke volume and CO

Diagnosis based on presence of pulmonarycongestion, pulmonary hypertension, ventricular

hypertrophy

normal ejection fraction (EF)


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Mixed systolic and diastolic failure Seen in disease states such as dilated

cardiomyopathy (DCM)

Poor EFs (


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Systolic and diastolic heart failure are treatedwith different types of medications

In both types, blood may back up in the lungs

causing fluid to leak into the lungs (pulmonaryedema)

Fluid may also build up in tissues throughout thebody (edema)


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American Heart

Assn-Media files

Animations


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Pathophysiology A. Cardiac compensatory mechanisms

1.tachycardia

2.ventricular dilation-Starlings law

3.myocardial hypertrophy

Hypoxia leads to dec. contractility


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B. Homeostatic Compensatory mechanisms Sympathetic Nervous System

1. Vascular system- norepinephrine- vasoconstriction 2. Kidneys A. Dec. CO and B/P > renin angiotensin release B. Aldosterone release > Na and H2O retention

3. Liver- stores venous volumeCounter-regulatory- Inc. Na > release of ADH (diuretics) Release of atrial natriuretic factor > Na and H20 excretion,


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Compensatory mechanisms- activated tomaintain adequate cardiac output Neurohormonal responses: Endothelin -stimulated

by ADH, catecholamines, and angiotensin II >

Arterial vasoconstriction

Inc. in cardiac contractility

Hypertrophy


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Compensatory mechanisms- activated tomaintain adequate CONeurohormonal responses: Proinflammatory

cytokines (e.g., tumor necrosis factor) Released by cardiac myocytes in response to cardiac

injury

Depress cardiac function > cardiac hypertrophy,contractile dysfunction, and myocyte cell death


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Compensatory mechanisms- activated tomaintain adequate CO

Neurohormonal responses: Over time > systemicinflammatory response > results

Cardiac wasting

Muscle myopathy

Fatigue


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**Counter regulatory processesNatriuretic peptides: atrial natriuretic

peptide (ANP) and b-type natriuretic peptide

(BNP)- *also dx test for HF

Released in response to increased in atrial volume andventricular pressure

Promote venous and arterial vasodilation, reduce

preload and afterload Prolonged HF > depletion of these factors


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Compensatory mechanisms- activated tomaintain adequate CO

Neurohormonal responses: Over time > systemicinflammatory response > results

Cardiac wasting

Muscle myopathy

Fatigue


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Counter regulatory processes Natriuretic peptides- endothelin and

aldosterone antagonists

Enhance diuresis Block effects of the RAAS

Natriuretic peptides- inhibit development ofcardiac hypertrophy; may have

antiinflammatory effects


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Decreased contractility Increased preload (volume) Increased afterload (resistance) **Ventricular remodeling

Ventricular hypertrophy

Ventricular dilation


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Result of

Compensatory

Mechanisms

>

Heart FailureHeart Failure

Explained


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Aurigemma GP, Gaasch WH. NEJM 2004;351:1097-

105.


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Coronary artery disease(ischemic cardiomyopathy)

Hypertension(hypertensive cardiomyopathy)

Valvular disease (valvular CM)

Infectious (e.g., viral myocarditis,Chagas) Cardiotoxins (e.g., alcohol,

chemotherapy) Infiltrative (e.g., amyloidosis,

sarcoidosis, hemochromatosis, Wilsons) Peripartum CM Stress-induced CM Genetic (Familial) Idiopathic (Dilated) CM

2/3


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Usually occurs as a result of left heart failure

The right ventricle pumps blood to the lungs foroxygen

Occasionally isolated right heart failure can occurdue to lung disease or blood clots to the lung

(pulmonary embolism)


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Usually a chronic disease

The heart tries to compensate for the loss inpumping function by:

Developing more muscle mass Enlarging

Pumping faster

Worsening

the HF


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Health conditions that either damage the heart ormake it work too hard

Coronary artery disease

Heart attack High blood pressure

Abnormal heart valves

Heart muscle diseases (cardiomyopathy)

Heart inflammation (myocarditis)


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Congenital heart defects

Severe lung disease

Diabetes

Severe anemia Overactive thyroid gland (hyperthyroidism)

Abnormal heart rhythms


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Coronary artery disease Cholesterol and fatty deposits build up in the hearts

arteries Less blood and oxygen reach the heart muscle

This causes the heart to work harder andoccasionally damages the heart muscle


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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 harderto keep up


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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 largerand weaker


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Abnormal heart valves

Heart muscle disease

Damage to heart muscle due to drugs, alcohol orinfections

Congenital heart disease

Severe lung disease


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Diabetes Tend to have other conditions that make the heart

work harder Obesity

Hypertension

High cholesterol


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Severe anemiaNot 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 maynot be able to pump enough blood to the body


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~25% in HF population Etiology: hemodilution, Fe or Epo deficiency, CKD

1-g/dL Hgb reduction associated with a 20%increase in risk of death

Tang WH et al, JACC 2008;51:569-576; Anand I et al, Circulation 2004;110:149-154Treatment is relatively easy

Iron supplementation

IV iron (short-term)

Erythropoiesis-stimulating agents (short term)


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Shortness of Breath (dyspnea) WHY?Blood backs up in the pulmonary veins because the

heart cant keep up with the supply an fluid leaks intothe lungs

SYMPTOMS Dyspnea on exertion or at rest

Difficulty breathing when lying flat

Waking up short of breath


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Persistent Cough or Wheezing WHY?

Fluid backs up in the lungs SYMPTOMS

Coughing that produces white or pink blood-tinged

sputum


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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


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Tiredness, fatigue WHY?

Heart cant 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


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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


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Confusion/ Impaired thinking WHY?

Changing levels of substances in the blood ( sodium)

can cause confusion SYMPTOMS

Memory loss or feeling of disorientation

Relative or caregiver may notice this first


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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


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Hunt SA et al. ACC/AHA Guidelines 2005 & 2001; Circulation

2001;104:2996.Farrell MH, Foody JM, Krumholz HM. JAMA 2002;287:890


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Class % ofpatients

Symptoms

I 35% No symptoms or limitations in ordinary physicalactivity

II 35% Mild symptoms and slight limitation duringordinary activity

III 25% Marked limitation in activity even during minimalactivity. Comfortable only at rest

IV 5% Severe limitation. Experiences symptoms even atrest


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Electrocardiogram (ECG) may show acuteischaemia, arrhythmias, left ventricularhypertrophy, left bundle branch block, or prior MI.

Heart failure is unlikely if the ECG is normal,and the diagnosis should be reconsidered in this

situation. Chest X-ray (CXR)

pulmonary vascular congestion (upper lobe diversion), pulmonary oedema effusions

cardiomegaly


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Cardiac function/structure ECHO (Cardiac MRI, MUGA)

Etiology

R/O CAD: cath vs stress vs CT Serologies: TSH, ANA, Ferritin, HIV, SPEP/UPEP

Cardiac MRI

Family Hx: Genetic testing?


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Jessup M, Brozena S. NEJM 2003;348:2007

ICD

Stem cells?

Hemofiltration?

all

ARB, H/I in some.


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Guidelines ACC/AHA: 1995, 2001, 2005, 2009 HFSA: 1999, 2006, 2010

Medications Diuretics, ACE inhibitors* &/or Angiotensin receptor

blockers* &/ or Hydralazine/Nitrates*, Beta-blockers*,Aldosterone antagonists*, Digoxin

Electrophysiology (EP) Devices Implantable cardioverter defibrillator (ICD) Biventricular pacemaker (CRT)

Surgery Revascularization Ventricular restoration (Dor procedure) Mitral valve surgery Cardiac transplantation Mechanical circulatory support (VAD)


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Kittleson MM, Kobashigawa JA, Circulation 2011;123:1569-1574

, B-blockers


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Treat the cause

Combination of diuretic therapy and ACE-I If ACE-I is contraindicated use vasodilators

Add beta blocker if the patient was stabilized Start with low dose

Spironolactone has shown 30% reduction in mortalitywhen administered with the conventional therapy If the above drugs dont relieve the symptoms use

digoxin Positive inotropic agents must be used for short time

If the patient condition become worse make surgeryintervention


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Preload reduction: reduction of excessplasma volume and edema fluid

Afterload reduction: lowered bloodpressure


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Thiazide For mild fluid retention

Furosemide More effective than thiazide

Rapid onset and short duration Potassium sparing diuretics

Use to along with the above diuretics to preventelectrolyte imbalance

Spironolactone have beneficial effect on heartremodeling


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Aldosterone antagonist, K-sparing diuretic Prevention of aldosterone effects on:

Kidney

Heart

Aldosterone inappropriately elevated in CHF Mobilizes edema fluid in heart failure Prevention of hypokalemia induced by loop

diuretics (protection against digitalis toxicity?) Prolongs life in CHF patients


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First line treatment Lower the morbidity and mortality rate

among HF pts Afterload reduction

Preload reduction Reduction of facilitation of sympathetic

nervous system Reduction of cardiac hypertrophy


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Standard -blockers: Reduction in damaging sympathetic influences in

the heart (tachycardia, arrhythmias, remodeling) inhibition of renin release

Carvedilol: Beta blockade effects peripheral vasodilatation via

1-adrenoceptor

blockade (carvedilol)


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10 mg bid

50 mg tid*

5 mg bid

20 mg qd

4 mg qd20-40 mg bid

*affected by food, ** depends on weight no mortality data, not in guideline

Enalapril (Vasotec)

Captopril (Capoten)

Ramipril (Altace)

Lisinopril (Prinivil, Zestril)

Trandolapril (Mavik)Quinapril (Accupril)

Bisoprolol (Zebeta)

Carvedilol (Coreg)Metoprolol XL/CR (Toprol XL)

Metoprolol (Lopressor)

Atenolol (Tenormin)

10 mg qd

25-50 mg bid **200 mg qd

100 mg bid

100 mg qd

ACE-I

BB


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Mechanism of action: reduce preload andafterload

Sodium nitroprusside

Hydralazine Nitrates

Alpha1 blocker

Ca2+ channel blockers must be avoided


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1. Cardiac glycosides: Digitalis derivatives :

Digoxin

Digitoxin

Nondigitalis derivatives: Ouabain


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Congestive Heart Failure Atrial fibrillation Atrial flutter


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cardiac output cardiac efficiency heart rate cardiac size

NO survival benefit


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Restoration of baroreceptor sensitivity Reduction in sympathetic activity

increased renal perfusion, with edemaformation

Increase parasympathetic outflow


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Digoxin has a long enough half life (24-36 hr.) and high enough bioavailabilityto allow once daily dosing

Digoxin has a large volume ofdistribution and dose must be based onlean body mass

Increased cardiac performance can

increase renal function and clearance ofdigoxin

Eubacterium lentum


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Cardiac AV block Bradycardia Ventricular extrasystole Arrhythmias

CNS toxicity Delirium Confusion and somnolence

GI Anorexia ,nausea and vomitting

Blurred vision Tendency to yellow-green vision Photophobia

K+

Digitalis competes for K binding at Na/K ATPase Hypokalemia: increase toxicity Hyperkalemia: decrease toxicity

Mg2+

Hypomagnesemia: increases toxicity Ca2+

Hypercalcemia: increases toxicity


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Bile resins or activated charcoal Atropine: advanced heart block

KCl: increased automaticity Antiarrythmics: ventricular arrhythmias Fab antibodies: toxic serum

concentration; acute toxicity


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Amrinone Milrinone

PDE 3 inhibitor


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Inhibition of type III phosphodiesterase increase intracellular cAMP activation of protein kinase A

o Ca2+

entry through L type Cachannelso inhibition of Ca2+ sequestration bySR

increase cardiac output

decrease peripheral vascular resistance

short term support in advanced cardiac failure


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Cardiac arrhythmias GI: Nausea and vomiting Sudden death


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Dobutamine

Dopamine


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Beta 1 agonist Administered as IV infusion Used in acute HF Can induce arrhythmias

Stimulation of cardiac 1adrenoceptors: inotropy > chronotropy

peripheral vasodilatation

myocardial oxygen demand Dobutamine: management of acute failureonly


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Stimulation of peripheral postjunctionalD1 and prejunctional D2 receptors

Splanchnic and renal vasodilatation Dopamine: restore renal blood in acute

failure


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DobutamineTolerance

Tachycardia

Dopamine

tachycardia arrhythmias

peripheral vasoconstriction if given at high doses


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Not followed as standard regimen only inpts with prior embolic events


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Treatment optionsNot 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)

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