Heart Failure Dg 2010

8/9/2019 Heart Failure Dg 2010

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Heart Failure

Definition:

A state in which the heart cannotprovide sufficient cardiac output to

satisfy the metabolic needs of the body

HF is a complex 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.

Heart Failure vs. Congestive Heart Failure

Because not all patients have volume overload at

the time of initial or subsequent evaluation, the

term heart failure is preferred over the older

term congestive heart failure.

Etiology

It is a common end point for manydiseases of cardiovascular system

It can be caused by :

-Inappropriate work load (volume or pressureoverload)

-Restricted filling

-Myocyte loss


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Causes of chronic leftventricular failure

Volume overload: Valve regurgitationHigh output status

Pressure overload: Systemic hypertensionOutflow obstruction

Loss of muscles: Post MI, Chronic ischemiaConnective tissue diseases

Infection, Poisons(alcohol,cobalt,Doxorubicin)

Restricted Filling: Pericardial diseases, Restrictivecardiomyopathy, tachyarrhythmia

Pathophysiologicalmechanisms

Pathophysiologicalmechanisms Pathophysiology

Hemodynamic changes

Neurohormonal changes

Cellular changes


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Pathophysiology:

The inciting event in HF is inadequate adaptationof the cardiac myocytes to increased wall stress in

order to maintain adequate cardiac outputfollowing myocardial injury

whether of acute onset or over several months to years

whether a primary disturbance in myocardial contractility

or an excessive hemodynamic burden placed on theventricle.

Pathophysiology:compensatory mechanisms

(1) Frank-Starling mechanism, in which anincreased preload helps to sustain cardiac

performance

(2) myocardial hypertrophy with or withoutcardiac chamber dilatation, in which the massof contractile tissue is augmented

(3) release of norepinephrine (NE) byadrenergic cardiac nerves, which augmentsmyocardial contractility activation (RAAS)

Pathophysiology: The primary myocardial response to chronic

increased wall stress includes myocytehypertrophy and remodeling, usually of theeccentric type.

The reduction of cardiac output followingmyocardial injury sets into motion a cascade ofhemodynamic and neurohormonal

derangements that provoke activation ofneuroendocrine systems, most notably theabove-mentioned adrenergic systems andRAAS.

Pathophysiology:

The release of epinephrine (E) and NE,along with the vasoactive substancesendothelin-1 (ET-1) and vasopressin(V), causes vasoconstriction, whichincreases afterload.

Pathophysiology:

Increase in cyclic adenosinemonophosphate (cAMP), causes anincrease in cytosolic calcium entry. Theincreased calcium entry into themyocytes augments myocardialcontractility and impairs myocardialrelaxation (lusitropy).

Pathophysiology:

Calcium overload induce arrhythmiasand lead to sudden death.

Increase in afterload and myocardialcontractility (known as inotropy)+myocardial lusitropy= increasemyocardial energy expenditure anddecrease in cardiac output.

Myocardial cell death, increased neurohumoralstimulation, adverse hemodynamic and myocardialresponses.


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Pathophysiology: RAAS activation: preload and myocardial

energy expenditure.

in renin= delivery of chloride to the maculadensa, and beta1-adrenergic activity as aresponse to cardiac output, angiotensin IIand aldosterone levels.

Ang II, along with ET-1, is crucial in maintaining effectiveintravascular homeostasis mediated by vasoconstriction andaldosterone-induced salt and water retention.

Pathophysiology:

Ang II mediates myocardial cellularhypertrophy and may promote

progressive loss of myocardial function

Neurohumoral factors lead to myocytehypertrophy and interstitial fibrosis,resulting in increased myocardialvolume and increased myocardial mass,as well as myocyte loss.

Pathophysiology:

Remodeling process leads to early adaptivemechanisms:

Augmentation of stroke volume (Starlingmechanism) Increasing venous return to the LV increases

LVEDP and volume, thereby increasing ventricularpreload. This results in an increase in stroke

volume (SV). The normal operating point is atLVEDP of 8 mmHg, and a SV of 70 ml/beat.

Pathophysiology:

Remodeling process leads to early adaptivemechanisms:

Decreased wall stress (Laplace mechanism; P= T/R,where P= pressure, T=tension in the wall, R=radius). A dilated ventricle requires more tension inthe wall to generate the same pressure.

Increased myocardial oxygen demand, myocardial

ischemia, Impaired contractility, and arrhythmogenesis.

Pathophysiology:

Heart failure advances and/or becomesprogressively decompensated and causedecline in the counterregulatory effects ofendogenous vasodilators: NO PGs BK atrial natriuretic peptide (ANP) B-type natriuretic peptide (BNP).

Pathophysiology:

Occurs simultaneously with the increase invasoconstrictor substances from the RAASand adrenergic systems.

Increases in vasoconstriction and thuspreload and afterload, leads to cellularproliferation, adverse myocardialremodeling, and antinatriuresis with totalbody fluid excess and worsening CHFsymptoms.


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Pathophysiology:

Both systolic and diastolic heart failureresult in a decrease in stroke volume.

Elevation in plasma NE directly correlateswith the degree of cardiac dysfunctionand has significant prognosticimplications.

Pathophysiology:

Abnormal levels of NE are toxic for cardiacmyocytes

Down-regulation of beta1-adrenergic receptors,uncoupling of beta2-adrenergic receptors, andincreased activity of inhibitory G-protein.

Changes in beta1-adrenergic receptors resultin overexpression and promote myocardialhypertrophy.

Pathophysiology:

ANP and BNP are endogenously generatedpeptides activated in response to atrial andventricular volume/pressure expansion.

ANP and BNP are released from the atria andventricles, respectively, and both promotevasodilation and natriuresis.

Their hemodynamic effects are mediated by

decreases in ventricular filling pressures,owing to reductions in cardiac preload andafterload.

Pathophysiology:

BNP, in particular, produces selective afferentarteriolar vasodilation and inhibits sodiumreabsorption in the proximal convolutedtubule.

BNP inhibits renin and aldosterone releaseand, possibly, adrenergic activation as well.

ANP and BNP are elevated in chronic heart

failure. BNP, in particular, has potentially important

diagnostic, therapeutic, and prognosticimplications

Pathophysiology: Othervasoactive systems in CHF

ET receptor system adenosine receptor system tumor necrosis factor-alpha (TNF-alpha).

ET, a substance produced by the vascular endothelium, maycontribute to the regulation of myocardial function, vasculartone, and peripheral resistance in CHF.

Pathophysiology: Othervasoactive systems in CHF

Elevated levels of ET-1 closely correlate with theseverity of heart failure.

ET-1 is a potent vasoconstrictor and has exaggeratedvasoconstrictor effects in the renal vasculature,reducing renal plasma blood flow, glomerular filtrationrate (GFR), and sodium excretion.

TNF-alpha levels seem to correlate with the degree ofmyocardial dysfunction.

Local production of TNF-alpha have toxic effects onthe myocardium.


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Pathophysiology:

In systolic dysfunction, neurohormonalresponses to decreased stroke volume result

in temporary improvement in systolic bloodpressure and tissue perfusion.

Neurohormonal responses acceleratemyocardial dysfunction in the long term.

Pathophysiology:

Pathophysiology:

In diastolic heart failure, altered relaxation ofthe ventricle (due to delayed calcium uptakeby the myocyte sarcoplasmic reticulum anddelayed calcium efflux from the myocyte)occurs in response to an increase inventricular afterload (pressure overload). Theimpaired relaxation of the ventricle leads to

impaired diastolic filling of the left ventricle(LV).

Pathophysiology:

Pathophysiology:

In systolic dysfunction, left ventricular contractility is depressed, and the end-systolic pressurevolume line is displaced downward and to the right; as aresult, there is a diminished capacity to eject blood into the high-pressureaorta. The ejection fraction is depressed, and the end-diastolic pressure is

normal.

Pathophysiology:

In diastolic dysfunction, the diastolic pressurevolume line isdisplaced upward and to the left; there is diminished capacity tofill at low left-atrial pressures. The ejection fraction is normal andthe end-diastolic pressure is elevated.


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Neurohormonal changes

After loadVasoconstrictionVREndothelin

ApoptosisMay have roles in myocytehypertrophy

interleukins &TNF

Same effectSame effectVasopressin

Vasoconstriction

after load

Salt & water retentionVRRenin-Angiotensin

Aldosterone

Arteriolar constriction

After load workload O2 consumption

HR , contractility,

vasoconst. V return, filling

Sympathetic activity

Unfavor. effectFavorable effectN/H changes

Biomarkers of Inflammation in HF he Cytokine Hypothesis of HF

Cellular changes

Changes in Ca+2handling.

Changes in adrenergic receptors:

Slight in 1 receptors

1 receptors desensitization followed by down regulation

Changes in contractile proteins

Program cell death (Apoptosis)

Increase amount of fibrous tissue


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Pathophysiology Acute Pulm.Edema

In the normal lung fluid moves continuously outward from the vascular to the interstitialspace according to the net difference between hydrostatic and protein osmoticpressures, as well as to the permeability of the capillary membrane. The factors thatdetermine the amount of fluid leaving the vascular space are - the net transvascularflow of fluid, - the membrane permeability, the hydrostatic pressure in the microvessels,the hydrostatic pressure in the perimicrovascular interstitium, the plasma proteinosmotic pressure in the circulation, and the protein osmotic pressure in theperimicrovascular interstitium.

Pathophysiology APEWhen hydrostatic pressure increasesin the microcirculation, the rate oftransvascular fluid filtration rises.When lung interstitial pressureexceeds pleural pressure, fluid movesacross the visceral pleura, creating

pleural effusions. Since thepermeability of the capillaryendothelium remains normal, thefiltered edema fluid leaving thecirculation has a low protein content.The removal of edema fluid from theair spaces of the lung depends onactive transport of sodium andchloride across the alveolar epithelialbarrier.

Pathophysiology APE

The primary sites of sodium andchloride reabsorption are the epithelial

ion channels located on the apicalmembrane of alveolar epithelial type Iand II cells and distal airway epithelia.

Sodium is actively extruded into theinterstitial space by means of theNa+/K+ATPase located on the

basolateral membrane of type II cells.Water follows passively, probablythrough aquaporins, which are water

channels that are found predominantlyon alveolar epithelial type I cells

Factors aggravating heartfailure

Myocardial ischemia or infarct

Dietary sodium excess

Excess fluid intake

Medication noncompliance

Arrhythmias

Intercurrent illness (eg infection)

Conditions associated with increased metabolic demand (eg

pregnancy, thyrotoxicosis, excessive physical activity) Administration of drug with negative inotropic properties or

fluid retaining properties (e. NSAIDs, corticosteroids)

Alcohol

Stages of Heart Failure

Designed to emphasize preventability of HF

Designed to recognize the progressive

nature of LV dysfunction


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Acute Heart Failure/AcutePulmonary Edema)

Often precipitated by a myocardial infarction.

Signs include: Severe breathlessness Frothy pink sputum Cold clammy skin Tachycardia Low blood pressure

Lung crepitations

Raised jugularvenous pressure

Third heart sound

Confusion

Chronic Heart Failure

The likelihood of heart failure in the presence ofsuggestive symptoms and signs is increased ifthere is ahistory of myocardial infarction (MI) or angina, an abnormal

ECG, or a chest X-ray showing pulmonary congestion orcardiomegaly. Symptoms include:

Shortness of breath on exertion (sensitivity 66%, specificity52%)

Decreased exercise tolerance (often simply 'fatigue') Paroxysmal nocturnal dyspnoea (sensitivity 33%, specificity

76%) Orthopnoea (sensitivity 21%, specificity 81%) Ankle swelling (sensitivity 23%, specificity 80%)

Chronic Heart Failure The most specific signs are:

Laterally displaced apex beat

Elevated jugular venous pressure

Third heart sound

Less specific signs include: Tachycardia

Lung crepitations

Hepatic engorgement (tender hepatomegaly)

Peripheral oedema

Anorexia,nausea,

abdominal fullness

Rt hypochondrial pain

Framingham Criteria forDiag. of Heart Failure

Major Criteria:

Paroxysmal nocturnal dyspnoea

JVD

Rales

Cardiomegaly

Acute Pulmonary Edema

S3 Gallop

Positive hepatic Jugular reflex

venous pressure > 16 cm H2O

Diag. 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

Initial Clinical Assessment of PtsPresenting With HF

Measurement of natriuretic peptides (B-type

natriuretic peptide (BNP) or N-terminal pro-

B-type natriuretic peptide (NT-proNBP)) can

be useful in the evaluation of patients

presenting in the urgent care setting in

whom the clinical diagnosis of HF is

uncertain. Measurement of natriuretic

peptides (BMP and NT-proBNP) can be

helpful in risk stratification.

Measurement of BNP and Noninvasive Imaging

III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII

Modified


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Forms of Heart Failure

Systolic & Diastolic

High Output Failure Pregnancy, anemia, thyrotoxisis, A/V fistula,

Beriberi, Pagets disease

Low Output Failure

Acute large MI, aortic valve dysfunction---

Chronic

Forms of heart failure( cont.)

Right vs Left sided heart failure:

Right sided heart failure :

Most common cause is left sided failure

Other causes included :Pulmonary embolisms

Other causes of pulmonary htn.

RV infarction

Mitral Stenosis

Usually presents with: LL edema, asciteshepatic congestion

cardiac cirrhosis (on the long run)

Differential Diagnosis

Other causes of shortness of breath on exertion

Pulmonary disease

Obesity

Unfitness

Volume overload from renal failure or nephroticsyndrome

Angina Anxiety.


Other causes of peripheral oedema

dependent oedema

nephrotic syndrome

pericardial diseases

liver diseases

protein losing enteropathy.


Non-cardiac diseases causing high-outputcardiac failure

Anaemia

Thyrotoxicosis

Septicaemia

Paget's disease of bone

Arteriovenous fistulae.


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Diff.Diag.APE

Laboratory Findings

Laboratory Findings


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The diagnosis of heart failure is primarily based on signs and

symptoms derived from a thorough history and physical exam.

Clinicians should determine the following:

a. adequacy of systemic perfusion;b. volume status;

c. the contribution of precipitating factors and/or co-

morbidities

d. if the heart failure is new onset or an exacerbation

of chronic disease; and

e. whether it is associated with preserved normal or

reduced ejection fraction.

The Hospitalized PatientNew


Diagnosis of HF

Chest radiographs,

echocardiogram, andechocardiography are key tests in

this assessment.

The Hospitalized Patient

Diagnosis of HF


New

Concentrations of BNP or NT-proBNP should be

measured in patients being evaluated for dyspnea

in which the contribution of HF is not known. Final

diagnosis requires interpreting these results in the

context of all available clinical data and ought not to

be considered a stand-alone test.


New


Acute coronary syndrome precipitating HF

hospitalization should be promptly identified by

electrocardiogram and cardiac troponin testing,and treated, as appropriate to the overall

condition and prognosis of the patient.


New

Patients Being Evaluated for Dyspnea

It is recommended that the following common

potential precipitating factors for acute HF be

identified as recognition of these comorbidities, is

critical to guide therapy:

acute coronary syndromes/coronary

ischemia

severe hypertension

atrial and ventricular arrhythmias

infections pulmonary emboli

renal failure

medical or dietary noncompliance


New


Precipitating Factors for Acute HF

ECGChest X-ray

Size and shape of heart

Evidence of pulmonary venouscongestion (dilated or upperlobe veins perivascularedema)

Pleural effusion


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Echocardiogram Function of both ventricles

Wall motion abnormality that may signify CAD

Valvular abnormality

Intra-cardiac shuntsSist.HF

Patterns o LV D asto c F ng asshown by standard Doppler echo.

Adams KF, LindenfeldJ, et al. HFSA 2006 ComprehensiveHeart Failure Guideline. J Card Fail 2006;12:e1-e122.

EvaluationExercise Testing

Exercise testing is not recommended as part ofroutine evaluation in patients with HF.

Exercise testing with physiologic testing forinducible abnormality in myocardial perfusion orwall motion abnormality should be considered toscreen for the presence of coronary arterydisease with inducible ischemia.

Strength of Evidence = C


EvaluationExercise Testing

Specific circumstances in which maximal exercise testing withmeasurement of expired gases should be considered include:

Assessing disparity between symptomatic limitation and objectiveindicators of disease severity

Distinguishing non HF-related causes of functional limitation,specifically cardiac vs. pulmonary

Considering candidacy for cardiac transplantation or mechanicalintervention

Determining the prescription for cardiac rehabilitation

Addressing specific employment capabilitiesStrength of Evidence = C


EvaluationEndomyocardial Biopsy

Endomyocardial biopsy should be considered in patients:

With rapidly progressive clinical HF or ventricular dysfunction,despite appropriate medical therapy

Suspected of having myocardial infiltrative processes, such assarcoidosis or amyloidosis

With malignant arrhythmias out of proportion to LV dysfunction,where sarcoidosis and giant cell myocarditis are considerations

Strength of Evidence = C


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Cardiac Catheterization

When CAD or valvular is suspected

If heart transplant is indicated

Pulmonary-ArteryCatheterization

- used to assess the pulmonary-artery occlusionpressure, is considered the gold standard fordetermining the cause of acute pulmonary edema.

- permits monitoring of cardiac filling pressures, cardiacoutput, and systemic vascular resistance duringtreatment.-a pulmonary-artery occlusion pressure above 18 mm Hgindicates cardiogenic pulmonary edema or pulmonaryedema due to volumeoverload.- common complications include: hematoma at the insertion site,arterial puncture, bleeding, arrhythmias, and bloodstreaminfection.

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Heart Failure Dg 2010