8/9/2019 Heart Failure Dg 2010
1/15
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
8/9/2019 Heart Failure Dg 2010
2/15
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
8/9/2019 Heart Failure Dg 2010
3/15
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.
8/9/2019 Heart Failure Dg 2010
4/15
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.
8/9/2019 Heart Failure Dg 2010
5/15
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.
8/9/2019 Heart Failure Dg 2010
6/15
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.
8/9/2019 Heart Failure Dg 2010
7/15
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
8/9/2019 Heart Failure Dg 2010
8/15
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
8/9/2019 Heart Failure Dg 2010
9/15
8/9/2019 Heart Failure Dg 2010
10/15
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
8/9/2019 Heart Failure Dg 2010
11/15
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.
Differential Diagnosis
Other causes of peripheral oedema
dependent oedema
nephrotic syndrome
pericardial diseases
liver diseases
protein losing enteropathy.
Differential Diagnosis
Non-cardiac diseases causing high-outputcardiac failure
Anaemia
Thyrotoxicosis
Septicaemia
Paget's disease of bone
Arteriovenous fistulae.
8/9/2019 Heart Failure Dg 2010
12/15
Diff.Diag.APE
Laboratory Findings
Laboratory Findings
8/9/2019 Heart Failure Dg 2010
13/15
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
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
Diagnosis of HF
Chest radiographs,
echocardiogram, andechocardiography are key tests in
this assessment.
The Hospitalized Patient
Diagnosis of HF
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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.
The Hospitalized Patient
New
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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
The Hospitalized Patient
New
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
Precipitating Factors for Acute HF
ECGChest X-ray
Size and shape of heart
Evidence of pulmonary venouscongestion (dilated or upperlobe veins perivascularedema)
Pleural effusion
8/9/2019 Heart Failure Dg 2010
14/15
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
Adams KF, LindenfeldJ, et al. HFSA 2006 ComprehensiveHeart Failure Guideline. J Card Fail 2006;12:e1-e122.
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
Adams KF, LindenfeldJ, et al. HFSA 2006 ComprehensiveHeart Failure Guideline. J Card Fail 2006;12:e1-e122.
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
8/9/2019 Heart Failure Dg 2010
15/15
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.