Introduction to heart failure

Introduction to heart failure, CHF, CCF, Congestive HF

1. Heart Failure
Mr. Jaineel Dharod
Dept. of Pharmacology

2. Common Terms related to Heart
•Cardiac output
•Heart Rate
•Force of Contraction
•Peripheral vascular resistance
•Preload
•Afterload
•Stroke volume
•Systole
•Diastole
•EDV
•ESV
•Congestion

3. •CardiacOutputTheamountofbloodtheheartpumpsthroughthe
circulatorysysteminaminute.
•Heartrateisthespeedoftheheartbeatmeasuredbythenumber
ofcontractionsoftheheartperminute.
•Cardiaccontractilitycanbedefinedasthetensiondevelopedand
velocityofshortening(i.e.,the“strength”ofcontraction)of
myocardialfibersatagivenpreloadandafterload.
•Vascularresistanceistheresistancethatmustbeovercometopush
bloodthroughthecirculatorysystemandcreateflow.
•Preloadistheamountofsarcomerestretchexperiencedbycardiac
musclecells,calledcardiomyocytes,attheendofventricular
fillingduringdiastole
•Afterloadisthepressurethattheheartmustworkagainsttoeject
bloodduringsystole.

4. •Strokevolumeisthevolumeofbloodpumpedfromtheleft
ventricleperbeat.
•Systoleiscontractionofhearttopumpthebloodoutofheart
•Diastoleistherelaxationofheartafteracontraction(atrium
emptyingbloodintoventricles)
•EDV:Enddiastolicvolumeisvolumeofbloodinsideheartaftera
diastole
•ESV:Endsystolicvolumeisvolumeofbloodinsideheartaftera
Systole
•Congestion:Theblockageofsomethingorpassageofsomethingis
calledcongestion.

5. Calculations
Stroke Volume (ml/beat) = EDV –ESV
Cardiac output (CO) (ml/min) = Stroke volume * Heart Rate (bpm)
CO = SV x HR
EDV and ESV are measured by Echocardiograph in which sound
waves depicts the image of heart.

6. HEART FAILURE: PATHOPHYSIOLOGY

7. Heart Failure
•Thetermheartfailureliterallymeansaconditioninwhichthe
bodyisunabletopumpthesufficientamountofbloodtomeetthe
metabolicdemandsofthebodyandalsounabletoreceiveitback,
becauseeverytimeafterasystole,someresidualbloodremainsin
itsventricles.
•Inpast,itwastermedascongestiveheartfailurebecauseoffluid
retentionandedematousstateleadingtopulmonaryand
peripheralcongestion,butnowpreciselyitiscalled‘heartfailure’
becauseallpatientsdonotshowfluidoverloadinitially.

10. Comparison

11. Low vs High Output (HF)
•HFissyndromewithmultiplecauses(MI,HT,Angina,ventricular
tachycardia,DM,hyperthyroidism,anemia,etc.),thatmayinvolve
rightventricle,leftventricleorboth.
•LowcardiacoutputHFismostcommonHF,wherethemetabolic
demandsofbodyareinnormallimit,buttheheartisunableto
meetthem.

12. Low vs High Output (HF)
•HighcardiacoutputHFoccursrarely.
•Insomecoexistingconditions(hyperthyroidism,anemiaand
arteriovenousshunt),themetabolicdemandsofthebodyare
excessivethatevenincreasedCOisinsufficienttomeetthem.
•Ascomparedrolowoutputfailureitshouldbetreatedby
correctingtheunderlyingcause.

13. Left vs Right Sided (HF)
•Signandsymptomsusuallyresultfromeffectsofbloodbackingup
behindthefailingventricles(exceptinhighoutputHF)
•LeftandrightsidedHFareusuallynotseparatebecauseoverthetime
rightsidedHFcausesleftsidedandviceversa
•Ifthebloodcannotbepumpedadequatelyfromtheleftventricletothe
peripheralcirculation,apartofitwillberetainedinleftventricle
duringsystole.
•Becauseofthisleftventriclewillnotbeabletoreceivecompleteblood
fromleftatriumandlungs.
•HenceleftsidedHFischaracterizedbypresenceofpulmonary
congestionandoedema(presentedasshortnessofbreathanddyspnoea)

14. Left vs Right Sided (HF)
•Ontheotherhand,whenbloodcannotbepumpedfromright
ventricleintolungs,apartofitretainsinrightventricle.
•Becauseofthisaccumulation,therightventriclewillbeunableto
acceptbloodfromperipheralorgans,henceitischaracterizedby
peripheraloedema.

15. Compensatory Mechanisms
•The failing heart evokes the following compensatory mechanisms
to enhance the CO
•CO = Stroke volume x HR
•If this mechanisms are able to restore the CO, the heart failure is
said to be compensated.
•In long term this compensations rather increase the work load of
the heart and cause worsening cardiac performance.

16. Compensatory Mechanisms
1.Increased Sympathetic activity
2.Activation of RAAS
3.Ventricular Remodeling

18. Increased Sympathetic Activity
•BaroreceptorssenseadecreaseinBPandtriggeractivationofBeta1-
adrenoceptorsintheheartresultinginanincreaseinheartrate(HR)and
contractility.
•Inaddition,alpha1receptormediatedvasoconstrictionenhancesvenous
returnwhichincreasespreload.
•TheincreaseinHR,contractilityandpreloadinitiallyincreasestheCO.
•Vasoconstrictionalsoincreasesarterialtone,whichresultsinanincrease
inafterloadandadecreaseinejectionfraction.

19. Increased Sympathetic Activity
•COfinallydecreases,whichreducesrenalperfusion.
•Aftersometime,thereisadown-regulationofBeta1receptors,
whichnegatesthestimulatoryeffectofsympatheticdischarge.
•Sustainedincreaseinsympatheticactivity,however,increasesthe
workloadonthefailingheartandthereforecontributesadversely
tothecardiacperformanceultimately.

20. Activation of Renin-Angiotensin Aldosterone
System (RAAS)
•AfallinCOdecreasesbloodflowtokidneys.
•Thispromptsreninrelease,synthesisofangiotensinII,andrelease
ofaldosterone.
•ThisresultsinanincreaseinPVRwithNa
+
andwaterretention.
•Thusbloodvolumeincreasesandmorebloodreachestheheart(in
preload).SinceafterloadalsoincreaseswithincreaseinPVR,the
heartisunabletopumpthisextravolume.

21. Activation of Renin-Angiotensin Aldosterone
System (RAAS)
•Theresultingfluidback-upbetweentheleftventricleandthelungs,
anduptorightventriclefromperipheralcirculation,causes
pulmonaryandperipheraloedema.
•AlthoughatrialnatriureticpeptideisalsoincreasedinHF,owingto
increasedarterialpressure,paradoxicallyitdoesnotproduce
natriureticorvasodilatoryeffectsinpatientsofHF.
•Excessivecompensatoryneurohormonalactivity,therefore,ultimately
depressescardiacfunctions.

22. Ventricular Remodeling
•Themostimportantintrinsiccompensatorymechanismis
myocardialhypertrophywitharesultantincreaseinamore
sphericalshapeoftheheartreferredtoas"cardiacremodeling"
whichmeansatypeofdilatationotherthanthatduetopassive
stretchofheartmuscle.
•Duringremodelingthereisproliferationoftheconnectivetissue
cellsaswellasofabnormalmyocardialcellsundertheinfluenceof
Ang-II.
•Initially,theincreaseinmusclemasshelpstomaintaincardiac
performance.

23. Ventricular Remodeling
•Butaftertheinitialbeneficialeffects,hypertrophycanleadto
ischaemicchangesandalterationsinventriculargeometry.
•Theventricularwalltensionincreases,mechanicalperformanceof
heartdecreasesandbloodinboththeventriclesisretainedwhich
ultimatelyworsenstheremodelingprocess.
•Overtime,themyocytesinthefailingheartdiethrough
apoptosisleavingtheremainingmyocytessubjecttoevengreater
workload.
•Hence,remodelingalso,ultimatelyworsensthecardiac
performance.

24. PHENOMENON OF DECOMPENSATED HEART
FAILURE
•Aftercertainperiod,thecompensatorymechanismsbecome
exhaustedandincreasinglyineffective,enteringaviciouscircleof
decompensationinwhichthecompensatorymechanismsbecomeself
defeating.
•Asthestraincontinues,totalperipheralresistance(TPR)and
afterloadincrease,therebydecreasingtheejectionfractionper
heartbeat.
•PreloadisalsoincreasedinHFbecauseofincreasedbloodvolumeand
venoustone.
•Ultimately,astagecomeswhentheadaptivemechanismfailto
maintaintheCO.TheHFnowistermedas"decompensated".

25. Sign & Symptoms of Decompensated HF
Asthebloodvolumeexpands,thedecompensatedheartisunabletopumpand
producessignsandsymptomsofHFlike:
a.Pulmonaryandperipheraloedema(asdiscussedabove).
b.Dyspnoeawithcyanosis,duetohypoxiaasaresultofinadequate
oxygenationofblood.
c.Hepatomegalyduetohepaticcongestion.
d.Cardiomegalyduetomyocardialhypertrophyandcardiacremodeling.
e.ReflextachycardiaduetohypoxiaanddecreasedCOinducedsympathetic
discharge.
f.Decreasedurineformationduetorenalcongestion.
g.DecreasedexercisetoleranceandmusclefatigueduetodiminishedCO.

26. Management of HEART FAILURE (HF)
•ThetherapeuticgoalinthemanagementofHFistoincrease
cardiacoutput(CO)anyhow.Abetterunderstandingofpreload,
afterloadandmyocardialcontractilityhasencouragedthe
judicioususeofthefollowingdrugsforthetreatmentofheart
failure:

27. DRUGS USED IN HEART FAILURE (HF)
I. Drugs with positive inotropic effects:
a) Cardiac Glycosides: DIGOXIN, DIGITOXIN and QUABAIN.
b) Bipyridines or Phosphodiesterase Inhibitors: INAMRINONE, MILRINONE,
LEVOSIMENDAN and ENOXIMONE
c) B-Adrenergic Agonists: DOPAMINE, DOBUTAMINE and DOPEXAMINE

28. DRUGS USED IN HEART FAILURE (HF)
II. Drugs without positive inotropic effects:
a) Diuretics: BUMETANIDE, FUROSEMIDE, HYDROCHLOROTHIAZIDE,
METOLAZONE and SPIRONOLACTONE
b) ACEIS: ENALAPRIL, LISINOPRIL and RAMIPRIL
(also AT receptor antagonist, e.g., LOSARTAN
c) B-Adrenoceptor Antagonists: BISOPROLOL, CARVEDILOL and METOPROLOL
d) Vasodilators: HYDRALAZINE, SODIUM NI NITROPRUSSIDE, ISOSORBIDE
DINITRATE and NESIRITIDE
e) Vasopressin Receptor Antagonists: CONIVAPTAN and TOLVAPTAN