Cardiac failure

By Dr. Osman Bukhari

Cardiac failure: Occurs when the heart is unable to maintain sufficient cardiac output to .meet the demands of the body .Incidence increases with age .Many pts. are admitted repeatedly Despite improvement in management mortality is still high

.Pathophysiology

:Manifestations of cardiac failure

:Left cardiac failure- 1 ymptoms include: fatigue! e"ertional dyspnoea! orthopnoea # paro"ysmal . nocturnal dyspnoea igns include: $ardiomegaly with displaced # often sustained apical impulse! triple # gallop rhythm! basal lung crac%les! pulsus alternans! .functional M& # pulmonary edema -

Cardiomegaly

LVF & pulmonary oedema

:-$auses
.()- ' .Ischemic heart disease- * .,o stenosis # regurgitation- + .Mitral regurgitation- .$ardiomyopathy- . Myocarditis. .arrhythmias (igh output states 2anemia ! ,-3 fistula! thyroto"icosis! PD,! pagets disease of bone! beri-beri # gram .4negative septicemia

0- - / -1

:Right cardiac failure- 2

ymptoms include: - fatigue! anore"ia and nausea related to distension and fluid accumulation .in areas drained by systemic veins &t hypochondrial pain swelling of of the 55s -

igns: include: - increased 63P tender smooth hepatomegaly dependent pitting edema ascites # pleural transudates tachycardia. 5P(! )&! &t. +

Pitting oedema of the LL

$auses
5t heart failure- ' 4 $hronic lung disease 2core pulmonale- * Pulm embolism- + Pulm ()- .)ricuspid valve dis- . Pulm valve dis- / 5t to &t shunts 2 , D ! 3 D4 1- isolated &t. 3ent. $ardiomyopathy -0

.I(D- 7 $onstrictive pericarditis # cardiac . tamponade .(igh output states- ''

- '8

.$$9: $ombines both 5t # &t (9- +

Acute heart failure

.:"tensive acute MI- ' .&upture of I3 producing 3 D- * Papillary or chordal rupture in -+ endocarditis producing M& -udden ,o valve rupture in endocarditis .,cute pulmonary embolism # cardiac .tamponade In all these conditions the heart si;e is . relatively normal

High output states are associated with tachycardia! gallop rhythm # patients .are often warm with distended veins

Factors precipitating HF in controlled .patients . Increased salt inta%e- ' .<ncontrolled ()- * .,naemia # pregnancy- + .9luid overload- .MI- . .,rrhythmias specially ,9- / .Pulm. :mbolism- 0

Infections sp. chest infections causing - 1 hyperdynamic circulation. 7.)hyroto"icosis .Drug non compliance- '8 &enal failure secondary to diuretic - '' induced volium depletion or due to . intrinsic renal disease

Investigations in HF )his is to confirm (9 # to establish the .underlying cause $=&: hows cardiac si;e # evidence of - ' pulmonary congestion 2upper lobe venous diversion> bat win appearance 4in pulm oedema :$?: hows arrhythmias! ischemia ! - * . chamber hypertrophy etc :cho: 2*- dimentional # doppler echo4 - + show valves! chambers si;e! e@ection . fraction! intracardiac thrombi

CXR with right apical fibrosis

Electrocardiogram

Echocardiography

.$A$! 59) # blood urea # electrolytes- $ardiac en;ymes in acute MI- . .$ardiac catheri;ation- / ,mbulatory :$? monitoring in -0 . suspected arrhythmias . tress :$?- 1

Coronary angiography

Treatment of HF Preventive measures in HF include: - $essation of smo%ing $ontrol of DM :ffective treatment of () )& of hypercholesterolemia .pharmacological )& following MI

TR of chronic HF aims at: - &elieving symptoms! &etarding disease progression! $orrection of the cause ! -)& of aggravating factors! $ompliance with drug therapy. ! Improving survival

:?eneral )&- '

Physical activity: ranges from bed rest in severe (9 to low level e"ercise in compensated (9 . ,void strenuous .e"ercise Dietary modifications: B) reduction! salt restriction! alcohol abstinence # fluid restriction in severe (9 .and dilutional hyponatraemia .:ducation -

4Drug )& Of (92 Pharmacotherapy- *

Diuretics 3asodilators Digo"in ,ntiarrhythics,nticoagulants Inotropic drugs AAtatins -

4Drug )& Of (92 Pharmacotherapy- *

:Diuretics- '
,ct by promoting renal e"cretion of salt and water reducing preload # rapidly improves dyspnoea # systemic congestion. )hey also cause arteriolar . vasodilatation reducing after load 5oop diuretics: e.g. frusemide 2lasi"4 have a rapid onset of action # short duration of action.)hey cause 4hypo%alaemia 2 add slow-C

b-)hia;ide diuretics: e.g. hydrochlorothia;ide and $hlorthalidone have mild diuretic effect! but act synergistically when combined with loop diuretics. Dot effective in renal impairment. Metola;one is a powerful thia;ide # is combined with loop diuretics in severe . and resistant (9 Loop & thiazide diuretics have no proven E survival benefit. They give symptomatic relieve

c- Potassium sparing diuretics: $are with ,$:-I # avoided in renal impairment . pironolactone reduces mortality in doses of up to *. mg when added to conventional therapy in moderate to severe (9. &is% of hyper%alaemia is ..high with doses of F .8 mg ,meloride # triamterene are wea% but useful when combined with loop ..diuretics

:3asodilater therapy- * a- ,$:-Is reduce after load # pre load - reduce circulating levels of catecholamines! reduce AP reduce cardiac dilatation # $$9 after e"tensive MI improve e"ercise tolerance # survival . in pts. with severe (9

,$:-I should be carefully introduced in pts. on high doses diuretics # in the presence of hyponatraemia. .$are with C- sparing diuretics

b- ,&As have similar effects to ,$:-I but . do not affect brady%inin metabolism c- ,lpha bloc%ers 2pra;ocin4 # direct smooth muscle rela"ants 2hydrala;ine4 are not very effective in (9. $$As reduce after load but have no prognostic benefit in (9. Diltia;em and .verapamil are $I in (9 d- Ditrates 2glyceride trinitrates and isosorbide mononitrates4 reduce preload and reduce pulm edema.Only

combination with hydrala;ine have . proven prognostic value AA used in pts. with chronic stable (9 2e.g. metoprolol! bisoprolol! atenolol and carvedilol4! improve symptoms! e"ercise tolerance! 53 function and mortality in pts. with (9. .Initial doses should be low

-+

:Inotropic drugs- Digo"in - ympathomimetic-

Digo"in : cardiac glycoside! It bloc%s ,3 node and increases myocardial contractility. used in severe (9 with conventional therapy! ,9! atrial flutter # 3). 78G is e"creted unchanged in urine and accumulation can occur in renal failure. Digito"in is used In renal failure. <sual dose is 8.'*.-8.*. mgHd. with dose of 'mg in emergency

:Dose is reduced in elderly renal failure hyperthyroidism -- Iuinine therapy electrolyte disturbance e.g. (ypo%al # hypo Mg. .$a is dangerous in digitali;ed pts

*-- ' -+ -. I3

: of Digo"in include: (,! fatigue! muscle wea%ness! abd. .Pain! D! 3! Bt. loss # gynaecomastia Digo"in to"icity include: anore"ia! D! 3! coloured vision with halo around ob@ects 2"anopsia4! arrhythmias # fits. - )& of digo"in to"icity: Ay stopping the drug! restoration of ser. C and management of arrhythmias. Digo"in abs. in life .threatening to"icity

,dr.! dobutamine! dope"opamine # dopamine are I3 adrenergic agonist. )hey increase $O # improve perfusion but increase myocardial O* reIuirements # aggravate cardiac ischemia. 3olume depletion should be corrected before their use. Main use in pts. with acute 539! following cardiac surgery # in pts. with end .stage (9 as a bridge to transplantation

Dobutamine is a A* agonist increasing cardiac contraction # has vasodil. effect by alpha bloc%er effect. Dose *..-'8 .mcgH%gHminute

Dope"amine is A* agonist with additional action on peripheral dopamine receptors .improving renal perfusion Dopamine in low dose 2*-- mcgH%gHmin.4 improves renal perfusion. In dose of -'8 mcgH%gHmin. increases (& # cardiac contractility. (igher doses increase AP at . the e"pense of tissue perfusion Doradr. &aise AP by peripheral .vasoconstriction

,nticoagulants to prevent

thromboembolism in pts. with ,9 ! endocardial thrombus # P( of .thromboembolism

-.

:,ntiarrhythmic agents- /
Drugs - D$ shoc% Implantable cardiovertor - defibrillator 4I$D 2 tatins- 0 -

BB !"#$% statins & spironolactone may .reduce sudden death in pts. &ith '% and HF

Don-pharmacological )r. of (9:

.'- &evasculari;ation

.Pacema%er or I$D- * 3alvular surgery # correction of other . causes of (9 .$ardiac transplantation- .<ltra-filtration- . .Intra-aortic balloon pump- /

-+

Pace ma er

In summary:

'-

,ll pts. with clinical (9 should receive diuretics # ,$:-I. *Patients with ,9 should be .digitali;ed Pts. in & improve with addition of - + . Digo"in or AA Pts. with asymptomatic 53 -dysfunction benefit from prophylactic ,$:- I therapy or ,&A

Pts. with ischemic (9 # intolerant to - . ,$:-I or in whom it is $I may benefit from nitrateH hydrala;ine . therapy . pironolactone should be added- /

Pulmonary edema
.5ife-threatening emergency .<sually preceded by PDD Interstitial edema usually occurs with . capillary pressure of *8 mm(g ,lveolar edema occurs with pressure of . *.-+8 mm(g $auses are those of 539! M # increased pulmonary capillary 4.permeability 2,dult &D

Pulmonary oedema

:$linical features include :"treme OA - .Bhee;ing .,n"iety # sweating .$ough with frothy blood tinged sputum )achypnea! cyanosis! tachycardia and . gallop rhythm .$rac%les # whee;e in ; chest .5ow arterial PO* $=& shows diffuse ha;iness # bat wing . appearance

:)reatment Include ,dmission in $$<. - .$ardiac bed $ontinuous flow high O* conc and in .severe cases pt. is ventilated 4. I3 morphine '8-'. mg2 J antemetic ,voided if AP K 78 I3 loop diuretic which produces immediate vasodilt. In addition to . more delayed diuresis 3enodilt. # arterial vasodilators to . decrease pre-load # after load

,minophylline . mgH%g I3 2 *.8-.884 slowly to avoid the ris% of precipitating ventricular arrhythmias. It is bronchodilator.! vasodilt. # increases cardiac contractility. <sually used when .bronchospasm is present .Monitor rhythm! O* saturation 3enesection # mechanical methods of reducing venous return are ineffective . and rarely used )reat precipitating factors 2arrhythmias! .4 chest infection! etc

$orrect the underlying cause of increased pulmonary capillary permeability 2to"ins! hypo"ia! .4. infections! DI$! etc