Syndrome of heart Syndrome of heart failurefailure

DR A SUNDASDR A SUNDASDEPT OF INTERNAL MEDICINE DEPT OF INTERNAL MEDICINE

GREYSGREYS20 SEPTEMBER 200620 SEPTEMBER 2006

INTRODUCTIONINTRODUCTIONHEART FAILUREHEART FAILURE ………Pump failure/ inadequate ………Pump failure/ inadequate `pump function of heart`pump function of heart

-- A complex blend of structural, functional and biological A complex blend of structural, functional and biological alteratiomyocardium. Is a common end point of most of the alteratiomyocardium. Is a common end point of most of the cardiac cardiac diseases,diseases,

-- A major cause of cardiovascular morbidity & mortality.A major cause of cardiovascular morbidity & mortality.-- Results in more than one million hospitalizations/years.Results in more than one million hospitalizations/years.-- The most common discharge diagnosis among patients older The most common discharge diagnosis among patients older

than 65 years. than 65 years. -- With very high mortality rate with 50% patients dead after With very high mortality rate with 50% patients dead after

five years.five years.-- Cost of management is huge. Cost of management is huge.

CLASSIFICATION CLASSIFICATION –– A COMPLEX ISSUEA COMPLEX ISSUE

a.a. Acute heart failure Acute heart failure vsvs chronic heart failurechronic heart failure

b.b. Left heart failure Left heart failure vsvs right heart failureright heart failure

c.c. Diastolic heart failure Diastolic heart failure vsvs systolic heart failuresystolic heart failure

d.d. Forward failure Forward failure vsvs backwards failurebackwards failure

e.e. High output failure High output failure vsvs low output failurelow output failure

Causes of heart failureCauses of heart failure

1.1. volume overloadvolume overloada.a. RegurgitantRegurgitant valves( valves( mitralmitral or tricuspid valve)or tricuspid valve)b.b. High out put states( anemia thyrotoxicosis)High out put states( anemia thyrotoxicosis)

2.2. Pressure overloadPressure overloada.a. Systemic hypertensionSystemic hypertensionb.b. Outflow tract Outflow tract obstruction(aorticobstruction(aortic stenosisstenosis, ASH), ASH)

3.3. Loss of muscleLoss of musclea.a. MI,connectiveMI,connective tissue disease, SLEtissue disease, SLE

4.4. Loss of contractility Loss of contractility a.a. Poison ,Poison ,alcohol,cobalt,doxorubicinalcohol,cobalt,doxorubicinb.b. Infections; viral bacterialInfections; viral bacterial

5.5. Restricted fillingRestricted fillingaa MitralMitral stenosisstenosis,,b.b. Pericardial Pericardial disease,constrictivedisease,constrictive pericarditis& pericardial pericarditis& pericardial

temponadetemponadec.c. Infiltrative diseases like Infiltrative diseases like amyloidosisamyloidosis..

Pathophysiology of heart failurePathophysiology of heart failure

Should be understood at multiple levelsShould be understood at multiple levelsHeart failure

Homodynamic changes

Neurohumorol changes

Cellular changes

PathophysiologyPathophysiologyHemodyanamic ChangesHemodyanamic Changes

a. Systolic a. Systolic DysfxDysfxb. Diastolic b. Diastolic DysfxDysfx

a.a. Systolic Systolic DysfxDysfxOnce forward pump function is impaired. Once forward pump function is impaired. isovolumetric systolic pressure curve of pressure isovolumetric systolic pressure curve of pressure volume relationship is shifted downwards. Decrease volume relationship is shifted downwards. Decrease in stroke volumein stroke volumeheart can respond with 3 compensatory mechanisms.heart can respond with 3 compensatory mechanisms.

1).1). Increase preload Increase preload ––Frank starling law but it occurs at Frank starling law but it occurs at the cost of Increase end diastolic pressure.the cost of Increase end diastolic pressure.

2).2). Increase release of catecholamines that increase Increase release of catecholamines that increase cardiac out put.cardiac out put.

3). Hypertrophy of cardiac muscle & incr3). Hypertrophy of cardiac muscle & increase ease ventricular volume.ventricular volume.

Diastolic dysfunctionDiastolic dysfunction

restricted relaxationrestricted relaxation

-- systolic isovolumetric curve remains unchanged but pressure systolic isovolumetric curve remains unchanged but pressure volume curve is shifted to left with increase in left ventriculavolume curve is shifted to left with increase in left ventricular r end end diastolic pressure & this lead to symptoms of heart diastolic pressure & this lead to symptoms of heart failure.failure.

-- Conditions like hypertension & myocardial ischemia can cause Conditions like hypertension & myocardial ischemia can cause diastolic dysfunction. Ischemia can cause both systolic & diastolic dysfunction. Ischemia can cause both systolic & diastolic dysfunctiondiastolic dysfunction..

Ventricular remodelingVentricular remodeling

1) concentric hypertrophy (pressure overload) 1) concentric hypertrophy (pressure overload)

2) eccentric hypertrophy ( volume overload)2) eccentric hypertrophy ( volume overload)3) mixed picture (e.g. in MI)3) mixed picture (e.g. in MI)pressure overload cause myocyte hypertrophy while volume pressure overload cause myocyte hypertrophy while volume overload causes elongation of myocyte via different signaling overload causes elongation of myocyte via different signaling pathways.pathways.

Neurohumorol changesNeurohumorol changesrelease of cytokines & hormonesrelease of cytokines & hormones

11) ) sympathetic activitysympathetic activity lead to increase preload & lead to increase preload & peripheral vascular resistance. peripheral vascular resistance.

2) 2) renin angiotensin aldosteronerenin angiotensin aldosterone synthesis via arterial synthesis via arterial under under filling causes salt & water retention & increase filling causes salt & water retention & increase preload.preload.

3)3) increase release of vasopressinincrease release of vasopressin vasoconstriction & vasoconstriction & increase water resorption from distal nephronincrease water resorption from distal nephron

4)4) increase release of inflammatory cytokines increase release of inflammatory cytokines like TNF like TNF alpha, alpha, ILsILs lead to myocyte hypertrophy & apoptosis.lead to myocyte hypertrophy & apoptosis.

5) 5) increase release of endothelinsincrease release of endothelins increase myocyte increase myocyte growth &collagen deposition also lead to endothelial growth &collagen deposition also lead to endothelial hypertrophy & pulm hypertension.hypertrophy & pulm hypertension.

Cellular changesCellular changes

1)1) Decrease level of mRNA for calcium channels.Decrease level of mRNA for calcium channels.

2) 2) Decrease level of mRNA for phospholambin & calcium Decrease level of mRNA for phospholambin & calcium ATPaseATPase

3) 3) Up regulation of alpha 1 receptors & down regulation of Up regulation of alpha 1 receptors & down regulation of beta 1 beta 1 receptorsreceptors

4) 4) Up regulation of inhibitory G protein which causes Up regulation of inhibitory G protein which causes decrease myocyte contractility.decrease myocyte contractility.

5) 5) Re expansion of fetal & neonatal forms of myosin & Re expansion of fetal & neonatal forms of myosin & troponin under the influence of inflammatory troponin under the influence of inflammatory cytokines & increase cytokines & increase activity of cactivity of c--fos, cfos, c--myc & cmyc & c-- junjun..

6) 6) Increase apoptosis lead to holes formation secondary to Increase apoptosis lead to holes formation secondary to hypertrophic signal like TNF alpha & a vicious circle start hypertrophic signal like TNF alpha & a vicious circle start where where increase hypertrophic signals cause more & more increase hypertrophic signals cause more & more apoptosis.apoptosis.

7)7) Increase in fibrous tissueIncrease in fibrous tissue secondary to collagen deposition secondary to collagen deposition because of fibroblast proliferation & myocyte death & increase because of fibroblast proliferation & myocyte death & increase endothelin release. Fibrosis cause increase chamber stiffness.endothelin release. Fibrosis cause increase chamber stiffness.

8) 8) Myocyte slippageMyocyte slippage because of activation of collagenases that because of activation of collagenases that disrupt the collagen network.disrupt the collagen network.

ESC guidelines for acute heart failureESC guidelines for acute heart failure

a.a. Acute heart failure is defined as rapid onset of symptoms & signAcute heart failure is defined as rapid onset of symptoms & signs s secondary to abnormal cardiac function.secondary to abnormal cardiac function.

b.b. It may occur with or without previous cardiac disease.It may occur with or without previous cardiac disease.

c.c. It can be related to systolic or diastolic dysfunction of heart,It can be related to systolic or diastolic dysfunction of heart,rhythm abnormality or preload after load mismatch.rhythm abnormality or preload after load mismatch.

d.d. It is life threatening & need urgent intervention.It is life threatening & need urgent intervention.

PRESENTATIONSPRESENTATIONS

1)1) Acute decompensated heart failureAcute decompensated heart failure

(a)(a) De novoDe novo

(b) (b) As decompensation of chronic heart failure which doesn’t fit As decompensation of chronic heart failure which doesn’t fit in the in the criterion of pulmonary edema, cardiogenic shock or criterion of pulmonary edema, cardiogenic shock or hypertensive crisishypertensive crisis

2)2) Hypertensive acute heart failureHypertensive acute heart failure

heart failure accompanied by high blood pressure & relatively heart failure accompanied by high blood pressure & relatively preserved left ventricular function. CXR shows features of acutepreserved left ventricular function. CXR shows features of acutepulmonary edema.pulmonary edema.

3)3) Pulmonary Edema Pulmonary Edema confirmed on CXR orthorpnoea oxygen confirmed on CXR orthorpnoea oxygen saturation of <90% on room air prior to treatmentsaturation of <90% on room air prior to treatment

4)4) Cardiogenic shock Cardiogenic shock Evidence of tissue hypoperfusionEvidence of tissue hypoperfusion

systolic BP of <90 & a drop in MAP of >30 or low urine output systolic BP of <90 & a drop in MAP of >30 or low urine output <0,5ml/kg/hr & pulse of >60bpm<0,5ml/kg/hr & pulse of >60bpm

5)5) High out put failureHigh out put failure feature of high output( warm peripheries, feature of high output( warm peripheries, pulmonary congestion & sometimes low BP as in septic shock) pulmonary congestion & sometimes low BP as in septic shock) ,fast heart rate. Condition like anemia thyrotoxicosis paget’s ,fast heart rate. Condition like anemia thyrotoxicosis paget’s disease.disease.

6)6) Right heart failureRight heart failure raised jvp low output increase liver size.raised jvp low output increase liver size.

CLASSIFICATIONCLASSIFICATION1. 1. Forward failureForward failure Right & left heart failure. can be mild Right & left heart failure. can be mild moderate or severe presents with;moderate or severe presents with;

-- FatigueFatigue

-- Decrease tissue perfusion at rest with Decrease tissue perfusion at rest with -- Weakness Weakness -- DrowsinessDrowsiness

-- Cold clammy skin low BP weak pulse oliguriaCold clammy skin low BP weak pulse oliguria..-- Pallor with peripheral cyanosisPallor with peripheral cyanosis

-- Culminate in cardiogenic shockCulminate in cardiogenic shock-- Clinical signs will reveal the cause like temponade Clinical signs will reveal the cause like temponade

infection like IE trauma or pulmonary embolus.infection like IE trauma or pulmonary embolus.

Backwards FailureBackwards Failure

Left heartLeft heart . Patient presents with exertional dyspnoea pulmonary . Patient presents with exertional dyspnoea pulmonary oedema, cyanosis, dry cough or frothy sputum. Pallor, cold, skinoedema, cyanosis, dry cough or frothy sputum. Pallor, cold, skin, fine , fine rales & congestion on CXR.BP may be normal or rales & congestion on CXR.BP may be normal or elevated. Conditions elevated. Conditions like ischemia infarct, aortic or like ischemia infarct, aortic or mitralmitral valve dysfunction rhythm valve dysfunction rhythm disturbance or tumor of left heart are related to this conditiondisturbance or tumor of left heart are related to this condition..

Right heartRight heart . Related to pulmonary & right heart dysfunction. Related to pulmonary & right heart dysfunctionincluding acute exacerbation of COAD, pulmonary hypertension, including acute exacerbation of COAD, pulmonary hypertension, massive pneumonia,RV infarct& tricuspid valve malfunction, revermassive pneumonia,RV infarct& tricuspid valve malfunction, reverse se shunt in congenital heart diseases, advance left heart failure pshunt in congenital heart diseases, advance left heart failure progress rogress to to rtrt heart failure nephritic/ nephritic syndrome, end stage liver heart failure nephritic/ nephritic syndrome, end stage liver disease and various vasoactive peptide secreting tumors.disease and various vasoactive peptide secreting tumors.presents with fatigue, pitting oedema liver congestion SOB and presents with fatigue, pitting oedema liver congestion SOB and anasarca.anasarca.Treatment of Cause is required.Treatment of Cause is required.

PathophysiologyPathophysiology1.1. Myocardial Stunning.Myocardial Stunning. Is myocardial dysfunction secondary to Is myocardial dysfunction secondary to prolong ischemia which may persist when normal flow is restored.prolong ischemia which may persist when normal flow is restored.

2.2. HibernationHibernation.. Impairment of myocardial function due to Impairment of myocardial function due to severely reduced coronary flow although myocardial cells are stiseverely reduced coronary flow although myocardial cells are still intact. ll intact. By improving the flow and oxygenation hibernating myocardium canBy improving the flow and oxygenation hibernating myocardium canrestore the function.restore the function.Both stunning and hibernation can co exist.Both stunning and hibernation can co exist.

3.3. Vicious Circle in AHFVicious Circle in AHF.. Final common denominator in syndrome Final common denominator in syndrome of AHF is a critical inability of myocardium to maintain output of AHF is a critical inability of myocardium to maintain output to meet to meet the demands. If not appropriately treated can lead to CHF and dethe demands. If not appropriately treated can lead to CHF and death.ath.

DiagnosisDiagnosis1.1.Clinical Evaluation.Clinical Evaluation. Assessment of;Assessment of;

a.a. Peripheral Circulation Peripheral Circulation b.b. Venous Filling Venous Filling c.c. Peripheral TemperaturePeripheral Temperature

ARHFARHFJVP is elevated JVP is elevated Caution.Caution. Interpretation of high CVP in ARHF can Interpretation of high CVP in ARHF can reflection of reflection of decreased venous compliance and decreased venous compliance and decreased RV compliance even in the presence of low decreased RV compliance even in the presence of low RV fillingRV filling

ALHFALHFChest auscultation reveals rales indicating high Chest auscultation reveals rales indicating high pressure pressure Confirmation is done with x rayConfirmation is done with x rayS3, S4 may be present S3, S4 may be present Murmurs bruits and missing pulse should be corelated Murmurs bruits and missing pulse should be corelated

2) 2) ECGECGNo specific changesNo specific changes

Changes help only to establish the underlying etiology like Changes help only to establish the underlying etiology like strain pattern, ischemia, myopathies, pericarditis or arrythmiastrain pattern, ischemia, myopathies, pericarditis or arrythmiass

3)3) CXR & ImagingCXR & Imagingshould be performed earlier to assessshould be performed earlier to assess

a.a. cardiac sizecardiac sizeb.b. pulmonary congestionpulmonary congestion

4)4) EchocardiogramEchocardiogramEvaluate structural & functional changes associated with heart Evaluate structural & functional changes associated with heart failure also assesses;failure also assesses;a.a. Ejection fraction Ejection fraction b.b. ValvesValvesc.c. Wall hypokinesisWall hypokinesisd.d. Aneurysmal dilatationAneurysmal dilatatione.e. Pulmonary artery pressurePulmonary artery pressure

5)5) Lab EvidenceLab Evidencea. FBCb. Plateletsc. INRd. CRPe. D- Dimersf. U & Eg. Glucoseh. Cardiac Troponini. ABGj. Transaminasek. Plasma BNP or NT pro BNP

6) Othersa. Coronary angiogram b. Insertion of pulmonary artery catheter

GOLES OF TREATMENT IN AHFGOLES OF TREATMENT IN AHF

1.1. Clinical improvementClinical improvement2.2. Lab parameters improvementLab parameters improvement3.3. Hemodyanamic stability PCWP < 18Hemodyanamic stability PCWP < 184.4. Improved outcomeImproved outcome5.5. Tolerability Tolerability

TREATMENT OF AHFTREATMENT OF AHF1.1. General MeasuresGeneral Measures

a.a. Treatment of underlying cause like treatment of infection, Treatment of underlying cause like treatment of infection, correction of valve abnormality.correction of valve abnormality.

b.b. To manage catabolic state To manage catabolic state c.c. Treat renal failure and good control of diabetesTreat renal failure and good control of diabetes

2.2. Ventilatory SupportVentilatory Supporta.a. Maintain sats 95Maintain sats 95--98% to maximize oxygen delivery to the 98% to maximize oxygen delivery to the

tissues.tissues. It may include;It may include;1)1) Face mask Face mask 2)2) CC-- PAP or NIPPVPAP or NIPPV

3)3) Endotracheal intubation.Endotracheal intubation.CC--PAP or NIPPV are first choice PAP or NIPPV are first choice CC--PAP causes pulmonary recruitment and increase FRC. It PAP causes pulmonary recruitment and increase FRC. It decreases overall work of breathing and decrease the need decreases overall work of breathing and decrease the need for intubationfor intubation

4)4) Intubation and mechanical ventilation should be used for Intubation and mechanical ventilation should be used for AHF induced resp. muscle fatigue and should only be used AHF induced resp. muscle fatigue and should only be used if all other majors fail or patient has acute if all other majors fail or patient has acute STEMI with heart failure. STEMI with heart failure.

3.3. Pharmacological TreatmentPharmacological Treatment

a.a. Morphine and its analoguesMorphine and its analoguesVenodilator and mild arterial dilator and reduced heart rateVenodilator and mild arterial dilator and reduced heart rate

b.b. Anti CoagulationAnti Coagulation. LMWH or unfractionated heparin. Placebo . LMWH or unfractionated heparin. Placebo controlled studies show no clinical improvement but there is a controlled studies show no clinical improvement but there is a decreased venous thrombosis. LMWH is contra indicated if decreased venous thrombosis. LMWH is contra indicated if creatinine clearance below 30.creatinine clearance below 30.

c.c. VasodilatorVasodilator. Used as first line therapy in most of AHF if . Used as first line therapy in most of AHF if hypoperfusion if associated with adequate BP and signs of hypoperfusion if associated with adequate BP and signs of congestion with low diuresis;congestion with low diuresis;

1)1) NitratesNitrates. Relives pulmonary congestion without . Relives pulmonary congestion without compromising stroke volume or increasing myocardial compromising stroke volume or increasing myocardial oxygen demand. Decrease preload and after load without oxygen demand. Decrease preload and after load without impairing tissue perfusion. Two randomize trials show impairing tissue perfusion. Two randomize trials show

efficacy of nitrates if > lasix in treatment of pulmonary efficacy of nitrates if > lasix in treatment of pulmonary oedema. Nitrates should be reduced if systolic BP falls oedema. Nitrates should be reduced if systolic BP falls below 90.below 90.

2)2) Sodium NitroprussideSodium Nitroprusside. 0.3 micro gm/ kg /min upto 1 . 0.3 micro gm/ kg /min upto 1 micro gmmicro gm-- 5 micro gm. Specially in the patients 5 micro gm. Specially in the patients with predominantly increased after load control with predominantly increased after load control trials with SNP are lacking in AHF.trials with SNP are lacking in AHF.

3)3) NesiritideNesiritide.. New class of vasodilator is a recombinent New class of vasodilator is a recombinent human BNP. It is venous arterial and coronary vasodilator human BNP. It is venous arterial and coronary vasodilator causes hypotension. It is superior to Nitroglycerin.causes hypotension. It is superior to Nitroglycerin.

4)4) Calcium Antagonist.Calcium Antagonist. Are not recommended in AHF. Are not recommended in AHF. Dihydropyridines should be considered contra indicated. Dihydropyridines should be considered contra indicated.

d.d. ACE Inhibitors.ACE Inhibitors. Are not indicated in the early stabilization of Are not indicated in the early stabilization of patients with AHF, however these drugs have a role in early patients with AHF, however these drugs have a role in early management of AHF because of MI. they is debate on the selectionmanagement of AHF because of MI. they is debate on the selectionof patient and timing of starting of ACE Inhibitors. All studiesof patient and timing of starting of ACE Inhibitors. All studies with with ACE inhibitors in heart failure after MI have focused on long teACE inhibitors in heart failure after MI have focused on long term rm affects but a recent meta analysis found a decrease mortality ataffects but a recent meta analysis found a decrease mortality at30 days with P value < 0.004. They should be used with caution 30 days with P value < 0.004. They should be used with caution with marginal cardiac output as they may significantly reduced with marginal cardiac output as they may significantly reduced GFR. The initial dose of ACE inhibitors should below and increasGFR. The initial dose of ACE inhibitors should below and increased ed progressively after early stabilization within 48 hours with progressively after early stabilization within 48 hours with monitoring of BP and renal function. monitoring of BP and renal function.

e.e. Diuretics.Diuretics. Indicated in patients with acute and acutely Indicated in patients with acute and acutely decompensated heart failure in the presence of symptoms. Loop decompensated heart failure in the presence of symptoms. Loop diuretic are preferred choice in patients with AHF. Combination diuretic are preferred choice in patients with AHF. Combination

of loop diuretics with ionotropes and nitrates is also a of loop diuretics with ionotropes and nitrates is also a therapeutics approach. Diuretic resistance can be therapeutics approach. Diuretic resistance can be encountered. New diuretic agents like V2 receptor encountered. New diuretic agents like V2 receptor antagonist BNP and adenosine receptors antagonist are antagonist BNP and adenosine receptors antagonist are under investigation.under investigation.

f.f. BetaBeta-- BlockersBlockers. In patient with overt AHF beta blockers . In patient with overt AHF beta blockers should be used with caution. IV Metoprolol can be should be used with caution. IV Metoprolol can be considered in patients with on going ischemia, however in considered in patients with on going ischemia, however in patients with AMI who stabilize after developing AHF beta patients with AMI who stabilize after developing AHF beta blockers should be started early and the dose should be blockers should be started early and the dose should be built up gradually. And up titration should be based on built up gradually. And up titration should be based on individual response.individual response.

g.g. Ionotropes.Ionotropes. Indicated in the presence of peripheral Indicated in the presence of peripheral hypoperfusion or pulmonary oedema refractory to diuretics hypoperfusion or pulmonary oedema refractory to diuretics and vasodilators. Include dopamine, dobutamine and vasodilators. Include dopamine, dobutamine phosphodiesterase inhibitors type 3. Levosimendan is phosphodiesterase inhibitors type 3. Levosimendan is indicated in patients with systolic dysfunction. indicated in patients with systolic dysfunction.

h.h. Vasopressors Vasopressors (Catecholamines).(Catecholamines). Used in cardiogenic Used in cardiogenic shock after the failure of combination of ionotropes and shock after the failure of combination of ionotropes and fluids.fluids.

i.i. Cardiac Glycosides.Cardiac Glycosides. In acute heart failure they increase In acute heart failure they increase in cardiac output. Their indication is AHF secondary to in cardiac output. Their indication is AHF secondary to arrythmias. Cardiac Glycosides cannot be recommended in arrythmias. Cardiac Glycosides cannot be recommended in AHF in particular following AMI.AHF in particular following AMI.

4.4. Other Treatments.Other Treatments. Specific treatments for arrythmias ischemia or Specific treatments for arrythmias ischemia or control of BP, surgical correction of valve problem and ventricucontrol of BP, surgical correction of valve problem and ventricular lar assist devices or in extreme cases heart transplant.assist devices or in extreme cases heart transplant.

SUMMARYSUMMARYThe clinical syndrome of AHF may be denovo or as The clinical syndrome of AHF may be denovo or as decompensation of CHF with forward or backward decompensation of CHF with forward or backward dominance. Patient requires immediate diagnostic dominance. Patient requires immediate diagnostic evaluation and resuscitative measures. Initial assessment evaluation and resuscitative measures. Initial assessment included clinical examinations supported by history, ECG, included clinical examinations supported by history, ECG, CXR, plasma BNP and other lab tests. Echo should be CXR, plasma BNP and other lab tests. Echo should be performed ASAP. Oxygenation vasodilatation with nitrates, performed ASAP. Oxygenation vasodilatation with nitrates, diuretics, morphine and appropriate medical treatment diuretics, morphine and appropriate medical treatment with beta blockers are required along with control with beta blockers are required along with control complicating conditions. complicating conditions.