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Congestive heart failure


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Congestive heart failure

  2. 2. 2 MAGDI AWAD SASI HEART FAILURE 2013DEFINITIONHeart (or cardiac) failure: pathophysiological state in which the heart isunable to pump blood at a rate commensurate with the requirements ofthe metabolizing tissues or can do so only from an elevated fillingpressureAccording to AHA,HF is a clinical syndrome including circulatory congestion or inadequatetissue perfusion , due to abnormal heart function and associatedneurohormonal abnormalities.An inadequate or decreased cardiac output which causes an increase inthe blood volume within the vascular system. The resulting congestionwithin the venous system interferes with the movement of body fluids,resulting in fluid accumulation in the tissue spaces, causing edemaFrequency : United States• More than 3 million people have congestive heart failure (CHF), and morethan 400,000 new patients present yearly. The prevalence rate is 1-2%.RaceBlacks are 1.5 times more likely to die of CHF than whites are.Nevertheless, black patients appear to have similar or lower in-hospitalmortality rates than white patients.SexPrevalence is greater in males than in females in patients aged 40-75 yrs.No sex predilection is noted among patients older than 75 years.AgePrevalence of CHF increases with increasing age and affects about 10% ofthe population older than 75 years
  3. 3. 3 MAGDI AWAD SASI HEART FAILURE 2013Mortality/MorbidityApproximately 30-40% of patients with congestive heart failure (CHF) arehospitalized every year. CHF is the leading diagnosis-related group (DRG)among hospitalized patients older than 65 years. 35% will die within oneyear of diagnosis. Less than 50% of patients with HF have typical physicalsigns. Less than 50% of patients being correctly identified during the initialconsultation. 50% readmission rate within 6 months50% of HF patients will die 5 years after the diagnosisThe most common cause of death is progressive heart failure, but suddendeath may account for up to 45% of all deaths.Patients with coexisting insulin-dependent diabetes mellitus have asignificantly increased mortality rate.Cardiac Physiology(remember this?)• CO = SV x HR• HR: parasympathetic andsympathetic tone• SV: preload, afterload,contractilityPreload• Def: Passive stretch of muscle prior to contraction• Measurement: Swan-Ganz– LVEDP( venous return)• Really a function of diastole
  4. 4. 4 MAGDI AWAD SASI HEART FAILURE 2013• Affected by compliance– Low compliance = higher LVEDP with lower LVEDVAfterload• Def: Force opposing/stretching muscle after contraction begins• Measurement: SVRContractility• Def: Normal ability of the muscle to contract at a given force fora given stretch, independent of preload or afterload forces• In other words:– How healthy is your heart muscle?• Ischemia,infarction, Hypertrophy (?), Muscle lossPathophysiology• Hemodynamic changes• Neurohormonal changes• Cellular changes1.Hemodynamic changes:• HF can be secondary to systolic dysfunction or diastolic dysfunction• 2. Cellular changes• Changes in Ca+2handling• Changes in adrenergic receptors:Slight in α1 receptors
  5. 5. 5 MAGDI AWAD SASI HEART FAILURE 2013β1 receptors desensitization followed by down regulation• Changes in contractile proteins• Program cell death (Apoptosis)• Increase amount of fibrous tissue• 3. Neurohormonal changesNeurohormonal changesN/H changes Favorable effect Unfavorable effectSympathetic activity HR , contractility,vasoconst. Venousreturn,fillingArteriolar constrictionAfter load workloadO2 consumptionRenin-Angiotensin –AldosteroneSalt & water retentionVenous ReturnVasoconstrictionafter loadVasopressin Same effect Same effectinterleukins &TNF- May have roles in myocytehypertrophyApoptosisEndothelin Vasoconstriction VR After loadClassifying Heart Failure• Forward Vs Backward• Rt. Vs Lt. sided HF• Acute Vs Chronic HF• Low Vs High output HF• Systolic Vs Diastolic HF
  7. 7. 7 MAGDI AWAD SASI HEART FAILURE 2013• A etiology It is a common end point for many diseases of cardiovascular system1. Vascular –Ischemic heart disease,myocardial infarction2. Valvular –stenosis/regurgitation(RHD, infectiveendocarditis)3. Preesure- hypertension4.Muscle-cardiomyopathy5. Rhythm- atrialfibrillationSymptoms:Left ventricular failure-The patient present with chest symptoms which may delay the diagnosis andkeep the patient to seek chest consultants advice.Failure of forward flow from left ventricle into the aorta result into pulmonarycongestion with chest symptoms.Since the left ventricle does not empty completely, it cannot accept bloodreturning from the lungs via the pulmonary veins. The pulmonary veins becomeengorged and fluid seeps out through the veins and collects in the lungs.LVF can be acute or chronic depending on the underlying cause of heart diseaseLVF= CHEST SYMTOMS= D/D OF ALL LUNG DISEASES= CHEST FINDING
  8. 8. 8 MAGDI AWAD SASI HEART FAILURE 2013LVF symptoms are:Dyspnea at restDyspnea upon exertion: This has been found to be the most sensitivesymptom reported, yet the specificity for dyspnea is less than 60%.Orthopnea and paroxysmal nocturnal dyspnea (PND): These symptomsare observed; however, the sensitivity for orthopnea and PND is only 20-30%.Cough: Cough that produces pink, frothy sputum is highly suggestive ofcongestive heart failure (CHF).The sputum is whitish , soap like , watery.Wheezing= new onset of wheezing above age of 60 years or wheezing inelder diabetic or wheezing all of a sudden in HTN patient is cardiacasthma until prove other wise.Palpitation in arrhythmiaChest pain or tightness especially if the cause is vascular(IHD/ACS).Non specific symptoms of low COPMalaise, Weakness,Light headedness, fatigue, dizziness ,sweating ,lose of effort.
  9. 9. 9 MAGDI AWAD SASI HEART FAILURE 2013Right ventricular heart failureThe patient present with abdominal symptoms which may delay the diagnosisand keep the patient to seek gastroenterologist advice.Failure of forward flow from right ventricle into the pulmonary artery resultsinto systemic congestion with abdominal symptoms.Failure of the right ventricle to maintain a normal output of blood.Since the right ventricle does not empty completely, it cannot fully accept bloodreturning from the body. Pressure builds in the veins of the body causing fluid toseep out and collect in the cells of the body – especially the extremities.Engorgement of the systemic veins produces pitting edema, enlargement of theliver, and ascites.
  10. 10. 10 MAGDI AWAD SASI HEART FAILURE 2013RVF can be acute or chronic depending on the underlying cause of heart diseaseRVF= ABDOMENAL SYMTOMS= D/DOF ABDOMENAL DISEASES= ABD FINDING.Right-sided or right ventricular (RV) heart failure usually occurs as a result ofleft-sided failure. When the left ventricle fails, increased fluid pressure is, ineffect, transferred back through the lungs, ultimately damaging the hearts rightside. When the right side loses pumping power, blood backs up in the bodysveins. This usually causes swelling in the legs and ankles.RVF symptoms are:Abdominal distentionRight hypochondrial painEpigastric fullness, early satiety , nausea , vomiting(stomach congestion)Change of bowel habit –constipation, diarrhea, malabsorptionBilateral leg swellingYellowish coloration of scleraChange of urine frequency and colourThese symptoms are caused by internal abdominal organs congestionAnd can be mistaken for local abdominal pathology.RVF is caused by:1. Left ventricular failure - most common cause- mitral stenosis2. Pulmonary hypertension caused by chronic lung disease(cor pulmonale)3. Cardimyopathies andmyocarditis
  11. 11. 11 MAGDI AWAD SASI HEART FAILURE 2013SIGNS:General appearancePatients with mild heart failure appear to be in no distress after afew minutes of rest, but they may be obviously dyspneic during andimmediately after moderate activity. Patients with LV failure maybe dyspneic when lying flat without elevation of the head for morethan a few minutes. Those with severe heart failure appear anxiousand may exhibit signs of air hunger in this position.Patients with recent onset of heart failure are generally wellnourished, but those with chronic severe heart failure are oftenmalnourished and sometimes even cachectic.Chronic marked elevation of systemic venous pressure may produceexophthalmos and severe tricuspid regurgitation and may lead tovisible pulsation of the eyes and of the neck veins.Central cyanosis, icterus, and malar flush may be evident in patientswith severe heart failure.In mild or moderate heart failure, stroke volume is normal at rest;in severe heart failure, it is reduced, as reflected by a diminishedpulse pressure and a dusky discoloration of the skin.With very severe heart failure, particularly if cardiac output hasdeclined acutely, systolic arterial pressure may be reduced. Thepulse may be weak, rapid, and thready; the proportional pulsepressure (pulse pressure/systolic pressure) may be markedlyreduced. The proportional pulse pressure correlates reasonablywell with cardiac output.Evidence of increased adrenergic activityIncreased adrenergic activity is manifested by tachycardia,diaphoresis, pallor, peripheral cyanosis with pallor and coldness ofthe extremities, and obvious distention of the peripheral veinssecondary to venoconstriction.Diastolic arterial pressure may be slightly elevated.Pulmonary rales =LVFRales heard over the lung bases( bilateral basal end inspiratory) arecharacteristic of heart failure of at least moderate severity.The absence of rales certainly does not exclude elevation ofpulmonary capillary pressure due to LV failure.
  12. 12. 12 MAGDI AWAD SASI HEART FAILURE 2013Protodiastolic (S3) gallop: This is the earliest cardiac physical finding indecompensated heart failure in the absence of severe mitral or tricuspidregurgitation or left-to-right shunts.LVF=CHEST-B/L BASAL INSPIRATORY CREPITATION + HEART-S3Systemic venous hypertension: This is manifested by jugular venousdistention. Normally, jugular venous pressure declines with respiration;however, it increases in patients with heart failure, a finding known as theKussmaul sign. This reflects an increase in right atrial pressure andtherefore right-sided heart failure.Hepatojugular reflux: This represents distension of the jugular veininduced by applying manual pressure over the liver. The patients bodyshould be positioned at a 45 º angle. This is found in patients withelevated left-sided filling pressures and reflects elevated capillary wedgepressure and left-sided heart failure.EdemaBilateral pitting pedal odema.Usually, a substantial gain of extracellular fluid volume (ie, aminimum of 5 L in adults) must occur before peripheral edema ismanifested.Edema, in the absence of dyspnea or other signs of LV or RV failure,is not solely indicative of heart failure and can be observed in manyother conditions, including chronic venous insufficiency, nephroticsyndrome, or other syndromes of hypoproteinemia or osmoticimbalance.HepatomegalyHepatomegaly is prominent in patients with chronic right-sidedheart failure, but it may occur rapidly in acute heart failure.When occurring acutely, the liver is usually tender.In patients with considerable tricuspid regurgitation, a prominentsystolic pulsation of the liver, attributable to an enlarged right atrialV wave, is often noted. A presystolic pulsation of the liver,attributable to an enlarged right atrial A wave, can occur intricuspid stenosis, constrictive pericarditis, restrictivecardiomyopathy involving the RV, and pulmonary hypertension(primary or secondary).
  13. 13. 13 MAGDI AWAD SASI HEART FAILURE 2013Hydrothorax (pleural effusion)Hydrothorax is most commonly observed in patients withhypertension involving both systemic and pulmonary systems.Hydrothorax is usually bilateral, although when unilateral, it isusually confined to the right side of the chest.When hydrothorax develops, dyspnea usually intensifies because offurther reductions in vital capacity.AscitesThis finding occurs in patients with increased pressure in thehepatic veins and in the veins draining into the peritoneum.Ascites usually reflects long-standing systemic venoushypertension.Pulsus alternans ( one strong and one weak beat)Pulsus alternans occurs most commonly in heart failure due to increasedresistance to LV ejection, as occurs in hypertension, aortic stenosis,coronary atherosclerosis, and dilated cardiomyopathy.It is usually associated with an S3 gallop, signifies advanced myocardialdisease, and often disappears with treatment of heart failure.Accentuation of P2 heart sound, S3 gallop, and systolic murmursThis accentuation is a cardinal sign of increased pulmonary arterypressure. It disappears or improves after treatment of heart failure.Mitral and tricuspid regurgitation murmurs are often present inpatients with decompensated heart failure because of ventriculardilatation. These murmurs often disappear or diminish whencompensation is restored. Note that correlation between theintensity of the murmur of mitral regurgitation and its significancein patients with heart failure is poor. Severe mitral regurgitationmay be accompanied by soft murmur.The presence of an S3 gallop in adults is important, pathologic, andoften the most apparent finding on cardiac auscultation in patientswith significant heart failure.Cardiac cachexiaCardiac cachexia is found in long-standing heart failure, particularlyof the RV, because of anorexia from hepatic and intestinalcongestion and sometimes because of digitalis toxicity.Occasionally, impaired intestinal absorption of fat and (rarely)protein-losing enteropathy occur.
  14. 14. 14 MAGDI AWAD SASI HEART FAILURE 2013Left heart failureIHD, Myocarditis,Valvular heart diseasesForward failure Backward failure↓ cardiac outputTissue anoxia↓ renal perfusionActivation of RAASPULMONARYCONGESTION andOEDEMANa+, H2O retentionResidual blood in left ventricle Left atrial pressure and volume Pressure in pulmonary venous circulationPulmonary arterial hypertension Right ventricular pressureSYSTEMIC VENOUSCONGESTION andPERIPHERAL OEDEMARight heart failureRight side valvular diseaseRt side myocardial diseasePulmonary hypertension
  15. 15. 15 MAGDI AWAD SASI HEART FAILURE 2013Precipitating Factors• Infection Sodium Intake• Medications!!! Anemia• Thyroid disorders Endocarditis• Pulm Embolus Noncompliance• Arrhythmia Myocardial Infarction• Stress reactionDiagnosis of CHF / Routine Tests:CBC count INVESIVEElectrolytes 1. Exercise stress testRenal function tests 2. Cardiac catheterizationLiver function tests 3. Holter monitorB-type natriuretic peptideECGChest x-rayEchocardiogramCXRCardiomegalyVascular redistributionKerley B linesInterstitial edemaPeri-bronchial “cuffing”Effusions
  17. 17. 17 MAGDI AWAD SASI HEART FAILURE 2013Chest radiographs in patients with abrupt onset are usually helpful but can belimited because a delay of as long as 12 hours is possible from the onset ofdyspnea due to acute heart failure to the development of classic abnormalfindings on radiographs.Classic radiographic findings demonstrate cardiomegaly (in patients withunderlying CHF) and alveolar edema with pleural effusions and bilateralinfiltrates in a butterfly pattern. The other signs are loss of sharp definition ofpulmonary vasculature, haziness of hilar shadows, and thickening ofinterlobular septa (Kerley B lines).In long standing biventricular chronic heart failure, chest radiographs may onlyshow cardiomegaly without alveolar edema or pleural effusions due toadaptive lung mechanism with increased arterial vasoconstriction andlymphatic drainage.
  18. 18. 18 MAGDI AWAD SASI HEART FAILURE 2013Electrocardiographyo The presence of left atrial enlargement and LV hypertrophy issensitive (although nonspecific) for chronic LV dysfunction.o ECG may suggest an acute tachyarrhythmia or bradyarrhythmia.o ECG may aid in the diagnosis of acute myocardial ischemia orinfarction as the cause of heart failure or may suggest the likelihoodof prior myocardial infarction or presence of coronary arterydisease as the cause of heart failure.o ECG is of limited help when an acute valvular abnormality or LVsystolic dysfunction is considered to be the cause of heart failure;however, the presence of left bundle branch block (LBBB) on anECG is a strong marker for diminished LV systolic functionEchocardiogramChamber enlargementWall motion abnormalitiesDiminished ejection fractionPossible LVHPossible valvular problemsAssess diastolic dysfunction
  19. 19. 19 MAGDI AWAD SASI HEART FAILURE 2013Heart disease(any)HypertensionDiabetes,HypercholesterolemiaAsymptomaticLV dysfunctionSystolic / DiastolicMarked symptomsat rest despitemax. therapyDyspnea, FatigueReduced exercisetoleranceStages in the Evolution of Heart FailureABCDAHA guidelines 2001Treatment Goals• Improve symptomsA. Enhance well-being and quality of lifeB. Increase exercise tolerance• Improve survivalA. Prevent progressive heart failureB. Prevent sudden deathC. Prevent thromboembolic episodes
  20. 20. 20 MAGDI AWAD SASI HEART FAILURE 2013• Treatment ::• Oxygen – nasal, BiPAP, intubation• Fluid BalanceRestrict fluid- 1000ml daily/ salt intakeMonitor Input/Outputs and daily weightDialysis if needed -Critical renal failure patientsAspirin 75mg Promoting Rest and Activity Bed rest or limited activity may be necessary during the acutephase Provide an overbed table close to the patient to allow resting thehead and arms Use pillows for added support. Gradual ambulation is encouraged to prevent risk of venousthrombosis and embolism due to prolonged immobility Activities should progress through dangling, sitting up on a chairand then walking in increased distances under close supervision. Assess for signs of activity intolerance (dyspnea, fatigue andincreased pulse rate that does not stabilize readily) Providing Skin Care Edematous skin is poorly nourished and susceptible to pressuresores Change position at frequent intervals Assess the sacral area regularly Use protective devices to prevent pressure sores Promoting Elimination Advise to avoid straining at defecation which involves Valsalvamanoeuvre. Administer laxative as ordered Encourage use of bedside commode
  21. 21. 21 MAGDI AWAD SASI HEART FAILURE 2013Preload Reduction– Loop diuretics Lasix 20-200mg IV (q 6-8 hours)– Nitrates -Nitroglycerin IV:10-200 mcg/min– ACEi / ARB Captopril 6.25-50mg PO q8hEnalapril 2.5-20mg PO BIDAfterload Reduction– IV NTG, Nitroprusside– Hydralazine 10-100mg PO q6-8 h– ACE-I / ARBIonotropic Support– Dopamine / Dobutamine 500mg in 250cc D5W3-10 cg/kg/min
  22. 22. 22 MAGDI AWAD SASI HEART FAILURE 2013– Amrinone / Milrinone n Digoxin (chronic)– Mechanical (ABP) Cardiogenic shock unresponsive to above txA.-----------Diuretics• volume overload , sodium overload , preload reductionAdvantages• Highly effective in most classes• Essential with fluid retention• Well tolerated, simple to useDisadvantages• Electrolyte abnormalities Na, k ,Ca ,Mg• Hypovolemia, hypotension, renal dysfunction• Activation of neurohormaonal systemAIM----Elimination of symptoms and/or signs of congestion• Avoid volume depletionA. Postural hypotension B. Increase in heart rateC. Increase in BUN/Cr D. Neuroendocrine activationThiazide Diuretics-----Hydrochlorothiazide, Chlorthalidone , MetolazoneLoop Diuretics----------Furosemide , TorsemidePotassium Sparing Diuretics---Spironolactone , Triamterene , AmilorideSpironolactone :Aldosterone inhibition minimize potassium loss, prevent sodium and waterretention, endothelial dysfunction and myocardial fibrosis.
  23. 23. 23 MAGDI AWAD SASI HEART FAILURE 2013B-------------ACE InhibitorsACE inhibitors should be the initial treatment for heart failure• Improve hemodynamic status• Attenuate neurohumoral abnormalities• Improve symptoms, left ventricular ejection fraction .• Reduce incidence of hospitization• Slow progression• Reduce mortalityNeurohormonal Changes• Decreased angiotensin II.• Reduction in arterial resistance (afterload).
  24. 24. 24 MAGDI AWAD SASI HEART FAILURE 2013• Reduction in venous tension (preload).• Inhibition of cardiac and vascular remodeling .• Increased bradykinin• Decreased or no change in aldosterone• Decreased norepinephrineReduction in Sudden Death/Potential Mechanisms• Increase in serum/total body potassium• Decreased adrenergic stimulation• Reduced heart size and decrease in ventricular hypertrophy• Prevention of myocardial ischemia• Prevention of progressive myocardial damageFDA Approved• Captopril ,Enalapril ,Lisinopril ,Quinapril ,Trandolapril ,FosinoprilAdverse effects : Dry irritating persistent cough Hyperkalemia Angioedema Fetal toxicity
  25. 25. 25 MAGDI AWAD SASI HEART FAILURE 2013CHF: ACE Inhibitor DoseagesCaptoprilEnalaprilLisiniprilQuinapril• Start: 6.25 bid/tid• Usual: 6.25-50 bid/tid• Start: 2.5 qd/bid• Usual: 2.5-10 bid• Start: 2.5-5 qd• Usual: 5-20 qd• Start: 5 bid• Usual 10-20 bidC---------------Beta Blockers• Primary mechanism is inhibition of down regulation of beta receptors• Additional mechanismsA. Restore receptor densityB.Protect against cardiotoxicity of catecholeaminesC. Improve systolic/diastolic function in ischemic myocardium• First Generation: Beta 1 and Beta 2Propranolol/Timolol• Second Generation: Beta 1Metoprolol/Atenolol• Third Generation: Vasodilating PropertiesCarvedilolImprove symptoms and clinical class
  26. 26. 26 MAGDI AWAD SASI HEART FAILURE 2013• Degree of benefit appears to relate to degree of disability beforetreatment• Should be used in all stable Class II/III patients unless contraindicated• Treatment should not be initiated in patients with acutelydecompensated CHF• Clinical response may take 2 to 3 monthsRisks of Treatment• Hypotension Fluid retention and worsening CHF• Bradycardia and heart block
  27. 27. 27 MAGDI AWAD SASI HEART FAILURE 2013CHF: Beta Blockers• Carvedilol• Metoprolol• Bisoprolol• Start: 3.125 mg bid• Usual: 25 mg bid• Start: 12.5-25 mg qd• Usual: 50-100 mg bid• Start: 1.25 mg qd• Usual: 5-10 mg qd Start at low dose and monitor for bradycardia Carvedilol and Metoprolol are the most commonly used for CCF amongstbeta blockersD------------Angiotensin Receptor AT-1 blockers (ARB) :Losartan, Irbesartan, Candesartan Competitive antagonists of Angiotensin II (AT-1). No inhibition of ACE or Cough.
  28. 28. 28 MAGDI AWAD SASI HEART FAILURE 2013 E--------------Vasodilators : Isosorbide dinitrate and hydralazine also used specially in patients whocannot tolerate ACE inhibitors. Amlodipine and prazosin are other vasodilators can be used in CCF.
  29. 29. 29 MAGDI AWAD SASI HEART FAILURE 2013F-------Cardiac glycosides : Digoxin : Inhibition of Na/K ATPase pump increase intracellular sodiumconcentration – eventually increase cytosolic calcium. It restores the vagal tone and abolishes the sympathetic over activity. Has positive inotropic (strengthens force of cardiac contractility) andnegative chronotropic effects (decreases heart rate. Increase the refractoriness of AV node thus decrease ventricular responseto atrial rate.
  30. 30. 30 MAGDI AWAD SASI HEART FAILURE 2013 Digoxin is used as a first-line drug in patients with congestive heart failurewho are in atrial fibrillation.Adverse effects / Precautions : Nausea, vomiting, gynecomastia, visual disturbances and psychosis. Ventricular bigeminy, AV block and bradycardia. Antidote for Toxicity: Digibind Nursing ResponsibilitiesAssess heart rate before administration; if below 60bpm or above 120 bpm, withhold the drug.Monitor serum potassiumAssess for signs of Digitalis toxicity- Bradycardia- GI manifestations (anorexia, nausea, vomiting anddiarrhea)- Dysrrhythmias- Altered visual perceptions- In males: gynecomastia, decreased libido andimpotence Amiodarone and verapamil can increase the plasma concentration ofdigoxin by inhibiting its excretionIN DIASTOLIC FAILURE;USE B-BLOCKER, ACE-I , CALCIUM CHANNEL BLOCKER RATE LIMITING• Difficult to treat• Diuretics for volume overload. Avoid volume depletion• Prevent tachycardia• Rate-limiting calcium channel blockers first choice• Beta 1 beta blockers second choice
  31. 31. 31 MAGDI AWAD SASI HEART FAILURE 2013ADVERSE PROGNOSTIC MARKERS IN CHRONIC HEART FAILURE• Old Age,• Severity of heart failure (NYHA class)• Left ventricular dysfunction,• Diabetes Mellitus,• Raised creatinine,• Hyponatremia , Hypoalbuminaemia,Anaemia• Presence of arrhythmia : AF / VTCauses of Mortality in Heart Failure• Pump failure• Arrhythmia• Severe Anaemia• Associated serious co-morbidities i.e. Renal failureCardiac Inotropes =• Dopamine acts at a variety of receptors (dose dependant)• Rapid elimination- can only be administered as a continuous infusionDobutamine• Stimulates beta-adrenergic receptors and produces a positive inotropicresponse• Unlike the vasoconstriction seen with high doses of dopamine,dobutamine produces a mild vasodilatation .
  32. 32. 32 MAGDI AWAD SASI HEART FAILURE 2013PDE Phosphodiesterase inhibitors• Inamrinone (amrinone) and Milrinone (bipyridines)• Acts by inhibiting the enzyme Phosphodiesterase• Thus lead to increase of intracellular concentrations of cAMP• cAMP is responsible for the conversion of inactive protein kinase to activeform• Protein kinases are responsible for phosphorylation of Ca channels• Thus causing increased Ca entry into the cell.MECHANISM OF ACTION:• Increase myocardial contractility by increasing the Ca influx during AP• Also have vasodilating effect• Selective for PDE isoenzyme-3 (found in cardiac and smooth muscle)ADVERSE RECTIONS• Inamrinone: nausea, vomiting, arrhythmias, thrombocytopenia and liverenzyme changes• Withdrawn in some countries• Milrinone: arrhythmias, less likely to cause other ADRNiseritide• Brain (B-type) natriuretic peptide (BNP) is secreted constitutively byventricular myocytes in response to stretch• BNP binds to receptors in the vasculature, kidney, and other organs,producing potent vasodilation with rapid onset and offset of action byincreasing levels of cGMP
  33. 33. 33 MAGDI AWAD SASI HEART FAILURE 2013• Niseritide is recombinant human BNP approved for treatment of acutedecompensated CHF.• It reduces systemic and pulmonary vascular resistances, causing anindirect increase in cardiac output and diuresis.• Effective in HF because cause reduction in preload and afterload• ADR- hypotensionOTHERS;Implantable cardioverter-defibrillatorPacemakers, Biventricular pacemakerHeart transplantCardiac Resynchronisation Therapy