Presentation on theme: "Congestive Heart Failure and Cardiomyopathy"— Presentation transcript:
1Congestive Heart Failure and Cardiomyopathy Mark BromleyPGY-1
2Case 1 A 63-year-old male presents with breathlessness x 3 days. ?Approach, ?HxPMHx: MI 3 years ago4-vessel CABGasymptomatic since surgery with no complaints of CPHPI: Over the last 3 months, the patient notes onset of shortness of breath while unloading groceries, and walking stairs.2 weeks ago, he was unable to complete his daily one-mile walk at the high school track. He noted swelling in his feet and ankles.4 days ago he woke at 2 am short of breath and had to sleep in his recliner the rest of the night. He has been unable to lay flat in bed at night since then and has slept on 3 pillows.Yesterday, he became breathless walking from one room to anotherHe presents today with extreme shortness of breathHe denies chest pain
3BP 108/52 P 140, irreg. R 30 and labored Temp 99°F Ht: 5'8" Wt: 210. General: Breathless, moderately obese male in acute distress sitting upright complaining "I am going to die. Please help me."Chest: Scattered rhonchi throughout, rales bilateral one third lower bases. Cough is productive and frothy.CVS: Tachycardia and irreg. Grade 3/6 systolic murmur at LSB, S3 gallop noted. JVP to jawAbd: Liver palpable three centimeters below right costal margin. HJR. Extremities: 4+ pitting edema of lower extremities to the knees. Pulses intact.
4Organization of CHFImportancePathophysiologyDiagnosisEtiologies – DecompensationManagementCardiomyopathy
5Importance Increasing burden Aging population Improved survival (Hypertension/CAD)Nationwide, heart failure affects more than Canadians1(10% of those >75)> new cases are diagnosed /yr1
6Bad Disease Mortality ED visits 1 year – 10-20% 6 year – 60-80% 20% new diagnosis80% repeat visit (decompensation)
7Definition CHF Pulmonary Edema Inability of the heart to maintain adequate vital organ perfusion at normal filling pressuresDecreased exercise capacityAssociated neurohumoral-endocrine changes, initially compensatory but ultimately maladaptivePulmonary EdemaA condition associated with increased loss of fluid from the pulmonary capillaries into the pulmonary interstitium and alveoli
8The heart is a pump that works together with the lungs The heart is a pump that works together with the lungs. It pumps blood in 2 waysIt pumps blood from the heart to the lungs to pick up oxygen. The oxygenated blood returns to the heartIt then pumps blood out into the circulatory system of blood vessels that carry blood through the body
9In HF the pumping action of the heart becomes less and less efficient/powerful The heart does not pump blood as well as it shouldWhen this happens, blood does not move efficiently through the circulatory systemIt starts to back up, increasing the pressure in the blood vessels, forcing fluid from the blood vessels into body tissues.
20Classification of Heart Failure Low OutputCardiac output is low, but demand for blood flow is normalThe heart is unable to meet this demand and failsDx: IHD, HTN, dilated cardiomyopathy, valvular and pericardial dzHigh OutputHigh-output heart failure Cardiac output is normal or a little bit highDemand for blood flow is abnormally high(hyperthyroidism, anemia, severe infections)The heart is unable to deliver the increased amount of blood and failsDx: hyperthyroidism, anemia, pregnancy, AV fistulas, beriberi, & Paget’sRx: ↓volume overload and correct the underlying disorder
21Classification of Heart Failure AcuteMI, Acute Valve Dysfunctionlargely systolicsudden reduction in cardiac output often results in systemic hypotension without peripheral edemaChronicCardiomyopathyarterial pressure tends to be well maintained until very late in the coursethere is often accumulation of peripheral edemaChordae Tendonae Rupture. Large enough area of ischemia.
22Classification of Heart Failure Right Sided (right ventricle)(pulmonic stenosis or pulmonary hypertension)When the right side of the heart starts to fail, fluid collects in the feet and lower legsAs the heart failure becomes worse, the legs swell and eventually the abdomen collects fluid (ascites, hepatic congestion)Weight gain accompanies the fluid retention and is an excellent measure of how much fluid is being retained.Left Sided (left ventricle)left ventricle is mechanically overloaded (aortic stenosis) or weakened (post MI)When the left side of the heart starts to fail, fluid collects in the lungs (Orthopnea/PND)Breathing becomes more difficult, and the patient may feel short of breath, particularly with activity or lying downThis extra fluid in the lungs makes it more difficult for the airways to expand on inhalation↓O2 diffusionHowever, when heart failure has existed for months or years, biventricular failure usually results. For example, patients with long standing aortic valve disease or systemic hypertension may have ankle edema, congestive hepatomegaly, and systemic venous distention late in the course of their disease, even though the abnormal hemodynamic burden initially was placed on the left ventricle.
23Classification of Heart Failure SystolicThe heart has difficulty contracting and pumping out enough bloodweakness, fatigue and decreased ability to exercise↓Ejection fraction = (stroke volume)/(end diastolic volume)A normal ejection fraction is greater than 50%Systolic heart failure has a ↓EF < 50%.DiastolicThe heart is unable to fill properly during diastole↑ filling pressureThis impedes blood filling into the heart → backup into the lungs → CHF symptoms↑ in patients > 75 years; women; HTNEjection fraction is normal
24Classification of Heart Failure Directional Heart FailureBackwards heart failureThe ventricle is not pumping out all the blood that comes into it. ↑ ventricular filling pressure and systemic or pulmonary edemaIn fact, the heart can only meet the needs of the body if the ventricular filling pressure is highForward heart failureThe heart is not pumping out enough blood to meet the needs of the body↓ blood reaches the kidneys, they conserve salt and water, which contributes to excess fluid retention and edemaForward failure also decreases the blood flow to various organs, causing weakness and fatigue
40Etiology Decompensation/Causes of exacerbation FAILURE: Forgot medication Arrhythmia/ Anemia Ischemia/ Infarction/ Infection (Pneumonia)Lifestyle: taken too much saltUp-regulation of CO: pregnancy, hyperthyroidism Renal failure Embolism: pulmonaryInappropriate treatmentFailure to seek care25%10%25%Other 10%10%20%
41Case 1 ManagementA 63-year-old male presents with breathlessness x 3 days.?Approach, ?HxPMHx: MI 3 years ago4-vessel CABGasymptomatic since surgery with no complaints of CPHPI: Over the last 3 months, the patient notes onset of shortness of breath while unloading groceries, and walking stairs.2 weeks ago, he was unable to complete his daily one-mile walk at the high school track. He noted swelling in his feet and ankles.4 days ago he woke at 2 am short of breath and had to sleep in his recliner the rest of the night. He has been unable to lay flat in bed at night since then and has slept on 3 pillows.Yesterday, he became breathless walking from one room to anotherHe presents today with extreme shortness of breathHe denies chest pain
42Management Treat the maladaptation ? LMNOP ↑ Vascular resistance ↑ Sympathetic tone↑ Total blood volume? LMNOP
43Management Nitrates O2 Ventilation Assist Devices ACE I Diuretics MorphineInotropes
44Airway/Breathing Non-rebreather facemask delivering 100% O2 Once initial therapy has begun, oxygen supplementation can be titrated in order to keep the patient comfortable and arterial oxygen saturation above 90 percent.O2 increases PCWP
45NIPPVIf respiratory distress and/or hypoxia persist, consider non-invasive PPV↓ preload, ↓ afterload, and ↑ left ventricular performanceMeta-analysis of 15 clinical trials: ↓mortality and ↓intubation with NPPV compared to conventional therapyPatients who fail/do not tolerate/have contraindications to NPPV should be intubatedPositive end-expiratory pressure is often useful for improving oxygenation
46Cardiogenic Pulmonary Edema Emergency Department Multi-centre RCT130 ptsCardiogenic Pulmonary EdemaEmergency DepartmentMedical therapy+O2 (65 pts)non-invasive pressure support ventilation (65 pts)Primary outcome – need for intubationItalian study – 5 departments
47Loop Diuretics ↑Na & H2O excretion Useful in volume overload Rapid onsetMild vasodilator↑1/2 life in CHF …be carefulDepletion of K + and Mg++
48Loop Diuretics Dosing – not well established High dose Lasix and low dose Nitro has worse outcomes than low dose Lasix and high dose Nitro
56Nesiritide Recombinant BNP ↓ Aldosterone ↓ Endothelin ↑ Na & H2O excretion – no reflex tachyGood for Nitro contraindications
57VMAC Randomized, Double Blind 489 inpatients IV Nisiritide vs IV Nitrates vs PlaceboPCWP and DyspneaImprovement in PCWP – 2mm 6hNo change in DyspneaProblems:↓Nitro dosingProlonged HypotensionNot ED patientsIndustry sponsored
58Vosodilator Therapy: Nesiritide Efficacy Phase432 patientsIn the efficacy phase, 127 patients underwent hemodynamic monitoring with a pulmonary artery catheterA six hour infusion of nesiritide (0.015 and 0.03 µg/kg per min) decreased pulmonary capillary wedge pressure(6 and 10 mmHg versus an ↑ of 2 mmHg for placebo)Improved the clinical status in a greater number of patients (60% and 67% versus 14%)Comparative phase305 patientsRandomly assigned to nesiritide or standard vasoactive agents for seven days without hemodynamic monitoringCompared to standard treatment with a single vasoactive agent (dobutamine, milrinone, nitroglycerin, or nitroprusside)nesiritide produced a similar significant improvement in clinical status and reduction in dyspnea and fatigue that persisted during the entire infusion period.Asymptomatic, dose-related hypotension was the most common side effect
59RR from meta-analysis: 1.74 Death within 30 days tended to occur more often among patients randomized to nesiritide therapy35 [7.2%] of 485 vs 15 [4.0%] of 377 patientsRR from meta-analysis: 1.74(95% confidence interval [CI], ; P = .059)Hazard ratio after adjusting for study, 1.80(95% CI, ; P = .057)
63placebo-controlled, randomized, double-blind study Placebo-Controlled, Randomized, Double-Blind Study of Intravenous Enalaprilat Efficacy and Safety in Acute Cardiogenic Pulmonary EdemaThe purpose of this study was to evaluate the efficacy and safety of a single IV 2-hour infusion of enalaprilat (1 mg)placebo-controlled, randomized, double-blind study20 CHF patients (NYHA class III or IV)Compared with placebo, enalaprilat↓ pulmonary capillary wedge pressure (-37% versus -10%, P=.001),↓ diastolic and mean systemic blood pressures (-21% vs 0%, P=.009, and -18% vs -1%, P=.026)↓ diastolic and mean pulmonary blood pressures (-21% vs -8%, P=.040; -18% vs -9%, P=.046)↓ brachial and renal resistances (-44% versus -14%, P=.017, and -22% versus -2%, P=.014)↑ brachial and renal blood flows (+77% versus +8%, P=.036, and +12% versus 0%, P=.043)↑ arterial oxygen tension (+2% versus -16%, P=.041)↑ arterial oxygen saturation (+1% versus -2%, P=.045)Enalaprilat did not affect CO or carotid or hepatosplanchnic hemodynamicsExcluded those already on ACE I
64BNP Why do we need another diagnostic test? How uncertain are we? Diagnostic uncertaintyHow uncertain are we?How uncertain should we be?ER docs are rarely wrong when they rate the probability of HF as very high or very low2ER docs are uncertain of the diagnosis in the in-betweeners (30%)2The degree of clinical certainty (or uncertainty) is determined by comparing the clinical impression with an independent validated criterion (gold) standard. Because there is no validated criterion standard for the diagnosis of HF, previous natriuretic peptide studies have compared the ED diagnosis with a retrospective diagnosis by 2 cardiologists who reviewed the medical records and were blinded to natriuretic peptide results and ED diagnoses. This unvalidated criterion standard has been assumed, although never proven, to be more accurate than the diagnostic impression of physicians in the ED.
71Breathing Not Properly - Analysis BNP brings us closer to the “gold standard”Low Prob -EP17% had CHF90% would have been corrected by BNPHigh Prob -EP4% did not have CHF80% would have been corrected by BNPUncertain -EPBNP correctly classified 74%Misclassified 7%
72BNPLevels < 100 pg/ml may prompt clinician to focus on alternative diagnosis (COPD)Reasonable neg pred valuePrognostic Value?Variation with Age/Gender/Kidney fxn
73Prospective, Randomized, Controlled Single blind452 Pts with dyspneaDiagnostic Strategy (BNP) vrs Standard AssessmentTold EP if <100 CHF unlikely, >500 CHF likely, indeterminateEnd Points: Time to D/C & Total CostSafety: SimilarConclusion: BNP improved evaluation thereby improving time to D/C and cost – no change in safety
77CasePreviously well 10 year old girl presents with 2 weeks of progressive right sided ABD pain. General malaise. Mild fatigue on exertion.Parents report mild lethargy, pallor and decreased PO intake over same period. Shallow rapid breathing, worse when reclining at night.37.8oC /54Pale irritableHEENT: MMM. No adenopathyCVS: regular S1S2, no murmer, PPPx4, no edemaCHEST: AE=AE slight decrease at basesABD: palpable liver edge below umbilicusEKG: sinus tach, LAD, flattened T-waves, decreased voltages.
79Dilated Cardiomyopathy Most common CM30% idiopathicHereditaryX-linked (dystrophin gene)BoozeHeavy MetalDrugsInfectiousViralChagasPost partumCollagen vascular diseaseGlycogen storage diseaseThiamine, PO4, zinc deficiencyAmyloidosisNeuromuscular disorders
80Dilated Cardiomyopathy Biopsy helpful for etiologyRx same as other CHFMDC (Metoprolol in Dilated CM)34% reduction in DeathMulticenter Myocarditis Treatment Trialno benefit of corticosteroids and azathioprine for Rx of biopsy-proven inflammation in dilated CM
81HCM Inappropriate hypertrophy w/o stimulus Usually asymmetric 4% mortality per year (sudden death)
82HCM 50% familial (Dominant Inheritance) Mechanism Abn Ca++ kinetics Abn sympathetic stimAbn CoronariesSubendocardial ischemiaStructural abn
83HCM25% 1st relatives of HCMUsually 3rd decade – not alwaysM>F
90Restrictive Idiopathic restrictive cardiomyopathy EndoMyocardial FibrosisLoeffler eosinophilic endomyocardial diseaseSecondary restrictive cardiomyopathyRadiationHemochromatosisAmyloidosisSclerodermaCarcinoid heart diseaseGlycogen storage disease of the heart
91Diagnosis Chest x-ray Electrocardiogram Absence of cardiomegaly, normal cardiac silhouetteCHFElectrocardiogramLBBB common, RBBB possibleLow voltageNonspecific ST-T changesVarious arrhythmiasChamber enlargement
92Echocardiography Normal to symmetrically thickened walls Rapid early-diastolic filling, slow late-diastolic fillingNormal or slightly reduced ventricular volume and systolic function
93Cardiac catheterization Elevated ventricular end-diastolic pressureDip and plateau configuration of the diastolic portion of the ventricular pressure pulseNormal to slightly decreased ejection fractionProminent x and y descent
94Endomyocardial biopsy May detect typical eosinophil infiltration in the inflammatory stageMay detect myocardial fibrosis in later-stage casesNegative findings do not exclude diagnosis
95Treat underlying cause if possible Therapy similar for other causes of CHFConsider anticoagulation as prone to stasisthromboembolism
97ReferencesKostuk WJ. Congestive heart failure: what can we offer our patients? CMAJ 2001;165(8):1053-5Schwam E. B-type natriuretic peptide for diagnosis of heart failure in emergency department patients: a critical appraisal. Acad Emerg Med 2004;11: