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Congestive Heart Failure and Cardiomyopathy Mark Bromley PGY-1.

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Presentation on theme: "Congestive Heart Failure and Cardiomyopathy Mark Bromley PGY-1."— Presentation transcript:

1 Congestive Heart Failure and Cardiomyopathy Mark Bromley PGY-1

2 Case 1 A 63-year-old male presents with breathlessness x 3 days. ?Approach, ?Hx PMHx: MI 3 years ago 4-vessel CABG asymptomatic since surgery with no complaints of CP HPI: 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 another –He presents today with extreme shortness of breath –He denies chest pain

3 BP 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 jawsystolic murmur Abd: Liver palpable three centimeters below right costal margin. HJR. Extremities: 4+ pitting edema of lower extremities to the knees. Pulses intact.

4 Organization of CHF Importance Pathophysiology Diagnosis Etiologies – Decompensation Management Cardiomyopathy

5 Importance Increasing burden Aging population Improved survival (Hypertension/CAD) Nationwide, heart failure affects more than Canadians 1 (10% of those >75) > new cases are diagnosed /yr 1

6 Bad Disease Mortality 1 year – 10-20% 6 year – 60-80% ED visits 20% new diagnosis 80% repeat visit (decompensation)

7 Definition CHF –Inability of the heart to maintain adequate vital organ perfusion at normal filling pressures Decreased exercise capacity Associated neurohumoral-endocrine changes, initially compensatory but ultimately maladaptive Pulmonary Edema –A condition associated with increased loss of fluid from the pulmonary capillaries into the pulmonary interstitium and alveoli

8 The heart is a pump that works together with the lungs. It pumps blood in 2 ways 1.It pumps blood from the heart to the lungs to pick up oxygen. The oxygenated blood returns to the heart 2.It then pumps blood out into the circulatory system of blood vessels that carry blood through the body

9 In HF the pumping action of the heart becomes less and less efficient/powerful The heart does not pump blood as well as it should When this happens, blood does not move efficiently through the circulatory system It starts to back up, increasing the pressure in the blood vessels, forcing fluid from the blood vessels into body tissues.

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11 Physiology ↓ CO = HR X Stroke Volume SV = preload + contractility - afterload

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13 Preload –initial stretching of the cardiac myocytes prior to contraction

14 Afterload –the "load" that the heart must eject blood against –Aortic pressure –Hypertrophy is a mechanism that allows more muscle fibers to share the work Stroke Volume

15 Contractility –ability of a cardiac muscle fiber to contract at a given fiber length catecholamines (norepi and epi) sympathetic stimulation Ca ++

16 Copyright ©2000 BMJ Publishing Group Ltd. Jackson, G et al. BMJ 2000;320: Neurohormonal Activation

17 Copyright ©2000 BMJ Publishing Group Ltd. Jackson, G et al. BMJ 2000;320: [Nor-epi] and Mortality

18 Copyright ©2000 BMJ Publishing Group Ltd. Jackson, G et al. BMJ 2000;320: Sympathetic Activation

19 Copyright ©2000 BMJ Publishing Group Ltd. Jackson, G et al. BMJ 2000;320: Remodelling Post MI

20 Classification of Heart Failure Low Output Cardiac output is low, but demand for blood flow is normal The heart is unable to meet this demand and fails Dx: IHD, HTN, dilated cardiomyopathy, valvular and pericardial dz High Output High-output heart failure Cardiac output is normal or a little bit high Demand for blood flow is abnormally high (hyperthyroidism, anemia, severe infections) The heart is unable to deliver the increased amount of blood and fails Dx: hyperthyroidism, anemia, pregnancy, AV fistulas, beriberi, & Paget’s Rx: ↓volume overload and correct the underlying disorder

21 Classification of Heart Failure Acute MI, Acute Valve Dysfunction largely systolic sudden reduction in cardiac output often results in systemic hypotension without peripheral edema Chronic Cardiomyopathy arterial pressure tends to be well maintained until very late in the course there is often accumulation of peripheral edema

22 Classification 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 legs As 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 down This extra fluid in the lungs makes it more difficult for the airways to expand on inhalation ↓O 2 diffusion

23 Classification of Heart Failure Systolic –The heart has difficulty contracting and pumping out enough blood weakness, 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%. Diastolic –The heart is unable to fill properly during diastole –↑ filling pressure –This impedes blood filling into the heart → backup into the lungs → CHF symptoms –↑ in patients > 75 years; women; HTN –Ejection fraction is normal

24 Classification of Heart Failure Directional Heart Failure Backwards heart failure –The ventricle is not pumping out all the blood that comes into it. ↑ ventricular filling pressure and systemic or pulmonary edema –In fact, the heart can only meet the needs of the body if the ventricular filling pressure is high Forward heart failure –The 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 edema –Forward failure also decreases the blood flow to various organs, causing weakness and fatigue

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26 Diagnosis History Phsyical EKG CXR

27 History Prior Heart Dz, Dyspnea, PND, Orthopnea, Fatigue, Cough, Bloating, Angina, ↑Wt/↑Girth, Nocturia Precipitants –↑salt, non-compliance, new meds, NSAIDs, palpitations, angina Comorbidities (COPD, Renal Dz, DM)

28 PE ↑HR ↑RR JVP HJR Precordial exam: –Apical impulse Location, Size, Sustained (45’ LLD position – exp) –Loud P2 –S3 (ventricular vibration with rapid filling) Low pitched (bell) 45’ LLD position Lungs: –Cracks / Wheezes Peripheral Edema

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31 58 F with known Idiopathic Dilated Cardiomyopathy Cardiac Cath (05): N coronaries LVEF 35% Meds: ACE-I, Diuretics, Digoxin ↑SOBOE x 3weeks OE: Displaced MPI Soft S3 Pre-sacral edema Case 2

32 Case 3 70 M – Obese SOBOE and fatigue x 3 months No Orthopnea/PND PMHx: Smoke x 40 pack-years, HTN (poorly controlled) DMII OE: BP 180/100 Sustained MPI Bilateral Rales Mild/Moderate Pretib Edema

33 X-ray Cardiomegally –↑LV or hypertrophied ventricular wall –Cardiothoracic Ratio > 50% Redistribution (cephalization) –Systolic dys-fxn → ↑filling pressure –Upper lobe vessels > Lower lobe vessels Blunting of costophrenic Angle Peribronchial cuffing Kerly-B lines

34 Peri-Bronchial Cuffing

35 “First, strike for the jugular and let the rest go!” Oliver W. Holmes Jr.

36 Etiology Dysrhythmia –Tachy ↓Diastolic filling time +/- atrial kick ↓CO ↓Coronary perfusion ↑ Myocardial O 2 demand –Brady ↓HR ↓CO = SV x ↓HR

37 Infection ↑ systemic met demands Pulm infection = ↓O 2 Tachycardia Anemia Isovolumic hemodilution ↑CO meet O 2 demands ↓Coronary O 2 delivery

38 Pregnancy ↑ demand for CO Acute Myocarditis ↓ contactility Acute valvular dysfunction 2 o to MI ↑preload or ↑↑afterload

39 PE ↓O2 supply ↑ Pulmonary Hypertension Pharmacologic ↓ inotropic effects ↑ Na / H 2 O retention

40 Etiology Decompensation/Causes of exacerbation FAILURE: Forgot medication Arrhythmia/ Anemia Ischemia/ Infarction/ Infection (Pneumonia) Lifestyle: taken too much salt Up-regulation of CO: pregnancy, hyperthyroidism Renal failure Embolism: pulmonary Inappropriate treatment Failure to seek care 25% 20% 10%

41 Case 1 Management A 63-year-old male presents with breathlessness x 3 days. ?Approach, ?Hx PMHx: MI 3 years ago 4-vessel CABG asymptomatic since surgery with no complaints of CP HPI: 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 another –He presents today with extreme shortness of breath –He denies chest pain

42 Management Treat the maladaptation ↑ Vascular resistance ↑ Sympathetic tone ↑ Total blood volume ? LMNOP

43 Management Nitrates O2 Ventilation Assist Devices ACE I Diuretics Morphine Inotropes

44 Airway/Breathing Non-rebreather facemask delivering 100% O 2 Once initial therapy has begun, oxygen supplementation can be titrated in order to keep the patient comfortable and arterial oxygen saturation above 90 percent.

45 NIPPV If respiratory distress and/or hypoxia persist, consider non-invasive PPV –↓ preload, ↓ afterload, and ↑ left ventricular performance –Meta-analysis of 15 clinical trials: ↓mortality and ↓intubation with NPPV compared to conventional therapy –Patients who fail/do not tolerate/have contraindications to NPPV should be intubated –Positive end-expiratory pressure is often useful for improving oxygenation

46 Multi-centre RCT 130 pts Cardiogenic Pulmonary Edema Emergency Department Medical therapy+O2 (65 pts) non-invasive pressure support ventilation (65 pts) Primary outcome – need for intubation

47 Loop Diuretics ↑Na & H 2 O excretion Useful in volume overload Rapid onset –Mild vasodilator ↑1/2 life in CHF …be careful Depletion of K + and Mg ++

48 Loop Diuretics Dosing – not well established High dose Lasix and low dose Nitro has worse outcomes than low dose Lasix and high dose Nitro

49 Morphine Controversial Weak vasodilator / ↓ Resp Drive ↑ ICU admisssions (OR = 3) Sacchetti ?Anxiolytic

50 Nitrates low dose high dose

51 Nitrates - Route SL/Spray ( mg / 5 min) x3 –50-100ug/min IV Drip (5-10ug/min) –titrate to effect –( ug) Transdermal –Peripherally shut down –Unreliable absorption Contraindications / Cautions –Viagra –RV MI –Fixed Aortic Lesions

52 Case 4 67 M ↑SOB Visibly Distressed /110 75% ORA PMHx: HTN, DM II EKG:

53 Nitroprusside Direct smooth muscle relaxant Balanced reduction of pre/after load Continuous pressure monitoring – good –Avoid hypotension

54 Case 5 67 M ↑SOB Visibly Distressed /90 75% ORA PMHx: HTN, DM II Meds: Inconsistent

55 Copyright ©2000 BMJ Publishing Group Ltd. Jackson, G et al. BMJ 2000;320: Natriuretic Peptide

56 Nesiritide Recombinant BNP ↓ Aldosterone ↓ Endothelin ↑ Na & H 2 O excretion – no reflex tachy Good for Nitro contraindications

57 VMAC Randomized, Double Blind 489 inpatients IV Nisiritide vs IV Nitrates vs Placebo PCWP and Dyspnea –Improvement in PCWP – 2mm 6h –No change in Dyspnea Problems: ↓Nitro dosing Prolonged Hypotension Not ED patients Industry sponsored

58 Vosodilator Therapy: Nesiritide Efficacy Phase –432 patients –In the efficacy phase, 127 patients underwent hemodynamic monitoring with a pulmonary artery catheter –A 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 phase –305 patients –Randomly assigned to nesiritide or standard vasoactive agents for seven days without hemodynamic monitoring –Compared 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

59 Death within 30 days tended to occur more often among patients randomized to nesiritide therapy –35 [7.2%] of 485 vs 15 [4.0%] of 377 patients RR from meta-analysis: 1.74 –(95% confidence interval [CI], ; P =.059) Hazard ratio after adjusting for study, 1.80 –(95% CI, ; P =.057)

60 Vasodilator Therapy Nitroglycerin: ↓preload ↓afterload Nitroprusside: ↓ ↓ afterload Nesiritide - BNP

61 ACE Inhibitors Clear longterm benefits 1.Vasodilate 2.Block Aldosterone 3.Bradykinin System 4.↓ Remodeling Take longer to work than nitrates (peak effect 45min)

62 Copyright ©2000 BMJ Publishing Group Ltd. Jackson, G et al. BMJ 2000;320: Effect of ACE-I

63 Placebo-Controlled, Randomized, Double-Blind Study of Intravenous Enalaprilat Efficacy and Safety in Acute Cardiogenic Pulmonary Edema The 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 study –20 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 hemodynamics Excluded those already on ACE I

64 BNP Why do we need another diagnostic test? –Diagnostic uncertainty How 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 low 2 –ER docs are uncertain of the diagnosis in the in-betweeners (30%) 2

65 BNP ↑Ventricular pressure & ↑Stretch –Pro-BNP → Nt-BNP(↑spec) & BNP(↑sens)

66 Prospective, Blinded 1586 pts presenting with acute dyspnea ED Study Bedside assay “Gold Standard” = 2 cardiologists Breathing Not Properly

67 ad

68 Breathing Not Properly

69 Prospective diagnostic test evaluation 7 centers 1586 patients BNP – blinded Gold Standard – Cardiology Chart Review 97% certainty by ED physician At “80%” EP certainty Sens: 49% Specificity: 96% At 100 pg/ml Sens: 90% Specificity: 73%

70 adf

71 Breathing Not Properly - Analysis BNP brings us closer to the “gold standard” Low Prob -EP 17% had CHF 90% would have been corrected by BNP High Prob -EP 4% did not have CHF 80% would have been corrected by BNP Uncertain -EP BNP correctly classified 74% Misclassified 7%

72 BNP Levels < 100 pg/ml may prompt clinician to focus on alternative diagnosis (COPD) Reasonable neg pred value Prognostic Value ?Variation with Age/Gender/Kidney fxn

73 Prospective, Randomized, Controlled Single blind 452 Pts with dyspnea Diagnostic Strategy (BNP) vrs Standard Assessment Told EP if 500 CHF likely, indeterminate End Points: Time to D/C & Total Cost Safety: Similar Conclusion: BNP improved evaluation thereby improving time to D/C and cost – no change in safety

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75 BNP strong prognostic indicator in symptomatic and asymptomatic individuals Death or Cardiac Death Additive to LVEF

76 Cardiomyopathy /MedMovieRedirect.aspx?ClientID=27http://www.medmovie.com/mmdatabase /MedMovieRedirect.aspx?ClientID=27

77 Case Previously 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. –37.8 o C /54 –Pale irritable –HEENT: MMM. No adenopathy –CVS: regular S1S2, no murmer, PPPx4, no edema –CHEST: AE=AE slight decrease at bases –ABD: palpable liver edge below umbilicus EKG: sinus tach, LAD, flattened T-waves, decreased voltages.

78 Post Myocarditis

79 Dilated Cardiomyopathy Most common CM –30% idiopathic –Hereditary X-linked (dystrophin gene) –Booze –Heavy Metal –Drugs –Infectious Viral Chagas –Post partum –Collagen vascular disease –Glycogen storage disease –Thiamine, PO4, zinc deficiency –Amyloidosis –Neuromuscular disorders

80 Dilated Cardiomyopathy Biopsy helpful for etiology Rx same as other CHF MDC (Metoprolol in Dilated CM) – 34% reduction in Death Multicenter Myocarditis Treatment Trial – no benefit of corticosteroids and azathioprine for Rx of biopsy-proven inflammation in dilated CM

81 HCM Inappropriate hypertrophy w/o stimulus Usually asymmetric 4% mortality per year (sudden death)

82 HCM 50% familial (Dominant Inheritance) Mechanism –Abn Ca++ kinetics –Abn sympathetic stim –Abn Coronaries –Subendocardial ischemia –Structural abn

83 HCM 25% 1st relatives of HCM Usually 3rd decade – not always M>F

84 HCM - Presentation Sudden Death Dysrhythmia CHF Presyncope / Syncope Angina

85 HCM CHF Sx OE: ↑JVP – prominent “a” wave Double impulse pulse PMI laterally displaced and increased SEM / HSM Split S2

86 HCM Genetic Studies ECG Echo –LV outflow gradient >50mmHg –Diastolic dysfunction –HOCM: septum >1.4:1 ratio to post wall

87 HCM – Approach/Mgmt ABCD Normal CHF / CAD Rx Myomectomy Catheter septal ablation MV replacement ICD B-blockade CCB Anti-arrhythmias

88 Restrictive Least common CM Incidence – likely under diagnosed Poor prognosis

89 Cardiomyopathy /MedMovieRedirect.aspx?ClientID=27http://www.medmovie.com/mmdatabase /MedMovieRedirect.aspx?ClientID=27

90 Restrictive Idiopathic restrictive cardiomyopathy –EndoMyocardial Fibrosis –Loeffler eosinophilic endomyocardial disease Secondary restrictive cardiomyopathy –Radiation –Hemochromatosis –Amyloidosis –Scleroderma –Carcinoid heart disease –Glycogen storage disease of the heart

91 Diagnosis Chest x-ray –Absence of cardiomegaly, normal cardiac silhouette –CHF Electrocardiogram –LBBB common, RBBB possible –Low voltage –Nonspecific ST-T changes –Various arrhythmias –Chamber enlargement

92 Echocardiography –Normal to symmetrically thickened walls –Rapid early-diastolic filling, slow late- diastolic filling –Normal or slightly reduced ventricular volume and systolic function

93 Cardiac catheterization –Elevated ventricular end-diastolic pressure –Dip and plateau configuration of the diastolic portion of the ventricular pressure pulse –Normal to slightly decreased ejection fraction –Prominent x and y descent

94 Endomyocardial biopsy –May detect typical eosinophil infiltration in the inflammatory stage –May detect myocardial fibrosis in later-stage cases –Negative findings do not exclude diagnosis

95 Treat underlying cause if possible Therapy similar for other causes of CHF Consider anticoagulation as prone to stasis –thromboembolism

96 Thanks Shawn for the resources!

97 References 1.Kostuk WJ. Congestive heart failure: what can we offer our patients? CMAJ 2001;165(8): Schwam E. B-type natriuretic peptide for diagnosis of heart failure in emergency department patients: a critical appraisal. Acad Emerg Med 2004;11:

98 Copyright ©2000 BMJ Publishing Group Ltd. Jackson, G et al. BMJ 2000;320: Risk of HF after AMI

99 20 pts Pulmonary Edema Looked like needed intubation 2 intubated Also had COPD Mean Treatment Duration 2 ½ h


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