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 jaw
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 Canadians1
(10% of those >75)
> new cases are diagnosed /yr1

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

7. Definition CHF Pulmonary Edema
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
The heart is a pump that works together with the lungs. It pumps blood in 2 ways
It pumps blood from the heart to the lungs to pick up oxygen. The oxygenated blood returns to the heart
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.

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

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

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

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

19. Remodelling Post MI Jackson, G et al. BMJ 2000;320:167-170
Copyright ©2000 BMJ Publishing Group Ltd.

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
Chordae Tendonae Rupture. Large enough area of ischemia.

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
↓O2 diffusion
However, 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.

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

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: Lungs: Peripheral Edema
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
Beware of AP films and poor inspiration (FP)

29. Precision improves with further training (i. e
Precision improves with further training (i.e. Medical students<Residents<Staff<Cardiologists)

30. Precision improves with further training (i. e
Precision improves with further training (i.e. Medical students<Residents<Staff<Cardiologists)

31. Case 2 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

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 Redistribution (cephalization)
↑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 Brady
↓Diastolic filling time +/- atrial kick
↓CO
↓Coronary perfusion
↑ Myocardial O2 demand
Brady
↓HR
↓CO = SV x ↓HR

37. Infection Anemia ↑ systemic met demands Pulm infection = ↓O2
Tachycardia
Anemia
Isovolumic hemodilution
↑CO meet O2 demands
↓Coronary O2 delivery

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

39. PE Pharmacologic ↓O2 supply ↑ Pulmonary Hypertension
↓ inotropic effects
↑ Na / H2O 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%
10%
25%
Other 10%
10%
20%

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 ? LMNOP ↑ 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% 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

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. Cardiogenic Pulmonary Edema Emergency Department
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
Italian study – 5 departments

47. Loop Diuretics ↑Na & H2O 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 (0.1 - 0.4mg / 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 96 28 200/110 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 96 28 140/90 75% ORA
PMHx: HTN, DM II
Meds: Inconsistent

55. Natriuretic Peptide Jackson, G et al. BMJ 2000;320:167-170
Copyright ©2000 BMJ Publishing Group Ltd.

56. Nesiritide Recombinant BNP ↓ Aldosterone ↓ Endothelin
↑ Na & H2O 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. RR from meta-analysis: 1.74
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
Vasodilate
Block Aldosterone
Bradykinin System
↓ Remodeling
Take longer to work than nitrates
(peak effect 45min)

62. Effect of ACE-I Jackson, G et al. BMJ 2000;320:167-170
Copyright ©2000 BMJ Publishing Group Ltd.

63. placebo-controlled, randomized, double-blind study
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? How uncertain are we?
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 low2
ER docs are uncertain of the diagnosis in the in-betweeners (30%)2
The 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.

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

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

67. Breathing Not Properlyad

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 <100 CHF unlikely, >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

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

76. Cardiomyopathy

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.
37.8oC /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

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 Electrocardiogram
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
Kostuk WJ. Congestive heart failure: what can we offer our patients? CMAJ 2001;165(8):1053-5
Schwam E. B-type natriuretic peptide for diagnosis of heart failure in emergency department patients: a critical appraisal. Acad Emerg Med 2004;11:

98. Risk of HF after AMI Jackson, G et al. BMJ 2000;320:167-170
Copyright ©2000 BMJ Publishing Group Ltd.

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