Heart failure is a condition where the heart is unable to pump enough blood to meet the body's needs. It can result from any structural or functional issues impairing the ventricle's ability to eject or receive blood. Treatment involves controlling risk factors, lifestyle changes, and medications like diuretics, ACE inhibitors, beta blockers, and aldosterone antagonists. Complications include fluid retention, arrhythmias, hepatic and renal dysfunction. Refractory cases may require devices, transplantation, or palliative care.

1. Congestive Heart Failure &
Cor Pulmonale
MARCH 2021

2. Heart failure - Definition
 Impaired cardiac pumping such that heart
is unable to pump adequate amount of
blood to meet metabolic needs
 Not a disease but a “syndrome”
2

3. Heart Failure
 Results from any structural or functional
abnormality that impairs the ability of the
ventricle to eject blood (Systolic Heart
Failure) or to fill with blood (Diastolic
Heart Failure).
3

4. Heart Failure (HF) - Key Concepts
 CO = SV x HR-becomes insufficient to
meet metabolic needs of body
 SV- determined by preload, afterload
and myocardial contractility
 *Classifications HF
 Systolic failure- decreased contractility
 Diastolic failure- decreased filling
 Mixed
4

5. 90/140= 64% EF> 55-65 (75) normal
5

6. Preload
 Volume of blood in ventricles at end
diastole
 Depends on venous return
 Depends on compliance
Afterload
•Force needed to eject blood into circulation
•Arterial B/P, pulmonary artery pressure
•Valvular disease increases afterload
Factors effecting heart pump effectiveness
6

7. Heart Failure
Etiology and Pathophysiology
 Primary risk factors
 Coronary artery disease (CAD)
 Advancing age
 Contributing risk factors
 Hypertension
 Diabetes
 Tobacco use
 Obesity
 High serum cholesterol
 African American descent
 Valvular heart disease
 Hypervolemia
7

8. Result of
Compensatory
Mechanisms
8

9. The Vicious Cycle of Congestive Heart
Failure
Decreased Blood Pressure and
Decreased Renal perfusion
Stimulates the Release
of renin, Which allows
conversion of
Angiotensin
to Angiotensin II.
Angiotensin II stimulates
Aldosterone secretion which
causes retention of
Na+ and Water,
increasing filling pressure
LV Dysfunction causes
Decreased cardiac output
9

10. HF Pathophysiology - summary
 A. Cardiac compensatory mechanisms
 Tachycardia
 Ventricular dilation - Starling’s law
 Myocardial hypertrophy
 Hypoxia leads to decreased contractility
10

11. HF pathophysiology-Summary
 B. Homeostatic Compensatory mechanisms
Sympathetic Nervous System -(Rx –b-blockers)
 Vascular system- norepinephrine-
vasoconstriction (increases after load)
Kidneys
 A. Decreased CO and B/P- Increase renin
angiotensin release ( Rx -ACE i)
 B. Aldosterone release > Na and H2O retention
(Rx ARB)
11

12. HF pathophysiology-Summary
Liver - stores venous volume (ascites, +HJR,
Hepatomegaly- can store 10 L. check liver
enzymes.
 Counter-regulatory-mechanisms
• Increased Na reabsorption >release of ADH
(Rx -diuretics)
• *Release of atrial natriuretic factor (ANP) >
Na and H20 excretion, (prevents severe
cardiac decompensation)
12

13. Types of Heart Failure
 Low-Output Heart Failure
 Systolic Heart Failure:
• Decreased cardiac output
• Decreased Left ventricular ejection fraction
 Diastolic Heart Failure:
• Elevated Left and Right ventricular end-diastolic
pressures
• May have normal LVEF
 High-Output Heart Failure
• Seen with peripheral shunting, low-systemic vascular
resistance, hyperthryoidism, beri-beri, carcinoid,
anemia
• Often have normal cardiac output
 Right-Ventricular Failure
• Seen with pulmonary hypertension, large RV
infarctions. 13

14. Causes of Low-Output Heart Failure
 Systolic Dysfunction
• Coronary Artery Disease
• Idiopathic dilated cardiomyopathy (DCM)
• 50% idiopathic (at least 25% familial)
• 9 % mycoarditis (viral)
• Ischemic heart disease, perpartum,
hypertension, HIV, connective tissue disease,
substance abuse, doxorubicin
• Hypertension
• Valvular Heart Disease
 Diastolic Dysfunction
• Hypertension
• Coronary artery disease
• Hypertrophic obstructive cardiomyopathy (HCM)
• Restrictive cardiomyopathy
14

15. Systolic HF -DCM
15

16. Staging of Heart Failure Disease
 ACC/AHA Guidelines
 Stage A – High risk of HF, without structural
heart disease or symptoms
 Stage B – Heart disease with asymptomatic
left ventricular dysfunction
 Stage C – Prior or current symptoms of HF
associted with underlying heart disease
 Stage D – Advanced heart disease and
severely symptomatic or refractory HF
16

17. Clinical staging of Heart Failure symptoms
 New York Heart Association (NYHA)
 Class I – symptoms of HF only at levels that
would limit normal individuals.
 Class II – symptoms of HF with ordinary
exertion
 Class III – symptoms of HF on less than
ordinary exertion
 Class IV – symptoms of HF at rest
17

18. NY ASSN Funct Class
ACC/AHA Stages

19. Heart Failure manifestations
19

20. Clinical Presentation of Heart Failure
 Due to excess fluid accumulation:
 Dyspnea (most sensitive symptom)
 Edema
 Hepatic congestion
 Ascites
 Orthopnea, Paroxysmal Nocturnal Dyspnea (PND)
 Due to reduction in cardiac ouput:
 Fatigue (especially with exertion
 Weakness
20

21. Physical Examination in Heart Failure
 S3 gallop - Low sensitivity, but highly specific
 Cool, pale, cyanotic extremities
 Have sinus tachycardia, diaphoresis and peripheral
vasoconstriction
 Crackles or decreased breath sounds at bases
(effusions) on lung exam
 Elevated jugular venous pressure
 Lower extremity edema
 Ascites,Hepatomegaly,Splenomegaly
 Displaced Apex beat - Apical impulse that is laterally
displaced past the midclavicular line is usually indicative
of left ventricular enlargement.
21

22. Measuring Jugular Venous Pressure
22

23. JVD
23

24. 24

25. Lab Analysis in Heart Failure
 CBC
• Since anemia can exacerbate heart failure
 Serum electrolytes and creatinine
• before starting high dose diuretics
 Fasting Blood glucose
• To evaluate for possible diabetes mellitus
 Thyroid function tests
• Since thyrotoxicosis can result in A. Fib,
and hypothyroidism can results in HF.
 Iron studies
• To screen for hereditary hemochromatosis as
cause of heart failure.
 ANA
• To evaluate for possible lupus
 Viral studies
• If viral mycocarditis suspected 25

26. Laboratory Analysis (cont.)
 BNP
• With chronic heart failure, atrial
mycotes secrete increase amounts of
atrial natriuretic peptide (ANP) and
brain natriuretic pepetide (BNP) in
response to high atrial and ventricular
filling pressures
• Usually is > 400 pg/mL in patients with
dyspnea due to heart failure.
26

27. Chest X-ray in Heart Failure
 Cardiomegaly
 Cephalization of the pulmonary vessels
 Kerley B-lines
 Pleural effusions
27

28. Cardiomegaly
28

29. Pulmonary Edema due to Heart Failure
29

30. Kerley B lines
30

31. Cardiac Testing in Heart Failure
 Electrocardiogram:
 May show specific cause of heart failure:
• Ischemic heart disease
• Dilated cardiomyopathy: first degree AV block, LBBB,
Left anterior fascicular block
• Amyloidosis: pseudo-infarction pattern
• Idiopathic dilated cardiomyopathy: LVH
 Echocardiogram:
 Left ventricular ejection fraction
 Structural/valvular abnormalities
31

32. But
32

33. Further Cardiac Testing in Heart Failure
 Exercise Testing
 Should be part of initial evaluation of all patients with
CHF.
 Coronary arteriography
 Should be performed in patients presenting with
heart failure who have angina or significant ischemia
 Reasonable in patients who have chest pain that
may or may not be cardiac in origin, in whom cardiac
anatomy is not known, and in patients with known or
suspected coronary artery disease who do not have
angina.
 Measure cardiac output, degree of left ventricular
dysfunction, and left ventricular end-diastolic
pressure.
33

34. Further testing in Heart Failure
 Endomyocardial biopsy
• Not frequently used
• Really only useful in cases such as
viral-induced cardiomyopathy
• In endomyocardial fibrosis
34

35. Chronic Treatment of Systolic HF
 Correction of systemic factors
• Thyroid dysfunction
• Infections
• Uncontrolled diabetes
• Hypertension
 Lifestyle modification
• Lower salt intake
• Alcohol cessation
• Medication compliance
 Maximize medications
• Discontinue drugs that may contribute to heart
failure (NSAIDS, antiarrhythmics, calcium
channel blockers) 35

36. Order of Therapy
1. Loop diuretics
2. ACE inhibitor (or ARB if not tolerated)
3. Beta blockers
4. Digoxin
5. Hydralazine, Nitrate
6. Potassium sparing diuretcs
36

37. Diuretics
 Loop diuretics
• Furosemide, buteminide
• For Fluid control, and to help relieve symptoms
 Potassium-sparing diuretics
• Spironolactone, eplerenone
• Help enhance diuresis
• Maintain potassium
• Shown to improve survival in CHF
37

38. ACE Inhibitor
 Improve survival in patients with all
severities of heart failure.
 Begin therapy low and titrate up as
possible:
• Enalapril – 2.5 mg po BID
• Captopril – 6.25 mg po TID
• Lisinopril – 5 mg po QDaily
 If cannot tolerate, may try ARB
38

39. Beta Blocker therapy
 Certain Beta blockers (carvedilol, metoprolol,
bisoprolol) can improve overall and event free
survival in NYHA class II to III HF, probably in class
IV.
 Contraindicated:
• Heart rate <60 bpm
• Symptomatic bradycardia
• Signs of peripheral hypoperfusion
• COPD, asthma
• PR interval > 0.24 sec, 2nd or 3rd degree block
39

40. Hydralazine plus Nitrates
 Dosing:
 Hydralazine
• Started at 25 mg po TID, titrated up to 100 mg po TID
 Isosorbide dinitrate
• Started at 40 mg po TID/QID
 Decreased mortality, lower rates of
hospitalization, and improvement in
quality of life.
40

41. Digoxin
 Given to patients with HF to control
symptoms such as fatigue, dyspnea,
exercise intolerance
 Shown to significantly reduce
hospitalization for heart failure, but no
benefit in terms of overall mortality.
41

42. Other important medication in Heart Failure
 Statin therapy is recommended in CHF for
the secondary prevention of
cardiovascular disease.
 Some studies have shown a possible
benefit specifically in HF with statin
therapy
• Improved LVEF
• Reversal of ventricular remodeling
• Reduction in inflammatory markers (CRP, IL-6,
TNF-alphaII)
42

43. Meds to AVOID in heart failure
 NSAIDS -Can cause worsening of preexisting
HF
 Thiazolidinediones
• Include rosiglitazone (Avandia), and
pioglitazone (Actos)
• Cause fluid retention that can
exacerbate HF
 Metformin - people with HF who take it are at
increased risk of potentially lethal lactic acidosis
43

44. Heart Failure Complications
 Pleural effusion
 Atrial fibrillation (most common
dysrhythmia)
 Loss of atrial contraction (kick) -reduce CO
by 10% to 20%
 Promotes thrombus/embolus formation
increase risk for stroke
 Treatment may include cardioversion,
antidysrhythmics, and/or anticoagulants
44

45. Heart Failure Complications
 **High risk of fatal dysrhythmias (e.g., sudden
cardiac death, ventricular tachycardia) with
HF and an EF <35%
 HF lead to severe hepatomegaly, especially
with RV failure
• Fibrosis and cirrhosis - develop over time
 Renal insufficiency or failure
45

46. Rx for arrhythmias -Implantable
Cardioverter-Defibrillators (ICD)
 Sustained ventricular
tachycardia is associated with
sudden cardiac death in HF.
 About one-third of mortality in
HF is due to sudden cardiac
death.
 Patients with ischemic or
nonischemic cardiomyopathy,
NYHA class II to III HF, and
LVEF ≤ 35% have a
significant survival benefit
from an implantable
cardioverter-defibrillator (ICD)
for the primary prevention of
SCD.
46

47. Management of Refractory Heart Failure
 Inotropic drugs:
 Dobutamine, dopamine, milrinone, nitroprusside,
nitroglycerin
 Mechanical circulatory support:
 Intraaortic balloon pump
 Left ventricular assist device (LVAD)
 Cardiac Transplantation
• A history of multiple hospitalizations for HF
• Escalation in the intensity of medical therapy
• A reproducable peak oxygen consumption with
maximal exercise (VO2max) of < 14 mL/kg per min.
(normal is 20 mL/kg per min. or more) is relative
indication, while a VO2max < 10 mL/kg per min is a
stronger indication.
47

48. Acute Decompensated Heart Failure
(ADHF)
 Occurs in known stable HF patients
 Cardiogenic pulmonary edema is a
common and sometimes fatal cause of
acute respiratory distress.
 Characterized by the transudation of
excess fluid into the lungs secondary to
an increase in left atrial and subsequently
pulmonary venous and pulmonary
capillary pressures.
48

49. ADHF Causes
 Infections
• Acute MI
• Rupture of chordae tendinae/acute
mitral valve insufficiency
• Volume Overload
• Transfusions, IV fluids
• Non-compliance with diuretics, diet
(high salt intake)
• Worsening valvular defect
• Aortic stenosis 49

50. ADHF
 Symptoms
 Severe dyspnea
 Cough
 Clinical Findings
 Tachypnea
 Tachycardia
 Hypertension/Hypotension
 Crackles on lung exam
 Increased JVD
 S3, S4 or new murmur 50

51. ADHF/Pulmonary Edema(advanced LVF)
 When PA WEDGE pressure is approx
30mmHg
 Signs and symptoms
• wheezing
• Pallor, cyanosis
• Increased HR and BP
• S3
• Rales,copious pink, frothy sputum
51

52. Labs/Studies in ADHF
 U/E/C, CBC
 EKG
 Chest X-ray
 May consider cardiac enzymes
 2D-Echo
52

53. ADHF Treatment
 Strict I’s and O’s, daily weights
 Oxygen, mechanical ventilation if
needed
 Loop diuretics (furosemide)
 Morphine
 Vasodilator therapy (nitroglycerin)
 Nesiritide (BNP) – can help in acute
setting, for short term therapy
53

54. Heart Failure (ADHF) Pneumonic
(emergency mgmt)
U Upright Position
N Nitrates
L Lasix
O Oxygen
A ACE, ARBs, Amiodorone
D Digoxin, Dobutamine
M Morphine Sulfate
E Extremities Down 54

55. Right heart failure / Cor Pulmonale
•Results from diseased right
ventricle
•Blood backs up into right atrium
and venous circulation
•Causes
LVF
Cor pulmonale
RV infarction
55

56. Cor Pulmonale
 Right Sided Heart Disease, secondarily
caused by abnormalities of lung
parenchyme, airways, thorax, or
respiratory control mechanisms.
 No evidence of other heart conditions,
 May be Acute or Chronic
56

57. Etiology of Cor Pulmonale
Lung and
Airways
 COPD
 Asthma
 Bronchiectasis
 DILD
 Pulmonary
tuberculosis
Vascular
Occlusion
 Multiple Emboli
 Schistosomiasis
 Filariasis
 Sickle Cell
 P. Pulmonary
Hypertension 57

58. Thoracic Cage
 Kyphosis > 100 o
 Scoliosis > 120 o
 Thoracoplasty
 Pleural fibrosis
N-M Disease
 Polio Myelitis
 Myasthenia
Gravis
 ALS
 Muscular
Dystrophy
Etiology of Cor Pulmonale
58

59. Abnormal Respiratory Control
 Idiopathic hypoventilation Syndrome
 Obesity hypoventilation syndrome
(Pick-Wickian syndrome)
 Cerebrovascular disease
Etiology of Cor Pulmonale
59

60. Pathophysiology
 Pulmonary disease can produce
physiologic changes that in time affect the
heart and cause the right ventricle to
enlarge and eventually fail.
 Any condition that deprives the lungs of
oxygen can cause hypoxemia and
hypercapnia resulting in ventilatory
insufficiency.
60

61. Pathophysiology..
 Hypoxemia and hypercapnia cause
pulmonary arterial vasoconstriction and
possibly reduction of the pulmonary
vascular bed e.g in COPD or pulmonary
Embolism.
 Right ventricular hypertrophy may result,
followed by right ventricular failure.
61

62. Pathophysiology..
In summary, cor pulmonale results from
pulmonary hypertension, which causes the
right side of the heart to enlarge because of
the increased work required to pump blood
against high resistance through the
pulmonary vascular system.
.
62

63. Natural History
 Several months to years to develop
 All ages from child to old people
 Repeated infections aggravate RV strain
into RV failure
 Initially responds well to therapy but
progressively becomes refractory
63

64. Clinical features of RHF/Cor pulmonale
 Fatigue, lethergy, anorexia
 Venous congestion
• Peripheral edema
• Weight gain
• Ascites
• Hepatomegaly
• Splenomegaly
• Jugular venous distension
 Rx – mainly diuresis 64

65. Lab. Findings
 X-Ray : Prominent pulmonary hilum
pulmonary artery dilatation
Rt MPA > 20 mm
 EKG : P- pulmonale, RAD, RVH
 Echocardiography : RVH, TR, Pulm.
Hypertension
 ABG : Hypoxemia, Hypercapnea,
Respiratory acidosis
 CBC : polycythemia
 Cardiac catheterization 65

66. Treatment of Cor Pulmonale
 Treat Underlying Disease : COPD Tx, Steroid,
Infection control, theophylline, B2 adrenergic
agonists, medroxyprogesterone,
 Continuous O2 : < 2-3L/min
 Diuretics
 Phlebotomy
 Digoxin : controversial
 Pulmonary Vasodilators
 Anticoagulation
 Reduce Ventilation/Perfusion imbalance :
Amitrine bimesylate 66

67. Prognosis
 1960-1970 : 3 yr mortality 50-60%
 Recent times : 5 - 10 years or more
67