This document discusses heart failure (CHF) and summarizes key points about clinical syndromes, diagnostic syndromes, and treatment options for CHF. There are three main clinical syndromes - pure right ventricular failure causing leg swelling, left ventricular failure causing pulmonary edema and shortness of breath, and low output failure causing weakness. Diagnostically, CHF can be systolic or diastolic dysfunction. Treatment for systolic dysfunction focuses on ACE inhibitors while diastolic dysfunction is best treated with ACE inhibitors, beta blockers, and calcium channel blockers.

1. HEART FAILURE
Jorge Garcia, MD
November 22, 2002

4. CHF: we will talk about:
Part 1. Clinical Syndromes: Left
ventricle vs Right Ventricular Failure.
Part 2. Diagnostic Syndromes: Systolic
vs. Diastolic Failure.
Part 3. Treatment options.

5. Part 1. There are 3 clinical
“CHF” syndromes:
1. Pure RV failure.
2. Pulmonary edema.
3. Low output failure.
What are the symptoms of
these?

6. What are the symptoms of pure
Right Ventricle failure?

7. Pure Right Ventricle failure:
1. JVD.
2. Dependent Pedal
Edema.

8. What are the symptoms of
“CHF” caused by pulmonary
edema?

9. Pulmonary Edema causes
Dyspnea:
Initially, DOE.
then PND.
Then dyspnea at rest.
Caused by…?

10. Pulmonary Edema causes
Dyspnea:
Initially, DOE.
then PND.
Then dyspnea at rest.
Caused by…LV failure.

12. (Why does the patient experience
dyspnea?)

13. (Why does the patient experience
dyspnea?)
Not hypoxia, but interstitial fluid causing
stiff lungs and increased work of
breathing.
Don’t be reassured by a decent O2 sat.

14. So the first distinction is between
pure right ventricular failure and
pure left ventricular failure:
RV failure causes pedal edema.
LV failure causes pulmonary edema.

15. Third “CHF” syndrome:
Low cardiac output (pump failure)
What are the symptoms?

16. Low cardiac output (pump
failure) causes:
Dyspnea
Swelling of the legs
Weakness, fatigue, lethargy,
lightheadedness, and
confusion

17. Low output CHF syndrome is
often mixed right and left heart
failure.
most common.
patients have mix of symptoms.

18. Do rales=CHF?
?

19. Rales
Rales present in < 25% of patients with
HF, and absence does not rule it out.

20. When else do you hear rales?

21. When else do you hear rales?
Rales can be present in other lung
conditions, such as pulmonary fibrosis,
especially if not basilar, or present in
entire respiratory cycle.

22. What is the more reliable sign of
“CHF”?

23. S3
S3 gallop in adults is considered
pathognomonic for heart failure.
S3 in children and adolescents can be
normal, and does not imply heart
failure.
S4 in elders can be a result of long
standing HTN, and not imply heart
failure.

24. What is the best way to hear
an S3?

25. Hearing an S3:
S3 is heard best heard with the bell,
with the patient in a left lateral decubitus
position.

26. How do you check for JVD and
HJR?

27. How do you check for JVD and
HJR?
Look at the internal jugular.

28. What is the most common cause
of pedal edema?

29. What is the most common cause
of pedal edema?
Venous insufficiency.

31. Another common sign of “CHF”
is the new onset of tachycardia.
Why do you get sinus tachycardia
with CHF?

32. Sinus Tachycardia.
CO = HR x SV. If SV is reduced and
fixed by heart failure, then an increase
in CO will require an increase in HR.
Always suspect HF in a
patient with unexplained
sinus tachycardia.

33. Part 2: the pathology of
“CHF.”
The distinction between systolic
and diastolic dysfunction.

34. Systolic dysfunction
Close to what was originally thought of
as “CHF.”
After infarction, muscle “scar” is
thinner and less contractile. After
several MI s one is left with a large
flabby heart.
Other causes of dilated
cardiomyopathy:

37. Diastolic dysfunction
May be the more common form of CHF.
Thick stiff heart after long history of
HTN.

40. Systolic dysfunction in more
detail...
• Diffuse dilation of three (if not all
four) heart chambers.
• Thin ventricular walls, poor global
contractility.
• Chest x-ray with cardiac enlargement,
pear shaped heart: DDx includes
pericardial effusion.

43. Systolic dysfunction
• Most common cause is CAD and
infarctions, with remodeling of the
ventricular wall.
• Cardiomyopathies can also cause
systolic dysfunction CHF.
The heart no longer works well in
systole: it does not contract well.

44. Diastolic dysfunction in more
detail…
What is the pathophysiology of
diastolic dysfunction?

45. Diastolic dysfunction:
The ventricle “fights” against
hypertension and against increased
afterload by becoming “stronger” and
the heart muscle hypertrophies.
Concentric hypertrophy, directed
inwardly, encroaches on the LV cavity.
Stiff, fibrotic LV muscle does not relax
in diastole, does not fill enough.
Thus, reduced end diastolic volume.

47. Diastolic dysfunction over time:
• Reduced stroke volume, reduced
cardiac output.
• As it progresses, CAD will often
develop and the pathology will overlap
with systolic dysfunction.

48. Diastolic dysfunction:
• Common, especially in elders with long
standing HTN.
Can’t be distinguished on exam from
systolic dysfunction:
Chest film: the heart often looks normal.
need an echo

49. Diastolic dysfunction on echo:
• Contractility is preserved and ejection
fraction is usually normal.
• Concentric hypertrophy on echo.
Inwardly directed ventricular
hypertrophy.

50. How can diastolic dysfunction
lead to atrial fibrillation?

51. A. Fib.
• In the normal heart, left ventricle fills
passively, right after the mitral valve
opens.
• In diastolic dysfunction, the stiff LV
does not relax, fills more slowly.
• Left atrium “tries” to overcome this by
dilating, which increases risk of
developing atrial fibrillation.

52. A. Fib.
• The cardiac output becomes
increasingly “dependent” on this
atrial kick.
• When the atrial kick is lost suddenly
with A. Fib, your patient may rapidly de-
compensate, and develop clinical heart
failure that was masked by the atrial
kick.

54. Summary of diastolic vs systolic
dysfunction.
Diastolic:
Cause: HTN.
Result: thick LV.
Muscle does not
relax.
Failure of diastole.
Systolic:
Cause: MI
Result: thin LV wall.
Muscle does not
contract.
Failure of systole.

55. Part 3. Treatment

56. What is the treatment of
systolic dysfunction?

57. The treatment of systolic
dysfunction?
ACE-I is the drug of choice: Start Rx
early.

58. The treatment of systolic
dysfunction?
ACE-I is the drug of choice: Start Rx
early
Used in the immediate post MI setting,
ACE-I will prevent remodeling and thus
prevent CHF.
May use an ACE-I alone if no signs of
volume overload.

59. The treatment of systolic
dysfunction?
Diuretics only in patients with volume
overload or acute pulmonary edema.
Cautious use of beta-blockers.
(Negative inotrope.)

60. The treatment of systolic
dysfunction?
What about dig?

61. Digoxin can be used as a positive
inotrope.
 It also controls ventricular rate in A Fib.
 Forth line therapy, after ACE-I, beta-
blockers, diuretics. Never proven to
decrease mortality.
 Avoid in patients in sinus with diastolic
dysfunction.

62. What is the prognosis of patients
with systolic dysfunction?

63. Px of patients with systolic
dysfunction
terrible:
“cardiac cancer.”
Progressive deterioration over a few
years, to death.

64. How do we treat diastolic
dysfunction?

65. Treatment of diastolic
dysfunction:
• Empiric treatment options only – no
decent data.
• The problem is not a weak pump, but a
stiff, un-relaxing pump.
• Making the heart pump harder will
make things worse: positive inotropic
agents, such as digoxin, are
contraindicated.

66. Treatment of diastolic
dysfunction:
• ACE-inhibitors are treatment of
choice,
because they reverse ventricular
hypertrophy.

67. Treatment of diastolic
dysfunction:
Negative inotropic agents can help:
beta-blockers and Calcium channel
blockers (Verapamil and Diltiazem).

68. Treatment of diastolic
dysfunction:
• Nitrates can help, but as in all cases,
need to avoid excess lowering of BP.
• In addition, maintain your patient in
sinus rhythm and keep the atrial kick.

69. What is the prognosis of diastolic
dysfunction?

70. What is the prognosis of diastolic
dysfunction?
can be OK, with treated patients
surviving years.

71. • When do you suspect
diastolic dysfunction?

72. When do you suspect diastolic
dysfunction?
• History of HTN.
Intermittent pulmonary edema.
• Sudden CHF episodes, with little
warning.
“Flash Pulmonary edema.”

73. When do you suspect diastolic
dysfunction?
• Worsening failure despite seemingly
appropriate therapy with dig and
diuretics.
Again, need echo in all new cases of
HF. This is the only way to determine if
dysfunction is diastolic or systolic.

74. Summary of treatment of CHF:
Systolic Failure:
ACE-I
diuretic
Beta-blocker
dig
Diastolic disfunction:
ACE-I
beta-blocker
Ca Ch. Blocker
nitrates.

75. Which ACE-I should be used?

76. Which ACE-I should be used?
• Look at cost, duration of action,
convenience. Otherwise, fairly
comparable.
• Dosing: usually under used and under
dosed. Aim for maximum dose
tolerated by BP.

77. Hey, what about ARBs?

78. ARBs (Angiotensin-II Receptor
Blockers)
might work as well, but not yet proven.
They don’t lead to accumulation of
bradykinins.

79. ARBs
Bradykinins are great for decreasing
blood pressure and preserving renal
function, but also responsible for cough
and angioedema of ACE-I.
No mortality study, and only Losartan
shown to benefit in HF in a drug
company sponsored study.

80. What are the contraindications
to ACE-I?

81. Contraindications to ACE-I:
• Allergy
angioedema
neutropenia
severe skin eruptions – all very rare.

82. Relative contraindications to
ACE-I
Hypotension
Hyperkalemia – care with K+
supplements or K sparing diuretics.
Dysgeusia.

83. Relative contraindications to
ACE-I: CRI
CRI: with creatinine 1.5-2.5, use with
caution and monitor creatinine.
Avoid with creat > 2.5. Often,
increasing creatinine can be caused by
over diuresis and renal hypo-perfusion.
May try to back off on diuretics first.

84. What about cough with ACE-I?
What is the most common cause of
cough in a patient with CHF on ACE-I?

85. Cough with ACE-I
most common cause of cough in a
patient with HF and ACE-I is
pulmonary edema

86. If ACE-I can not be used?
What can be used instead?

87. If ACE-I can not be used?
• Hydralazine and Nitrates. These have
been shown to decrease mortality, but
less than ACE-I.
• Hydralazine dosed multiple times per
day, can cause head aches,
palpitations, nasal congestion, reflex
tachycardia, tachyphylaxis.

88. What about diuretics? Can they
be used first, and alone in
treatment of HF?
??

89. What about diuretics? Can they
be used first, and alone in
treatment of HF?
No.

90. Diuretics and CHF:
• Still best for acute symptoms of volume
overload.
• Not to be used alone long term. Can be
counter-productive, in decreasing
volume, renal perfusion, activating RAA,
promoting tachycardia.

91. Diuretics and CHF
• Used alone, they become increasingly
ineffective. Addition of ACE-I can
restore effectiveness.
• Loop diuretics most potent. Double the
dose of Lasix until effective. Single
daily does is best. (Lasix is short acting
[“Lasts Six – hours”] and not great for
BP control, but decent for diuresis.)

92. Diuretics and CHF
• Can often combine types for better
effect.
• Renal function may dictate type:
Creatinine Clearance of > 30 ml/m –
may use thiazides. ClCr of 20-30, may
use Lozol(indapamide) and
Zaroxolyn(metolazone). Lower ClCr
may use loops until you need dialysis.

93. Diuretics and CHF
• Spironolactone 25 mg PO qd has been
shown to reduce mortality (by 27%,
1600 patients, RALES study NEJM,
1999) but best effect in Class III & IV
heart failure. May be useful in other
patients. Again, blocks the aldosterone
of the RAA system. Can’t use if
Creatinine is greater than 2.0.

95. When can one use Dig?
?

96. When can one use Dig?
• Systolic dysfunction, as a positive
inotrope.
• Reduce HR in A Fib.
• Forth line therapy, after ACE-I, beta-
blockers, diuretics. Never proven to
decrease mortality.
• Avoid in patients in sinus with diastolic
dysfunction.

97. When to use beta-blockers?

98. When to use beta-blockers?
• Best for patients with diastolic
dysfunction, tachycardia. Use full
doses as for HTN.
• Can be used in systolic dysfunction,
with caution. Start low dose, and titrate
slowly, over months. Have been shown
to reduce mortality. Mechanism not
clear, perhaps restoring body’s
sensitivity to catecholamines.
• Don’t start during decompensation.

99. Can we use Calcium Channel
Blockers, and if so, which?
?

100. CCBs in CHF
• Think of CCB as two types:
–1. Verapamil and Diltiazem
–2. everything else…(Nifedipine,
etc…)

101. CCBs in CHF
• Verapamil: most negative inotropic, not
useful in systolic dysfunction, but useful
in diastolic dysfunction.
• Diltiazem. Less negative than
Verapamil, used in the same way.

102. CCBs in CHF: Everything else...
• Dihydropyridines: Nifedipine and all
other CCB. Should not be used with
HF. Can cause vaso-dilation, and reflex
tachycardia. Can cause non-cardiac
edema – complicating evaluation.
• Amlodipine may be different (Norvasc)
but best to group with Nifedipine.

104. Treatment can save lives:
NNT (Number needed to treat)
ACE-I: NNT for 4 years to save one live
is 20.
Spironolactone: in Class IV only, NNT
for 2 years of treatment to save one life
is 9.
Beta-blocker: NNT for 9 months to save
one life is ~30.