1. Cardiac Failure
and the
Therapeutics of
Failure
Rebecca E.
Gompf

2. Normal Heart Function
 Maintain blood pressure
 Perfuse lung and tissues
 Maintain normal venous pressure
 Maintain systemic and pulmonary
capillary pressures

3. Abnormal Heart
Function
 Low blood pressure
 Decreased tissue perfusion
 Increased venous pressures
 Increased capillary pressures

4. Factors of Cardiac
Performance
 Cardiac output = heart rate X
stroke volume
 Stroke volume = end diastolic
volume-end systolic volume

5. Stroke Volume
SV = contractility X preload
afterload
Since CO = HR X SV
Then
CO = heart rate X contractility X PL
afterload

6. Preload
 Force that stretches ventricular
fibers
 Increases contractility at first
 Increases stroke volume
 Estimated as end diastolic
volume

7. Afterload
 Impedes ventricular contraction
and ejection of blood
 Due to vascular resistance
 Increases ventricular wall stress
 Increases work load of heart
 Decreases stroke volume

8. Contractility
 Sarcomere contraction
 Many factors affect it—cardiac
and systemic factors
 Increased contractility increases
stroke volume and vice versa

9. Compliance
 Pliability of the ventricles so that
they can fill.
 Influenced by wall thickness
 Also influenced by pericardial
diseases

10. Heart Rate
 Influenced by many factors
 Increased heart rate will increase
cardiac output up to a point
 Decreased heart rates can
decrease cardiac output

11. Synergy
 Coordinated function of the atria
and ventricles to optimize heart
function
 Arrhythmias disrupt synergy and
decrease cardiac output

12. Heart Disease
 Abnormal heart
 Heart may or may not be in
failure
 Congenital
 Acquired
 10% of dogs have heart disease

13. Circulatory Failure
 Insufficient cardiac output of any
cause
 One cause is heart failure

14. Heart Failure
 Heart cannot pump blood
presented to it-congestive
 Or heart cannot meet body’s
needs- output failure

15. Heart Failure
 Venous overload results in
congestion
 Inadequate perfusion

16. Heart Failure
 Normal heart=low diastolic size
and low venous pressure
 Failing heart=high diastolic size
and high venous pressure
 Failing heart=cardiac reserve is
used at rest

17. Heart Failure
 Congestive failure--edema,
effusions
 Low output failure

18. Heart failure
 Clinical syndrome
 Not a specific disease!

19. Left sided Congestive
Heart Failure
 Left sided congestive heart failure
(CHF)
 Cascade of events that starts
with increased left ventricular
diastolic pressure

20. Left sided congestive heart
failure
 Increased LV diastolic pressure
 Increased LA diastolic pressure
 Increased pulmonary venous
pressure

21. Left sided congestive
heart failure
 Increased pulmonary capillary
hydrostatic pressure
 Fluid into interstitial and alveolar
areas
 Pulmonary edema

22. Causes of increased LV
diastolic pressure
 Increased preload
 Decreased compliance
 Increased afterload
 Combinations of the above

23. Right sided congestive
heart failure
 Increased right ventricular diastolic
pressures
 Increased right atrial diastolic
pressure
 Increased central venous pressure

24. Right sided Congestive
Heart Failure
 Increased systemic capillary bed
pressure
 Edema (pleural effusion, ascites)

25. Causes of Right Sided
CHF
 Increased preload
 Decreased compliance
 Increased afterload
 Combination of above

26. Biventricular Heart
Failure
Both sides of the heart fail

27. Low output failure
 Either right or left side cannot
pump enough blood to perfuse
tissues
 Dilated cardiomyopathy (end
stage)

28. Causes of Heart Failure
 Pressure overload
 Volume overload
 Pump failure

29. Causes of Heart Failure
 Arrhythmias
 Myocardial restriction
 High output states

30. Pressure Overload
 Excessive afterload
 diastolic dysfunction
 Contractility ok
 Examples: subaorticstenosis,
pulmonicstenosis, hypertension

33. Volume Overload
 Excessive preload
 Systolic dysfunction
 Contractility ok at first
 Examples: Mitral regurgitation,
patent ductus arteriosus

35. Pump Failure
 Insufficient contractility
 Systolic dysfunction
 Low output failure
 Also, congestive failure

36. Pump Failure
 Dilated cardiomyopathy
 Ischemia/infarcts
 Chronic heart disease
 Dysenergy
 Drugs

38. Arrhythmias
 Changes in rate, rhythm, or
conduction
 Affects heart rate, synergy, and
ventricular filling
 Examples: tachycardias,
bradycardias, heart blocks

40. Myocardial Restriction
 Interferes with ventricular filling
 Diastolic dysfunction
 Contractility ok
 Examples: hypertrophic
cardiomyopathy, pericardial
effusion

43. High output states
 Increased need for tissue blood
flow
 Heart is normal until later
 Examples: hyperthyroidism,
chronic anemia, chronic fever

45. Classes of Heart Failure
 Mild
 Moderate
 Severe
 Modified NYHA Classes

46. Compensatory
Mechanisms
 Sympathetic Nervous System
 RAAS system activation
 Myocardial remodeling

47. Sympathetic Nervous
System
 Heart rate increased due to
stimulation of Beta1 receptors on
SA and AV nodes
 Increases cardiac output at up to
2 ½ times normal rate

48. Sympathetic Nervous
System
 Increased contractility by
stimulation of Beta1 receptors
and epinephrine and
norepinephrine
 Effects blunted in chronic disease
and can make things worse

49. Sympathetic Nervous
System
 Causes peripheral arteriolar
vasoconstriction by stimulation of
Alpha1 receptors
 Prevents hypotension
 Creates increased afterload and
increased workload on the heart

50. RAAS System
 Increases preload to try to
increase cardiac output
 Activated by decreased renal
perfusion
 Renin released, converted to
angiotension I converted to
angiotension II by ACE

51. RAAS System
 Angiotension II is potent
vasoconstrictor which increases
afterload and preload
 Angiotension II has adrenals
release aldosterone so that
sodium and water retained which
also increases preload

52. RAAS System
 In early heart disease, can return
CO to normal
 In later heart disease, increases
preload which increases cardiac
work load and increases failure

53. RAAS System
 Antidiuretic hormone (ADH)
released by increased
angiotension II
 ADH causes renal retention of
fluid which increases preload

54. Myocardial Remodeling
 Chronic volume overload
increases diastolic stress
 Heart lays down more sarcomers
end to end
 Result is dilation of the heart and
eventually some hypertrophy
(eccentric hypertrophy)

55. Myocardial Remodeling
 Chronic pressure overloads
 Heart lays down more sarcomers
in parallel so that wall becomes
thicker
 Concentric hypertrophy

57. Side Effects of Remodeling
 Dilated ventricle eventually has
decreased contractility
 Excessively hypertrophied
ventricle results in decreased
lumen size, stiff ventricle, and
decreased coronary artery filling

58. Clinical Signs of Heart
Failure
 Decreased cardiac output
(exercise intolerance)
 Pulmonary congestion (coughing,
dyspnea)

59. See notes on hormones
and cardiac failure p.96

60. Physical Exam Findings
with Left Heart Failure
 Possible murmur or gallop
 Tachycardias or bradycardias
 Coughing and/or dyspnea are the
main 2 signs

61. Physical Exam Findings
with Left Heart Failure
 Pulmonary crackles (rales), not
always
 Prolonged capillary refill time =>
decrease CO
 Weak femoral pulses (not
always)

64. Physical Exam Findings
with Right Heart Failure
 Systemic congestion (ascites in
dogs, pleural effusion in cats,
peripheral edema in horses, cows)
 Hepatomegaly, splenomegaly
 Distended jugular veins
 Cardiac cachexia

69. Cats with Left or Right
Heart Failure
 Dyspnea is primary sign**
 Cats may or may not cough with
left heart failure (usually not
detected)

72. Therapy Goals
 Reduce congestion
 Increase cardiac output
 Decrease cardiac work load
 Control arrhythmias, heart rate
 Treat cause of heart failure

73. Therapy Goals
 Modify the neurohormonal
compensation
 Modify cardiac remodeling
 Improve the patient’s quality of
life
 Increase patient’s longevity

74. RAAS
 Beta blockers decrease renin
release
 ACE inhibitors interupt
conversion of AGI to AGII
 ARBs (angiotension receptor
blockers)
 Aldosterone antagonists

75. Sympathetic Stimulation
 Beta blockers prevent stimulation
of heart by sympathetic system
 Alpha antagonists block alpha
one receptors in arterioles (over
50% dogs will get hypotensive).
ACE I don’t cause hypotension.

76. Water retention
 Diuretics counteract it
 ACE inhibitors also counteract it

77. Cardiac Remodeling
 ACE inhibitors and aldosterone
antagonists
 Beta blockers
 Arteriolar dilators to reduce
afterload
 Reduce preload with ACE
inhibitors and diuretics

78. Reduce Preload
 Diuretics
 ACE inhibitors
 Venodilators
 Low salt diet
 Do not reduce preload too
much!b/c these rely on preload
for CO

79. Afterload Reduction
 ACE inhibitors - dilate
 Arteriolar dilators
 Must treat other diseases causing
the increased afterload.
Hyperthyroid in cats
 Don’t overdo it as get
hypotension.

80. Increase Contractility
 Digoxin (wk. positive inotrope)
 Pimobendan (st. pos. inotrope)
 Catetcholamines IV
 Increases myocardial oxygen
demand and ATP consumption
(down side)
 Find and treat underlying disease

81. Increasing Compliance
 Calcium channel blockers may
relax heart
 Decrease heart rate so heart can
fill
 Remove pericardial effusion. This
is easy to do and rewarding.
 Find cause and treat

82. Heart Rate
 Must treat tachycardias or
bradycardias
 Antiarrhythmic therapy if needed.
 Find and treat any underlying
systemic problem contributing to
the change in heart rate.

83. Restore Synergy
 Treat significant arrhythmias with
appropriate drugs
 Treat heart blocks

84. Stabilize Patient
 Diuretics
 Cage rest
 Oxygen
 Venodilators
 Find and treat underlying problem

85. Positive Inotropes
 Digitalis
 Pimobendan (newest ones)
 Catecholamines (emergency)
 Others

86. Positive Inotropes
 Affect calcium in some manner
 Used only with systolic function
with decreased contractility
 Increases oxygen and energy
used by heart, so heart works
harder
 Arrhythmogenic

87. Positive Inotropes
 Do not cure disease!!***
 Efficacy varies b/t patients
 Give symptomatic improvement
is the goal of Tx

88. Digitalis
 Increases contractility in normal
and failing hearts
 Only increases cardiac output in
failing hearts
 Weak positive inotrope

89. Digitalis
 Negative chronotrope
 Increases myocardial excitability
 Better for volume overloads and
myocardial disease. Not good for
pressure overloads.

90. Digoxin ECG Changes
 Seen mainly with toxicity
 Slower heart rate
 First degree heart block
 Mild ST changes (depression)
 Arrhythmias

91. Digitalis
 Digoxin
 Digitoxin
 Oral drugs
 Well absorbed but, absorption
decreased by food, drugs, and
malabsorption states

92. Digitalis
 Digoxin eliminated by kidneys
 Slow oral method of dosing
 Cats (sick) are more intolerant of
digoxin. Don’t use it.

93. Digitoxicity
 Vomiting, diarrhea, anorexia
 Arrhythmias
 Negative inotrope
 Enhanced by hypokalemia, low
magnesium, hypercalcemia, and
alkalosis

94. Digoxin Drug
Interactions
 Quinidine
 Aspirin (high levels)
 Amiodarone (same class w/
Sotalol)
 Spironolactone
 Cimetidine (decreases absorp of
Dig)
 Verapamil

95. Digoxin
 Crosses placenta
 Older dogs less tolerant of
digoxin
 Giants breeds need less
 Hypothyroid dogs have problems
unless being treated

96. Digoxin Levels
 Run in human hospitals
 Low therapeutic index

97. Indications for Digoxin
 SVT (Supraventricular
tachycardia) or
 Hearts with decreased
contractility
 Does not prevent progression of
the disease process

98. Contraindications for
Digoxin
 Ventricular arrhythmias (severe)
 Animals with just a murmur
 Pericardial disease
 Restrictive cardiomyopathy
 Sinus node disease

99. Contraindications for
Digoxin
 AV blocks
 Hypertrophic cardiomyopathy
 Aortic stenosis
 Pulmonic stenosis
 Pulmonary hypertension

100. Pimobendan
 Inodilator = positive inotrope and
peripheral vasodilator
 Increases cardiac output
 Decreases preload and afterload
 Increases efficiency of cardiac
cells

101. Pimobendan
 Oral drug
 Well absorbed
 Out via feces
 Used in addition to other
medications (instead of digoxin)

102. Pimobendan
 No drug interactions
 But, it is a vasodilator so when
using other vasodilators, be
careful of hypotension.
 Negative inotropes may attenuate
its positive inotropic effects

103. Pimobendan Side Effects
 Uncommon – yea!
 Vomiting/diarrhea-uncommon
 Polyuria/polydipsia-uncomon
 Anorexia-uncommon
 Sinus tachycardia at high doses
 Usually doesn’t worsen VPCs,
but can cause them at high doses

104. Pimobendan
 Efficacy in cats being studied
 Does not stop the progression of
the disease process
 Can accelerate the progression
of mitral regurgitation (murmurs)
if used too soon in the disease.
Don’t start p on this drug if just
has murmurs.

105. Catecholamines
 Stimulates beta receptors and
cyclic AMP
 Synergistic with digoxin
 Metabolized in the liver (IV drugs)

106. Catecholamines
Contraindications
 Hypotension or hypertension
 Sinus tachycardia
 Arrhythmias
 Cardiac disease with mechanical
obstruction (aortic stenosis)
 With beta blockers

107. Epinephrine
 Increases heart rate (thru beta
receptors)
 Increases blood pressure
 Increases cardiac output
(contractility thru beat receptors)
 Increases arrhythmias
 Used mostly in CPR

108. Isoproterenol
 Increases contractility
 Increases heart rate
 Increases cardiac output
 Causes hypotension
 Used for heart block

109. Dopamine
 Increases contractility
 Increases heart rate (sinus
tachycardia)
 Increases blood pressure
(vasoconstricts) (dose
dependent)

110. Dopamine Side Effects
 Tachycardias--high doses
 Arrhythmias--high doses
 Hypotension--low doses
 Hypertension--high doses
(vasoconstriction)
 Increases pulmonary capillary
pressure--high doses. Right
heart to work against increased

111. Dobutamine
Hydrochloride
 Increases contractility
 No vasodilatation or
vasoconstriction
 Cats can seizure or vomit
 Dogs can vomit

112. Dopamine versus
Dobutamine
 Same price now
 Dobutamine does not induce
tachycardias or affect peripheral
vasculature
 Both cannot be used more than
72 hours b.c they up regulate
beta receptors and the receptors
then become ineffective

113. Amrinone
 Increases contractility
 Vasodilates
 Expensive

114. Diuretics
 To relieve excessive fluid
accumulation
 Decrease preload
 Relieve signs of failure only

115. Types of Diuretics
 Xanthine derivative
 Thiazides
 Aldosterone inhibitors
 Ethacrynic acid
 Loop diuretics—furosemide –
used the most - Lasix

116. Xanthines
Bronchodilators
 Weak diuretics
 Weak positive inotropes
 Dilates coronary, pulmonary ,
renal, and systemic arterioles
and veins (v little effect)
 Bronchodilator

117. Bronchodilators
 Aminophylline
 Theophylline

118. Bronchodilators
 Metabolized in the liver
 Side effects: vomiting, sinus
tachycardia, hyperexcitability
(MAY happen and could last for 8
hrs.)

119. Thiazide Diuretics
 Effects are not dose dependent
 Not as potent as furosemide but
have a more sustained diuretic
effect
 New lipid soluable ones
 Not effective with compromised
renal function

120. Thiazides
 Side effects uncommon
 Cheap
 No drug tolerance develops
 Can be used with other diuretics
 Well tolerated
 Effects aren’t dose related

121. Thiazides
 Only disadvantage--only oral
form
 Drug interactions--penicillins

122. Aldosterone Inhibitors
Spironolactone
 Takes 2-3 days to be effective
 Weak diuretic
 Used in combination with other
diuretics
 Other benefits being explored
 Drug interactions—ACE inhibitors

123. Furosemide
 Loop diuretic
 Effect is dose dependent
 Will dehydrate animal
 Comes in IV and oral forms
 Inexpensive

124. Furosemide
 Side effects--hypokalemia,
hyponatremia, dehydration,
prerenal azotemia
 Tolerance develops
 Drug interactions--cephaloridine,
polymixins, aminoglycosides

125. Vasodilators
 Arterial dilators
 Venodilators
 Mixed vasodilators

126. Arterial dilators
 Counteract reflex
vasoconstriction of heart failure
 Decreases work load of left
ventricle
 Improves tissue perfusion
 Decreases mitral regurgitation
(indirectly)
 Side effect is hypotension

127. Venodilators
 Increase vascular capacity
 Decrease venous pressure (less
bld goes back to the heart)
 Decrease preload
 Decreases pulmonary edema
indirectly
 Side effect is decreased CO (be
careful with this)

128. Vasodilator Uses
 Chronic, congestive heart failure
 Valvular heart disease (leaky
valves)
 Congenital heart problems (PDA,
VSD)
 Pulmonary hypertension (some)
 Cardiac arrhythmias due to
hypoxia

129. Vasodilator
Contraindications
 Hypotension
 Coronary artery disease (some)
 Poor cardiac contractility
 Tachycardias

130. Vasodilator Net Effects
 Decreased preload
 Decreased afterload
 Increases cardiac output
 Decreased workload of heart
 Antiarrhythmic

131. Hydralazine
 Pure Arterial dilator
 Uses--dogs with mitral
regurgitation, hypertension
 Side effects in 50%--hypotension,
GI side effects, increased
pulmonary artery pressures

132. Nitrates
 Nitroglycerine ointment--
venodilator, no side effects,
topical
 Sodium nitroprusside--IV, mixed
vasodilator, metabolized to
cyanide

133. Prazosin
 Arterial and venous dilator
 Metabolized in the liver
 Does not cause a reflex
tachycardia
 Unknown if animals develop a
tolerance to it or not.

134. Angiotension
Converting Enzyme
Inhibitors (ACE)
 Captopril (not used much b/c had
many problems)
 Enalapril
 Benazapril
 Lisinopril
 Other ―Pril‖ drugs

135. ACE Inhibitors
 Stop conversion of angiotensin I
to angiotensin II in lungs
 Decreases plasma aldosterone
levels
 Increases blood flow to kidneys
 Effects are progressive

136. ACE Inhibitors
 Increases effects of thiazide
diuretics
 Causes retention of potassium
 Does not cross blood brain
barrier

137. ACE Inhibitors Used in:
 Dilated cardiomyopathy
 Mitral regurgitation
 Volume overloaded hearts
(shunts such as PDA, VSD)
 Advanced heart disease in
people

138. Enalapril
 Side effects uncommon--
hypotension
 Improves heart failure and
increases survival
 Takes 7-10 days to reach
maximum benefits
 Only one clinically tested in
animals

139. Enalapril
 Hard to use in renal patients so
use benazepril
 Improves dog’s quality of life and
increases longevity
 Use in cat needs more study
 Not effective in horses, not
absoped well in their GI tract

140. Beta Blockers’ Actions
 Decrease contractility (negative
inotrope)
 Decrease heart rate
 Decreases myocardial oxygen
consumption
 Blocks sympathetic stimulation of
heart

141. Beta Blockers
 Used to slow AV conduction and
slow heart rate with SVT
 Also used in hypertrophic
cardiomyopathy

142. Beta Blockers
 Propranolol
 Atenolol
 Metroprol
 Carvedilol
 Other ―–ol‖ drugs

143. Beta Blockers Side Effects
 Blocking beta 1 receptors in heart
will decrease contractility and
heart rate
 Blocking beta 2 receptors cause
bronchoconstriction
 Heart blocks
 Heart failure

144. Carvedilol
 Blocks beta 1 and beta 2
receptors
 Extends life span in people
 May help in dogs—studies
ongoing

145. All Beta Blockers
 Start at low dose and increase
gradually
 Do not stop abruptly
 Don’t start until heart failure
under control

146. Additional Therapy
 Cage rest
 Low sodium diet
 Narcotics
 Removing accumulated fluids

147. Acute Pulmonary Edema
 Diuretics
 Cage rest with oxygen
 Nitrol ointment
 ACE inhibitors
 Hydralazine or nitroprusside
 Catecholamines

148. Pleural Effusion
 Thoracentesis—but do NOT
stress
 Cage rest and diuretics

149. Chronic CHF Therapy
 Diuretics
 Venodilators—ACE inhibitors
 Treat the underlying heart
disease with appropriate drugs
 Beta blockers

151. Pressure Overload
 Excessive afterload
 Systolic dysfunction
 Subaortic stenosis or pulmonic
stenosis
 Pulmonary hypertension
 Systemic hypertension

152. Volume Overload
 Excessive preload
 Systolic dysfunction
 Mitral or tricuspid regurgitation
 Shunts--PDA, VSD

153. Pump Failure
 Systolic dysfunction
 Cardiomyopathies--dilated,
myocarditis
 Chronic heart disease
 Dysynergy
 Drugs

154. Arrhythmias
 Changes in rate, rhythm, or
conduction
 Affects heart rate, synergy and
filling of the ventricles
 Effect depends on ventricular
heart rate
 Bradyarrhythmias,
tachyarrhythmias

155. Myocardial Restriction
 Diastolic dysfunction
 Restrictive cardiomyopathy
 Pericardial disease
 Tumors infiltrating myocardium
 Hypertrophic cardiomyopathy

156. High Output States
 Excessive tissue demands
 Shunts
 Anemia
 Fever
 Hyperthyroidism

158. Cardiac Preformance
 Preload
 Afterload
 Contractility

159. Cardiac Performance
 Distensibility
 Heart rate
 Synergy