Cardiac failure occurs when the heart cannot pump enough blood to meet the body's needs. It can be due to low cardiac output or congestion within the heart or vessels. Therapy aims to reduce preload and afterload on the heart, increase contractility, control arrhythmias, and treat the underlying cause. Positive inotropes like digoxin increase contractility but do not cure the disease and can cause toxic side effects at high levels. Diuretics, ACE inhibitors, beta blockers, and other drugs target compensatory mechanisms and remodeling processes to improve cardiac function.

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