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Pharmacology I > Lecture 20/21 - CHF Drugs > Flashcards

Lecture 20/21 - CHF Drugs Flashcards

1
Q

What major molecule controls the contractility of the heart?

A

Calcium

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2
Q

What six aspects can be alter cardiac contractility?

A 
Sensitivity to Ca 
Amount of Ca released from SR 
Amount stored in SR 
Amount of trigger Ca 
Na/Ca exchanger activity 
Intracellular Na concentration
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3
Q

What are the four components of cardiac performance?

A

Preload
Afterload
Contractility
Heart rate

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4
Q

What occurs in cardiogenic shock in regards to stroke work?

A

even with LV filling pressure increasing heart can’t counteract with increased work force

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5
Q

What are the three aspects of pressure of fluid movement within the capillaries?

A

Hydrostatic
Colloid
Tissue

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6
Q

What is normal transudation pressure?

A

10 to 15 mmHg

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7
Q

Drug type that works on: Decreased CO

A

Positive inotropic drugs

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8
Q

Drug type that works on: Na + Water retention

A

Diuretics

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9
Q

Drug type that works on: RAA system

A

ACE inhibitors

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10
Q

Drug type that works on: Cardiac remodeling

A

ACE inhibitors + B-blockers

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11
Q

Drug type that works on: Congestion + Edema

A

Diuretics

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12
Q

Drug type that works on: Increased venous volume + pressure

A

Vasodilators

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13
Q

Drug type that works on: Increased afterload

A

Vasodilators

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14
Q

What are the nine drug groups that can be used to treat CHF, or other cardiac conditions? (nine)

A 
Diuretic
ACE inhibitors 
Calcium sensitizers
Digitalis 
Sympathomimetics 
Inodilators 
Beta blockers 
Alpha/Beta blockers 
Calcium channel blockers
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15
Q

List the drugs: Diuretics

A

Furosemide
Spironolactone
Hydrochlortiazide

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16
Q

List the drugs: ACE inhibitors

A

“-prils”
Enalapril
Benazepril
Captopril

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17
Q

List the drugs: Calcium sensitizer

A

Pimobendan

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18
Q

List the drugs: Digitalis

A

Digoxin

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19
Q

List the drugs: Sympathomimetics

A

Dobutamine

Dopamine

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20
Q

List the drugs: Inodilators

A

“-nones”
Amrinone
Milrinone

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21
Q

List the drugs: Beta Blockers

A

“-olol”
Atenolol
Propranolol
Metoprolol

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22
Q

List the drugs: A/B blockers

A

Carvedilol

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23
Q

List the drugs: Calcium channel blockers

A

Diltiazem

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24
Q

What characterizes CHF?

A

High cardiac filling pressure –>

Leading to venous congestion + Tissue fluid accumulation

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25
Q

Where, in regards to the CHF, does venous congestion occur?

A

Behind the affected side of the heart

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26
Q

What condition normally underlies CHF that can cause further progression of the disease?

A

Poor contractility

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27
Q

What can stimulate compensatory mechanisms to begin in CHF?

A

Chronic cardiac overload (Volume or Pressure)

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28
Q

What are the major signs of left-sided CHF?

A

Pulmonary venous congestion + edema

Cough + Pulmonary crackles + etc.

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29
Q

What occurs with chronic pulmonary venous congestion?

A

Pulmonary hypertension

Sometimes right sided CHF can begin

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30
Q

What are the major consequences of right-sided CHF?

A

Systemic venous hypertension
Jugular venous distension
Hepatic congestion + Pleural effusion

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31
Q

What are the three goals in the treatment of Acute CHF?

A

Decrease pulmonary edema
Increase CO
Oxygenate patient

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32
Q

What is acute CHF characterized by?

A

Severe cardiogenic pulmonary edema with poor CO
+/- pleural effusion
+/- abdominal effusion

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33
Q

What changes with chronic CHF even with medical management?

A

Even with drugs on board

Will still see pleural effusion + ascites

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34
Q

What is a very important medication in Chronic heart failure for support of myocardial function?

A

Pimobendan

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35
Q

What can be given with Pimobendan if CHF is severe?

A

Digoxin

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36
Q

What are two examples of diastolic dysfunction?

A

Hypertrophic cardiomyopathy
– and –
Cardiac tamponade

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37
Q

What is the treatment for cardiac tamponade?

A

Pericardiocentesis - to relive the pressure on the heart and allow it to fill normally
No medical management

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38
Q

What specific animal tends to suffer from hypertrophic cardiomyopathy the most?

A

Maine Coon Cats

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39
Q

What does hypertrophic cardiomyopathy impair in the heart?

A

Ventricular filling

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40
Q

What is a major overall goal when treating hypertrophic cardiomyopathy?

A

Slow the heart rate - allows for increased filling time + reduces occurance of ischemia

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41
Q

What is a goal of a drug used to treat hypertrophic cardiomyopathy?

A

Improve cardiac relaxation

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42
Q

What medications are most helpful when treating hypertrophic cardiomyopathy?

A

Furosemide
– and –
ACEi

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43
Q

When would you most use furosemide in treating hypertrophic cardiomyopathy?

A

When CHF begins to develop

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44
Q

Why are diuretics used to treat CHF?

A

Control edema + effusion

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45
Q

Describe: Furosemide

A

Loop-diruetic

Used mostly in cases of cardiogenic edema/effusion

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46
Q

What are the recommendations for Furosemide use in chronic HF?

A

not used as monotherapy

47
Q

What is Furosemide used for in regards to acute CHF?

A

Sudden onset pulmonary edema

48
Q

What is the primary use of Furosemide in racing horses?

A

Excercise induced pulmonary hemorrhage

49
Q

What is an adverse effect of Furosemide?

A

Excessive fluid and/or electrolyte loss

50
Q

Describe: Spironolactone

A

K-sparing diuretic, little effect in dogs though

51
Q

What are the adverse effects of Spironolactone?

A

Excess K retention + GI disturbances

52
Q

What are contrindicated uses of Spironolactone?

A

Hyperkalemic patients

Patients on ACEi + K supplements

53
Q

What specific disease processes is Spironolactone used for?

A

Chronic refractory HF

54
Q

When is a thiazide diuretic used?

A

In dogs that have become resistant to furosemide

55
Q

What is occurring biochemically with ACEi?

A

Inhibits ACE

Decreasing ANGII + Increase Bradykinin

56
Q

Why does bradykinin increase with ACEi?

A

ACE normally degrades Bradykinin

57
Q

What is a contraindication for ACEi? Why?

A

Liver insuffiency, ACEi are pro-drugs and need to be metabolized by the liver

58
Q

What are the main benefits of ACEi use?

A

Reduce neurohormonal activation
– and –
Art/Venous vasodilation

MAY stop abnormal CV remodeling changes

59
Q

What type of diuretic effect does ACEi have?

A

Renal Na retention

60
Q

What are the specific therapeutic uses of ACEi?

A

Chronic management of CHF
Dilated cardiomyopathy
Valvular insufficiency
Hypertrophic cardiomyopathy

61
Q

What disease is ACEi the first drug of choice to treat?

A

Dogs: Systemic arterial hypertension

62
Q

What adverse effects are seen in ACEi use?

A

Hypotension + GI upset + Hyperkalemia

63
Q

What happens to treatment regimine if azotemia develops?

A

Diuretic dose decreased first!

then ACEi is reduced or removed

64
Q

Characteristics: Enalapril

A

most excreted in kidney

2hr half life

65
Q

Characteristics: Benazepril

A

Much longer 1/2 in cats (up to a day)

Renal + Hepatic excretion

66
Q

What is pimobendan?

A

Inotropic drug + Vasodilating properties

67
Q

How does pimpbendan work?

A

Inhibits phosphodiesterase III = vasodilation
Increase cAMP = Increase L Ca2+ channels
Increase myofiliament sensitivity to Ca

68
Q

What is the therapeutic use for Pimobendan?

A

CHF –
Dilated cardiomyopathy
Chronic mitral valve disease

69
Q

Pharmokinetics: Pimobendan

A

> 90% protein bound
Excretion through feces
Delay from peak concentration + maximal effect

70
Q

What are the adverse effects of pimobendan?

A

not many lethargy, diarrhea, dyspnea

Rare: Azotemia

71
Q

What do glycocides contain?

A

Aglycon

Three digitoxose

72
Q

What plant contains glycosides?

A

Foxglove

73
Q

What is the main function of Digoxin?

A

Positive iontropic effect

74
Q

What is the mechanism of action for digoxin?

A

Bind to Na/K ATPase channel on myocardial membrane

Decrease Na transport leading to increased intracellular Ca

75
Q

What does digoxin have anti-arrhythmic effects towardS?

A

Supraventicular tachyarrhythmia

76
Q

By what mechanisms does digoxin have anti-arrhythmic effects?

A

Improves arterial baroreceptor sensitivity

Increased vagal activity

77
Q

What is the primary use for Digoxin when wanted for its anti-arrhythmic effects?

A

Artrial fibrillations - Dilated cardiomyopathy or MVD

78
Q

What is a contrindiation for digoxin usage?

A

Cats with hypertrophic cardiomyopathy

79
Q

Why do you see increased serum levels of digoxin with dog and cats that have renal problems?

A

Reduced body clearance
– and –
Volume of distribution

80
Q

What does Digoxin bind to mostly in the body? Why is this a problem?

A

Skeletal muscle

– if animal has wasting, decreased effect of the drug

81
Q

What is the treatment for digoxin toxicity?

A

Intravenous K
Lidocaine + Propranolol + Phenytonin
Immunotherapy

82
Q

What is the biggest adverse effect of Digoxin?

A

Cardiac toxicity

83
Q

What are some arrhythmias that Digoxin stimulate?

A

Sinus bradycardia
Ectopic ventricular beats
AV block

84
Q

What is the most common arrhythmia due to Digoxin that can cause death?

A

Ventricular fibrillation

85
Q

What causes a decrease in digoxin absorbtion?

A

Antacids
Kaolin-pectin
Food

86
Q

How long does it take for Digoxin to reach SS in the blood of: Horse, Dog, and Cat

A

Horse - 3 days ~
Dog - 7 days
Cat - 10 days

87
Q

What is the main method of excretion of Digoxin?

A

renal

88
Q

How is Digoxin transported?

A

Pgp

89
Q

What seven things can increase digialis toxicity?

A 
Hypokalemia 
B-antagonist 
Calcium channel blockers 
Decrease plasma protein 
Decrease renal excretion 
Altered GI flora 
Sensitizing myocardium
90
Q

What are the two ways K interacts with digitalis?

A

Inhibit each other binding to Na/K ATPase receptor
– and –
K reduces cardiac automaticity

91
Q

What other compound decreases digitalis toxicity?

A

Mg

92
Q

What compound SHOULD NOT BE GIVEN with digitalis?

A

Calcium

93
Q

What is the standard drug therapy for heart failure?

A

Diuretics
ACEi
Pimobendan

94
Q

What breaks down cAMP?

A

PDE

95
Q

What does cAMP phosphorylate?

A

PKA + CREB

96
Q

What creates cAMP, what does it make it from?

A

Adenylyl cyclase

Uses ATP

97
Q

Drug for goal of therapy: Reduced preload

A

Diuretic
– and –
Venodilator

98
Q

Drug for goal of therapy: Reduced afterload

A

Arteriodilator

99
Q

Drug for goal of therapy: Increased contractility

A

Inotropic drug

100
Q

Drug for goal of therapy: Reduced energy expenditure

A

B-adrenergic antagonist

101
Q

What CHF effect causes the need for reduced preload?

A

Increased BV + Venous tone

102
Q

What CHF effect causes the need for reduced afterload?

A

Increased Aortic impedance + Arterial contriction

103
Q

What CHF effect causes the need for increased contractility?

A

Ventricular dilation + Reduced pumping force

104
Q

What CHF effect causes the need for reduced energy expenditure?

A

Increase HR due to reflex tachycardia via SNS hyperactivity

105
Q

What drug group can be used to slow HR and reduce myocardial O2 comsumption?

A

B-blocker

106
Q

What do calcium entry blockers do to the heart?

A

Coronary + Systemic vasodilation

Enhanced myocardial relaxation

107
Q

What is a good use for a calcium entry blocker, what drug?

A

Diltiazem

Hypertrophic cardiomyopathy

108
Q

What is contraindicated with diltiazem?

A

B-blockers

109
Q

What are important myocardial protective agents?

A

Some B-blocker s

Carvedilol + Metoprolol

110
Q

When do you need myocardial protective agents?

A

Dilated cardiomyopathy
– and –
Chronic valve disease

111
Q

How do the inodilators, Amrinone + Milrinone, work?

A

Inhibit phosphodiesterase III

112
Q

What effects do Amrinone + Milrinone have?

A

Increase myocardial contractility
– and –
Vasodilation

113
Q

What are adverse effects of Amrinone + Milrinone?

A

Worsen ventricular tachyarrhythmias

Reflex tachycardia

114
Q

Which, Amrinone or Milrinone, last the longest?

A

Amrinone

Pharmacology I (21 decks)

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