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Pharmacology > Lecture 17: Drugs for Heart Failure > Flashcards

Lecture 17: Drugs for Heart Failure Flashcards

1
Q

What class/type are the following drugs: furosemide, spirnolactone, hydrochlrothiazide

A

Diuretics

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2
Q

What class/type are the following drugs: enalapril, benazepril, lisinopril, ramipril

A

ACEI

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3
Q

What class/type is the following drug: pimobendan

A

Calcium sensitizer

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4
Q

What class/type is the following drug: Digoxin

A

Digitalis

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5
Q

What class/type are the following drugs: dobutamine and dopamine

A

Sympathomimetics

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6
Q

What class type/are the following drugs: atenolol, metoprolol, propanolol

A

Beta blockers

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7
Q

What class/type is the following drug: carvedilol

A

Alpha and beta blocker

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8
Q

What class/type is the following drug: diltiazem

A

Calcium channel blockers

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9
Q

Describe the steps in cardiac muscle contraction

A

Na+ channels open, depolarize and open voltage gated calcium channels that then release more calcium from sarcoplasmic reticulum. Results in myosin-actin interaction causing contraction

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10
Q

What are the 4 factors that affect cardiac performance

A
  1. Preload
  2. After load
  3. Contractility
  4. Heart rate
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11
Q

How does and increase preload affect contractility and cardiac output

A

Increase both

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12
Q

What is afterload

A

Peripheral resistance in the left ventricle

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13
Q

Afterload regulates __pressure

A

Diastolic

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14
Q

What regulates afterload

A

SNS tone which is regulated by contractility

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15
Q

How does increase in contractility affect SNS and diastolic pressure

A

Increase both

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16
Q

What regulates heart contractility

A

Filling pressure, distention of heart and SNS tone

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17
Q

How does vagal tone regulate HR

A

Regulates HR at much lower rate by controlling SA node

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18
Q

What are the 2 regulatory response systems to heart failure

A
  1. SNS activation
  2. RAAS activation
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19
Q

Failure of __ dysfunction is characterized by high cardiac filling pressure which leads to venous ____ and ___ accumulation

A

Systolic, congestion and tissue fluid accumulation

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20
Q

Poor contractility is often results from chronic ___

A

Cardiac overload

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21
Q

What are the signs of left sided heart failure

A

Pulmonary venous congestion and edema often resulting in cough, tachypnea, dyspnea, pulmonary crackles, etc.

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22
Q

What are the signs of right sided heart failure

A

Systemic venous hypertension resulting in jugular vein distension, pleural effusion, ascites

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23
Q

How is acute heart failure characterized

A

Cardiogenic pulmonary edema, with or without pleural and/or abdominal effusion and poor cardiac output

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24
Q

In acute heart failure, what is the therapy aimed at

A

Rapidly clearing pulmonary, improved oxygenation and optimizing cardiac output

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25
Q

Hypertrophic cardiomyopathy impairs ___filling

A

Ventricular

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26
Q

How is the ejection fraction from the LV impacted in hypertrophic cardiomyopathy

A

Heart will want to maintain 65% ejection fraction, it will maintain 65% but will be smaller volume due to decreased total volume in HCM

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27
Q

What are the goals of the drugs to treat hypertrophic cardiomyopathy

A

Avoid elevated HR, increase filling time, reduce ischemia, improve cardiac relaxation

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28
Q

What drugs may be effective in tx of hypertrophic cardiomyopathy

A

ACEI and furosemide

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29
Q

What is cardiac tamponade a result of

A

Hole in the ventricle that is causing blood to go into pericardial sac instead of aorta

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30
Q

How do you treat cardiac tamponade

A

Pericardiocentesis with or without subsequent pericardiectomy

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31
Q

What is the main goal of diuretic therapy

A

Control edema and effusion in HF

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32
Q

What does furosemide do to treat HF

A

Reduces Na+ reabsorption and therefore decreases fluid retention, also synthesizes prostaglandins which vasodilate reservoir veins, decrease filling pressure of heart

33
Q

When is furosemide most commonly used

A
  1. Animals with cardiogenic edema or effusion, usually acute HF
  2. Exercise induced pulmonary hemorrhage
34
Q

How is furosemide used to treat acute heart failure vs chronic heart failure

A

Acute heart failure: aggressive furosemide indicated for acute pulmonary edema

Chronic heart failure: should not be monotherapy

35
Q

What are the adverse effects of furosemide

A

Excessive fluid and electrolyte losses

Loss of Na+ thicken blood, increases peripheral resistance and BP. Decreases contractility of LV

36
Q

What type of diuretic is spironolactone

A

K sparing diuretic

37
Q

What is spironolactone used for

A

Adjunct therapy for chronic refractory heart failure

38
Q

When is spironolactone contraindicated

A

Hyperkalemic patients

39
Q

What does spironolactone antagonize

A

Aldosterone, which controls K+ excretion in CD

40
Q

What are the adverse effects of spironolactone

A

Excess K+ (effects membrane potential) and GI disturbances

41
Q

What are thiazide diuretics recommended for

A
  1. Dogs and cats that have become refractory to furosemide
  2. Hyperkalemic periodic paralysis in horses
42
Q

How does ACE inhibitors work

A

Block conversion of inactive Angiotensin I to active angiotensin II, therefore decrease actions of RAAS

43
Q

ACEI degrade ___ contributing to vasodilatory effect

A

Bradykinins

44
Q

Most ACEi’s are prodrugs that are converted to their active form in the ___. How is the conversion location important

A

Liver, important to consider for liver dysfunction that might inhibit this conversion

45
Q

How do ACEi impact CV remodeling changes

A

Oppose remodeling changes by decreasing BP/afterload which cause hypertrophy

46
Q

When are ACEi’s used

A

Chronic heart failure, expected DCM, chronic valvular insufficiency and HCM

First choice agent in management of systemic arterial hypertension in dogs

Cats with hypertension

Chronic renal disease

47
Q

What is the drug of choice for systemic arterial hypertension in dogs

A

ACE inhibitors

48
Q

What are some adverse effects of ACEi’s

A

Hypotension, GI upset, renal function deterioration, Hyperkalemic

49
Q

Which ACEi is labeled use for dogs

50
Q

How does pimobendan work

A
  1. Increases myocardial contractility by increasing myofilament sensitivity to Ca2+
  2. Inhibits PDE III, so increase cAMP—> activates pKA which activates L-type Ca2+ channels and increases myocardial contractions
51
Q

When is pimobendan indicated

A

Labeled use in dogs (ELDU cats) with HF from DCM of chronic mitral valves disease

52
Q

How does digoxin work

A

Competitively binds and inhibits Na+/K+ ATPase, decrease Na+ extracellular transport and causes accumulation of Ca2+ intracellularly, increased Ca2+ available to contractile proteins

53
Q

What arrhythmias is digoxin useful for

A

Supraventricular tachyarrythmias

54
Q

What mediates supraventricular tachyarrythmias

A

Increased PNS tone to the SA band AV nodes and atria

55
Q

Digoxin improves arterial ___ sensitivity to increase vagal activity in HF

A

Baroreceptor

56
Q

When is digoxin primarily used

A

Atrial fibrillations with concurrent HF secondary to DCM or MVD

57
Q

When is digoxin contraindicated

A

Hypertrophic cardiomyopathy

58
Q

What is the dose for digoxin

A

0.25mg/dog- should never exceed this

59
Q

How does renal dysfunction and decrease muscle mass affect digoxin

A

Both can lead to increase toxicity since the drug is processed through the renal system and binds to skeletal muscle

60
Q

Elimination of digoxin is mainly __

61
Q

What are the adverse effects of digoxin

A

Cardiac toxicity, sinus bradycardia, ectopic ventricular beats, AV block, ventricular fibrillation

62
Q

Why should digoxin not be given with a drug that causes hypokalemia

A

Digoxin inhibits Na+/K+ ATPase so decrease K+ intracellularly don’t want to exacerbate

63
Q

Why should digoxin not be given with a B-antagonist

A

B-antagonist will decrease HR, SA and AV node activity. Digoxin increases PNS tone to AV and SA node which decrease HR

64
Q

Digoxin should not be given with __channel blockers

65
Q

Why should digoxin not be given with quinidine

A

Decrease plasma protein binding and increase toxicity

66
Q

What does dopamine do at low levels

A

Stimulate D1 receptors and cause vasodilation in kidney

67
Q

What does dopamine do at medium doses

A

Stimulates B receptors, producing positive inotropic effect

68
Q

What does dopamine do at high doses

A

Stimulates alpha1 receptors causing vasoconstriction

69
Q

What does dobutamine do

A

Stimulates b1 receptors increases contractility

70
Q

When is dobutamine and dopamine indicated

A

Myocardial failure, short term treatment

71
Q

Why is the use of catecholamines for heart failure limited

A

Downregulation of B receptors

72
Q

What are the adverse effects of dopamine and dobutamine

A

Arrhythmias, increased myocardial O2 demand, tachycardia, tachyphylaxis, necrosis, seizures

73
Q

What drugs are often used to decrease HR and myocardial O2 consumption

A

B-blockers (atenolol, propanolol, metoprolol)

74
Q

What do calcium entry blockers do

A

Cause coronary and systemic vasodilation, enhanced myocardial relaxation and sometimes reduced cardiac contractility

75
Q

Concurrent use of B-blocker with ___ is avoided

76
Q

ACEi inhibitors are increasingly being used in management of HF from ___

77
Q

Certain ___ may be useful in long term management of CDM, CVD by reducing effects of chronic SNS activation

A

Beta blockers- carvedilol and metoprolol

78
Q

What is the standard drug therapy for heart failure

A
  1. Diuretics (furosemide)
  2. ACEI
  3. Pimobendan

Pharmacology (14 decks)

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