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Pharmacology II > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What treatment options exist to manage a bradyarrythmia such as “Sick Sinus Syndrome”?

A

Medical management is usually unrewarding
Test dose of atropine, if responsive, try propantolene orally
Usually requires pacemaker surgery

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2
Q

Name the basic mechanism for the four different classes of antiarrhythmics.

A

Class I: sodium-channel blockade
Class II: Beta blockade
Class III: potassium-channel blockade
Class IV: calcium-channel blockade

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3
Q

Why do excessively high heart rates have a deleterious impact on cardiac output?

A

They do not allow for adequate ventricular filling

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4
Q

What drug is most commonly used to manage atrial fibrillation when there is underlying myocardial disease?

A

Digoxin

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5
Q

What drug is most commonly used to convert idiopathic atrial fibrillation to a normal sinus rhythm, and what are its main toxicities?

A

Amiodarone

High incidence of side-effects including hepatotoxicity

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6
Q

What is the initial drug of choice in treating nearly all PVCs during hospitalization?

A

Lidocaine

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7
Q

What is an “escape beat” on an ECG and how does its presence impact the use of antiarrhythmics?

A

An escape beat is depolarization that occurs after a long pause that can help rescue the heart from complete standstill
Ventricular antiarrhythmics can cause cardiac arrest

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8
Q

Is lidocaine useful to treat ventricular arrhythmias, supraventricular arrhythmias, or both?

A

Ventricular arrhythmias

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9
Q

Is procainamide or mexiletine useful to treat ventricular arrhythmias, supraventricular arrhythmias, or both?

A

Ventricular arrhythmias

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10
Q

Is solatlol useful to treat ventricular arrhythmias, supraventricular arrhythmias, or both?

A

Both

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11
Q

Is amidoraone useful to treat ventricular arrhythmias, supraventricular arrhythmias, or both?

A

Both

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12
Q

Name the therapeutic goals in the management of hypertrophic cardiomyopathy (HCM) and what drugs we commonly use to accomplish these.

A 
Treat underlying cause
Decrease LA (and LV) pressure: Oxygen, Furosemide, low dose opioid (butorphanol)
Relax cardiac muscle (positive lusitropy): Diltiazem (calcium channel blocker)
Slow HR (negative chronotropy): Dilatiazem, beta 1 blocker (atenolol), nonselective beta blockers
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13
Q

Contrast the merits of diltiazem versus atenolol use in HCM.

A

Atenolol decreases the effects of catecholamine in hyperthyroidism and is give every 12 hours. The benefit of dilatiazem over atenolol has been questioned. Dilatiazem is given every 8 hours.

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14
Q

In early congestive heart failure (systolic heart failure) physiologic changes occur that allow “compensated” heart failure to exist. Explain those physiologic changes and how eventually overexaggerated responses lead to decompensated heart failure.

A

Heart failure –> reduced CO –> reduced BP –> reduced renal perfusion with activation of RAAS and activation of sympathetic nervous system –> salt and water retention and systemic arteriolar vasoconstriction
Salt water retention–> excessive preload
Systemic arteriolar vasoconstriction –> increased total peripheral resistance –> excess afterload

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15
Q

What are the therapeutic goals in the management of CHF (systolic heart failure)?

A 
Decrease preload
Decrease afterload
Increase force of contraction 
Slow HR
Decrease pulmonary edema
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16
Q

What drugs decrease preload?

A

Nitrates (Nitroglycerine, Nitroprusside)
Diuretics (Furosemide, Torsemide, Thiazides, Postassium-sparing (sprinolactone, triamterene, amiloride), Aldactazide (sprinolactone and hydrochlorothiazide))

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17
Q

What drugs decrease afterload?

A

Amlodipine

Hydralazine

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18
Q

What drugs increase the force of contration?

A

Dobutamine
Dopamine
Pimobendan
Digitalis glycosides (Oubain, Digitoxin, Digoxin)

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19
Q

Does nitroglycerine alter preload, afterload, or both?

A

Decreases preload

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20
Q

Does nitroprusside alter preload, afterload, or both?

A

Affects both

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21
Q

Do diuretics alter preload, afterload, or both?

A

Decrease preload

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22
Q

Does amlodipine alter preload, afterload, or both?

A

Decrease afterload

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23
Q

Does hydralazine alter preload, afterload, or both?

A

Decrease afterload

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24
Q

Do ACE inhibitors alter preload, afterload, or both?

A

Both

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25
Q

Do angiotensin II receptor antagonists alter preload, afterload, or both?

A

Both

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26
Q

Salt (sodium) restriction has historically been a method used in heart failure to reduce preload. What disadvantages might it however pose?

A

Palatability problems

Many cardiologists now feel that sodium restriction may activate RAAS too early especially if diuretics are used

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27
Q

Does nitroglycerin decrease afterload, preload, or both?

A

Preload

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28
Q

Furosemide decreases preload. What additional benefit does it provide when pulmonary edema is present?

A

Causes the release of vasodilatory prostaglandins in the lungs to lower pulmonary arterial pressure to help diminish pulmonary edema

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29
Q

For what group of cardiac drugs does tachyphylaxis limit the duration of their usefulness?

A

Nitrates

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30
Q

Why are hydrochlorothiazide or spironolactone seldom used as a sole diuretic in congestive heart failure (CHF), yet are commonly used as adjunct diuretics with furosemide, especially when pulmonary edema occurs despite furosemide therapy.

A

They cause weak diuresis, so it is often combined with furosemide in refractory cases

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31
Q

Explain how an Angiotensin converting enzyme (ACE) inhibitor, by virtue of inhibiting conversion of angiotensin 1 to angiotensin 2, has a beneficial effect in CHF.

A

It causes less vasoconstriction (both arteriolar (afterload) and venous (preload)) and it decreases aldosterone which will decrease sodium retention

32
Q

How might NSAIDs interfere with ACE inhibitors?

A

NSAIDs may inhibit vasodilatory PG thereby decreasing GFR and/or inhibit the release of natriuretic PGs causing increased sodium retention

33
Q

When might benazepril be preferred over enalapril as an ACE inhibitor?

A

In renal failure patients because enalapril can affect the kidney

34
Q

Describe how renal function and body weight impact the dosing of digoxin

A

Renal function affects digoxin elimination

Dose on lean body weight

35
Q

What benefit besides inotropy does digoxin provide in CHF?

A

Sensitizes baroreceptors –> increased parasympathomimetic effect –> slows conduction at AV node –> slowing of HR

36
Q

Which electrolyte abnormality predisposes to digoxin toxicity?

A

Hypokalemia

37
Q

Pimobendan is an oral inotrope. What other beneficial effect does it have?

A

It is also a vasodilator, decreasing afterload and preload

Absorption is enhanced and consistent in an acid stomach

38
Q

What receptors are stimulated by dobutamine?

A

Selective stimulates a subset of beta1 receptors. Some beta 2 activity occurs

39
Q

What are the clinical indications for dobutamine?

A

Target to raise systolic BP to 100-120 mmHg

40
Q

What is a dobutmaine holiday?

A

Accumulates in cardiac muscle so that residual inotropy occurs after infusion

41
Q

What are the receptors stimulated by dopamine?

A

Low doses stimulate beta1 and dopamine receptors

42
Q

What is the dopamine therapeutic window?

A

Higher doses stimulate alpha receptors resulting in an increase in peripheral vascular resistance

43
Q

Why are opioids often beneficial in pulmonary edema other than for sedation?

A

Morphine decreases preload by splanchnic vasodilation

Desensitizes CO2 receptors

44
Q

What drug is used for left atrial enlargement with mild clinical signs?

A

Enalapril

45
Q

What drug is used for left ventricular enlargement with systolic impairment?

A

Pimobendan/digoxin

46
Q

What drug is used for atrial fibrillation with a high heart rate?

A

Digoxin and diltiazem

47
Q

What drug is used for early pulmonary edema?

A

Furosemide

48
Q

What drug is used for refractory pulmonary edema?

A

Chlorothiazide or spironolactone to furosemide

49
Q

What drug is used for PVCs?

A

Procainamide or sotolol

50
Q

How do pulmonary vessels differ in their response to hypoxia versus other vessels in the body?

A

Pulmonary vessels undergo vasoconstriction

51
Q

What is considered the vasodilator of choice in the management of pulmonary hypertension?

A

Oxygen

52
Q

Which breed of dog may be more prone to digoxin toxicity?

A

Dobermans

53
Q

What drugs are used as vasopressors?

A 
Dobutamine
Epinephrine
Norepinephrine
Vasopressin
Dopamine
Phenylephrine
Ephiderine
54
Q

How does dobutamine works as a vasopressor?

A

Acts to raise blood pressure by increasing CO. Not a vasoconstrictor

55
Q

How does epinephrine works as a vasopressor?

A

Stimulates the heart and vasoconstricts

56
Q

How does norepinephrine works as a vasopressor?

A

Stimulates alpha1 and beta1 receptors with modest activity on beta2 receptors. Causes vasoconstriction and cardiac stimulation

57
Q

How does vasopressin works as a vasopressor?

A

Causes vasoconstriction without cardiac stimulation

58
Q

How does dopamine works as a vasopressor?

A

High dose: alpha1 receptor stimulation causes vasoconstriction

59
Q

How does phenylephrine works as a vasopressor?

A

Causes vasoconstriction without cardiac stimulation

60
Q

How does ephiderine works as a vasopressor?

A

Causes indirect effect by the release of norepinephrine at the postsynaptic alpha and beta receptors

61
Q

Why are vasopressors used only after more conservative measures have failed to adequately raise blood pressure?

A

Vasoconstricting vasopressors may decrease perfusion to some tissue

62
Q

What is the rationale for using epinephrine IV for cardiac asystole?

A

Stimulates the heart and vasoconstricts

Encourages preload to return to the heart during preload

63
Q

What is the rationale for using epinephrine IM for anaphylaxis?

A

Raises BP while avoiding ventricular fibrillation

Beta2 are in muscle blood vessels- so it causes rapid onset IM and avoids cardiac effects.

64
Q

What is the rationale for using epinephrine SQ for acute bronchoconstriction without hypotension?

A

Reverses bronchocontrction

Blood vessels are primarily alpha1 receptors. So you get slower absorption, less risk of cardiac effects

65
Q

Discuss the preference of amlodipine versus enalapril in the management of hypertension in the dog versus cat.

A

Dog: enalopril first, add amlodipine if necessary
Cat: Amlodipine first, enolapril or beta-blocker may be combine with amlodipine in refractory cases

66
Q

How do aspirin and clopidogrel have their anticoagulant effect?

A

Aspirin: inhibits platelet function by its effects on thromboxane
Clopidogrel: Inhibits platelet function by irreversibly inhibiting ADP receptors on the platelet membrane

67
Q

Why is low molecular weight heparin often preferred over regular unfractionated heparin? What clotting factors are affected?

A

Low molecular weight heparins inactivate factor Xa activity but not thrombin activity and are less likely to cause accidental hemorrhage unlike unfractioned heparin
It inactivates factor Xa activity, but not thrombin activity

68
Q

Why is warfarin not used therapeutically as an anticoagulant in animals?

A

The small therapeutic index makes it difficult to adjust the dose for the anticoagulant effect without causing bleeding

69
Q

What ophthalmic indication is tPA used for?

A

Hyphema (blood in anterior chamber). Injected into anterior chamber to decrease risk of glaucoma

70
Q

What is “reperfusion injury” as it relates to tPA use?

A

We hoped that tPA, as a thrombolytic, would break down saddle thrombus in cats. While it did, the cats died from reperfusion injury due to the thrombus having cut off blood supply to the hind limbs for so long. Also, those that did survive the reperfusion injury ended up with a saddle thrombus again.

71
Q

What evidence supports the use of acepromazine in laminitis?

A

Shown to increase blood flow to laminae in healthy horses through vasodilation

72
Q

What evidence supports the use of nitroglycerine in laminitis?

A

Shown to increase blood flow to laminae in healthy horses through vasodilation
Limited and conflicting evidence for use

73
Q

What evidence supports the use of isoxsuprine in laminitis?

A

Peripheral vasodilator; unclear mechanism involving either beta receptor stimulation or alpha receptor antagonism
Limited and conflicting evidence for use

74
Q

What evidence supports the use of DMSO in laminitis?

A

Given IV early in laminitis as anti-inflammatory and mild platelet inhibitor
Limited and conflicting evidence for use

75
Q

What evidence supports the use of pentoxyfylline in laminitis?

A

Increases flexibility of the RBC membrane leading to increased flow through narrow vessels
Limited and conflicting evidence for use

Pharmacology II (18 decks)

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