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Pharmacology > Exam 2- Cardiovascular > Flashcards

Exam 2- Cardiovascular Flashcards

1
Q

Proposed benefit of Acepromazine use for treating equine laminitis

A

Increases blood flow to the laminae

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2
Q

Proposed benefit of Nitroglycerin for treating equine laminitis

A

Limited evidence on the benefit

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3
Q

Proposed benefit of Isoxsuprine for equine laminitis

A

Limited evidence, peripheral vasodilation

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4
Q

Proposed benefit of IV DMSO in treating equine laminitis

A

Limited evidence, anti-inflammatory & mild platelet inhibition

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5
Q

Proposed benefit of Pentoxifylline in treating equine laminitis

A

Limited evidence, hemorheologic, increases RBC membrane flexibility to increase blood flow through narrow vessels

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6
Q

Three hemostatics that act systemically & the evidence supporting their use

A

A. Aminocaproic acid- decreased fibrinolysis & post-op healing
B. Yunnan baiyao- Chinese herbs, variable evidence but suggested to increase clot strength
C. IV formalin- 81.25% cured in 4d, while <50% of untreated cows cured in 7-8d

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7
Q

This hemostatic can be used to treat hemorrhagic cystitis

A

Diluted formalin

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8
Q

What are two topical hemostatic agents & how do they work?

A

a. Silver nitrate- caustic

b. Styptic powder- anhydrous aluminum sulfate, acts as vasoconstrictor decreasing blood flow

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9
Q

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

A

a. When toxic substances that have built up in an area are released all at once
b. tPA used against clots w/ bad results= reperfusion shock & death

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10
Q

What ophthalmic indication is tPA used for?

A

a. Management of hyphema

- Injected into anterior chamber to decrease risk for glaucoma

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11
Q

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

A

Has a small therapeutic index, prone to drug interactions, & has an impact on the diet

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12
Q

Why is LMW heparin often preferred over regular unfractionated heparin? What clotting factors are affected?

A

a. Less likely to cause accidental hemorrhage/iatrogenic bleeding
b. Inactivates factor Xa activity, but not thrombin activity

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13
Q

How do aspirin & clopidogrel produce anticoagulant effects?

A

Aspirin- inhibits platelet function by its effects on thromboxane; interferes with cyclooxygenase, inactivating the platelet
Clopidogrel- causes anticoagulant effects through the ADP pathway; inhibits platelet function by inhibiting ADP receptors on the platelet membrane

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14
Q

Preference of Amlodipine vs. Enalapril in hypertension management for the dog vs. cat

A

Dog- Enalapril first, Amlodipine if necessary

Cat- Amlodipine first, Enalapril used in refractory cases

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15
Q

Epinephrine injected by different routes- why?

A

a. Cardiac asystole- IV or intratracheally
i. Stimulates heart & vasoconstricts, do not give intracardiac unless visualizing left ventricles
b. Anaphylaxis- IM
i. Provides a more rapid increase in plasma & tissue concentrations
c. Acute bronchoconstriction w/o hypotension- SQ
i. Rapid uptake into the system
d. Rate of absorption differs with each route of administration
i. More side effects can occur when epinephrine is absorbed too fast inappropriately

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16
Q

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

A

May decrease perfusion to some tissues

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17
Q

This vasopressor works to raise the BP by increasing the CO, no vasoconstriction

A

Dobutamine

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18
Q

This vasopressor works by stimulating the heart & causing vasoconstriction

A

Epinephrine

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19
Q

This vasopressor works by stimulating alpha1 & beta1 receptors to create vasoconstriction & cardiac stimulation

A

Norepinephrine

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20
Q

Dopamine, when given at different doses, produces different effects, what are those?

A

Low dose- D1 dopamine receptors, vasodilation of renal & splanchnic vessels
Mid dose- beta1 receptor; increases heart inotropy
High dose- alpha1 receptors; vasoconstriction

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21
Q

This vasopressor causes vasoconstriction w/o cardiac stimulation

A

Phenylephrine

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22
Q

This vasopressor has an indirect effect by the release of NorEpi at the postsynaptic alpha & beta receptors

A

Ephedrine

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23
Q

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

A

Dobermans

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24
Q

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

A

Oxygen therapy

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25
Q

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

A

Hypoxia causes vasoconstriction of the pulmonary vessels to shunt blood towards healthy tissues

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26
Q

What drugs would be used for Left atrial enlargement w/ mild clinical signs?

A

Enalapril or Pimobendan

27
Q

What drugs would be used for left ventricular enlargement w/ systolic impairment?

A

Pimobendan or Digoxin

28
Q

What drugs would be used for atrial fibrillation w/ a high HR?

A

Digoxin or Diltiazem

29
Q

What drugs would be used to treat early pulmonary edema?

A

Furosemide or Torsemide

30
Q

What drugs would be used to treat refractory pulmonary edema?

A

Furosemide w/ Thiazide or Spironolactone

31
Q

What drugs would be used for treating premature ventricular contractions?

A

Procainamide or Sotalol

32
Q

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

A

a. Decreased air hunger
b. Morphine- decrease preload by splanchnic vasodilation
c. Desensitizes CO2 receptors

33
Q

Compare and contrast dobutamine versus dopamine as to receptors stimulated, clinical indications, existence of a “holiday”, and whether a “therapeutic window” exists.

A

a. Dobutamine
i. Selectively stimulates subset of β1 receptors→ increase in strength of contraction
1. Some β2 activity may also reduce afterload
ii. Normally it has minimal effects on the HR but can cause tachyarrhythmias→ monitor w/ ECG
iii. Constant IV infusion due to short plasma half-life
iv. Target to raise systolic BP 100-120mmHg
v. Accumulates in cardiac muscle→ Dobutamine holiday
b. Dopamine
i. Less selective than dobutamine
ii. Low doses stimulate β1 & dopamine receptors
1. Beta1 stimulation→ positive inotropic effects
2. Dopamine stimulation→ vasodilation of renal (dogs, not cats) & splanchnic vessels
iii. Therapeutic window relative to use in heart failure
1. Higher doses stimulate alpha receptors→ increase in peripheral vascular resistance
iv. Constant IV infusion→ short half-life

34
Q

Which electrolyte abnormality predisposes to digoxin toxicity?

A

Hypokalemia

35
Q

What benefit besides inotropy does digoxin provide for treating CHF?

A

Sensitizes baroreceptors → slows HR

36
Q

How does renal function & body weight impact dosing digoxin?

A

Dose made on lean body weight; renal function affects drug elimination

37
Q

When might Benazepril be preferred over Enalapril as an ACE inhibitor?

A

When the patient is in renal failure

38
Q

How might NSAIDs interfere w/ ACE inhibitors?

A

Inhibit vasodilatory PG → decreases GFR → inhibits release of natriuretic PGs

39
Q

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

A

Less conversion of angiotensin I to angiotensin II= less vasoconstriction

40
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

Weak diuretics

41
Q

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

A

Nitrates

42
Q

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

A

Produces vasodilatory prostaglandins

43
Q

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

A

Palatability problems

May activate Renin-Angiotensin system too early

44
Q

What cardiovascular drugs alter preload?

A

Nitroglycerine, Furosemide, Torsemide, Thiazides/hydrochlorothiazide, Spironolactone

45
Q

What cardiovascular drugs alter afterload?

A

Amlodipine, Hydralazine, Dobutamine

46
Q

What cardiovascular drugs alter preload & afterload?

A

Nitroprusside, ACE inhibitors, Pimobendan

47
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 over-exaggerated responses lead to decompensated heart failure.

A

a. Early CHF leads to a reduced cardiac output & reduced BP.
i. Causes the activation of both the RAAS & the sympathetic NS
ii. RAAS- salt & water retention leading to excessive preload
iii. SNS- systemic arteriolar vasoconstriction leading to increased total peripheral resistance causing excessive afterload

48
Q

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

A

a. Treat the underlying cause
b. Decrease the left atrial pressure
i. Oxygen
ii. Furosemide
c. Relax cardiac muscle (positive lusitropy)
i. Diltiazem
ii. Beta 1 blocker- Atenolol
iii. Nonselective beta blockers
d. Aspirin
i. Decreases risk of thromboembolism
e. Merits for treating HCM
i. Diltiazem & Atenolol→ positive lusitropy, relax the heart muscle
1. Diltiazem – calcium-channel block, q8hr dosing
2. Atenolol – beta1 block, q12hr dosing, decreases effects of catecholamines in hyperthyroidism

49
Q

What cardiac drugs are useful to treat ventricular arrhythmias?

A

Lidocaine, Procainamide/Mexiletine, Magnesium sulphate

50
Q

What cardiac drugs are useful to treat supraventricular arrhythmias?

A

Digoxin, Quinidine

51
Q

What drugs are useful to treat both supraventricular & ventricular arrhythmias?

A

Amiodarone, Sotalol

52
Q

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

A

Escape beat= 3rd degree heart block
i- P waves not coordinated w/ QRS complex
ii- bradycardia
iii- ventricular antiarrhythmics that can cause cardiac arrest

53
Q

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

A

Lidocaine

54
Q

What drug is most used to convert idiopathic a-fib to a normal sinus rhythm, & what are its main toxicities?

A

Amiodarone

  • hepatotoxic in dogs
  • causes diarrhea
55
Q

What drug is most used to manage a-fib when there is underlying myocardial disease?

A

Digoxin

-will not convert normal rhythm, but does slow conduction at the AV node

56
Q

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

A

They do not allow for adequate ventricular filling to occur

57
Q

What is the basic mechanism for the class I antiarrhythmics?

A

Sodium-channel blockade- reduce phase 0 slope & peak of action potential

58
Q

Basic mechanism for class Ia antiarrhythmic

A

Moderate Na-channel blockade- moderate reduction of phase 0 slope, increase APD & ERP

59
Q

Basic mechanism for class Ib antiarrhythmic

A

Weak Na-channel blockade- small reduction in phase 0 slope, reduce APD & decreases ERP

60
Q

Basic mechanism for class Ic antiarrhythmic

A

Strong Na-channel blockade- pronounced reduction in phase 0 slope, no effect on APD or ERP

61
Q

Basic mechanism for class II antiarrhythmics

A

Beta-blockade- blocks sympathetic activity, reduces rate & conduction

62
Q

Basic mechanism for class III antiarrhythmics

A

Potassium-channel blockade- delay repolarization (phase 3) & thereby increase action potential duration & effective refractory period

63
Q

Basic mechanism for class IV antiarrhythmics

A

Calcium-channel blockade- block L-type calcium-channels; most effective at SA & AV nodes; reduce rate & conduction

64
Q

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

A

Administer a test dose of atropine & then administer propantheline
Usually requires a pacemaker sx, medical management unrewarding

Pharmacology (4 decks)

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