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VETM 443 Clin Pharm Tox > Cardio > Flashcards

Cardio Flashcards

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1
Q

what is the relationship between cardiac output, heart rate, and stroke volume?

A

cardiac output = heart rate x stroke volume

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2
Q

Name at least 3 general mechanisms of heart failure (there are 6 total)

A

pump failure, forward obstruction to blood flow, regurgitant blood flow, congenital shunts, rupture of heart or vessel, conduction disorders

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3
Q

What triggers sympathetic nervous system activation in early heart failure?

A

Decreased cardiac output

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4
Q

What are 3 acute changes to compensate for early heart failure? (Hint, these occur due to sympathetic activation)

A

increase HR, increased CO (cardiac output), increased TPR

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5
Q

Name at least 2 effects of chronic SNS activation as they relate to worsening heart failure

A

Chronic activation of SNS results in persistent tachycardia, adrenal receptor down regulation, increased myocardial oxygen demand, and myocyte necrosis. (These all result in myocardial injury and therefore worsen heart failure)

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6
Q

In response to decreased BP, is the conversion of angiotensinogen to angiotensin 1 increased or decreased? what enzyme is responsible for this conversion?

A

increased conversion of angiotensinogen to angiotensin 1. by renin from the kidney.

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7
Q

name 3 effects of angiotensin II

A

SNS activation, vasoconstriction, increased production of aldosterone

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8
Q

what is the effect of increased aldosterone on the kidney? how does this effect relate to blood volume?

A

aldosterone increases renal retention of Na and H2O. increases blood volume

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9
Q

most common type of heart disease in dogs?

A

chronic valvular heart disease (CVHD), also known as endocardiosis or myxomatous valve degeneration, accounts for 75% of these cases (left AV valve is most common)

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10
Q

how does CVHD/myxomatous valve degeneration/endocardiosis affect the ventricles of the heart?

A

changes in mitral valve collagen result in valve prolapse and mitral regurgitation. this leads to ventricular remodelling and dysfunction due to increased cardiac work

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11
Q

what are 6 basic pharmacological mechanisms to modify cardiac function

A

chronotropy, ionotrophy, peripheral resistance, blood volume, rate of conduction, neurohormonal input to heart

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12
Q

pharmacological modification aims to change one or more of these 5 cardiac parameters

A

preload, afterload, rate or rhythm, contractility, sympathetic or neurohormonal input

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13
Q

term for amount of ventricular stretch at end of diastole

A

preload

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14
Q

as preload increases, does strength of cardiac muscle contraction (ionotropy) increase or decrease? what is the name of this mechanism?

A

increase; Frank-Starling law

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15
Q

what determines preload

A

amount of blood returned to heart prior to contraction

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16
Q

term for resistance the heart must pump against to send blood out of the left ventricle and into the aorta

A

afterload

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17
Q

what determines afterload?

A

total peripheral resistance

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18
Q

if you increase vasoconstriction and decrease vasodilation, what is the effect on after load?

A

increased afterload (due to increased total peripheral resistance)

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19
Q

what drug class affects contractility of the heart

A

ionotropes

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20
Q

when skeletal muscle contracts, is the calcium released by the SR sufficient to interact with all of the troponin? what proportion of actin-myosin interactions will occur?

A

yes, sufficient. all potential actin-myosin interactions will occur

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21
Q

when cardiac muscle contracts, does all troponin interact with calcium? what proportion of actin-myosin interactions will occur?

A

not all troponin interacts with calcium in cardiac muscle contraction. number of actin-myosin cross-bridges will depend on intracellular calcium availability

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22
Q

name at least 2 positive ionotropes intended for chronic use

A

digoxin, pimobendan, dobutamine, dopamine, epinephrine

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23
Q

name at least 1 positive ionotropes intended for short-term use

A

ephedrine, isoproterenol

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24
Q

before pimobendan was discovered, this was the only positive ionotrope available for chronic use; now it is infrequently used. what is this drug? what is it still used for?

A

digoxin. useful in animals with atrial fibrillation

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25
Q

how does digoxin facilitate more interactions between actin and myosin to improve contractility?

A

digoxin inhibits Na-K pump in cardiac myocyte cell membrane, increasing Na concentration in cell, slowing or reversing action of Na-Ca exchanger, increasing Ca concentration in cell, increasing actin-myosin interactions

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26
Q

name at least 2 adverse effects of digoxin

A

arrhythmias, electrolyte interactions, drug interactions (eg. furosemide), GI effects (eg. vomiting, anorexia).
this high incidence of adverse effects is why digoxin in infrequently used in vet med

27
Q

what is the positive ionotrope of choice in small animals

A

pimobendan

28
Q

mechanism of action of pimobendan on heart

A

sensitizes troponin C complex to calcium leading to increased contraction. also inhibits PDE3 and 5 in blood vessels, resulting in arterial and venous vasodilation, reducing preload and afterload

29
Q

what route of administration for the positive ionotrope beta 1 agonists, dopamine and dobutamine?

A

must be given IV

30
Q

the Frank Starling law states that

A

the stroke volume of cardiac contraction increases as preload increases

31
Q

dopamine1 (DA1) receptor activation causes vasodilation in which 4 organs

A

kidneys, mesentery, heart, brain

32
Q

consider dobutamine vs dopamine. which has more positive ionotropic effects? more chronotropic effects? dilates the renal vascular bed?

A

dobutamine has more positive ionotropic effects and does not dilate the renal vascular bed. dopamine has more chronotropic effects and dilates the renal vascular bed

33
Q

what two classes of drugs are used primarily as chronotropes

A

beta antagonists (beta blockers) and muscarinic antagonists (anticholinergics)

34
Q

what is the effect of beta antagonists on heart rate

A

reduce heart rate

35
Q

what is the therapeutic goal of the non-selective beta antagonists propranolol

A

negative chronotrope and negative ionotrope

36
Q

this drug can be given orally or IV, has a large first pass effect, and has adverse effects of bradyarrhythmias, hypotension, bronchospasm, negative ionotropy (effects of beta blockade)

A

propanolol

37
Q

you have concerns about pulmonary function. should you use atenolol or propranolol to treat Fluffington’s ventricular tachyarrythmia?

A

atenolol (because there are same beta 1 effects, but lacks the beta 2 effects)

38
Q

do anticholinergics increase or decrease heart rate

A

increase heart rate

39
Q

where are M2 receptors mainly located

A

in cells making up SA and AV nodes

40
Q

does atropine affect only cardiac M2 receptors or all muscarinic receptors? how does its receptor activity relate to its adverse effects?

A

affects all muscarinic receptors, therefore non-specific effects which can be undesirable (eg. GI effects can cause colic in horses, also contraindicated in animals with glaucoma)

41
Q

this drug is used for acute, short-term responses, increases cardiac output, used pre-anesthesia to decrease salivation and airway secretions, and is a positive chronotrope useful for treating bradycardia and asystole

A

atropine

42
Q

when is a cardiac myocyte unable to initiate an action potential?

A

effective refractory period which lasts from phase 0 to early phase 4

43
Q

what cells lack fast sodium channels

A

cardiac nodal cells

44
Q

what are 4 effects of antiarrhythmic drugs on heart (not classes, think in terms of physiological effects)

A

alter automaticity, alter conduction velocity, change excitability of cardiac cells during ERF, alter membrane ion conductance to affect action potential

45
Q

what are 5 classes of antiarrythmic drugs

A

class 1 sodium channel blockers, class 2 beta blockers, class 3 potassium channel blockers, class 4 calcium channel blockers, class 5 miscellaneous

46
Q

class 1 sodium channel blocker antiarrhythmic drugs change which phase of the action potential? what is their effect on action potential duration?

A

phase 0 (reduce slope and amplitude); may increase, decrease, or not change AP

47
Q

what class of antiarrhythmic drugs also has anticholinergic effects

A

class 1A

48
Q

this class 1B antiarrythmic drug is used to treat tachyarrythmias, especially during anesthesia, has a large first pass effect, and has a rapid onset after IV administration

A

lidocaine

49
Q

this class 1A antiarrythmic drug prolongs the ERP of atrial and ventricular muscle to allow atrial fibrillation conversion, is anticholinergic, and speeds AV conduction

A

quinidine

50
Q

this class 1A antiarrythmic has a similar mechanism of action to quinidine but is used for controlling ventricular arrhythmias rather than atrial arrhythmias

A

procainamide

51
Q

this class 3 antiarrhythmic prolongs the AP and slows depolarization, is also a beta blocker, and is used for control of ventricular arrhythmias

A

sotalol

52
Q

this class 4 antiarrythmic blocks slow calcium channels in cardiac cells, is the calcium channel blocker of choice for arrhythmias, and is used for atrial fibrillation in dogs and hypertrophic cardiomyopathy in cats

A

diltiazem

53
Q

name 3 ways vascular smooth muscle contraction can be triggered

A

passive stretching, electrical stimulation (AP), chemical stimulation (receptor binding triggering calcium release from SR)

54
Q

this calcium channel blocker has potent vasodilatory effects, less direct effects on the heart, and is used to treat systemic hypertension as weak as severe mitral regurgitation in dogs

A

amlodipine

55
Q

do alpha 1 antagonists have a greater dilation effect on arteries or on veins?

A

dilate both arteries and veins, but less of an effect on veins (therefore major effect is reduced preload)

56
Q

what are the 2 goals of using a diuretic

A

reduce blood volume and mobilize edema

57
Q

what is diuretic of choice for cardiovascular disease

A

furosemide

58
Q

what is the effect of ACE inhibitors on blood vessels

A

vasodilation

59
Q

what is the effect of ACE inhibitors on aldosterone

A

decrease aldosterone (so cause a diuretic effect)

60
Q

what is the effect of ACE inhibitors on sympathetic input to the heart

A

decrease

61
Q

ACE inhibitors are pro drugs, so they require a conversion to active metabolites. why does this matter clinically?

A

delayed onset of action, 1-2 weeks to see magnitude of response. they are for management rather than acute therapy.

62
Q

what ion controls cardiac contractility

A

calcium

63
Q

this drug is a positive ionotrope that does NOT increase heart rate at normal doses, can cause seizures in cats, and has a half-life of 2 minutes so is given as CRI

A

dobutamine

64
Q

glycopyrrolate is similar to atropine but is a less polar molecule. what effect does this have on distribution compared to atropine?

A

less CNS penetration, so fewer adverse CNS effects

VETM 443 Clin Pharm Tox (18 decks)

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