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Pharmacology > Cardiovascular - NICOLE > Flashcards

Cardiovascular - NICOLE Flashcards

1
Q

heart failure is

A

the inability of the heart to meet the metabolic needs of the peripheral tissues

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2
Q

pathophysiology of heart failure

A

-pump failure
- forward obstruction to blood flow
- regurgitant blood flow
-congenital shunts
- rupture of heart of vessels
- conduction disorders

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3
Q

decreased cardiac output leads to activation of what

A

sympathetic activation (a,B)

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4
Q

short and long term responses to underlying cardiovascular disease

A

increase heart rate
increase peripheral resistance
increase blood volume
redistribute blood flow
cardiac dilation
myocardial hypertrophy

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5
Q

pharmacological modification of cardiac function is usually achieved by modifying one or more of the following

A

chronotropy (heart rate)
inotropy (contractility)
peripheral resistance (vascular tone)
blood volume (diuresis, fluids)
rate of conduction (rhythm)
neurohormonal input to the heart

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6
Q

name some things you want to change with drugs?

A

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

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7
Q

Frank-Starling Law - Cardiac output increases with ________ and decreases with _______

A

exercise, disease

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8
Q

the cardiac output of the diseased heart is reduced at any ________

A

preload

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9
Q

changes in preload have less of an effect on the output of the __________than on the output of the healthy heart

A

diseased heart

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10
Q

neurohormonal activation and excessive sodium and water retention leads to

A

elevated intracardiac and venous pressure (backward failure). Intravenous pressures >25 mg Hg results in signs of congestion

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11
Q

Diuretics move performances leftward along the Frank-Starling by reducing

A

preload and moving performances to a position below the threshold for congestion. Diuretics have little effect on cardiac output

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12
Q

cardiac injury can also result in low cardiac output (forward failure). What helps with this?

A

positive inotropes improve cardiac contractility, which improves output at any preload

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13
Q

patients with severe heart failure can exhibit signs of poor cardiac output and congestion (forward and backward failure). These patients require

A

positive inotropes and diuretics to shift the curve/improve function

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14
Q

The Frank-Starling Law states that the stroke volume of cardiac contraction ______________ as preload increases

A

increases

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15
Q

Inotropes - what mechanism/drugs

A

adrenergic drugs, inodilators, cardiac glycosides

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16
Q

chronotropes - what mechanisms/drugs

A

adrenergic drugs
cholinergic drugs

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17
Q

antiarrthymics - what classes

A

class 1 - sodium channel blockers
class 2 - beta blockers
class 3 - potassium channel blockers
class 4 - calcium channel blockers

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18
Q

positive inotropes

A

increase contractility

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19
Q

negative inotropes

A

decrease contractility

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20
Q

positive inotropes are useful in clinical situations when

A

decreased cardiac output is due to decreased myocardial contractility - ex dilated cardiomyopathy

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21
Q

negative inotropes have limited usefulness as a

A

first-line therapy but can be useful to allow cardiac relaxation and filling in hypertrophic cardiomyopathy. They also decrease cardiac oxygen consumption

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22
Q

when skeletal muscle contracts the calcium released by the SR is sufficient to

A

interact with all of the troponin, causing ALL potential actin-myosin interactions to occur

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23
Q

in cardiac muscle, NOT ALL troponin interacts with

A

calcium; thus, more or fewer actin-myosin cross bridges may form depending on intracellular calcium availability

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24
Q

WHATEVER CONTROLS THE CALCIUM WILL CONTROL

A

Cardiac contractility

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25
Q

examples of positive inotropes

A

digoxin, pimobendan, dobutamine, dopamine, epinephrine

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26
Q

is digoxin a good positive inotrope?

A

NO! because of high incidence of adverse effects and current availability of better options, digoxin is used infrequently in vetmed

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27
Q

inotropic mechanism of digoxin action

A

inhibition of the NA/K pump in the cell membrane results in decreased K+ in the cells. This leads to lower resting membrane potential/hyper excitability. It also increases Na+ inside the cell, which slows the action of the Na/Ca exchanger, with the net effect of increasing calcium concentrations within the cell. This improves contractility

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28
Q

Pimobendan is a

A

positive inotrope and vasodilators

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29
Q

pimobendan is not recommended for animals with

A

hypertrophic cardiomyopathy, aortic stenosis - caution with arrhythmias

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30
Q

what is the positive inotrope of choice in small animals

A

pimobendan

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31
Q

pimobendan has been shown in clinical trials to enhance

A

survival in dogs with heart failure due to DCM or Mitral Valve Insufficiency (MVI)

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32
Q

pimobendan mechanism of action (long one sorry) 4 things

A
  1. sensitizes troponin C complex to calcium, leading to increased strength of contraction
  2. causes venous and arterial dilation via phosphodiesterase III & V inhibition (reduces preload & after load)
  3. increases cardiac contractility without increasing myocardial oxygen consumption
  4. Appears to modulate neurohormonal input to heart
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33
Q

cAMP is an important second messenger in the regulation of cardiac contraction. cAMP, through various interactions with other intracellular messengers, increases the

A

strength and rate of contraction as well as the conduction of action potentials. Phosphodiesterase (PDE) breaks cAMP down to AMP. PDE III is inhibited in cardiac myocytes

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34
Q

pimobendan should be administered

A

orally, 1 hour before feeding

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35
Q

is pimobendan protein bound

A

yes, approx 93%

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36
Q

pimobendan half life

A

short - 30 min in dogs - active metabolite has 2 hr half life

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37
Q

how is pimobendan excreted

A

fecal excretion

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38
Q

adverse effects - pimobendan

A

usually well-tolerated
GI effects
tachycardia
pu/pd
CNS toxicity

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39
Q

B1 agonists are what

A

positive inotropes

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40
Q

examples of B1 agonists

A

dopamine, dobutamine

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41
Q

B1 agonists like dopamine and dobutamine have low bioavailability so must be given

A

IV

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42
Q

B1 agonists are useful in

A

an in-hospital setting

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43
Q

B1 agonists act on

A

beta receptors in the heart and blood vessels

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44
Q

in the heart, activation of beta-1 receptors by norepinephrine (or a beta-1 agonist) increases

A

cAMP concentrations. This activates a protein kinase (PK-A) to phosphorylate calcium channels in the cardiac myocyte resulting in increased calcium entry into the cell which enhances calcium release from sarcoplasmic reticulum during action potentials and increases the force of contraction

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45
Q

in the blood vessels, activation of beta2 receptors results in

A

increased cAMP, which results in vasodilation. This is because increased cAMP in vascular smooth muscle inhibits myosin light chain kinase, which is involved in myocyte contraction.

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46
Q

dobutamine is a positive inotrope that

A

does NOT increase heart rate

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47
Q

half life dobutamine

A

2 minutes, given as CRI

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48
Q

adverse effects dobutamine

A

-correct hypovolemia before administration!!!!
-incompatible with bicarbonate
-at high doses, can cause tachycardia
- SEIZURES IN CATS

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49
Q

Dopamine interacts with which receptors

A

Dopamine 1 (DA1), B1, a1, a2
- becomes less DA1 selective with increasing dose

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50
Q

DA1 receptor activation causes

A

vasodilation in the kidneys, mesentery, heart, and brain

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51
Q

B1 causes increased _________ and a1 activation increases _________

A

cardiac contractility, peripheral vascular resistance

52
Q

dopamine half life -

A

very short half life - administer by CRI, less than 2 minutes

53
Q

adverse effects dopamine

A

high doses can cause renal vasoconstriction
extravascular administration causes tissue necrosis
arrhythmias

54
Q

dobutamine vs dopamine - which has more positive inotropic effects

A

dobutamine

55
Q

dobutamine vs dopamine - chronotropic effects

A

dobutamine - less chronotropic effects
dopamine - more chronotropic effects

56
Q

dobutamine vs dopamine which one dilates renal vascular bed

A

dopamine

57
Q

indications for dobutamine

A

cardiogenic shock, endotoxic/septic shock, short-term treatment of refractory CHF (with pimobendan)

58
Q

indications for dopamine

A

cardiogenic shock
endotoxic/septic shock
oliguria

59
Q

epinephrine - a non-selective adrenergic agonist - increases

A

-myocardial oxygen demand and energy consumption
-arrythmogenic

60
Q

epinephrine is used in

A

life threatening emergencies, not for management of CHF
- cardiac arrest, anaphylactic shock

61
Q

negative inotropes - drug classes

A

B antagonists (blockers)
calcium channel blockers
certain antiarrhythmics
(all are rarely used specifically for their negative inotropic effects)

62
Q

positive chronotropes

A

increase heart rate

63
Q

negative chronotropes

A

decrease heart rate

64
Q

negative chronotropes - drug classes

A

B antagonists (blockers)
muscarinic antagonists/anticholinergics

65
Q

examples of beta antagonists (negative chronotropes)

A

-propranolol
-atenolol
-carvedilol

66
Q

examples of anticholinergics (positive chronotropes)

A

atropine, glycopyrrolate

67
Q

B antagonists are competitive antagonists of B adrenergic receptors - can be

A

selective or non-selective

68
Q

B antagonists _________ heart rate

A

REDUCE

69
Q

propranolol - effects

A

negative chronotrope and inotrope (B1 antagonism)
vasoconstrictor and bronchoconstrictor (B2 antagonism)
antiarrythmic

70
Q

propanolol (non-selective, competitive beta blocker) is used for

A

-primarily used as an anti-arrhythmic
-sometimes used as short-term treatment for hypertension associated with thyrotoxicosis or pheochromocytoma
-treatment of CHF with tachycardia
-to slow ventricular rate during atrial fibrillation
- to decrease sympathetic input to heart

71
Q

propanolol can be given

A

IV or orally

72
Q

propanolol has a small/large first pass effect

A

large - oral doses are approximately 10X greater than IV doses

73
Q

propranolol adverse effects

A

can be predicted as are effects of B blockade
bradyarrythmias, hypotension
bronchospasm (especially of concern in patients with poor lung function
negative inotropy

74
Q

atenolol is a

A

beta 1 selective antagonist

75
Q

atenolol has same B1 effects as propanolol, without the

A

b2 effects

76
Q

uses of atenolol

A

treatment of tachyarrythmias and ventricular hypertrophy
treatment of hypertrophic cardiomyopathy in cats
adjunctive treatment for hypertension associated with chronic kidney disease (amlodipine first choice)

77
Q

atenolol is a better choice than propanolol IF

A

there are concerns about pulmonary function

78
Q

atenolol administered

A

orally - with excellent bioavailability

79
Q

muscarinic antagonists block the

A

effects of acetylcholine (Ach) on M2 receptors in the cardiovascular system

80
Q

the effects of M2 activation in the cardiovascular system are:

A
  • slow heart rate through effects on SA node
    -decreased atrial contractility and AP duration
    -decreased conduction velocity at AV node
    -decreased ventricular contractility
    -antagonists have OPPOSITE EFFECTS
81
Q

anticholinergics _____________ heart rate

A

increase

82
Q

M2 receptors are mainly located in

A

the cells making up the SA and AV nodes. There are also some M2 receptors in cardiac muscle, but fewer, so the effects on cardiac myocytes of M2 antagonists are less important than their effects on the SA and AV nodes

83
Q

Atropine is a

A

competitive muscarinic antagonist

84
Q

atropine prevents the interaction of Ach with

A

its receptor, which attenuates the physiologic response to parasympathetic nerve stimulation. Atropine affects all muscarinic receptors, not just cardiac M2 receptors.

85
Q

atropine has a non-specific nature, so its difficult to induce one of its effects without

A

inducing others, which can lead to undesirable side effects

86
Q

atropine clinical use - mainly used for

A

acute, short term response

87
Q

atropine is a positive chronotrope - useful for treating

A

bradycardia
increases cardiac output (bc of increase in HR)

88
Q

atropine old uses

A

was used pre-anasthesia to decrease salivation and airway secretions, now only used in select cases
- was occasionally used in treatment of asystole but clinical benefit not confirmed
useful in treatment of certain toxicities

89
Q

atropine adverse effects

A

due to non selective nature of atropine
-GI effects can cause colic in horses
-contraindicated in animals with glaucoma

90
Q

glycopyrrolate is a drug that is very similar to atropine but with less

A

CNS penetration

91
Q

Glycopyrrolate: basically the same as atropine but

A

more polar molecule - so less CNS penetration than atropine, less adverse CNS effects, does not cross placenta, and also lowers incidence of tachyarrythmias

92
Q

conduction velocity is influenced by

A

parasympathetic and sympathetic inputs

93
Q

ERP

A

effective refractory period - phase 0 to early phase 4
a new AP cannot be initiated during this time

94
Q

cardiac nodal action potentials - do not have

A

fast sodium channels (AP in the SA and AV nodes are determined mainly by slow Ca and K currents)
these cells do not have a true resting potential, they spontaneously depolarize

95
Q

causes of arrhythmia

A

-disturbances in automaticity of the pacemaker cells
-disturbances in impulse conduction or action potential generation

96
Q

ventricular arrthymias originate in

A

the ventricles

97
Q

atrial (supraventricular) arrhythmias originate in

A

the atria or atrial conduction system (can include AV node)

98
Q

anti arrhythmic drugs alter

A

automaticity
conduction velocity
change excitability of cardiac cells during ERP

99
Q

ALL anti arrhythmic drugs alter membrane ion conductance to

A

affect the action potential

100
Q

Class 1 (Na-Channel blockers) examples

A

lidocaine, quinidine, procainamide

101
Q

Na channel blockers bind to and block

A

fast Na channels responsible for rapid depolarization of cardiac myocytes. This reduces the slope and amplitude of phase 0 of the action potential - decrease conduction velocity in non-nodal cardiac tissue `

102
Q

Na channel blockers may increase, decrease, or not change the

A

action potential duration and ERP

103
Q

Na channel blockers reduce automaticity of

A

ectopic pacemakers

104
Q

class 1 subtypes are based on

A

effects of ERP - due to nature of Na channel block and presence or absence of K channel block

105
Q

class 1a also has

A

anticholinergic effects - ex quinidine

106
Q

class 1b - example

A

lidocaine

107
Q

lidocaine is used to treat

A

acute ventricular tachyarrythmias, particularly during anesthesia

108
Q

does lidocaine have any effect on artia?

A

no - effect primarily seen in ventricles

109
Q

lidocaine onset time

A

rapid onset after IV administration and quick metabolism (short half life)

110
Q

lidocaine has a large

A

first pass effect, therefore not given orally

111
Q

lidocaine adverse effects

A

vomiting, seizures, muscle fasciculation, usually stop when administration stopped

112
Q

quinidine - prolongs the

A

ERP of atrial and ventricular muscle - allows atrial fibriliation conversion

113
Q

procainamide - similar mechanism to quinidine but more effective for

A

controlling ventricular arrhythmias than atrial arrhythmias

114
Q

Quinidine - USED FOR

A

ATRIAL ARRHYTHMIAS

115
Q

Procainamide - USED FOR

A

VENTRICUALR ARRHYTHMIAS

116
Q

quinidine vs procainamide - how to give

A

quinidine - PO in horses, IM or IV
Procainamide - PO, IM, or IV

117
Q

K channel blockers - examples

A

sotalol

118
Q

K channel blockers - prolong the

A

action potential and slow repolarization by blocking K channels

119
Q

what is the most relevant class 3 anti arrhythmic in vet med

A

sotalol

120
Q

sotalol is not only a k channel blocker but also

A

a B blocker

121
Q

sotalol is used for control of

A

ventricular and some supra ventricular arrhythmias

122
Q

does sotalol has a first pass effect

A

no! high bioavailability

123
Q

calcium channel blockers - bind to and block

A

L-type Ca channels in vascular smooth muscle, cardiac myocytes, and cardiac nodal tissue

124
Q

Calcium channel blockers effect on blood vessels, chronotropy, inotropy

A

vasodilator, negative inotrope, negative chronotrope, negative dronotrope (decreases conduction velocity within the heart esp at AV node)

125
Q

class 4 calcium blocker of choice for arrhythmias

A

diltiazem

126
Q

diltiazem primarily acts on

A

the AV node

127
Q

clinical use of diltiazem

A

supra ventricular tachycardia / atrial fibrillation in dogs - heart rate control
hypertrophic cardiomyopathy in cats - control heart rate (slow down rate to allow cardiac filling)
-peripheral vasodilation (reduces after load)
- negative inotropic effect (may allow more effective filling of heart because increases relaxation of heart muscle

Pharmacology (11 decks)

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