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VETM 443 Pharmacology > Cardiac Pharmacology > Flashcards

Cardiac Pharmacology Flashcards

1
Q

List 6 mechanisms by which a heart can fail?

A

pump/mechanical failure

obstruction to. forward flow via stenosis or hypertension

regurgitant flow via valve dysfunction

congenital shunt causing volume overload in certain chambers

conduction disorders like arrhythmias

reduced fluid return from vessel rupture or vasodilation resulting in reducing preload

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2
Q

What are 6 compensatory mechanisms that occur in response to heart failure?

A

increase heart rate

increase peripheral resistance

redistribution of blood flow

increase blood volume

myocardial hypertrophy

cardiac dilation

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3
Q

Explain how cardiac function is controlled? How do acute and chronic outcomes compare?

A

PSNS reduces the heart rate via the vagus nerve

SNS increases heart rate and contractility via sympathetic cardiac nerves

acute increases in sympathetic tone result in
- increased heart rate
- increase cardiac output
- increase TPR

chronic increases in sympathetic tone result in
- persistant tachycardia
- adrenergic receptor downregulation
- increased myocardial oxygen demand
- myocyte necrosis

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4
Q

Define cardiac output

A

heart rate x stroke volume

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5
Q

What are the physiologic features of skeletal muscle?

A

they have
- intercalated discs/gap junctions
- branched
- central nucleus

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6
Q

Explain the mechanism of how heart disease causes congestive heart failure?

A

Heart disease reduces cardiac output

reduced cardiac output results in reduced blood pressure

low blood pressure causes:
- reduced renal perfusion and that stimulates renin production
- sympathetic activation (of alpha and beta receptors)

  1. Renin = increased angiotensin 2
    - stimulates increased aldosterone and ADH (also stimulate SNS activation and vassoconstriction)
    - water and Na retention
    - increase blood volume
    - increase hydrostatic and lower oncotic pressure
    - edema and increased preload
    - cardiac dilation = further reduces cardiac output
  2. SNS activation results in vasoconstriction and an increase in heart rate and TPR
    - vasoconstriction will increase heart rate and TPR
    - this increases afterload and cardiac work resulting in reduced cardiac output
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7
Q

Explain the steps of RAAS activation and its impacts on the heart.

A
  1. reduced blood pressure stimuli
  2. juxtaglomerular cells release renin
  3. renin converts angiotensinogen to angiotensin 1 in liver
  4. angiotensin 1 to angiotensin 2 converted in the lungs by angiotensin converting enzyme
  5. ACE interacts with bradykinin causing vasoconstriction
  6. angiotensin 2 causes vasoconstriction, SNS activation , increased aldosterone release
  7. aldosterone increases sodium and water retention = increasing blood volume

vasoconstriction will increase afterload

aldosterone will increase preload

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8
Q

What are the gross systemic effects of heart failure?

A

pulmonary edema from LS heart failure

liver congestion, subcutaneous edema, ascites from RS heart failure

edema is from increased preload

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9
Q

What is the most common kind of heart disease causing heart failure in dogs? How does the prevalence compare to other types of heart disease

A

myxomatous valvular degeneratioin

small dogs

mitral valve collagen degeneration causes valve regurgitation
- increases cardiac work
- ventricular remodeling and dysfunction

myxomatous > congenital heart disease > DCM > hemorrhagic pericardial effusion > neoplasia > dirofilaria

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10
Q

List the common causes of heart disease/failure in cats

A

HCM > DCM > hyperthyroid associated hypertrophy > congenital

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11
Q

List 6 factors that cardiac drugs can target

A

chronotropy

inotropy

peripheral resistance/vascular tone

blood volume (diuresis/fluid)

rate of conduction/rhythm

neurohormonal input

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12
Q

What are 5 potential goals of cardiac drugs

A

Modify (1+)

preload

afterload

rate/rhythm

contractility

SNS/neurohormonal input

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13
Q

Explain the frank starling law/mechanism is?

A

It says that by increasing preload it will increase cardiac output up until a certain point
- disease reduces the threshold of preload that will ‘max’ the capacity of cardiac output
(healthy animals are moderate, when exercising the threshold is increased)

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14
Q

How do cardiac drugs affect cardiac output in terms of the frank starling law

A

diuretics will act to reduce the preload

positive inotropes will increase cardiac output

mixed vasodilators will act to both increase cardiac output and reduce preload

On the frank starling curve, preload is on the x axis and cardiac output is on the y axis.

We are using these drug to optimize cardiac output and reduce increased blood pressure associated with high preload and CHF (>25mmHg)

If CHF is severe and has both forward and backwards failure you may need a diuretic and a positive inotrope

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15
Q

What is a physiologic reflex in response to drug administration? + example

A

It is an indirect response to a drug

furosemide will reduce blood volume
- renal vasodilation and reduced bp
- RAAS activation
- increasing SNS and heart rate

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16
Q

What are the categories of drugs that can directly target the heart? And the types/classes of drugs under each category

A

inotropes
- adrenergic
- inodilator
- cardiac glycoside

chronotropes
- adrenergic
- cholinergic

antiarrhythmics
class
1 - Na channel blocker
2 - beta blocker
3 - potassium channel blocker
4 - Ca channel blocker

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17
Q

Explain the process of cardiac muscle contraction

A

it is similar to skeletal muscle contraction except it is synchronous

  1. resting membrane potential = -90mV
    - because there is more extracellular potassium
  2. Na channel inactive while K and Ca channels are open
  3. Ca enters and triggers Ca release from sarcoplasmic reticulum
  4. Ca binds troponin which allows actin and myosin to interact
    - not all the troponin will interact with Ca so you can control muscle contraction by controlling the amount of Ca available
  5. Ca is removed by Na/Ca pump exchanger or returned to sarcoplasmic reticulum
  6. intracellular Na homeostasis returned via Na/K pump
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18
Q

What is the main function of positive and negative inotropes respectively

A

+ = used to treat reduced cardiac output

  • = can be used to reduce myocardial O2 consumption but not used as much
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19
Q

List 3 examples of short term positive inotropes

A

dobutamine
dopamine
epinephrine

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20
Q

List 2 examples of chronic use positive inotropes

A

digoxin
pimobendan

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21
Q

What is digoxin? What is its mechanism of action?

A

it is a cardiac glycoside from the foxglove plant

It inhibits Na/K pump causing an increase in intracellular sodium
- increased intracellular Na = reduced action of Na/Ca exchanger
= more intracellular Ca

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22
Q

What are the effects of digoxin

A

reduce heart rate
- restore baroreceptor sensitivity = reduced SNS and increase PSNS

increase inotropy

increase cardiac output

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23
Q

What is digoxin used for

A

atrial fibrillation (by increasing PSNS)

not normally used
its efficacy is not well studied

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24
Q

What are the adverse effects associated with digoxin

A

arrhythmias (impact K)

electrolyte interactions

drug interactions (careful with furosemide)

GI effects - v and anorexia

It has a long half life
- dog = 24-39h
- cat = 33-58h

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25
What are the effects of pimobendan
positive inotrope vasodilator This results in increased contractility without increased myocardial oxygen demand
26
What is the mechanism of action of pimobendan
Increase inotropy by... - sensitizes troponin C to Ca - inhibit phosphodiesterase 3 in heart = increase cAMP Reduce pre and afterload by... - inhibiting phosphodiesterase 3 and 4 = cAMP/cGMP accumulation = vein and artery dilation cAMP is made after norepinephrine binds the beta 1 receptor by adenylyl cyclase - result in increased cAMP, strength and rate of contraction, rate of AP conduction
27
In what cases is pimobendan contraindicated
HCM aortic stenosis arrhythmia = situations where increasing cardiac output could be bad
28
In what cases is pimobendan indicated
DCM mitral valve insufficiency
29
What are the pharmacokinetic features of pimobendan
short half life (30min in dogs with 2hrs of active metabolite) 93%/mostly protein bound excreted in feces
30
What are the instructions for pimobendan administration
PO 1hr before meal
31
What are the adverse effects of pimobendan
usually safe/well tolerated GI effects tachycardia - at high doses PU/PD CNS toxicity
32
Which 2 positive inotropes are B1 agonists? How are they administered?
dopamine and dobutamine IV only (low bioavailability)
33
What is the mechanism of action of dopamine/dobutamine? What class of drug are they?
beta agonists Heart - act on beta 1 receptors - norepi + B1 result in increased cAMP - result in phosphorylation of Ca channel by protein kinase A - increases Ca entry - increased Ca release from sarcoplasmic reticulum Vessels - B2 receptor targets - B2 activation results in increased cAMP - increased cAMP inhibits the myosin light chain - vasodilation B2 activation will also cause bronchodilation
34
What is the effect of dobutamine? How is it administered?
positive inotrope + no impact on heart rate (at normal doses) - no renal vasodilation CRI (because half life is 2 mins)
35
What are the adverse effects associated with dobutamine
seizures in cats* expensive don't use with bicarbonate tachycardia at high doses mut fix hypovolemia before administration
36
What cardiac conditions is dobutamine indicated for
cardiogenic or septic shock short term CHF treatment with pimobendan
37
What receptors does dopamine activate in the context of cardiac drugs? What are the effects of activation?
It act on many receptors dopamine 1 receptors - kidney vasodilation beta 1 receptor - increase inotropy alpha 1 receptor - increase peripheral vascular resistance alpha 2 receptors
38
How is dopamine administered and what are the adverse effects?
CRI because of short half life adverse - vasoconstriction of the kidney at high doses - extravascular administration will cause tissue necrosis - arrhythmia
39
What conditions may indicate the use of dopamine?
cardiogenic or septic shock oliguria
40
What are the effects of epinephrine administration?
bronchodilation via beta 2 receptors positive inotrope and chronotrope via beta 1 receptors increase peripheral resistance
41
What are the adverse effects of epinephrine administration
arrhythmia
42
What are the conditions that may indicate epinephrine administration
cardiac arrest anaphylactic shock
43
Give 3 examples of negative inotropes
beta antagonists calcium channel blockers some antiarrhymatics
44
What are 2 classes of chronotrope drugs
beta antagonists/blockers muscarinic antagonists/anticholinergics
45
List 3 negative chronotropic drugs commonly used
propranolol atenolol carvediol =beta antagonist
46
List 2 positive chronotropic drugs commonly used
atropine glycopyrrolate - anticholinergics
47
What is the mechanism of action of beta antagonists
They are competitive antagonists of beta receptors selective or non selective oppose normal action beta 1 - increase heart rate, contractility - increase conduction velocity beta 2 - smooth muscle relaxation resulting in peripheral vasodilation and bronchodilation beta antagonsists will oppose the above effects
48
What is the mechanism of action of propranolol? What are the effects?
It is a beta 1 and 2 antagonist - reduces chronotropy and inotropy - vasoconstriction and bronchoconstriction
49
What is propranolol primarily used for
antiarrhythmic short term treatment of hypertension secondary to thyrotoxicosis or pheochromocytoma CHF with tachycardia slow ventricular filling in atrial fibrillation to reduce SNS input to the heart
50
What are the adverse effects associated with propranolol
bradyarrhythmia hypotension bronchospasm (can be a problem if there is reduced lung function or pulmonary edema) reduced inotropy
51
What is the route of administration of propranolol
PO or IV large first pass effect so the dose for PO is much higher than for IV
52
What is the mechanism of action for atenolol? WHat are its effects?
It is a beta 1 selective antagonist - negative inotropy and chronotropy
53
What are the indications/situation for use of atenolol
tachyarrhythmia and ventricular hypertrophy HCM in cats hypertension secondary to CKD - amlodipine is the first choice tho it is a good choice if you have concerns about pulmonary function (vs. propranolol)
54
What is the mechanism of action of muscarinic antagonists on the heart? What are the effects?
block the effects of Ach on M2 receptors in the cardiovascular system normal functions (opposed) - reduce SA node depolarization - reduce atrial contractility and action potential duration - reduce AV node conduction velocity - reduce ventricle contractility M2 receptors are found mainly in the SA and AV node - normally when it is bound by Ach it reduces the amount of cAMP which causes reduced chronotropy and dromotropy (action potential conduction) there are less M2 receptors in the cardiac myoctes (not as important)
55
What is the mechanism of action of atropine? What are its effects?
It is a non specific muscarinic receptor antagonist - blocks Ach interaction with the receptor during PSNS stimulation dose dependent effects - low: impact salivary and sweat glands - higher: cardiac impacts like positive chronotropy and dromotropy and increased cardiac output along with non specific signs
56
What are the adverse effects of atropine
GI impact - can cause colic in horses anticholinergic toxidrome - delirium - ocular signs - dry mouth and skin - fever - constipation - tachycardia - urinary retention - cutaneous vasodilation
57
When is atropine contraindicated
for patients with glaucoma
58
What situations may indicate atropine use
acute treatments of - bradycardia - preanesthetic to reduce salivation and airway secretions (not used anymore) - sometimes asystole tx or toxicity tx
59
What is the mechanism of action of glycopyrrolate? How does it compare to atropine?
It is the same as atropine - non selective muscarinic receptor antagonist much more polar than atropine - less CNS penetration and related adverse effects - does not cross placenta - lower incidence of tachyarrhythmia - lower the volume of distribution (less movement out of vessels into tissue)
60
Explain how a normal cardiac rhythm is created
1. dominant pacemaker cells in the SA node regularly/spontaneously depolarize - cardiac myocyte RMP = -90 - depolarization threshold = -70 - creates long uniform AP with refractory periods 2. AP transmitted to the AV node 3. AP transmitted to bundle of His and purkinji fibres throughout the ventricles the velocity is determined by the PSNS and SNS inputs
61
What are the phases of a cardiac myocyte action potential? Compare this to a SA node action potential?
myocyte - phase 0 = Na influx - fast - phase 1 = K efflux - fast - phase 2 = slow Ca channel open - phase 3 = slow K efflux - phase 4 = restore RMP with Na/K ATPase effective refractory phase = from phase 0 - early 4 node - phase 0 = depolarization via Ca influx - phase 3 = repolarize via slow K efflux - phase 4 = slow Na influx/Ca influx no fast Na channel no true RMP due to spontaneous depolarization
62
What can cause arrhythmias
disruption of the pacemaker cells - ectopic pacemaker - abnormal impulse conduction or AP generation
63
How are arrhythmias classified?
ventricular - ventricular tachycardia or fibrillation - premature ventricular contractions atrial - supraventricular tachycardia or atrial fibrillation - premature atrial contraction - AV block
64
List 3 primary mechanisms that antiarrhythmic drugs use
change automaticity change conduction velocity change excitability of cells in effective refractory period all will change membrane ion conductance
65
Name 2 antiarrhythmic drugs that do not fall into one of the 4 classes
atropine - for bradycardia digoxin - for supraventricular arrhythmia (ex. fibrillation)
66
List 3 commonly used Na channel blockers
lidocaine quinidine procainamide
67
What is the mechanism of action of Na channel blockers? What is its effects?
They bind/block the fast Na channels to prevent depolarization of cardiac myocytes It will reduce the slope and amplitude of phase 0 AP thus reducing conduction velocity It can change the AP duration and effective refractory period by affecting K channels It will reduce automaticity of ectopic pacemakers
68
Of lidocaine, quinidine, and flecainide; what class of Na channel blockers are they and what are their respective effects?
class 1A = quinidine - increase ERP - modeate Na channel blocker - anticholinergic class 1B = lidocaine - reduce ERP - mild Na channel blocker class 1C = flecainide - ERP same - strong Na channel blocker
69
What is lidocaine used for?
ventricular tachyarrhythmia in anesthesia - minimal impact on atria local anesthetic
70
How is lidocaine administered?
IV no PO (high first pass effect)
71
What are the adverse effects associated with lidocaine
vomiting seizure muscle fasciculation - will stop when lidocaine stopped
72
What are the effects of quinidine administration?
increase ERP in atrium and ventricle - allow atrial fibrillation conversion anticholinergic increase AV conduction speed which increases the risk for ventricular tachycardia - can pretreat with digoxin to avoid (slow AV conduction) but be careful because quinidine will increase digoxin plasma concentrations
73
How is quinidine administered
PO in horses IM or IV in SA
74
What is quinidine used for
atrial arrhythmia
75
What is the mechanism of procainamide
same as quinidine
76
How is procainamide andministered
PO IM IV dogs are the only species that utilize it as a prodrug = they have special values for monitoring
77
What is procainamide used for
ventricular arrhythmias
78
What are beta blockers used for
atrial fibrillation
79
What is the mechanism of K channel blockers
block K channels slow down repolarization
80
What is a common K channel blocker? What is its mechanism of action?
sotalol it is a K channel blocker and a beta blocker it has no first pass effect = high bioavailability
81
What is sotalol used for
ventricular + some supraventricular arrhythmia
82
What is the mechanism of action of Ca channel blockers? What are the effects?
block L-type (slow) Ca channels in vascular smooth muscle, cardiac myocyes, and cardiac nodal cells vasodilation negative inotrope/chronotrope/dromotrope - must be cautious if using in CHF patient
83
What are Ca channel blockers used for
atrial fibrillation in dogs HCM in cats
84
What is an example of a common Ca channel blocker used? What is its mechanism of action?
diltiazem It is the main Ca channel blocker used for arrhythmias It blocks Ca channels mainly in the AV node
85
What are the effects of diltiazem
it has a minimal impact of inotropy - if they have myocardial disease it can have an effect vasodilation negative chronotrope/dromotrope
86
What is diltiazem used for
supraventricular tachycardia and atrial fibrillation in dogs - slow heart rate HCM in cats - control their heart rate to allow filling - peripheral vasodilation to reduce afterload - reduce inotropy to allow filling and let the heart relax

VETM 443 Pharmacology (23 decks)

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