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Pharmacology > Cardiac Pharm > Flashcards

Cardiac Pharm Flashcards

1
Q

What affects ability for heart to function?

A

1.Preload-pressure from venous system (great veins into right side of heart) into heart
**big determinant of CO
*can’t have too much because excess amount into heart overloads it (can’t stretch anymore, leads to remodelling and weakening of heart)

  1. Afterload- resistance in the arteries (aorta). If they are still, will make it more difficult to push blood forward.
    **harder work if afterload/hypertension is high
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2
Q

Hypertrophic cardiomyopathy (HCM)

A

-most common form of heart failure in cats

-thick walls- need to slow heart down and relax

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3
Q

Dilated cardiomyopathy (DCM)

A

-most common form of heart failure in dogs; certain breed dispositions (boxers, pinschers)
>linked with grain free diets/taurine
>taurine free diets in cats

-chamber is enlarged, need to increase hearts ability to create force and increase contractility

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4
Q

Volume Overload

A

Leads to increased diastolic pressure, addition of new sarcomeres, chamber enlargement
=eccentric hypertrophy

Dilated cardiomyopathy (DCM)

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5
Q

Pressure overload

A

Leads to increased systolic pressure, parallel addition of new myofibrils =wall thickening= concentric hypertrophy

**Hypertrophic cardiomyopathy

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6
Q

causes of Cardiac insuffiency/failure

A
  1. Reduced stroke volume, CO
    -reduced preload (ex. hypovolemia, HCM), impaired contractility (ex. DCM)
    -increased afterload (hypertension)
    -poor valve function
  2. Abnormal rates
    -bradycardia
    -tachycardia- not enough time for heart to fill, so SV and CO decrease
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7
Q

Heart failure symptoms

A

1.cardiomegaly

  1. Left ventricular failure
    -blood accumulates in lungs
    -pulmonary edema
    -poor peripheral perfusion

3.Right ventricular failure
-leads to edema in venous side
-SQ edema, ascites, hepatojugular reflex

**Failure on one side often leads to failure on the other side

  1. Arrhythmias (especially tachycardia)
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8
Q

Pimobendan

A

-phosphodiesterase inhibitor leads to increase in cAMP

-positive inotrope
-arterial vasodilator
-may enhance cardiac contractile protein sensitivity to calcium
-induces well being and increases appetite

**shown to increase survival/reduce morbidity in dogs with DCM or mitral valve insufficiency

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9
Q

Digoxin

A

-digitalis glycosides isolated from foxglove

-positive ionotropic effect
-negative chronotrophic (HR) and dromotropic (speed) effect
-increased parasympathetic tone; decreased sympathetic tone/ baroreceptor

-secondarily leads to increased peripheral tissue perfusion (eg. increased renal output)

**highly toxic!

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10
Q

Digoxin mechanism

A

1.inhibits Na/K ATPase. Leads to increase in Na. Increased Na causes Na/Ca exchanger to bring more Ca in to get rid of Na. Leads calcium induced calcium release= more calcium= enhanced contraction

2.Negative HR and speed because inhibits Na/K pumps in SA and AV nodes. Means it takes longer for everything to reset=increased refractory period. Longer for excitation to move through perkinjie fibers and reset

  1. Increased stretch on baroreceptors= decrease in sympathetic activation
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11
Q

Side effects of digoxin

A

-death
-anorexia
-vomiting and diarrhea
-AV block or ventricular arrhythmias
-hypokalemia can precipitate arrhythmias

**hyperkalemia blocks digoxin effects because high K will force Na/K to override and continue to function

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12
Q

Dobutamine

A

-causes positive inotropic actions via beta 1 adrenergic receptor agonist action

**Emergency use only
-arrhythmogenic

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13
Q

Dobutamine mechanism

A

Acts to increase stimulation of beta 1 adrenergic receptors resulting in increased cAMP, increase in Ca and therefore increase in myofibril contraction

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14
Q

Beta blockers in heart failure

A

Useful in chronic treatment of hypertrophic cardiomyopathy because:
-positive inotropes generally contraindicated
-often HR so high and heart wall so rigid that diastolic filling impaired
-blocks effects of compensatory overactivation of heart by sympathetic nervous system

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15
Q

Increasing use of beta 1 and alpha 1 antagonists

A

inhibition of alpha 1= reduces afterload

inhibiting beta 1 leads to normal treatment of beta blockers on heart failure

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16
Q

Why are beta blockers useful in both HCM and DCM?

A

They inhibit the beta1-stimulated renin release

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17
Q

Vasodilators

A

-ACE inhibitors

-Angiotensin type 1 receptor antagonists

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18
Q

ACE inhibitors

A

-enalapril, benazepril, imidipril

-prevent the formation of Ang II from Ang I by inhibiting angiotensin converting enzyme

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19
Q

Angiotensin type 1 receptor antagonists

A

-valsartan
-telmisartan

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20
Q

ACE inhibitors and AT1 receptor blockers function

A
  1. Vasodilation- reduce venous and arterial pressure and therefore edema
  2. Prevent aldosterone release and therefore decrease fluid retention/edema
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21
Q

Enalapril results

A

shown to significantly decrease clinical symptoms and extend survival time by 92% in dogs

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22
Q

Effects on RAAS system

A
  1. Beta adrenergic receptor antagonists- work in kidneys to prevent renin release
  2. Angiotensin receptor inhibitors (ARBs)
    - prevent Ang II effects on arterioles= no vasoconstriction
    -prevent Ang II effects on adrenal cortex- No aldosterone
  3. ACE inhibitors
    -prevents break down of bradykinin to inactive products
    *sometimes presents as tickle cough due to irritation from bradykinin inflammation/accumulation
23
Q

Tickle cough vs. productive cough

A

Productive cough linked with heart failure, fluid accumulation/edema.

Tickle cough=minor side effect to ACE inhibitors?

24
Q

Vasodilators for acute and/or severe cases

A

-nitroglycerin (venodilator)= metabolized into NO=dilation

-sodium nitroprusside (arteriolar/venodilator)- broken down into NO

25
Q

Older, cheaper vasodilators

A

1.alpha blockers (prazosin)- mainly arteriolar some venodilation

2.direct acting arteriolar dilators (hydralazine)- veno and arteriolar dilator

26
Q

Negative effects from vasodilators (older and acute, severe treatment drugs)

A

-excessive hypotension
-reflex tachycardia
-excessive activation of RAAS

**better for short term use, then move to other drugs for long term once more under control

27
Q

Vasodilator therapy options

A

1.ACE inhibitors- Prevents Ang II formation and therefore Ca levels and contraction
2. alpha 1 adrenergic receptor antagonist (prazosin)- prevents contraction from prevention of increased Ca
3. Direct acting smooth muscle relaxant- decreases Ca

28
Q

Drug therapy to increase NO

A

All drugs that can be used to form NO
-eg. Nitroprusside, nitroglycerin, isosorbide dinitrate

NO will result in increased vasodilation and relaxation

29
Q

Nitroprusside

A

-can be dangerous because also contains cyanide. Need to be limited in use… short term only!

30
Q

Phosphodiesterase inhibition on NO pathway

A

Ex. slidenafil

-Can result in prevention of degradation from cGMP to GMP and vasodilation

31
Q

Diuretics in heart failure therapy

A

Used for treatment of pulmonary edema
-beware of excessive diuresis leading to excessive loss of venous return
-beware of hypokalemia potentiating digoxin action

32
Q

Digoxin use

A

-heart failure and atrial fibrillation

-results in positive inotrope, negative chronotrope and dromotrope

33
Q

Mechanism of action of digoxin

A
  1. inhibits Na K ATPase
  2. increases intracellular Ca via Na/Ca exchanger
34
Q

Dobutamine use

A

-acute treatment of severe heart failure

-postive inotrope

35
Q

Dobutamine mechanism of action

A

beta 1 agonist

36
Q

Arrhythmias

A

-tachycardia
-bradycardia
-fibrillation
-conduction abnormalities

37
Q

Tachycardia

A

-heart rate too high

38
Q

Bradycardia

A

-heart rate too low

39
Q

Fibrillation

A

uncoordinated, rapid excitation/contraction

40
Q

Depolarization channels

A
  1. Phase 1: Depolarization of cell= influx of Na
  2. Phase 2: Depolarization=influx of Ca
  3. Phase 3: K efflux decreases membrane potential
  4. Phase 4: resting membrane potential (Na/K ATPase returns to normal)
41
Q

Phase 4 in Pacemakers

A

-Channels (Na and Ca funny channels) slowly leaking resulting in slow depolarization

42
Q

ECG

A

p wave= atrial depolarization
excitation occurs in SA node, passes to AV node. Small pause, then further passing on to purkinje

QRS wave: depolarization and excitation of purkinje and ventricles

T waves= repolarization

43
Q

Supraventricular tachycardia

A

Increased automaticity- caused by any change that decreases the time required for depolarization from the max diastolic potential to the threshold potential

44
Q

Premature ventricular contraction leading to ventricular tachycardia

A

Arise from damaged ventricular myocytes affecting repolarization
-often due to leaky Ca channels which excite ventricles pretty quickly after resting phase (therefore not all channels have reset)

Results in another QRS prior to the next P wave causing excitation

45
Q

Damage to purkinje fibers= ventricular tachycardia

A

-Damage to branches so spread is stopped to damaged side. So get normal side excitation and then spread to the damaged side…sets up self excitation loop. Will be at a higher excitation than normal

**most likely common cause of ventricular tachycardia

46
Q

Anti-arrhythmic drugs class I mechanisms

A

-Na channel inhibitor
-decreases Na current, prolongs QRS= reduced HR and cardiomyocyte excitability

ex. Quinidine, Procainamide, Lidocaine

47
Q

Effects of Class I anti-arrhythmics

A

1A: all cells; effects rate of depolarization/ amount needed to get action potential. Prolongs QRS and QT

1B: targets damaged ventricular myocytes. Drugs bind to Na channels that are not completely reset in resting membrane effect. No large effect

1C: targets all cells but prefers conduction cells. Slows rate of depolarization= prolongs QRS, QT

48
Q

Use of class I anti-arrhythmics

A

-mostly ventricular arrhythmias, mostly tachycardias

-some use in supraventricular arrhythmias

49
Q

Procainamides in dogs

A

-dogs have poor acetyltransferase and therefore this drug not well used in canines

50
Q

Class II anti-arrhythmics

A

-beta 1 adrenergic receptors antagonist

-results in negative chronotrope, domotrope, and inotrope

-metoprolol, atenolol

51
Q

Class III anti-arrhythmics

A

-K channel inhibitors (and some effects on beta adrenergic receptors and Na channels depending on drug)

-results in decreased K, therefore prolonging repolarization phase and reducing heat rate
-prolong refractory period

-amiodarone, bretylium, sotalol

52
Q

Class III anti-arrhythmics effects

A

-prolongs QT interval

53
Q

Class IV anti-arrhythmics

A

Ca channel inhibitors

-results in decrease Ca = negative chronotrope= slow spontaneous depolarization in pacemaker cells
-also some decrease in inotrope

-verapamil, diltiazem

54
Q

Effects of Class II and IV anti-arrhythmics

A

-prolonged PR and PP intervals

-decrease spontaneous depolarization prolonging time it takes for P wave to appear.

Pharmacology (19 decks)

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