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3. Clin Pharm 3 > Cardiovascular 1 > Flashcards

Cardiovascular 1 Flashcards

1
Q

when does heart disease become heart failure?

A

Heart disease becomes heart failure when the heart is unable to meet the body’s oxygen (metabolic) requirements

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2
Q

what is congestive heart failure?

A

when the heart cannot compensate for reduced CO resulting in venous congestion and edema

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3
Q

What causes the heart to fail?

A
  • Myocardial contractility failure
    > Weakened heart and reduced contractility
    => Dilated cardiomyopathy (DCM)
    => Taurine deficiency
    <><><><>
  • Systolic mechanical overload
    > Pressure versus volume overload
    => Altered preload and/or afterload
    => Valvular disorders
    <><><><>
  • Diastolic mechanical inhibition
    > Feline hypertrophic cardiomyopathy (HCM)
    > Pericardial disorders eg. pericarditis
    <><><><>
  • Electrical disorders
    > Dysrhythmias
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4
Q

preload

A

-work or stress the heart faces at the end of diastole

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5
Q

afterload

A

-resistance against which the heart must pump at systole

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6
Q

contractility

A

-the capacity of myocardium to contract

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7
Q

distensibility

A

-how easily the ventricles relax and fill

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8
Q

contraction synergy

A

-correlated/cooperative contraction of heart chambers

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9
Q

p What are the determinants of heart failure?

A

(1) preload

(2) afterload

(3) contractility

(4) distensibility

(5) heart rate

(6) contraction synergy

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10
Q

BP relationship to CO

A

CO x TPR
<><>
CO = SV x HR
<><><><>
- Reduced CO perceived as a decrease in mean arterial pressure (BP)

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11
Q

R-A-A-S activity - effects on the cardiovascular system

A

n increase Vasoconstriction
n increase Blood volume

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12
Q

SNS activity - effects on the cardiovascular system

A

n increase HR
n increase Contractility
n increase Vasoconstriction
n increase Renin

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13
Q

Congestive heart failure will manifest how?

A

clinical signs suggestive of poor cardiac performance:
- tachycardia
- decreased exercise tolerance
- peripheral and pulmonary edema
> dyspnea
- cardiac enlargement
- hypotension

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14
Q

Ideal approach to heart failure is to repair the primary abnormality
q Make the heart stronger if weak
q Make the heart fill better if indistensible
q Repair leaks if mitral or aortic valve insufficiency
<><>
q Full attainment of these goals are currently not possible; approach management with two aims:

A

q Improve hemodynamic performance
q Modify vascular volume

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15
Q

Positive Inotrope drug types

A
  • Na/K-ATPase Blockers
  • Drugs that increase cAMP
  • Caclium sensitizers
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16
Q

types of drugs that decrease preload

A
  • diuretics
  • venodilators and mixed vasodilators
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17
Q

drug classes that decrease afterload

A
  • arteriodilators and mixed vasodilators
18
Q

drug classes that treat reduced distensibility

A
  • beta-adrenergic blockers
  • Ca2+ channel blockers
19
Q

mechanism of positive inotropes

A

increase contractility > increase CO
<><>
- decreased SNS activity > decrease HR and TPR (afterload)
- increase renal blood flow > decrease R-A-A-S
> decrease edema and decrease blood volume (decrease preload)

20
Q

disadvantages and contraindications of positive inotropes

A

Disadvantages
- increased myocardial oxygen consumption
- Arrhythmogenic
<><><><>
Contraindicated
- Valvular stenosis
- Cardiac tamponade
- HCM

21
Q

Positive Inotropes
- i) Drugs that increase myocyte cAMP

A

beta-agonists (Sympathomimetics):
- Dobutamine
- Dopamine

22
Q

b-agonists (Sympathomimetics) mechanism, drawback

A

increase cAMP > increase intracellular Ca2+
> interaction of actin and myosin
> increase contractility
> However progression of heart failure and mortality often increases

23
Q

Dobutamine
- use
- admin
- receptors
- concerns

A
  • Use is limited to acute treatment of severe heart failure due to systolic dysfunction
    <><>
    Must be given by CRI in hospital setting
  • Onset of action is rapid (~2 min) as is offset due to short half-life (1-2 minutes)
    <><>
  • Direct b1-receptor activation; some b2 and a1
  • Tachycardia and arrhythmias are a concern
24
Q

Dopamine
- use, preference
- effects based on dose

A
  • Can also be used for short term tx in acute systolic heart failure— dobutamine preferred as less arrhythmogenic
    <><>
  • medium dose > increase inotropy
  • high dose > increase vasoconstriction
    <><>
  • Used in the management of acute oliguric renal failure in the dog
    > low dose > renal vasodilation
25
Q

Na+/K+-ATPase Blockers

A

Digoxin

26
Q

Digoxin
- type of drug

A

ii) Na+/K+-ATPase Blockers > cardiac glycoside

27
Q

Digoxin mechanism

A

Inhibits Na+/K+-ATPase pumps on myocytes
- Results in an increase in intracellular Na+ that decreases expulsion of intracellular Ca2+ from the Na+/Ca2+-exchanger
- Intracellular calcium levels increase and are sequestered in the sarcoplasmic reticulum
- Action potential sees greater calcium released, enhanced actin- myosin interaction and an increase in inotropy ie contractility
<><><><>
Beneficial effects of digoxin may also be due to increased vagal activity

28
Q

Digoxin
- use, replacement
- elimination

A

Use in the dog for heart failure has been replaced by Pimobendan as first line drug !!
- Used occasionally for treatment of heart failure in the horse
- May be used for treatment of arrhythmias (see arrhythmia notes)
- Primary route of elimination is renal excretion

29
Q

Digoxin toxicity and factors

A
  • long half life, hard to get out of the body when toxicity occurs
  • Narrow therapeutic range > monitor with TDM
  • Drug interactions > diuretics and hypokalemia
  • Arrhythmias: VPC’s, heart block, atrial & ventricular tachycardias
    > Ventricular arrhythmia’s > lidocaine
30
Q

Ca2+-sensitizers

A

Pimobendan

31
Q

Pimobendan mechanism

A
  • increase Ca2+-binding affinity of myocyte contractile proteins > increase inotropy without an increase in [Ca2+]IC
    > Effects do not increase MVO2 ie. myocardial oxygen consumption
    <><><><>
    Agents in this class also block PDE III enzymes
  • Produces balanced vasodilatory effects that can be beneficial in heart failure
  • These agents aka “Inodilators”
32
Q

Pimobendan seconday effects

A
  • Cytokine modulation
  • Positive lusitropy (rate of myocardial relaxation)
33
Q

pimobendan use

A

Licensed in dogs; valvular insufficiency & DCM
> Works rapidly; no additional monitoring needed

34
Q

pimobendan administration, safety, use with other drugs?

A
  • Available as oral capsule
  • Well tolerated and very good safety to date
  • Often used with diuretics, ACEi’s etc
35
Q

Drugs Used to Reduce Preload

A
  • Diuretics
  • Venodilators
36
Q

Diuretics
- what they do, which ones are commonly used?

A

Reduce fluid overload, resolve pulmonary edema in congestive heart failure
- Furosemide, Hydrochlorothiazide, Spironolactone

37
Q

Diuretics mechanism of action for heart failure
- dosing in combination?
- disadvantages?

A
  • Reduce preload primarily by diuretic effect
  • Furosemide venodilation aids acute relief of edema
  • Reduce initial doses of diuretics when combing agents—-furosemide and hydrochlorothiazide
  • Disadvantage is their activation of R-A-A-S
  • Hypokalemia and digoxin toxicity
38
Q

Venodilators
- ones we use

A
  • Nitroglycerin
  • Isosorbide
39
Q

Nitroglycerin mechanism of action for heart failure

A

At therapeutic doses is considered a selective venodilator > increase venous capacitance
<><>
- via relaxation of smooth muscle

40
Q

Nitroglycerin duration of action
- application

A
  • Nitrates tend to have a high first pass effect
  • Duration of action can be short (minutes)
    > ointment > apply to inner pinna
    > development of tolerance is possible with nitrates
41
Q

when are nitrates indicated?
used with what?
adverse effect?

A
  • Indicated in acute treatment of CHF
  • Usually used in conjunction with furosemide
    as nitroglycerin as monotherapy is limited
  • Hypotension can occur; headache in humans

3. Clin Pharm 3 (12 decks)

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