Cardiovascular 1 Flashcards
(41 cards)
when does heart disease become heart failure?
Heart disease becomes heart failure when the heart is unable to meet the body’s oxygen (metabolic) requirements
what is congestive heart failure?
when the heart cannot compensate for reduced CO resulting in venous congestion and edema
What causes the heart to fail?
- 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
preload
-work or stress the heart faces at the end of diastole
afterload
-resistance against which the heart must pump at systole
contractility
-the capacity of myocardium to contract
distensibility
-how easily the ventricles relax and fill
contraction synergy
-correlated/cooperative contraction of heart chambers
p What are the determinants of heart failure?
(1) preload
(2) afterload
(3) contractility
(4) distensibility
(5) heart rate
(6) contraction synergy
BP relationship to CO
CO x TPR
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CO = SV x HR
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- Reduced CO perceived as a decrease in mean arterial pressure (BP)
R-A-A-S activity - effects on the cardiovascular system
n increase Vasoconstriction
n increase Blood volume
SNS activity - effects on the cardiovascular system
n increase HR
n increase Contractility
n increase Vasoconstriction
n increase Renin
Congestive heart failure will manifest how?
clinical signs suggestive of poor cardiac performance:
- tachycardia
- decreased exercise tolerance
- peripheral and pulmonary edema
> dyspnea
- cardiac enlargement
- hypotension
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
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q Full attainment of these goals are currently not possible; approach management with two aims:
q Improve hemodynamic performance
q Modify vascular volume
Positive Inotrope drug types
- Na/K-ATPase Blockers
- Drugs that increase cAMP
- Caclium sensitizers
types of drugs that decrease preload
- diuretics
- venodilators and mixed vasodilators
drug classes that decrease afterload
- arteriodilators and mixed vasodilators
drug classes that treat reduced distensibility
- beta-adrenergic blockers
- Ca2+ channel blockers
mechanism of positive inotropes
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)
disadvantages and contraindications of positive inotropes
Disadvantages
- increased myocardial oxygen consumption
- Arrhythmogenic
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Contraindicated
- Valvular stenosis
- Cardiac tamponade
- HCM
Positive Inotropes
- i) Drugs that increase myocyte cAMP
beta-agonists (Sympathomimetics):
- Dobutamine
- Dopamine
b-agonists (Sympathomimetics) mechanism, drawback
increase cAMP > increase intracellular Ca2+
> interaction of actin and myosin
> increase contractility
> However progression of heart failure and mortality often increases
Dobutamine
- use
- admin
- receptors
- concerns
- 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
Dopamine
- use, preference
- effects based on dose
- 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