Term
| 3 component model of muscular contraction |
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Definition
1. Contractile element
2. Series Elastic Element
3. Parallel Elastic Element (tension supporting unit, maintains the geometry of the myocardium)
CE contracts, which pulls on the series elastic element and elongates it. However, the total length of the contractile unit stays the same until it generates a force greater than the afterload (isometric contraction). After it generates a force larger than the afterload, then the total contractile unit shortens (isometric contraction). |
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Term
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Definition
Force the contractile unit must overcome in order to isometrically contract and shorten. In heart, the left ventricle needs to overcome BP and valves (afterload) in order to open aortic valve and eject blood.
Has both intrinsic and extrinsic factors. |
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Term
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Definition
1. Depolarization triggers opening of Ca channels in sarcolemma.
2. CICR from sarcoplastic reticulum.
3. Binds to troponin C which moves tropomyosin in groove to expose actin binding sites.
4. Once contraction is over, Ca is actively resequestered inside the sarcoplastic reticulum. |
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Term
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Definition
| Overexpression of myosin leads to thickening of the myocyte. |
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Term
| Factors affecting Cardiac Output |
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Definition
1. Contractility
2. Preloading
3. Afterloading
4. Heart rate |
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Term
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Definition
| Force of contraction is proportional to fiber length, the more stretched a muscle fiber is, the more forcefully it will contract, acts like a rubber band. Preload measured by the wall stress at the end of diastole. |
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Term
| Factors affecting heart rate |
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Definition
| Autonomic regulation and peripheral metabolic requirements. |
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Term
| Factors affecting contractility |
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Definition
1. Sympathetic innervation
2. Heart rate
3. Strength of myocyte |
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Term
| Factors affecting preloading |
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Definition
| Venous return, the more EDV, the more forceful the contraction due to Starling law. |
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Term
| Cardiac modification of Ohm's law |
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Definition
I=V/R
CO=BP/R
Can lower the amount of work the heart has to do by lowering BP (afterload). |
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Term
| CO of right and left ventricles |
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Definition
They are the same (5L), must match each other.
Right ventricle is in pulmonary (low pressure) circuit, doesn't need to contract as forcefully to pump same amount of blood (less afterload).
Therefore, left ventricle has thicker muscular wall. |
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Term
| Clinically common reasons for increased afterload |
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Definition
1. Hypertension
2. Valvular (aortic) stenosis
3. Age
Heart needs to work harder to pump out same CO and SV, leads to LVH (form of hypertrophic myopathy). |
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Term
| Internal determinants of afterload |
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Definition
| Mainly consists of wall stress, less significant than extrinsic factors of afterloading. |
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Term
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Definition
Calculated by Law of LaPlace
(Pressure x Radius)/ (2x wall thickness)
Determines preload. |
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Term
| Extrinsic factors of afterloading |
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Definition
1. Aortic compliance (elasticity)
2. Vascular resistance
3. Impedance |
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Term
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Definition
Increased afterload (from high BP, etc.) leads to myocyte that is larger in volume but not in length.
Both concentric and eccentric hypertrophy results in fibroblast and collagen proliferation. |
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Term
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Definition
Regurgitant valves lead to blood moving back from semilunar valves to ventricles, increases EDV and myocyte length.
Both concentric and eccentric hypertrophy results in fibroblast and collagen proliferation. |
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Term
| Drug interventions for restored ventricular function |
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Definition
| High EDV and ventricular filling combined with low SV is sign of congestive heart failure. Can use drugs such as ionotropic agents (make heart contract more forcefully) and vasodilators (lowers afterload) to increase stroke volume to normal levels. |
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