Lecture 08 - Ventricular Function

Lecture 08 - Ventricular Function - L ecture 08 Ventricular...

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Lecture 08 - Ventricular Function Cardiac Output Cardiac Output (CO) = Heart Rate x Stroke Volume Normal CO (in man): Rest= 6.0 L/min +/- 1.3 Exercise - Can increase C.O. 400% (4-fold) Normalize CO to Metabolic Rate Normalize to compare people with different height/ body surface area Body Surface Area (BSA) BSA (M 2 )=0.007184 x weight 0.425 (kg) x height 0.725 (cm) Cardiac Index (CI) = CO / BSA ( normalized cardiac output) Normal CI = 3.4 ± 0.8 L / min / M 2 (2.6-4.2) Four Determinants of cardiac performance o Intrinsic properties of the heart (contractility) Functional Properties of the Myocyte and Heart - We try to understand how the cell start to collate with the intact heart - Mouse/human contracts the same Properties of Cardiac Muscle o The weight at the bottom is the preload Apparatus to measure force in a papillary muscle - o Think of this as a sacromere with 1.7 micrometers (if you do something to change it to 21 micro meters adding weight or you can add the microman and watch it contract Resting Cardiac Muscle Properties - o Passive force analogous to filling the ventricle , i.e. diastolic pressure or preload o Increase the preload and you’ll raise up the line o Raises exponentially with increasing sarcomere length Isometric Contraction: (iso=same, metric=length) - Muscle is stimulated (the man coming in to stimulate it), twitch occurs and force develops but shortening is PREVENTED. Force and Sarcomere Length - o Passive force is set by the stretch of the o Active force when we stimulate the Length-tension curve: Active tension (force) is Initial Sarcomere Length - - As we increase the length of the muscle increases tension - The descending limb never occur in cardiac muscle or intact heart - Concept of change in length before the heart contracts starling relationship Sliding Filament Model of Muscle Contraction - o If the muscle is stretch is at 3.7 microns there is no overlap between the two o 1.7 micron the thick and thin overlaps Key points: - Isometric contraction – twitch occurs, NO shortening - Active tension of the isometric muscle is set by the intiail sarcomere length or PRELOAD - Length changes in the muscle (both shortening and lengthening) occur by the relative sliding of the thick and thin filaments past each other. - Maximal overlap of cross-bridges between thick and thin filaments occurs at 2.2 μm. - The relaxed cardiac myocyte (no distending force) assumes a sarcomere length of about 1.7 μm - < 1.7 μm, thick filament hits the “Z-line” and recoils. - Cardiac muscle does not operate on the “Descending Limb” of the length-tension (force) curve (as compared to skeletal muscle) - Below 2.0 μm thin filaments from opposite sides of the sarcomere overlap and cross-bridge interaction is disrupted, leading to reduced force . This is termed: o Filament Interference: o Length-Tension and Cardiac Muscle: Length-Dependent Activation (or length-dependent Ca 2+ sensitivity) - o Stretching cardiac muscle lead to increase force that is out of proportion simply to the number of cross bridges
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o Why isn’t this curve is not linear =
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