Don's Lecture 10-13
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| show | atrial, ventricular, and specialized exciatory and conducting muscle fibers
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| atrial and ventricular muscle fibers contract the same as skeletal but | show 🗑
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| excitatory and conductive fibers exhibit | show 🗑
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| cardiac muscles are | show 🗑
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| cardiac muscle fibers are arranged in | show 🗑
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| show | actin & myosin filaments like skeletal muscle
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| show | cell membraines that seperate individual cardiac muscls from one another and form permeable gap junctions
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| Purpouse of intercalated discs and gap junctions formed | show 🗑
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| show | where cardiac cells are so interconnected, that when one cell becomes excited, the AP then spread throughout the lattice work.
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| show | atrial (2 walls of atria) and ventricular (2 walls of ventricle)
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| show | fibrous tissue and surrounds AV valves
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| show | atrial synctium to the ventricle synctium via the A-V bundle.
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| show | allows for the conduction from atria to ventricles
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| show | to contract a short time before ventricles
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| show | longer (15X)
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| show | higher more negative -70 to -90.
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| show | plateau
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| show | squeeze
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| show | fast Na+ channels & slow Ca++ channels (skeletal has only fast Na+)
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| Calcium channels are | show 🗑
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| show | depolarization or plateau
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| In addition the calcium that is entering the cell from these slow Ca+ channels also | show 🗑
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| Immediately after the onset of AP, the K permeability decreases causing | show 🗑
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| show | there is a rapid outflux of K+ and cell reaches resting potential.
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| show | 0.3 - 0.5 m/second
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| Velocity of perkinje fibers | show 🗑
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| Refactory period | show 🗑
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| Relative refractory period | show 🗑
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| Excitation coupling mechanism of cardiac muscle (mechanism by which AP causes contraction) | show 🗑
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| show | in the SR membrane, activated by influx of Ca++ and triggers a further release of Ca++ into the cell.
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| show | The SR in cardiac muscle is less developed than in skeletal, and not enough Ca++ would be provided for adequate contraction
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| show | T-tubles are larger in diameter, allowing for more Ca++ to diffuse in.
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| Strength of cardiac contraction is determined by? | show 🗑
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| show | Ca++ in skeletal muscle is release from SR inside the cell.
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| At end of plateau of the AP, influx of Ca++ is | show 🗑
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| 2 types of cardiac action potential | show 🗑
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| show | in R atrium near opening of the superior vena cava.
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| show | SA node
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| show | K+, Na+ and Ca+
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| SA spontaneous firing rate is | show 🗑
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| show | RIGHT vagus nerve
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| spontaneous SA rate can also be changed by | show 🗑
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| show | LEFT vagus nerve
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| show | recieves sensory input sending out PSNS (vagus) and SNS stimulation to heart to release catecholamines.
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| show | the atria to contract first before the ventricles
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| show | relation or filling
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| systole | show 🗑
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| show | no change in volume, ventricles are relaxed and the AV and semilunar valves remain closed
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| Ventricular filling or diastole | show 🗑
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| show | 110-120 mL in a normal heart
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| Isovolumetric Contraction in ventricular systole | show 🗑
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| S1 or "lub" | show 🗑
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| Ventricular ejection | show 🗑
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| Ventricular relaxation | show 🗑
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| show | dicrotic notch
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| AV (mitral & tricuspid) valves prevent backflow of blood from ventricles to atria during | show 🗑
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| Semilunar valves (aortic & pulmonic) valves prevent backflow from aorta and pulm areries into the ventricle during | show 🗑
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| Valves close when | show 🗑
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| Valves open when | show 🗑
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| AV valves are specialized b/c | show 🗑
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| purpose of the chordae tendinea | show 🗑
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| show | they have rapid closure (snap shut) due to a smaller opening in comparison to AV valves. Much more wear and tear on these valves.
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| CO = | show 🗑
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| show | volume of blood ejected per beat - if normal heart around 70.
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| Aortic stenosis patients are complicated to tx because | show 🗑
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| show | 1. Preload 2. Contractility 3. afterload
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| Preload | show 🗑
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| show | Greater the stretch, greater the contraction (withing reason, overstretch and will have problems)
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| show | preload
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| show | inotropic fx or chemical factors. Na+, K+, CALCIUM (biggest fx), epiniephrine, thyroxine
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| afterload | show 🗑
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| show | Afterload
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| Dehydrated, increased H&H, hypovolemic | show 🗑
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| Conditions that alter CO | show 🗑
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| show | causes heart to dialate and becomes flaccid. Slows HR, can block conduciton throug AV bundles, making contraction very weak
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| Heart effects from increased Ca++ | show 🗑
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| show | heart becomes flaccid
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| S1 | show 🗑
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| S2 | show 🗑
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| Split S2 | show 🗑
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| show | supplies anterior and L lateral portion of the L ventricle
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| RCA | show 🗑
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| Coronary circulation dependant on | show 🗑
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| show | diastole
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| How to improve collateral circulation | show 🗑
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| show | tachycardia and hypotension, (supply/demand)
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| Coronary circulation most important factor is a good | show 🗑
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| show | Cardiac output
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| Vasomotor center regulates | show 🗑
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| Cardiovascular center gets information from | show 🗑
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| Baroreceptorss are located | show 🗑
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| Chemoreceptors | show 🗑
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| show | 1.) juxtaglomerular cells secrete renin in kidneys. 2.) changes angiotensinogen to angiotensin I 3.) angiotensin I is converted to angiotensin II in lungs which constricts vessels & stim secretion of aldosterone from adrenal cortex
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| show | to hold onto Na+, H2O follows salt increasing blood volume.
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| show | secreted by hypothalamus, increases volume
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| Aterial natriuretic (ANP) | show 🗑
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| show | secreted by endothelial cells, causes vasodilation. Sets tone in blood vessels. Most potent vasodilator in the body.
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| Electrical current | show 🗑
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| show | measures electrical current, = coulombs/second
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| EKG measures | show 🗑
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| Phase I Action Potenial ions are | show 🗑
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| show | Ca+ in (plateau) K+ delayed to release but starts its move
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| Phase III of AP | show 🗑
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| Phase IV of AP | show 🗑
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