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29 Cards in this Set
- Front
- Back
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what accounds for the two heart sounds
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1st=begining of systole when AV (mitral, tricuspid) valve close, loudest at apex; 2nd=end of systole when aoric and pulmonic (semiunar) valves close, loudest at base
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describe the three types of cells foudn in the myocardium. Give thier location and function
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1. myocardial muscle in atria and ventricles generates force 2. conducting cells in the budle of HIs and purkinje fibers coordinate contraction by conducting the depolarization 3. Pacemaker cells in the SA and AV node initiate the heartbeat and controal heart rate
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What is the significance of intercalated discs in cardiac muscle
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the ID's are gap junctions that have low electrical resistance and allow ions to flow from cell to cell. This enables syncytial spread of action potential from cell to cell
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Describe the structure of the syncytia of the heart
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1. Atrial syncytium with anteror (bachmann) middle (wenchkebach) and posterior (thorel) tracks 2. AV node to AV bundle, slows conduction to allow atria to contract before ventricles 3. Bundleof His dristributes current to ventricles from bottom up 4. ventricular syncytium
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How does the peak voltage of the AP of cardiac muscle compare to that of skeletal
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cardiac mucle peaks ~15x higher
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Where does the calcium for cardiac muscle contraction come from
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The cardiac SR needs external "trigger calcium" to enter the cells via the L type Ca channels during the plateau phase of each AP to initiate Ca-induced Ca release, Ca is released form both the SR and the T tubules (which are much bigger than those in skeletal muscle)
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Explain how calcium initiates a contraction in cardiac muscle
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The AP spreads to the interior of the muscle fiber along the T tubule and then longitudinally along the SR. Extracellular calcium triggers release of Ca fro the SR, the Ca combines with troponin C. Troponin C undergoes a change in conformation and tugs on tropomyosin to expose the active sites of the actin. Myosin attaches to the actin and a contraction occurs
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define end diastolic volume
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Volume of blood in ventricle after filling 110-130 mL
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define stroke volume
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volume of blood ejected as ventricles contract during systole 70-90mL
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define end systolic volume
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volume of blood left in ventricles after contraction 40-50mL
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How is stroke volume calculated
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SV=EDV-ESV
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how is ejection fraction calculated
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EF=SV/EDV (what fraction of possible blood was actually ejected), normal is >55%
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how is stroke work calculated
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volume pressure work +acceleration of blood, w=SVxP +1/2mv^2
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Extrinsic control of the heat occusr via the sympathetic and parasympathetic nervous systems. What are three ways these systems can regulated the heart
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1. chronotropic-heart rate 2. inotropic-strength of contraction 3. lusitropic-rate of relaxation
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SV is determined by ESV and EDV. What are three factors that affect theses volumes and which does each factor effect?
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1. preload affects EDV 2. contractility and 3. afterload affect ESV
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describe the shape you would expect to see in a graph of ventricular output vs atrial pressure for the right and left ventricles
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The graph would show identical outputs but the right ventricle would be shifted left becasue it operates at lower volumes
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what parts of the heart does each division of the autonomic nervous system affect
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sympathetic- right and left ventricles increases both HR and SV, parasympathetic (vagus nerves)= SA and AV node
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how would an increase in afterload affect the shape of the pressure volume curve
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the curve would become taller and narrower, the stroke volume would decrease beacuse increased afterload decreases the amount of blood that can be ejected
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How would an increase in preload affect the shape of the pressure volume curve
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the curve would extend right because an increase in preload increases the stroke volume because EDV is higher
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how would a change in contractile state affect the shape of the pressure volume curve
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The curve would extend left because end systolic volume is lower, the curve would be wider because the stroke volume is increased because more blood is being squeezed out of the heart
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compare the action potential of the SA node to that of a ventricular myocyte
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The AP in the SA node has a more gradual rise and no plateau
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how long is the delay between the initiation of an AP in the SA node and the arrival of the impulse at the ventricle
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0.16 seconds, corresponds to the P-Q interval on the ECG
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why is the fibrous band between the atria and ventricles important
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the band acts as an insulator and forces the current to run through the conducting system rather than read randomly over the muscle. this allows for the coordianated contraction and twisitng motion of the ventricles
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what affect would excess potassium in the ECF have on the heart
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Excess potassium causes the heart to become dilated and flaccid and slows the heart rate. large quantities can block conduction of the impulse from the atria to the ventricles via the AV bundle. The high potassium in the ECF decreases the resting membrane potential/ partially depolarizes the cell. This decreases the intensity of the action potential and makes contraction of the heart weaker
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What afffect would an excess of Ca ions in the ECF have on the heart
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Extra calcium in the ECF has the opposite effect of K, extra Ca leads to spastic contraction because of the direct effect of Ca ions to initiate cardaic contraction
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What affect would a calcium deficiency have on the heart
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Cardiac flaccidity similar effect to that of potassium
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What affect does increasing atrial pressure have on cardiac output
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Little until it passes about 160mmHg, this emphasises that during normla function of the heart the cardiac output is determined almost entirely by the venous return rather than the afterload
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why do SA node and ventricular muscles have differnt shapes of AP upstroke
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The upstroke in the ventricle is rapid because it is caused by opening of fast sodium channels leading to rapid depolarization. In the SA nodes, these channels are inactive because of the less negative resting membrane potential. The more gradual depolarization in the SA node is due to the slow Na/Ca channels opening.
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Why is there a plateau in the ventricular AP but not in the NA nodal
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The plateau in the ventricular AP is cuased by the opening of th eslow Na/Ca channels. This does not occur in the SA node because these channels are responsible for the initial upstroke
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