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147 Cards in this Set
- Front
- Back
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semilumar valves prevent backflow by structure. AV valves prevent backflow by chordae tendonae
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right AV is tricuspid
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left AV valve
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bicuspid
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aortic and pulmonary semilunar valves have 3 lobes
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right atrium get blood from
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inferior and superior vena cava
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Cardiac pacemakers depolarize in response to an influx of Ca++
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to an influx of Ca++
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Contractile cardiac cells depolarize due to an influx of
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Na+.
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what plays a role in the prolonged depolarization of contractile cells.
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Ca++.
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Plateau period of cardiac cells is vital for complete pumping and allows ventricles to fill.
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6 regions of autorhythmic cells in elec cond. system: SA node, internodal pathway, interarterial pathway, AV node, bundle of His, and Purkinje fibers
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SA node
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right atrium, normal pacemaker of heart.
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Interatrial pathway
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goes from SA node in right atrium to the left atrium to make sure both depolarize together.
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Internodal pathway
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conducts action potential from SA to AV node.
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AV node
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small bundle of cells at the junction of the atria and ventricles. Only point where action potential from SA node can spread to ventricles.
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Bundle of His
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goes from AV node down the interventricular septum and transfer action potential to Purkinje fibers
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Purkinje fibers
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go from bundle of His to ventricles
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AV nodal delay makes sure ventricles fill.
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Whatever cell has the fastest inherent rate of depolarization is the pacemaker because if it goes off it will set everything else off. SA has fastest rate so it is the pacemaker.
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Inherent SA pacemaker
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70-80bpm
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Inherent AV pacemaker speed
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40-60 bpm
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speed the heart (ventricles) would beat at if the bundle of His was acting as the pacemaker pacemaker
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20-40 bpm
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If AV node is damaged
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Atria go at 70 bpm. Purkinje fibers make ventricles go much slower about 30 bpm.
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Ectopic focus
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A normally slower functioning tissue becomes excited and sets a faster pace.
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P wave
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atrial depolarization
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PR segment
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AV nodal delay
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QRS complex
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ventricular depolarization (atria repolarizing as well)
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ST segment
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ventricles contracting and emptying
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T wave
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ventricular repolarization
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TP interval
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time from vent repol. to atrial depolarization. ventricles relaxing and filling
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normal end diastolic volume
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about 135 mL
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Isovolumetric ventricular contraction
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none of the valves are open and ventricles are contracting. It lasts until the pressure of the ventricles becomes greater than that in the aorta and the valve opens
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end systolic volume
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about 65 mL
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dicrotic notch
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closing of the aortic vessel which makes the second heart sound.
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Frank starling law of the heart
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Increased venous return results in increased strength of contraction and increased stroke volume.
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stenotic valve
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narrowed valve that does not close completely
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heart failure
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inability of the cardiac output to keep up with demand
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epicardium
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thin external membrane covering the heart.
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endocardium
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lines entire circulatory system
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CHF
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inability for cardiac output to keep pace with need and blood dams up in the veins behind the failing heart
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diameter of systemic cappilaries
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7-10 microns
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venous blood is 60-70 in venules and small veins.
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arterial blood is 10 % of total blood.
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What buys time for the ventricles to fill
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slow conduction at the AV node
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myogenicity
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timing of sequential activitaion is a fxn of the ability of one group of cells to depolarize adjacent cells
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arterioles
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resistance vessels + controls distribution blood flow
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Venules & Small Veins
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capacitance vessels
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Large Veins
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collecting vessels that return blood to the heart.
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His Bundle & Bundle Branch System
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Composed of Purkinje Fibers. Specialized Ventricular Conducting System. – Purkinje Fibers can develop pacemaker
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Neural input can change heart rate, change activation, and change force of muscle contraction, but neural input not required
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Parameters that Determine Spread of Activation through Cardiac Tissue
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1. Rate of Rise and Amplitude of the Action Potential of Cells within a Tissue 2. Electrical Coupling among Cells – Presence and # of Low Resistance Junctions 3. Geometric Relationship among Cells with the Tissue 4. Refractory Properties of the Inward, Depolarizing, Current Channels
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Study slide 8 about different action potentials in the heart.
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Basic Principles in Understanding Ionic Generation of Cardiac Action Potentials
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1. Affect of inward and outward ionic current flow on the membrane potential referenced to the resting membrane potential (inside the cell negative). 2. For our purposes, current flow represents movement of + charge. • Inward ionic Current Flow Depolarizes the Cell – makes the inside of the cell less negative or more positive. • Outward ionic Current Flow Repolarizes the Cell – makes the inside of the cell less positive or more negative. 3. Depolarization occurs when there is net movement + charge into cell. 4. Repolarization occurs when there is net movement + charge out of cell.
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Ionic Current Carried by 3 ions and their ion Channels
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1. K ionic current through a number of K channels 2. Na ionic current through a few Na channels 3. Ca ionic current through a few Ca channels
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Depolarization of cardiac tissue
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Activation of Na and Ca Channels and Current Flow
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Repolarization
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Activation of K Channels and Current Flow
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Eq Ca++
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+30 mv
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Eq K for heart
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-95 mv
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P – R Interval
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Atrial – Ventricular Conduction time.
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Sympathetic stimulation of cardiac tissue
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increases the slope of the pacemaker potential
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Parasympathetic (vagal) stimulation of cardiac tissue
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Increases the maximum diastolic potential and decreases the slope of the pacemaker potential.
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ANS Affects on Conduction through the AV Node
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Effective refractory period
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The tissue behaves as if it is unexcitable. Action potential will not spread through the tissue.
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Relative refractory period
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Tissue is excitable but conduction velocity slowed & conduction time prolonged because time course for cell to cell spread of activation is prolonged
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If a cardiac cell is rel refract. it does not need a stronger stimulus to get it to depolarize.
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Absolute refractory period and diagram where on a graph of pressure in the ventricles the heart is absolutely refractory
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cell cannot be stimulated to produce an action potential. 2/3 of the time of the ventricular contraction the cells are in ARP.
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Maximum diastolic potential
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How far below the threshold for an action potential will go before it starts to depolarize again as seen in cardiac pacemaker cells.
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What determines Systolic Blood Pressure?
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What determines Diastolic Blood Pressure?
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Why is Systolic Blood Pressure higher than Diastolic Blood Pressure?
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If there is less volume of blood on the arterial side than on the venous side of the circulatory system, why is arterial pressure higher than venous pressure?
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Why are the arterioles considered the resistance elements within the circulatory system and not the capacitance elements?
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Why are the venules and small veins considered the capacitance elements within the circulatory system and not the resistance elements?
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If the capillaries are the smallest diameter blood vessels, why are they not the principle site of resistance to flow through the circulatory system?
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The outputs of the right and left hearts are equal over time. Why is the pressure in the pulmonary vascular system about 1/5 to 1/4 that of the systemic vascular system?
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Static Hemodynamic Properties
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Parameters that determine Pressure
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Pressure Function of
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1. Capacitance or Compliance of the vessels or chamber 2. & Volume contained within the capacitance or compliance Specifically, Pressure = Volume/Capacitance
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Dynamic Hemodynamic Properties
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Parameters that determine Flow (Vol/min)
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Flow Function of
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1. Pressure Gradient (P1 – P2) 2. & Resistance (Function of Length, Viscosity & Radius) Specifically, Flow = Pressure Gradient /Resistance
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Diagram the pressure wave associated with contraction
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1/3 is systole, 2/3 is diastole - half way through is dicrotic notch associated with closing of aortic valve
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Mean Circulatory Pressure
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average pressure for flow through Total Vascular System. dictated by the capacitance of the total vascular system and the total volume of blood contained within this capacitance
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What determines arterial and venous pressure when there is flow from the venous side to the arterial side of the vascular system?
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capacitance
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compliance - holding capacity
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resistance is a fuction of
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length, viscosity, radius.
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average resting pressure
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1/3 of 120 and 2/3 of 80
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What determines arterial and venous pressure when there is flow from the venous side to the arterial side of the vascular system?
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What do you predict will happen to venous pressure with decreases in volume as volume is transferred to the arterial side?
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What do you predict will happen to arterial pressure with the addition of this volume to the arterial side?
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What would you predict will happen to the relative magnitudes of pressure changes in the arterial and venous components with the transfer of a volume from the venous to the arterial components?
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Why, with the heart pumping, doesn’t the pressure in the vascular system return to the mean circulatory pressure between cardiac contractions & ejections of volume?
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Poisseulle’s Law
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Quantifies parameters that determine flow through a tube. Flow = Π/8 [(P1 – P2)R4]/Lη
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Contractility
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pressure generating capacity, the rate of cycling, of each Actin – Myosin Cross-Bridge.
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2 hearts anatomicall in parallel but functionally in series
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60-70% of blood in venules and small veins
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muscle cells
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generate pressure
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AV node is slow to provides time for atria to fill ventricles
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AV node has pacemaker cells but most of the time they are not activated
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HIS bundle and bundle branch system conducts electricity twice as fast as the conduction through the atria or ventricles.
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Time for conduction through the atria
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20-30 ms
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Time for conduction through the ventricles
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60-80 ms
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ventricular muscle mass compared to atrial muscle mass
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500-1000 times greater
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DEFINE EKG
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Neuro input can effect, heart rate, force of contraction and conduction
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Number of connexons has effect on time of conduction
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4 parameters for timecourse of spread of activation of the heart
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1) rate of rise of amplitude of action potentials. 2) electrical coupling among cells 3) geometric relationship of cells among tissues (straight line faster) 4) refractory properties of inward depolarizing current cells
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phase 4
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resting membrane potential - for SA nodal pacemaker cell it is the diastolic depolarization
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phase 0
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upstroke of cardiac action potential
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initial rapid repolarization
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phase 1
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plateau phase
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phase 2
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terminal repolarization
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phase 3
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duration of nerve AP vs cardiac AP
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1-2 ms for nerve 200-250ms for cardiac
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relative refractory period time duration for card. muscle
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30-50 ms and extends a little bit past the time where it reaches resting memb potential. Start of RRP is 2/3 of the peak contraction strength on the way down.
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cardiac cells are not all or none
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can get graded action potential during relative refractory period. Early in RRP the amplitude of an action potential would be small and it gets bigger as you go toward the end of the RRP.
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AV node can block or slow conduction to the ventricles
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have long absolute refractory period
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P wave
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sequential activation of atrial muscle (depolarization)
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QRS
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vent muscle depol.
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T
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replarization of vent.
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Do not see
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1) firing of SA node (too few cells) 2) activation of AV node or bundle branch 3) repolarization of atria because mass is too small and it takes too long
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if we see a P wave
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we know we had depolarization of SA node
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If we have P followed by QRS
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we can assume had spread through AV and His bundle bundle branch system.
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AV node depolarizes about
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middle of peak of P wave
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Why is the T wave positive?
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direction of repolization of T wave is opposite the direction of depolarization. Depolarization of ventricle starts at endocardium to epicardium. Repolarization goes from last part to be depolarized to the first part.
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PR interval
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Atrial conduction time. From inscription of P wave to activation of R wave. from activation of atrial to activation of ventricles. Changes by changes in AV nodal conduction time.
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Vent muscle contraction is Q wave
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EKG does not provide info about contraction of heart just about electronics.
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3 things you can assess from EKG
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1) Heart Rate 2) Rhythm 3) Conduction
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SA nodal pacemaker cells self depolarization to threshold
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diastolic depolarization or pacemaker potential
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How freq SA node depolarizes determines HR
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How does a heart speed up
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no change in maximum diastolic potential
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what increases rate (slope) of self depolarization to threshold
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sympathetic stimulation. This increases heart rate.
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Can parasympathetic stim stop heart
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yes
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How does parasympathetic stimulation effect heart
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Increases maximum diastolic potential; increases resting potentials closer to Eq pot. of K+. Slows rate (slope) of pacemaker potential.
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Stimulate Vagus nerve
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slow heart.
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different types of K+ channels have different times they stay open to effect timing of depolarization.
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parasympathetic effect on AV node
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can slow or even block conduction.
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sympathetic effect on AV node
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shortens conduction time, (P-R interval shortens)
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Effect on EKG when you have both sympathetic and parasymp.
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MUST BE ABLE TO SAY: what observe in EKG of parasymp effect to SA only, to AV only, or to both. What see in EKG if increase symp activity to SA pacemakers and not AV node. Increase in HR but not AV conduction time. MUST BE ABLE TO DRAW CONTROL AND THEN DRAW EFFECTS OF ALL OF THESE
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diameter of capillaries
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7-10 microns
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diff between systolic and diastolic
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pulse pressure.
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what determines pressure in arteries
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volume - capacitance is fixed
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If a fall in pressure from syst. to diast what happened
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volume decreased
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average arterial pressure
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93 mm Hg
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average venous pressure
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5 mm Hg
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average venule pressure
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10 mm Hg
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mean circulatory pressure
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average pressure for total vasc system. Measured when heart is not pumping. The reason for the pressure when the heart is not functioning is because the volume of blood stretches the entire system.
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start heart pumping again what happens to venous and arterial pressure?
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venous pressure goes down arterial goes up. Change in aterial pressure is greater than change in venule pressure because arterial capacitance is low
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