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50 Cards in this Set
- Front
- Back
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Heart muscel and resistance
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Has low resistance intercalated disks (1/400 the resistance of cell membrane
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Cardiac tissue electrically can be described as
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Cardiac tissue is an electrical syncytium
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Electrical threshold of cardiac tissue
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Resting membrane potential of cardiac muscle is -85 to -95 millivolts
Action potential is 105 millivolts Plateau lasts ~0.2 -0.3 sec in ventricular muscle (much longer than skeletal muscle) |
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Phases 0 - 4
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0-Fast Na+ channels open then slow Ca++ channels
1-K+ channels open 2-Ca++ channels open more 3-Resting membreane potential |
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Why don't atria trigger ventricles
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Fibrous insulator exists between atrium and ventricle
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Results of Action Potential
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Ca++ release from sarcoplasmic reticulum.
Ca++ release from T- tubules, which are large, are a very important source of Ca++. T-tubule Ca++ depends strongly on extracellular Ca++ concentration. Mucopolysaccharides bind Ca++. |
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EKG
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EKG - P - atrial depol QRS - Ventricular depol, atrial repol T - ventricular repolarization
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Systole
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Systole - muscle is stimulated by action potential and is contracting
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diastole
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muscle is reestablishing Na+/K+/Ca++ gradient and is relaxing
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Cardiac Cycle graph
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Isovolumic contraction
Ejection Isovolumic relaxation rapid inflow diastasis Atrial systole |
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Refractory period
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During During this time cardiac muscle tissue cannot be re-excited
Lasts 0.25-0.30 sec in ventricles Lasts 0.15 sec in atria |
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Excess K+
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lowers potential across the membrane and lessens likelihood of depolarization
causes dilation decreases contractility causes arrhythmias and fibrillation slows rate increases of 2-3x normal can block A-V bundle and cause death |
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Excess Ca++
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spastic contraction
opposite causes effects of K + |
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Atrial pressure waves
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a-wave - atrial contraction c-wave - ventricular contraction (A-V valves bulge) v-wave - flow of blood into atria
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Ventricular systole
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A-V valves close (ventricular press> atrial press)
Aortic valve opens Ejection phase Aortic valve closes |
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End diastolic volume (each ventricle
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120 ml
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End systolic volume
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50 ml
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Ejection volume (stroke volume)
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70 ml
120-50 (End diastolic volume - end systolic volume) |
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Ejection fraction
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70ml/120ml = 58% (Stroke volume/end diastolic volume)
normally 60%) |
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If heart rate (HR) is 70 beats/minute, what is cardiac output?
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HR X stroke volume = 70/min. X 70 ml = 4900ml/min.
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Total blood volume (ave
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5.5 liters
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If HR =100, end diastolic volume = 180 ml, end systolic vol. = 20 ml, what is cardiac output?
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C.O. = 100/min. * 160 ml = 16,000 ml/min
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Cardiac output
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HR X stroke volume
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Ejection volume (stroke volume)
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End diastolic volume - end systolic volume
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Valvular Function
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-To prevent back-flow.
-Chordae tendineae are attached to A-V valves. -Papillary muscle, attached to chordae tendineae, contract during systole and help prevent back-flow. -Because of smaller opening, velocity through aortic and pulmonary valves exceed that through the A-V valves. |
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Valvular Function and forces
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Work output is affected by preload (end-diastolic pressure) and afterload (aortic pressure)
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Frank - Starling
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states that the more the ventricle is filled with blood during diastole (end-diastolic volume), the greater the volume of ejected blood will be during the resulting systolic contraction (stroke volume).
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Pre-load and After-load
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preload is the volume of blood present in a ventricle of the heart, after passive filling and atrial contraction. reload is theoretically most accurately described as the initial stretching of cardiac myocytes prior to contraction. This cannot be measured in vivo. Preload is affected by venous blood pressure and the rate of venous return. These are affected by venous tone and volume of circulating blood
afterload is the tension produced by a chamber of the heart in order to contract |
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Sympathetic stimulation
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causes increased HR + increased contractility with HR = 180-200 and C.O. = 15-20 L/min.
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Parasympathetic stimulation
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decreases HR markedly and decreases cardiac contractility slightly. Vagal fibers go mainly to atria.
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Fast heart rate (tachycardia
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can decrease C.O. because there is not enough time for heart to fill during diastole.
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(allows atria to contract before ventricles)
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Impulse delayed in A-V node
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takes impulse into ventricles
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A-V bundle
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take impulses to all parts of ventricles
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Left and right bundles of Purkinje fibers
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S.A. Nodal cells
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Specialized cardiac/nerve cells within atrial muscle wall.
Acts as pacemaker because membrane leaks Na+ and membrane potential is -55 to -60mV When membrane potential reaches -40 mV, slow Ca++ channels open causing action potential. After 100-150 msec Ca++ channels close and K+channels open more, returning membrane potential to -55mV. Leaky |
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potentials
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sinoatrial (SA) node and travel across the wall of the atrium (arrows) from the SA node to the atrioventricular (AV) node.
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Discharge of a single atrial fiber compared to a ventricular fiber
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Resting potnetial, Threshold -40 mV, Na+ leak, slow Ca++channels open, K+ channels open more (~1 sec) Ventricular musecle fiber -72 mV (~0.5 sec)
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Internodal Pathways
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Transmit cardiac impulse throughout atria
Anterior, middle, and posterior internodal pathways Anterior interatrial band carries impulses to left atrium. |
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A-V Node
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Delays cardiac impulse
Most delay is in A-V node Delay AV node---0.09 sec. Delay AV bundle--0.04 sec |
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Purkinje System
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Fibers lead from A-V node through A-V bundle into Ventricles
Fast conduction; many gap junctions at intercalated disks |
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A-V Bundles
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Normally one-way conduction through the bundles
The only conducting path between atria and ventricles is A-V node and A-V bundle Divides into left and right bundles Transmission time between A-V bundles and last of ventricular fibers is 0.06 second (QRS time) |
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Discharge rates
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Normal rate of discharge in sinus node is 70-80/min.; A-V node - 40-60/min.; Purkinje fibers - 15-40/min.
Sinus node is pacemaker because of its faster discharge rate |
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S1
S2 |
AV valves close
Semilunar valves close |
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ST segment
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Depression: Ischemia
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1st, 2nd , 3rd degree AV blocks
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1.P-R exceeds 0.20 sec
2. only one out of several atrial waves get through the AV node 3. no atrial waves get through and venticles revert to baseline depolarization. |
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Main Arrival times
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S-A Node 0.00 sec
A-V Node 0.03 sec A-V Bundle 0.12 sec VentricularSeptum 0.16 sec |
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“Ectopic Foci
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This is a portion of the heart with a more rapid discharge than the sinus node.
Also occurs when transmission from sinus node to A-V node is blocked (A-V block). |
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Ectopic…
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During sudden onset of A-V block, sinus node discharge does not get through – and sinus is suppressed from previous over run, and next fastest area of discharge becomes pacemaker of heart beat (Purkinje system).
Delay in pickup of the heart beat is the “Stokes-Adams” syndrome. New pacemaker is in A-V node or penetrating part of A-V bundle. Person faints and/or dies |
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Parasympathetic effects
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Parasympathetic (vagal) nerves, which release acetylcholine at their endings, innervate S-A node and A-V junctional fibers proximal to A-V node.
Causes hyperpolarization because of increased K+ permeability in response to acetylcholine. This causes decreased transmission of impulses maybe temporarily stopping heart rate. Ventricular escape occurs.( Ventricles initiate their own depol |
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Sympathetic effects
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Releases norepinephrine at sympathetic ending
Causes increased sinus node discharge Increases rate of conduction of impulse Increases force of contraction in atria and ventricles |
