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61 Cards in this Set
- Front
- Back
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The heart is composed of three major types of cardiac muscle
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atrial muscle, ventricular muscle and specialized excitatory and conductive muscle fibers.
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syncytium is pronounced:
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sin sish' uhm
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action potential recorded in a VENTRICULAR muscle fiber averages about ___ mV which means that the intracellular potential rises from ____ mV to ____ mV
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averages about 105 mV
rises from -85 mV to +20 mV |
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After the initial spike, the ventricular muscle fiber remains depolarized for about:
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0.2 second, exhibiting a plateau followed at the end of the plateau by abrupt repolarization. This plateau in the action potential causes ventricular contraction to last as much as 15 times as long in cardiac muscle as in skeletal muscle
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The action potential of skeletal muscle is caused almost entirely by sudden opening of large number of _____
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fast sodium channels. Open for a few thousandths of a second and then abruptly close. At the end, repolarization occurs and the action potential is over within another thousandth of a second or so.
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In cardiac muscle, the action potential is caused by opening of 2 types of channels:
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1) fast sodium channels
2) slow calcium channels aka calcium-sodium channels |
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The slow calcium channels in cardiac muscle differs from the fast sodium channels in that they are
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slower to open and remain open for several tenths of a second. Lots of Ca+ and Na+ flow into the cardiac muscle & causes the plateau.
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Immediately after the onset of the action potential, the permeability of the cardiac muscle membrane for potassium ions
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decreases about fivefold. The decreased K+ permeability greatly decreases the outflux of positively charged K+ ions during the action potential plateau and thereby prevents early return of the action potential voltage to its resting level.
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Cardiac muscle refractory period is the interval of time during which a normal cardiac impulse cannot re-excite an already excited area of cardiac muscle. The normal refractory period of the ventricle is
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0.25 to 0.30 second which is about the duration of the prolonged plateau action potential. There is an additional relative refractory period of about 0.05 second during which the muscle is more difficult than normal to excite but nevertheless can be excited by a very strong excitatory signal.
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The refractory period of atrial muscle is
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about 0.15 second (much shorter than the ventricle muscle at 0.25-0.30 second)
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When an action potential passes over the cardiac muscle membrane, the action potential spreads to the interior of the cardiac muscle fiber along the membranes of the
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transverse (T) tubules which in turn act on the membranes of the sarcoplasmic tubules to cause release of Ca+ ions into the muscle sarcoplasm from the sarcoplasmic reticulum. Then these Ca+ diffuse into the myofibrils and catalyze the chemical reactions that promote sliding of the actin and myosin filaments along one another producing the muscle contraction.
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In addition to the Ca+ ions that are released into the sarcoplasm from the cisternae of the sarcoplasmic reticulum, a large quantity of extra calcium ions also diffuses into the sarcoplasm from the
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T tubules themselves at the time of the action potential. This extra Ca+ from the T tubules makes the contraction much stronger. This is necessary because cardiac sarcoplasm doesn't store enough Ca+. Therefore, the T tubules have a diameter 5 times as great as that of the skeletal muscle tubules, which means a volume 25 times as great.
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Strength of contraction of cardiac muscle depends to a great extent on
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the concentration of Ca+ in the extracellular fluids. Because the openings of the T tubules pass directly through the cardiac muscle cell membrane into the extracellular spaces surrounding the cells, allowing the same extracellular fluid that is in the cardiac muscle interstitium to percolate through the T tubules as well.
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At the end of the plateau, the influx of Ca+ to the interior of the muscle is suddenly cut off and the Ca+ in the sarcoplasm
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are rapidly pumped back out of the muscle fibers into both the sarcoplasmic reticulum and the T tubule/extracellular fluid space.
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The duration of contraction of cardiac muscle is mainly a function of the
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duration of the action potential, including the plateau -- about .2 second in atrial muscle and 0.3 second in ventricular muscle. (Cardiac muscle begins to contract a few milliseconds after the action potential begins and continues to contract until a few milliseconds after the action potential ends.
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The SA node is located
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in the superior lateral wall of the right atrium near the opening of the superior vena cava.
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There is a delay of more than ___ second in impulse from atria into the ventricles
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0.1 second. This allows the atria to contract ahead of ventricular contraction.
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The P wave is caused by
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spread of depolarization thru the atria
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About ___ second after the onset of the P wave, the QRS waves appear
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About 0.16 second after the onset of the P wave, the QRS waves appear as a result of electrical depolarization of the ventricles which initiates contraction of the ventricles. The QRS complex begins slightly before the onset of ventricular systole.
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Ventricular T wave is
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the stage of repolarization of the ventricles when the ventricular muscle fibers begin to relax. Therefore, the T wave occurs slightly before the end of ventricular contraction
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Atrial contraction usually causes an addition ___ filling of the ventricles
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20% (80% just goes into the ventricles directly)
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The period of rapid filling of the ventricles lasts for about
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the first third of diastole. During the middle third of diastole, only a small amount of blood normally flows into the ventricles; this is blood that passes directly into the ventricles from the vena cavae
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During the last 1/3 of diastole, the atria
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contract and give an additional thrust to the inflow of blood into the ventricles
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Immediately after ventricular contraction begins, the ventricular pressure rises abruptly causing
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the AV valves to close. Then an additional 0.02 to 0.03 second is required for the ventricle to build up sufficient pressure to push the semilunar valves open (aortic and pulmonary) (period of isovolumic (isometric) contraction)
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When the left ventricular pressure rises slightly above 80 mm Hg and the right ventricular pressure slightly above 8 mm Hg, the ventricular pressures
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push the semilunar valves open (aortic and pulmonary)
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Period of rapid ejection
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70% of the blood emptying from the ventricles occurs during the first third of the period of ejection
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Period of slow ejection
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30% of the blood emptying from the ventricles during 2/3 of the period of ejection
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Period of isovolumic or isometric relaxation
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Ventricle pressures decreases rapidly. Then the elevated pressures in the distended large arteries immediately push blood back toward the ventricles which snaps the aortic and pulmonary valves closed. For another 0.03 to 0.06 second, the ventricular muscle continues to relax, even though the ventricular volume does not change, giving rise to the period of isovolumic or isometric relaxation
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End-diastolic volume
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about 110-120 mL (when ventricles are at their fullest)
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stroke volume output
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As the ventricles empty during systole, the volume decreases about 70 mL. The remaining volume in each ventricle, about 40 to 50 mL, is called the end-systolic volume
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Ejection fraction
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The fraction of the end-diastolic volume that is ejected is called the ejection fraction -- usually equal to 60%
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By both increasing the end-diastolic volume and decreasing the end-systolic volume, the stroke volume output can be increased to
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more than double normal
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the AV values are aka
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tricuspid and mitral valves
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the semilunar valves aka
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the aortic and pulmonary artery valves
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The papillary muscles attach to the veins of the AV valves by the
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chordae tendineae. The papillary muscles contract when the ventricular walls contract, but they do not help the valves to close. Instead they pull the vanes of the valves inward toward the ventricles to prevent their bulging too far backward toward the atria during ventricular contraction
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The entry of blood into the arteries causes the walls of these arteries to stretch and the pressure to increase to about
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120 mm Hg
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The pressure curves in the right ventricles and the pulmonary artery are similar to those in the aorta, except that the pressures are only about
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1/6 as great
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For cardiac contraction, the preload
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is usually considered to be the end -diastolic pressure when the ventricle has become filled
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The afterload of the ventricle is
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the pressure in the artery leading from the ventricle (sometimes the afterload is loosely considered to be the resistance in the circulation rather than the pressure)
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In many abnormal functional states of the heart or circulation, the pressure during filling of the ventricle (preload) and the arterial pressure against which the ventricle must contract (afterload) is
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severely altered from normal
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Energy for the heart is derived mainly from oxidative metabolism of
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fatty acids
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At rest, the heart pumps only ____ per minute
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4 to 6 L of blood each minute
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During severe exercise, the heart may pump
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4 to 7 times the resting 4 to 6 L of blood
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The basic means by which the volume pumped by the heart is regulated are
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1) intrinsic cardiac regulation of pumping in response to changes in volume of blood flowing into the heart and
2) control of heart rate and strength of heart pumping by the autonomic nervous system |
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Each peripheral tissue of the body controls its
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own local blood flow
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Frank-Starling mechanism of the heart
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The intrinsic ability of the heart to adapt to increasing volumes of inflowing blood. Basically the greater the heart muscle is stretched during filling, the greater is the force of contraction and the greater the quantity of blood pumped into the aorta
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When an extra amount of blood flows into the ventricles, the cardiac muscle itself is stretched to greater length. This in turn causes the muscle to contract with increased force because
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the actin and myosin filaments are brought to a more nearly optimal degree of overlap for force generation.
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Stretch of the right atrial wall directly increases the heart rate by
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10-20%
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Strong sympathetic stimulation can
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increase the heart rate up to 180 to 200, rarely 250, in healthy, young adult humans. Also sympathetic stimulation increases the force of heart contraction to as much as double normal increasing the volume of blood pumped and increasing the ejection pressure.
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Under normal conditions, the sympathetic nerve fibers to the heart discharge continuously at a slow rate that maintains pumping at about ____ above that with no sympathetic stimulation.
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30%. (So if sympathetics are depressed, decreases in both heart rate and strength of ventricular muscle contraction. Can be as much as 30% below normal)
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The vagal fibers are distributed mainly to the
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atria and not much to the ventricles
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Strong parasympathetics to the heart can stop the heartbeat for a few seconds, but then the heart usually "escapes" and beats at a rate of
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20 to 40 beats per minute as long as the parasympathetic stimulation continues
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Figure 9-11. It shows four cardiac function curves:
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Maximum sympathetic stimulation 25L/min
normal sympathetic stimulation about 13L/min zero sympathetic stimulation about 10L/min parasympathetic stimulation about 8L/min |
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Both ___ and ___ change in response to parasymp and symp nerve stimulation
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changes in heart rate and from changes in contractile strength of the heart
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The concentration of K+ and Ca+ in the extracellular fluids
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have important effects on cardiac pumping
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Excess K+ in the extracellular fluids
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causes the heart to become dilated and flaccid and slows the heart rate. Large quantities also can block conduction of the cardiac impulse from the atria to the ventricles through the AV bundle. Only 2 to 3 times the normal value of K+ can cause such weakness of the heart and abnormal rhythm that this can cause death.
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High potassium concentration in the extracellular fluids
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decreases the resting membrane potential in the cardiac muscle fibers. As the membrane potential decreases, the intensity of the action potential also decreases, which makes contraction of the heart progressively weaker.
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An excess of calcium ions causes
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the heart to go toward spastic contraction. This is caused by a direct effect of Ca+ to initiate the cardiac contractile process.
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Deficiency of calcium ions causes
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cardiac flaccidity, similar to the effect of high potassium. However, Ca+ levels in the blood are regulated within a very narrow range. Therefore, cardiac effects of abnormal calcium concentrations are seldom of concern.
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Heat increases the permeability of the cardiac muscle membrane to ions that control heart rate resulting in the acceleration of the self-excitation process. Therefore, optimal function of the heart depends greatly on
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proper control of body temperature by the temperature control mechanisms.
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During normal function of the heart at normal systolic arterial pressures, the cardiac output is determined almost entirely
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by the ease of blood flow through the body's tissues, which in turn controls venous return of blood to the heart. (So arterial pressure load does not decrease the cardiac output - up to a limit, of course)
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