Cardiac M for physiology

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Last updated 6:19 AM on 10/10/26
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43 Terms

1
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functional syncytium

  • a group of individual, separate cells that are connected to work together as a single, unified unit

  • connected by intercalated disks

    • gap junctions, adhering junctions, desmosomes


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how are cardiac myocytes arranged

  • in series and parallel


<ul><li><p>in series and parallel</p></li></ul><p></p>
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2 syncytium:

  • atria

  • ventricles


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action potential

  • avg. 105 millivolts each beat

  • 0.2 sec depolarization (15x longer than skMSC)


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Phase 0 of depolarization

  • depolarizes to -20 from -80mv

  • by voltage activated fast sodium channels

    • open for 1/1000th of a second

    • same for Sk m.

  • L Type ca channels (calcium channels)

    • open for longer (1/10th of a second)

    • slower


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Phase 1: initial repolarization

  • fast sodium channels close, Ca channels stay open, and K leaves the cell


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Phase 2: plateau

  • Ca remains open

  • K channels close

  • reduced permeability of membrane to K

  • Reduction of efflux of K prevents early repolarization


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Phase 3: Repolarization

  • Calcium channels close

  • Calcium ceases to enter cell

  • Membrane permeability to K is restored, channels re-open, and cells rapidly repolarize Membrane permeability


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Phase 4:

  • Resting membrane potential


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<p>explain this chart</p>

explain this chart

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<p>explain this chart and how it correlates to other charge </p>

explain this chart and how it correlates to other charge

Na is phase 0

ca is phase 2

K+ balanced out after decreases is phase 3

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Velocity of action potential

  • 0.3-0.5 m/sec


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Refractory in nature?

  • Effective refractory period (ERPA)

    • from phase 0-2, cell cannot depolarize again until repolarization

  • 0.23-0.30 sec


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Relative refractory period

  • typically occur in phase 2

  • +0.05 sec

  • if stimulus is strong enough u can overcome RRP to get an early premature contraction

    • only during RRP


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<p>explain</p>

explain

knowt flashcard image
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can u get premature contractions to make wave summation?

no

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Excitation-contraction coupling and relaxation in cardiac muscle: explain

  • AP travels along membrane to transverse (T) tubules

  • Activation of voltage-dependent Ca channels

  • Travels along longitudinal sarcoplasmic tubules

  • Release of calcium from SR via ryanodine receptor (RyR) channels

  • Calcium in sarcoplasm binds troponin

  • Activation of actin-myosin complex

  • Relaxation occurs via Ca ATPase (SERCA) and Ca/Na exchanger


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T tubules:

  • Ca required from T tubules for full contraction strength.

  • T tubules retain calcium through electronegative mucopolysaccharides.

  • Diameter 5x and volume 25x compared to SkMsc.


<ul><li><p>Ca required from T tubules for full contraction strength. </p></li><li><p>T tubules retain calcium through electronegative mucopolysaccharides. </p></li><li><p>Diameter 5x and volume 25x compared to SkMsc.</p></li></ul><p></p>
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No ca what?

NO CA no HEAWRT BEAT

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Sarcomere

  • basic contractile unit of the myocyte


<ul><li><p>basic contractile unit of the myocyte</p></li></ul><p></p>
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Myosin combines (what is combined myosin called) o form?

  • combined myosin is called filament

  • combines to form thousands of cross bridges with actin


<ul><li><p>combined myosin is called filament </p></li><li><p>combines to form thousands of cross bridges with actin </p></li></ul><p></p>
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myosin is made of?

  • 2 heavy and 4 light chains

  • head has 2 flexible hinges at either side of the arm

    • contains ATPase enzyme

  • anchored by titin


23
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actin contains:

2 F actin and 2-tropomyosin molecules

  • F actin contains G actin + ADP (active site)

  • Tropomyosin lies on top of active sites at rest


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structure of actin and myosin?

both have twisted helix structure

<p>both have twisted helix structure </p>
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troponin complex

  • troponin I has high affinity for actin

  • troponin T has high affinity for tropomyosin

  • Troponin C has high affinity for calcium


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what happens at rest on troponin-tropomyosin complex

  • there is an inhibitory effect

  • 4 Ca ions induce a conformational change and the troponin complex pulls tropomyosin away from active sites

  • Active sites bind to myosin cross-bridges and contraction occurs

  • Cross-bridges are independent thus number in contact with actin filament correlates to force of contraction


<ul><li><p>there is an inhibitory effect </p></li><li><p>4 Ca ions induce a conformational change and the troponin complex pulls tropomyosin away from active sites </p></li><li><p>Active sites bind to myosin cross-bridges and contraction occurs </p></li><li><p>Cross-bridges are independent thus number in contact with actin filament correlates to force of contraction</p></li></ul><p></p>
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specific sequence of propagation of cardiac action pot.?



<p></p><p></p>
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Propagation of cardiac action potential is simultaneous: T/F

  • False


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Influence of voltage-gated Na channels absent in SA and AV node: T/F?

T

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which node is the primary pacemaker?

  • SA Node

  • connects directly to the atrial muscle fibers

  • sets normal sinus rhythm



<ul><li><p>SA Node </p></li><li><p>connects directly to the atrial muscle fibers </p></li><li><p>sets normal sinus rhythm</p></li><li><p></p></li></ul><p></p>
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phases in SA node :

  • Phase 0: Depolarization

    • L-type Ca channels open

  • Phase 1-2: Absent in SA

  • Phase 3: Repolarization

    • Ca channels close and K channels open

  • Phase 4: Return to resting membrane


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can SA node self excitate?

  • yes,

  • Resting potential is less negative

  • Leaky to sodium (funny currents) and calcium

  • Slight delay with K channels remaining open (hyperpolarization)


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what effect does neural control of SA node have

  • alters rate of depolarization, HR

  • sympathetic control

    • (mostly release NE, activates beta1 adrenergic receptors, increases rate of depolarization (note: circulating Epi also activates beta1-AR)

  • Parasympathetic control

    • Right = SA and Left = AV

    • Release Ach, activates muscarinic receptors and decreases rate of depolarization


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Neural control is needed to initiate action potential?

FALSE

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AP spreads thru atrial muscle cells and atria contract?

True

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what phases do atrial m AP phases exhibit?

  • typical phases of cardiac muscle


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Basal level of neural control

  • Strong vagal stimulation can decrease the strength of heart muscle contraction by 20% to 30%.

  • Can stop heart beat for a few seconds

  • Vagal fibers are distributed mainly to the atria so primary effect is on heart rate


<ul><li><p>Strong vagal stimulation can decrease the strength of heart muscle contraction by 20% to 30%. </p></li><li><p>Can stop heart beat for a few seconds </p></li><li><p>Vagal fibers are distributed mainly to the atria so primary effect is on heart rate</p></li></ul><p></p>
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Contraction movement of ventricle

  • by purkinje system and left ventricle rotation




<ul><li><p>by purkinje system and left ventricle rotation </p></li></ul><p></p><p></p><p></p>
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  • Purkinje System


  • Causes synchronous contraction of the ventricular muscle

  • Rapid conduction results in almost all parts of the ventricles contracting within a narrow time

  • First to last muscle fiber only 0.03-0.06 sec apart

  • Functional syncytium

  • Run ~1/3 of the way into ventricular muscle

  • Merge with ventricular muscle fibers

  • Muscle fibers conduct the action potential to the rest of the ventricular muscle mass



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Left ventricular rotation

  • During systole, the left ventricle contracts in a twisting motion

  • Counterclockwise rotation of the apex of the heart

  • Clockwise rotation of the base of the left ventricle during the ejection phase

  • Pulls base downward towards apex during systole (wrings it out)

  • Like a loaded spring, recoils (untwists) during diastole


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<p>Pressure across the Cardiac Cycle</p>

Pressure across the Cardiac Cycle

  • Pressure changes in the aorta (top dotted), left ventricle (red), and left atrium (bottom dotted)

  • Iso = equal or same

  • Atrial contraction usually causes an additional 20% filling of the ventricles

  • Approximately 60% of the blood in the ventricles at the end of diastole is ejected during systole


<ul><li><p>Pressure changes in the aorta (top dotted), left ventricle (red), and left atrium (bottom dotted) </p></li><li><p>Iso = equal or same </p></li><li><p>Atrial contraction usually causes an additional 20% filling of the ventricles </p></li><li><p>Approximately 60% of the blood in the ventricles at the end of diastole is ejected during systole</p></li></ul><p></p>
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systole vs diastole

  • Systole:

    • 60% volume ejected during period of rapid ejection (first 1/3 systolic time)

    • 30% volume ejected during period of slow ejection (last 2/3 systolic time)

  • Diastole

    • Ventricle fillin



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