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PHYSIO EXAM 2 > L15/16 Cardiac Electrophysiology And Excitation-Contraction > Flashcards

L15/16 Cardiac Electrophysiology And Excitation-Contraction Flashcards

1
Q

Cardiac muscle

A

Striated

ANS involuntary

Multi-nucleated

Junctions

Large mitochondria

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2
Q

Intercalated discs

A

Connect adjacent cardiac muscle fibers and form function syncytium

Two kinds of membrane junctions within them:
Desmosomes-mechanical junctions
Gap junctions- electrical junctions

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3
Q

Cardiac muscle looks similar to

A

Skeletal muscle

Sarcolemma

T-tubules

SR sacks

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4
Q

Sequence of electrical events in the heart

A 
SA node 
AV node
Bundle of His
Bundle branches (left and right) 
Purkinje fibers
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5
Q

Only way to guarantee ventricles aren’t contracting while atria are

A

Isolating electrical activity from one part of the heart from the other

Controls when ventricles get activated compared to atria

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6
Q

Bundle of his

A

On pathway between atria and ventricles

Delay in conduction of activity btw AV node and ventricles

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7
Q

Conduction of the cardiac AP

A

Atria - fast

AV node - slows down

His-purkinje - fastest

Ventricle - back to atria velocity

Due to how fast AP can depolarize and depolarize

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8
Q

AV node delay

A

AV node to bundle of his is Only point of electrical contact btw atria and ventricle

Very slow conduction

Allows adequate time for ventricular filling btw beats

Essential to synchronize atria and ventricular contractility

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9
Q

Purkinje fibers

A

Mesh of specialized fibers with very fast conduction

Rapidly spread impulse throughout much of left and right ventricles

Allows for efficient contraction and ejection of blood

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10
Q

Overdrive suppression

A

Phenomenon by which SA node drives heart rate and suppresses the latent pacemakers

Wait for impulses to be retrieved

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11
Q

SA node has

A

Fastest intrinsic firing rate

Damage to SA node, AV node may have control over heart rate

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12
Q

Ectopic pacemaker (ectopic focus)

A

Occurs when the latent pacemakers have an opportunity to drive the heart rate ONLY if

SA node firing rate decreases (vagal stimulation)
SA node firing stops completely (SA node destroyed, removed, etc)
Intrinsic firing of latent pacemakers become faster
Conduction of APs from SA node is blocked by disease

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13
Q

Types of myocardial cells

A

Pacemaker (nodal) cells

Conductile cells

Contractile cells

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14
Q

Pacemaker (nodal) cells

A

Pacemaker activity

Slow action potentials

SA node (primary) 
AV node
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15
Q

Conductile cells

A

Rapid spread of electrical signal

FAST AP

bundle of his
Purkinje fibers

No myosin or action

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16
Q

Contractile cells

A

Contraction (pumping)

FAST AP

Ventricular and atrial cells

Contain myosin and action

17
Q

Phases of fast AP

A

Phase 0: upstroke (similar to skeletal muscle AP) fast inward Na+ current

Phase 1: early repolarization
Transient K+ channels (Ito; outward)

Phase 2: plateau phase
L-type Ca2+ channel inward (depolarizes) and K+ (Ito, Ik, Ik1) currents outward (hyperpolarize)

Phase 3: repolarization
turn-off Ca current and increases K current

Phase 4: resting potential
Caused by large background K current

18
Q

Resting membrane potential of heart

A

-90

Due to many more leaky K channels (high permeability to K at rest)

19
Q

Phases of slow AP

A

Phase 0: upstroke
L-type Ca channel ( NOT Na - capacity lower)

Phase 1 and 2: absent

Phase 3: repolarization
K current

Phase 4: pacemaker potential (spontaneous depolarization)
“Funny” Na current (If) and a T-type (transient) Ca current

20
Q

Relationship of AP and refractory period to the duration of the contractile response in cardiac muscle

A

Because long refractory period occurs in connecting with prolonged plateau phase

Summation and that is of cardiac muscle is impossible

Ensures alternate periods of contraction and relaxation which are essential for pumping blood

21
Q

Excitation-contraction coupling in cardiac contractile cells

A
  1. Excitation AP causes depolarization of the membrane (Travels down T tubule)
  2. Entry of small amount Ca from ECF through L-type Ca channels
  3. Ca enters cell
  4. Ca-induced Ca release from SR (essential)
  5. SR releases large amount Ca through ryanodine receptors. Cytosolic Ca levels increase
  6. Ca binds troponin-tropomyosin complex in thin filaments pulled aside
  7. Cross bridge cycling btw thick and thin filaments
  8. Contraction
22
Q

Ca induced Ca release in cardiac muscle

A

Ca enters through L type Ca channel

Ryr receptor is close proximity to L type Ca channel but not physical connection

Necessary for contraction

23
Q

Mechanism for decreasing intracellular Ca in cardiac muscle

A

Decrease in contractile force occurs when conc intercellular Ca decreases

Cytosolic Ca conc decrease by:
SR Ca ATPase (SERCA)
Sarcolemmal Na/Ca exchanger (NXC)
Sarcolemmal Ca ATPase

Need Na/K ATPase for NCX

24
Q

Length tension relationship in cardiac muscle

A

Neither summation nor recruitment occurs

Force contraction is altered in others ways

Does not normally function at peak of Lo
Rather works in ascending limb
stretching cardiac muscle fibers (to a point) increase contraction

Force developed by contraction depends on initial fiber length

25
Q

Positive inotropic effect

A

Increase in contractility that involves an increase in the amount tension developed

Also an increased rate of tension development at a given fiber length

26
Q

Negative inotropic effect

A

Decrease in contractility that involves decrease in tension developing and a decrease in the rate of tension development at given fiber length

27
Q

Contractility state in cardiac muscle

A

Regulation of Ca flux from modulation of the L-type calcium channels and SR

A single AP provides sufficient free cytoplasmic ca to activate (at most) about 1/2 crossbridges

28
Q

How does heart function change?

A

Heart rate - chronotropy

AV conduction - dromotrophy

Electro-mechanical coupling - contractility - inotropy

29
Q

Autonomic effects in heart rate

SA node peacemaker activity

A

Sympathetic simulation - increase rate of phase 4 depolariziaton and increases frequency of AP

Parasympathetic- decreases rate of phase 4 depolarization and hyperpolarizes the maximum potential to decrease the frequency of AP

30
Q

SNS has what effect on contractility/inotrophy

A

Positive inotropic effect

Increased peak tension
Increased rate of tension development
Faster rate of relaxation (shorter contraction, more time for filling)

Mediated via beta1 receptors coupled with G protein to adenylyl cyclase
Increased cAMP
Activation of protein kinase A
Phosphorylation of proteins

31
Q

Phosphorylation of sarcolemma Ca channels

A

Increases Ca in cells , stronger contraction

Phosphorylation of phospholamban (on SERCA) drives Ca back into SR and always relaxation to happen faster

32
Q

PSNS has what effect on contractility/ inotropy

A

Negative inotropic effect on atria

Via muscarinic receptors coupled to G protein (inhibitory Gk) to adenylyl cyclase
Decreases cAMP
Reduced inward Ca current by AP plateau ACh
Increases IkACh thereby shortening the duration of AP and indirectly decreases inward Ca current (by shortening plateau phase)
Decrease Ca induced Ca released from SR

33
Q

PNS

A

M receptors
Decrease cAMP
Reduces Ca induced Ca release from SR

34
Q

CO to ventricular end diastolic volume

A

More volume , more CO

Fight/ flight increase CO (pos inotropic)

Rest/digest decrease CO (neg inotropic)

35
Q

Extra systole

A

Extra heart beat

Following beat goes up (more tension)

Extra heart beat allows more Ca to be released

And the following heartbeat tension goes up because now Ca induced Ca release adds to intercellular space Ca

36
Q

Common cardiac drugs

A

Na-K ATPase blocker

Ca-channel blockers

Beta-receptor agonists

37
Q

Na-K ATPase

A

Inhibits Na/K ATPase which increases the ICF Na concentration

Therefore reversing Na/Ca exchanges leading to higher intracellular [Ca]

Enhances contractility (pos inotropy)

Used in patients w contractility issues

38
Q

Ca-channel blockers

L type

A

Vascular effects:
Smooth muscle relaxation (vasodilation)
Hypertension

Cardiac effects:
Decreased contractility (neg inotropy) angina
Decreased heart rate (neg inotropy) angina
Decreased conduction velocity (neg dromotropy)

39
Q

Beta-agonists and contractility

A

Pos inotropy via cAMP pathway

Congestive heart failure, heart attack

Used to enhance contractility of the heart

PHYSIO EXAM 2 (5 decks)

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