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Physiology > Cardiac Excitation and Contraction I > Flashcards

Cardiac Excitation and Contraction I Flashcards

1
Q

Cardiac output vs Stroke volume vs Ejection fraction

A

CO: blood volume pumped by the heart in 1 min (~5L/min)

SV: blood volume ejected by left ventricle in 1 contraction (70mL)

EF: fraction of blood volume in left ventricle ejected in 1 contraction (60%)

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2
Q

Effective Refractory period (ERP)

A

Time period after an action potential (or QRS complex) during which the heart is refractory to another action potential

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3
Q

SA node

A
  • In the upper right atrium
  • Highest level of automaticity; “sets the pace” for heart rate
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4
Q

AVN / AV node

A
  • Between the atria & ventricles
  • Slow conduction & behaves like an electrical filter during high atrial rates (e.g. atrial fibrillation
  • Conduction here is mediated by L-type Ca current
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5
Q

Bundle of His & Bundle branches

A

Extends from distal end of the AV node & divides into smaller bundle branches in the ventricles, terminating in Purkinje fibers.

Specialized for rapid conduction of cardiac APs

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6
Q

Purkinje fibers

A

Specailized cardiac cells that spread out over the inner surface of the ventricles (endocardium).

Weakly contract, but are mostly specialized for rapid conduction of APs to the ventricular muscle.

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7
Q

The ___ is where the AP originates to stimulate heart contraction.

___ is specialized for slow conduction and prevents ventricles from being paced faster than they can fill with blood when atrial tachyarrhythmia occurs.

___ are specialized for rapid conduction & delives AP to the inner ventricular myocardium (nedocardium) via a web-like network of Purkinje fibers.

A

SA node- pace setter

AV node- slow conduction & prevents ventricles from pacing faster than they can fill during atrial tachyarrhythmia

His bundle- rapid conduction & delivery of APs to ventricles

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8
Q

Why do the ventricles have thicker walls (esp the left) than the atria?

A

They pump blood out of the heart into the rest of the body in systole

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9
Q

Steps of normal sinus rhythm

A
  1. Spontaneous apperance of APs in the SA node
  2. Spread of AP rapidly through the atria and into the AV node
    1. Slow conduction of AV node gives the atria time to contract and fill the ventricles
  3. AP reaches bundle of His, which divides into the left & right bundle branches on each side of the ventricular septum going toward the apex
  4. Divide into smaller Purkinje fibers that spread out all over the ventricular endocardium
    1. Conduction through HIs-Purkinje system is so fast that it basically simultaneously stimulates all muscle cells in both chambers
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10
Q

Intercalated discs between cardiac muscle fibers

A

Group of gap junctions between myocardial cells, allowing

  • excitation to spread through cardiac muscle in the direction that muscle fibers are oriented.
  • spread of metabolic or second msger signals btwn cells
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11
Q

Gap junctions of intercalated discs can “close” under conditions commonly produced during ____

A

myocardial ischemia

chronic depolarization of neighboring cells (depolarized resting potentials)

acidic conditions

high Cai

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12
Q

P wave

A

Atrial depolarization

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13
Q

PR interval

A

Delay in conduction that takes place in the AV node

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14
Q

QRS complex

A

Ventricular depolarization

Q wave: initial depolarization of septum before the ventricles

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15
Q

Things that widen the QRS complex (affects normal srpead of ventricular depolarization)

A

Na channel blocking drugs

Myocardial ischemia

Hyperkalemia

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16
Q

T wave

A

Ventricular repolarization

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17
Q

QT interval

A

time for complete ventricular repolarization

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18
Q

things that lengthen the QT interval

A

K-channel blocking drugs

Mutations in ion channels

long QT syndrome

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19
Q

Events that prolong the QT interval are typically proarrhythmic:

A

They increase the likelihood for multifocal ventricular arrhythmias such as Torsades de pointes –> life threatening

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20
Q

SAN, AVN, and Purkinje fibers all display

A

automaticity: ability to spontaneously depolarize an action potential

Demonstrated by the phase 4 depolarization

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21
Q

Action potentials in the SAN and AVN both have slow upstroke velocity caused by

A

L-type Ca current

22
Q

The upstroke of APs in cells outside of the node

A

Na current

23
Q

The 5 phases of a cardiac action potential

A
24
Q

Why do different regions of the heart show differently shaped action potentials?

A

Cells in different regions express varying densities of the various ion channels that regulate the shape of the cardiac action potential

Ex) Atrial cells’ APs are much faster due to differences in ion channel expression

25
Q

What ion channel is responsible for phase 4 when cardiac cells are left unstimulated?

A

The K-selective channel opens, producing an inwardly-rectifying K current called IK1

K ions leave the cell, but as they leave, other ions get stuck in the channel and block K+ efflux

26
Q

What ion channel is responsibnle for phase 0?

A

Na channels transiently opening while K channels are closed

27
Q

What maintains the plateau phase of the ventricular action potential (phase 2)?

A

Ito’s repolarizing effect is slowed by

  • Activation of an L-type Ca current (ICa) causing Ca influx
    • Inactivates slowly
  • There’s a small (~1%) fraction of Na channels that don’t fully inactivate after depolarization
28
Q

what is responsible for phase 1?

A

Ito: transient K efflux produces rapid repolarization

29
Q

What’s responsible for the rapid repolarization of phase 3?

A
  • Slow inactivation of the Ca current
  • Activation of additional outward K currents (IKr & IKs)
30
Q
A
31
Q

The resting potential is a function of ____ concentration

A

extracellular K concentration

32
Q

Hyperkalemia causes ______ of the resting potential

A

Depolarization

Hyperkalemia may result from

  • Renal failure
  • Addison’s disease (adrenal gland destruction)
  • K-sparing diuretics
33
Q

How does myocardial ischemia cause a depolarization of the resting potential?

A

Occlusion of a coronary artery will produce local tissue hyperkalemia

34
Q

Relative refractory period (RRP)

A

time after the ERP during which conduction occurs, but at a less than maximal velocity bc not all Na channels have recovered from inactivation yet

Beats originating during the RRP have a slower upstroke velocity and produce a wider QRS complex

35
Q

Avg resting heart is 70 bpm

Sympathetic nerves innervate the __; whereas, vagal nerves innervate the ___

A

Sympathetic innervates atria & ventricles

Vagal nerves innervate only the atria, SA node, AV node, and Purkinje fiber system

36
Q

Depolarized resting potentials are common in cells exposed to severe stretch (opens non-selective ion channels) , hyperkalemia, or ischemia.

Depolarized resting potentials has what impact on the Na current?

A

Na channel inactivation

  • Reduces Na current amplitude
  • Slower action potentials (may even block conduction)

note: “rested”=available to be opened

37
Q

Impact of neural stimulation on

  • heart rate
  • AV node ERP,
  • PR
  • contractility (SV)
A

note: vagal stimulation has little impact on contractility

38
Q

Right vs left vagal nerve

A

Right affects SA

Left affects AV

39
Q

Sympathetic stimulation: Norepinephrine binds to ____ receptors >__>__>__>___ phosphorylates the L-type Ca channel to allow Ca influx.

Parasympathetic: Acetylcholine binds to __ receptors >___> inhibits ___ & activates a ___

A
  • SYMP: Norepi
    • > Gs
    • > adenylate cyclase
    • > cAMP
    • > PKA phosphorylates L-type Ca channel
  • PARASYMP: Ach
    • > type 2 muscarinic receptors
    • > Gi
    • > inhibits adenylate cyclase and activates a K channel resulting in K efflux (IKAch)
40
Q

Why do cells at the nodes have a less negative diastolic membrane potential and slower upstroke velocity in phase 0 than atrial or ventricular cells?

A

Lower K+ permeability -> smaller IK1 -> less negative RP

Conduction is primarily Ca current-mediated -> slower upstroke velocity because the Ca current is much smaller than the Na current

41
Q

How does Ach prolong the AV node ERP?

A

Increasing K conductance & Decreasing Ca conductance

–> AV node cell will have to wait more time for enough Ca channels to regain their excitability for conduction

42
Q

Latent pacemakers

Ectopic pacemakers

A

Latent pacemaker: Cells outside the SAN that can become pacemakers

If SAN’s automaticity becomes depressed or cells outside the SAN become enhanced, then the region that starts generating APs outside the SAN is the ectopic pacemaker. AVN or Purkinje

43
Q

bpm of san, avn, and purkinje

A

SAN = 70bpm (impacted by autonomics)

AVN= 40-60 bpm

Purkinje = 15-40 bpm

44
Q

What is If?

A

funny, nonselective current that slowly activates upon hyperpolarization below a threshold of -50mV.

-> Na primarily enters ( depolarizing)

45
Q

What are the sources of depolarizing current during diastole (phase 4) in the SAN & Purkinje fibers?

A
  • SAN
    • Both T- and L-type Ca currents
    • If
  • ​​​Purkinje
    • Just If
46
Q

Ivabradine blocks If, thus __ the heart rate.

L-type Ca channel blockers will __ the heart rate due to their affect on ___.

A

Ivabradine reduces the heart rate

L-type Ca channel blockers also reduce HR thru their affect on the SAN (butalso by slowing conduction thru AV); can even cause bradycardia or asystole

47
Q

Vagal stimulation vs Sympathetic stimulation on the slope of the phase 4 depolarization

A

Vagal stimulation -> greater K efflux in SAN & Purkinje –> less steep slope

Symp stimulation -> greater L-type Ca current & If -> steeper slope

48
Q

How does hypokalemia result in development of an ectopic pacemaker activity?

A

Lowering [K]out causes EK and the maximum diastolic potential to be more negative.

-> Activates more If and reduces IKI

–> Enhances phase 4 depolarization in Purkinje (strong K permeability)

49
Q

What Ca channels are the trigger for the SR to release its Ca into the cytoplasm?

What is the mechanism?

A

It’s the calcium from the L-type Ca channels participating in calcium-induced calcium release:

  1. Ca influx during AP plateau triggers the release of SR’s Ca into the cytoplasm.
  2. Large rise in free cytosolic Ca activates contraction of the myofilaments (systole).
  3. Relaxation (diastole) occurs following the
    1. reuptake of cytosolic Ca into the SR via SERCA
    2. extrusion of Ca into the extracellular fluid via Na/Ca exchange.
50
Q

Excitation-Contraction Coupling

A

Infux of Ca from AP triggers release of Ca from the SR into the cytoplasm –> contraction

Reuptake of cytosolic Ca into the SR via SERCA and into the extracellular fluid via Na/Ca exchange –> relaxation

51
Q

The more Ca released into the cytoplasm (e.g. B-adrenergic agonists), the increased

A

force of contraction

52
Q

Contractility in cardiac tissue is sensitive both tot he amt of Ca influx, which regulates Ca-induced Ca released from the SR, as well as ___ because ___

A

intracellular & extracellular Na concentrations due to the role of the Na/Ca exchanger in clearing out the Ca afterwards

Physiology (42 decks)

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