Cardiac Ion Channels, Action Potentials, & Conduction Flashcards

1
Q

L-type Ca2+ channels

A

Voltage-activated Ca2+ channels

Allow influx of Ca2+ that is responsible for the plateau phase (2) of fast myocardial action potentials

Activate rapidly in response to depolarization and then inactivate

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2
Q

IKto Channels

A

K+ channels that produce a small, repolarization current following rapid depolarization of the fast myocardial action potential

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3
Q

IKr

A

Rapid K+ rectifier channel; responsible for plateau (2) and repolarization (3) phases of the mycardial action potential

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4
Q

IKs

A

Slow K+ rectifier channel; responsible for plateau (2) and repolarization (3) phases of the myocardial action potential

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5
Q

IK1

A

Inward rectifier K+ channel; readily conducts inward K+ current at potentials below Ek and only weakly passes outward K+ current at potentials positive to Ek; therefore responsible for maintenance of cell potential near Ek between depolarizations

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6
Q

If

A

Responsible for conducting the “funny” Na2+ current that is responsible for the slow creep of membrane potential toward threshold between beats in automatic cells; induced by hyperpolarization

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7
Q

T-Type Ca2+ channels

A

Activated by weak depolarizations; expressed in the SA node

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8
Q

IKAch

A

K+ channels that increase their outward current in response to ACh acting on muscarinic receptors; important for the ability of parasympathetic nervous system to slow pacemaker activity of the SA node

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9
Q

Absolute refractory period

A

The time during which a second action potential cannot be initiated, while most of the Na+ channels remain inactivated

On ECG, corresponds to the time from the Q wave to the peak of the T wave

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10
Q

Relative refractory period

A

The time during which the threshold for production of a second action potential remains elevated, prior to complete removal of Na+ channel inactivation and deactivation of IKr and IKs

On ECG, corresponds to the latter half of the T wave

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11
Q

First degree AV block

A

Conduction delayed but all P waves conduct to the ventricles and are followed by R waves

Lengthening of PR interval

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12
Q

2nd degree AV block

A

Some P waves conduct to ventricles and are followed by R waves while others do not

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13
Q

3rd degree AV block

A

None of the P waves conduct to the ventricles, no P waves are followed by R waves; ventricular pacemaker takes over

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14
Q

Right bundle branch block

A

Depolarization has to go through regular contractile myocytes rather than through Purkinje fibers; causes QRS widening with delayed conduction to right ventricle

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15
Q

Left bundle branch block

A

Depolarization has to go through regular contractile myocytes rather than through Purkinje fibers; causes QRS widening with delayed conduction to Left ventricle

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16
Q

How do disturbances in cardiac conduction cause tachyarrhythmias? 3 mechanisms

A
  1. Abnormal re-entry
  2. Ectopic foci
  3. Triggered activity
17
Q

Which L-type Ca2+ channel isoform predominates in the heart?

18
Q

Which RyR isoform predominates in the heart?

19
Q

Mechanism of cardiac EC coupling

A

Wave of depolarization triggers DHPR Ca2+ channel on the plasma membrane to open, allowing an influx of trigger Ca2+; trigger Ca2+ activates RyR2 on the SR to open, allowing a large flux of Ca2+ from the SR to the mycoplasma; Ca2+ activates contraction by binding to Tn-C on thin filaments

20
Q

SERCA2 pump

A

Located in SR membrane, pumps Ca2+ from the mycoplasma into the SR

21
Q

Calsequestrin

A

Low-affinity, Ca2+ binding buffer protein located in the SR of cardiomyocytes; keeps effective concentration of Ca2+ in the SR low to aid Ca2+ reuptake

22
Q

NCX

A

Located in plasma membrane and t-tubules of cardiomyocytes, pumps 1 Ca2+ out of the cell for every 3Na+ brought in

Runs backwards for a brief time during the action potential upstroke when Vm > Vr, supplying trigger Ca2+ to the activated cell

23
Q

4 targets of PKA

A
  1. LTCCs - increases amplitude of L-type Ca2+ current (trigger calcium); positive inotropic effect
  2. RyR2 - sensitizes RyR2 to lower levels of trigger Ca2+; positive inotropic effect
  3. Phospholamban - causes PLB to dissociate from SERCA, relieving its normal inhibition; positive inotropic & lusitropic effects
  4. Troponin - causes decreased affinity of Tn for Ca2+; positive lusitropic effect
24
Q

Timothy Syndrome

A

Caused by mutatiosn in the LTTC Cav1.2 which decreases voltage-dependent inactivation, leading to increased Ca2+ influx across an elongated action potential plateau

Patients display AV block, prolonged QT intervals, and episodes of ventricular tachycardia

25
Brugada Syndrome
AKA "Sudden Unexplained Death Syndrome" Caused by mutations of the cardiac sodium channel, Ikto channel, and ankyrin; the end result of these mutations is a large reduction in the magnitude of LTTC current (decreased duration of action potential plateau) with a shortened QT interval
26
Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT)
Caused by dominantly inherited mutations in RyR2 that increase the resting leak of Ca2+ out of the SR and/or render RyR2 more sensitive to activation by trigger Ca2+ B-adrenergic activity is pro-arrhythmogenic; it increases SR Ca2+ content as well as RyR sensitivity to Ca2+, resulting in inappropriate releases of Ca2+ that are not directly coupled to LTCC activation; extrusion of this Ca2+ via NCX results in inappropriate diastolic depolarizations that can trigger ectopic action potentials and arrhythmias