Dysrhythmia (lecture3)

Question 1

Absolute refractory period

Answer 1

• No impulse can generate depolarization event

–> Na+ channels are in Inactivated state

Question 2

describe relative refractory period

Answer 2

• requires greater impulse to generate a depolarization event
• corresponds to phase 3
• Na+ channels are in resting state

Question 3

describe the activation/inactivation of Na+ channels

Answer 3

1) impulse causes threshold to be met leading to activation of the resting Na+ channels undergoing conformational shift and opening up of the pore.
2) Na+ flow down concentration gradient into the cell
3) time dependent event occurs in which the inactivation gate blocks the pore leading to inactivation of Na+ channel
4) eventually the intracellular plug (gate) is removed and the channel goes back to resting phase

Question 4

describe the role of Ca+ in contraction

Answer 4

1) Calcium entry through VOCC
2) calcium release from Sarcoplasmic reticullum (binds to RyR2)
3) calcium interacts with troponin leading to contractile shortening of sarcomere

Question 5

describe Calcium role in relaxation

Answer 5

1) calcium dissociates from toponin
2) calcium is taken back up into store via SERCA
3) Calcium is bound to protein within SR (calsequestrin)
3) calcium is pumped out of the cell at the cell membrane (shuttles Ca out of cell)

Question 6

what effect does changing slope of phase 4 depolarization

Answer 6

• Lowering the slope of the phase 4 depolarization will cause a slower HR (longer refractory period)

Question 7

describe the effects of sympathetic/parasympathetic stimulation

Answer 7

• SYMPATHETIC:

–> stimulation causes increase in the slope of the phase 4 deoplarization leading to sinus tachycardia (INCREASED AUTOMATICITY)

• PARASYMPATHETIC:

–> stimualtion causes decrease in the slope of the phase 4 depolarization leading to sinus bradycardia (DECREASED AUTOMATICITY)

Question 8

effect of acetylcholine on automaticity

Answer 8

• released from parasymapthetic nerve terminals increases potassium current resulting in reducing the slope of the diastolic depolarization (PHASE 4) and reducing HR

Question 9

effect of hypokalemia on automaticity

Answer 9

• decreases the potassium current during phase 4 and decreases the time between subsequent action potentials
• leads to decreased in automaticity (bradycardia)

Question 10

effect of mild hyperkalemia on automaticity

Answer 10

• altered potassium gradient across the membrane increases the maximum diastolic potential (PHASE 4) and increases automaticity

Question 11

describe the effects of severe hyperkalemia on automaticity

Answer 11

• significantly depolarized membrane potential causes the cells to become inexcitable

Question 12

describe the effects of norepinephrine on automaticity

Answer 12

• causes increased calcium and funny current leading to an increased slope of phase 4 (increases automaticity

Question 13

describe Early afterdepolarization (EAD)

Answer 13

• Triggered activity
• generated during phase 2 or phase 3 caused by altered ion flux
• characteristically displays extended action potential duration (APD)
• accentuated at lower heart rates due to physiological prolonged APD

Question 14

describe teh causes of prolonged action potential duration

Answer 14

• reduced potassium current (repolarization takes longer than normal)
• increased cacium (more calciium extend plateau phase, can cause late sodium current at the end of phase 2)
• increased sodium-calcium exchanger activity (mutation can cause current during the end of phase 2; increased Na+ current)
• increased late sodium current (mutation can lead to altered kinetics of fast sodium channel generating a current during phase 3)

Question 15

describe Delayed afterdepolarizations

Answer 15

• arrhythmia is generated at a time when the cell is fully repolarized (DURING PHASE 4)
• related to conditions of improper calcium cycling (impaired calcium channels generate a depolarizing current within the cell which if strong enough can generate another AP)
• Exacerbated at high heart rates (not enough time to reduce intracellular calcium between beats)

Question 16

describe Anatomically define circuit

Answer 16

• you need a fixed pathway and an excitable gap
• ex: wolff-parkinson-white syndrome

Question 17

describe functionally defined circuit

Answer 17

• area of inexcitable tissue at core (circuit is not static in space
• Sets up a spiral wave reentry circuit

–> MONOMORPHIC VT = travels like a cone shape (tip of the cone around and out)

–> POLYMORPHIC VT/VF = meandering,drifting spiral waves (not static and causes dramatic loss of cardiac output

Question 18

define wolff-parkinson-white syndrome

Answer 18

• Anatomically defined reentric circuit
• Pathway links atria tissue to ventricular tissue (bypass AV node)

–> AV node functions is to slow conduction, therefore causing a abnormally fast HR

–> SEEN ON ECG AS SHORTENED PR INTERVAL!!!

(isnt seen in every heart beat)

Question 19

describe the formation of reentrant circuits

Answer 19

• NORMAL: circuit travels and encounters tissue in absolute refractory period and signal becomes terminated
• ABNORMAL:

–> if the refractory period is reduced, the propagating wavefront encounters tissue that can be excited and RENTER the intial point of stim

–> If the conduction velocity is reduced, the propagating wavefront will again encounter tissue that can be excited and REENTER the initial point of stimulation