Cardiac Eletrical Activity Flashcards

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1
Q

What are the Phases of the Fast Cardiac Action Potential? Which cell types experience these?

A

Normal atrial/ventricular myocytes; Purkinje fibers

Phase 0: Rapid Upstroke

Phase I: Early partial repolarization (Only fast reponse)

Phase II: Plateau of 0.1 - 0.2 seconds

Phase III: Membrane repolarization Slower than Phase 0

Phase IV: Resting state polarization

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2
Q

Which cells of the heart conduct slow potentials? What is the main difference from Fast to Slow potentials?

A

SA/AV Nodes

Slow Lack Phase I

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3
Q

What phase does cardiac muscle relaxation occur?

A

Phase IV

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4
Q

What major electrochemical changes occur for each phase in the Fast cardiac potential?

A

Phase 0: Opening of Fast Na channels resulting upstroke

Phase I: K+ efflux causes partial repolarization

Phase II: Ca channels open; Net flow of Ca in and K out

Phase III: Efflux f K predominate; Ca channels close

Phase IV: K efflux through channels predominates over influx

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5
Q

Which channels is responsible for the effective refractory period?

A

Na Channels

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6
Q

Describe L-type Calcium Channels.

A
  • Predominant type in Myocytes
  • Once open, inactivate slowly
  • Activates during AP upstroke when Vm is about -20 mV
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7
Q

Describe T-type Ca channels in the heart

A
  • Less abundant in heart
  • Activated at membrane potentials more negative than -70 mV
  • Inactivates more quickly
  • opening of Channels results in increase in Ca conductance and calcium current soon after action potential upstroke
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8
Q

What are the inward rectifying channels, and what are the types?

A

Potassium channels

  • iKS - Slowly activating
  • iKr rapidly activating
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9
Q

Which channel is responsible for restoring resting membrane potential in cardiac myocytes?

A

NA/K ATPase

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10
Q

What is Postrepolarization refractoriness?

A
  • Slow response action potential relative refractory period extends well beyond phase III;
  • After cell has completely repolarized, it may be difficult to evoke propagated response for some time
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11
Q

How does decreased cycle length affect action potentials?

A
  • Changes in cycle are important for terminating arrhythmia s
  • As cycle length diminishes, duration of AP decreases
  • K rectifier channels activate slowly and inactivates very slowly
  • AP occur earlier in activation period
  • As cycle length decreases, increase in K+ current shortens plateau
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12
Q

What is movement types toward a positive/negative pole?

A

Positive Deflection: Toward + Pole

Negative deflection: Toward (-) deflection

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13
Q

Where is the SA node located?

A

Les posteriorly in groove at junction btwn SVC + RA

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14
Q

What are the two principles cells of the SA Node?

A

1.
Small, round cells that have few organelles and myofibrils. Probably pacemaker cells. 2.
Slender, elongated cells that are intermediate in appearance between round and “ordinary” atrial myocardial cells. Conduct impulses within node and to the nodal margins.

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15
Q

Describe the affect of tetrodotoxin. Does it affect cardiac APs?

A
  • Tetrodoxon blocks fast Na+ Channels

- no effect on SA Nodes Slow Potential because upstroke is not due to inward Na via fast channels

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16
Q

What distinguishes pacemaker cell Action potential from other cardiomyocytes?

A
  • Phase IV in nonautomatic Cells remains the same

- pacemaker fibers is characterized by slow diastolic depolarization is phase IV

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17
Q

What three electrical factors can change pacemaker frequency?

A
  • Rate of depolarization during phase IV
  • Maximum negativity during phase IV
  • Threshold potential
18
Q

How does sympathetic stimulation affect NA Node?

A

When the cholinergic vagal fibers to nodal tissue are stimulated, the membrane becomes hyperpolarized and the slope of the prepotentials is decreased because the acetylcholine released at the nerve endings increases the K+ conductance of
nodal tissue.

19
Q

How does parasympathetic activation affect the SA Node?

A
  • M2 receptors aspen special K+ channels —> Slow depolarization
  • M2 —> decrease cAMP —> slowed Ca channels
  • Decreased firing rate
20
Q

What 3 ionic currents mediate slow diastolic depolarization?

A
  1. Outward K+. - iK
  2. Hyperpolarization induced inward current - if
  3. Inward Ca current ICa
21
Q

What is sick sinus syndrome?

A

SA node recovery time is prolonged resulting in period of asystole which may cause loss of consciousness

22
Q

What is overdrive suppression?

A
  • The automaticity of pacemaker cells diminishes after these cells have been excited at a high frequency
23
Q

What is Bachmann’s bundle?

A

Conducts impulses from SA node directly to left atrium

24
Q

Describe Wolff-Parkinson-White syndrome.

A
  • Congenital
  • Most common bypass tract of myocardial fibers becomes an accessory pathway
    between the atria and ventricles. Ordinarily causes no functional abnormality.
  • Preexcitation appears as a bizarre configuration in the QRS
25
Q

What can be triggered from electrical reentry?

A

Early Afterdepolarization - Occur in Phase 2 or Phase 3; Low HR + prolonged APs

Delayed afterdepolarization - Occur in Phase IV: High HR; elevated EC Ca

26
Q

What is Scalar ECG?

A

recording of changes in difference in potential between two points on the skin surface over time

27
Q

What do the different ECG waves represent?

A

P Wave: Atrial depolarization

QRS: Ventricular depolarization

PR/PQ interval: Time from onset of atrial depolarization to ventricular depolarization. Normally 0.12-.2 seconds

28
Q

What are the three ECG leads and degrees?

A

Lead I: RA —> LA 0 deg

Lead II: RA —> LL 60 deg

Lead III: LA —> LL 120 Deg

29
Q

Where are precordial leads connected? What are they for?

A
  • Applied to chest surface

- Used for saggital and transverse planes

30
Q

What are the routinely recorded limb leads?

A

AVR: Middle heart —> RA; LA/LL connected

AVL: Heart —> LA; RA/RL connected

AVF: Heart —> Foot; RA/LA connected

31
Q

What characterizes an AV Block?

A

First degree: Prolonged PR Interval; Block is above bundle of His

Second degree: All QRS are preceded by P waves, but not all P waves preceded by QRS; Block below bundle of HIS

Third degree: Complete heart block; Distal to bundle of His; Atrial and ventricular rhythms are entirely independent

32
Q

What is premature depolarization? Differentiate the types.

A
  • Premature depolarizations of the heart before normal heart rate

Coupled extrasystoles: Premature depolarization which reflect reentry

Parasystole: Occur at regular intervals or integral multiple of that interval

33
Q

What is paroxysmal tachycardia?

A
  • Tachycardia which originates in atria or AV Node

- QRS complexes are frequently normal because ventricular activation proceeds over usual pathways

34
Q

What is ventricular tachycardia?

A
  • Repeated bizarre QRS complexes which reflect abnormal intraventricular impulse conditions
  • Ectopic Foci
35
Q

What are Fibrillations?

A

Irregular contraction propelling blood ineffectively in antra and ventricles

36
Q

What is characteristic in Atrial vs Ventricular Fibrillation.

A

Atrial: Lack of a P Wave; reentry phenomenon—> atria do not contract and relax subsequently during each cycle and do not contribute to ventricular filling; Atria go through continuous uncoordinated rippling motion

Ventricular: Premature impulse arrives during vulnerable period, coincides with downslope of T Wave. APs are propagated in many irregular wavelets that travel along circuitous paths at various velocities.

37
Q

What is an ICD used for?

A

Long QT Syndrome

38
Q

What are the two types of 2nd degree AV Block?

A

Mobitz type I or Wenckebach: Intermittent conduction block within AV Nde resulting in failure to conduct impulse from A -> V

Mobitz Type II: Secondary to a disease involving His system resulting in failure to conduct

39
Q

What are the ECG Manifestations of Hyperkalemia?

A

> 5.5: Peaked T Waves

> 6.5: P widens; PR lengthens; P eventually disappear

> 7.0: Prolonged QRS with bizarre morphology; High grade AV Block; Bradycardia

> 9.0: Cardiac arrest; Asystole; VFib

40
Q

What is Brugada Syndrome?

A
  • Right BBB
  • Block QRS w/ ST elevation in V1-V3
  • Sudden Arrest
  • No Coronary obstruction