Cardiac EP Flashcards by Vanessa Copes

What is conduction pathway of the heart?

SA>AV>Bundle HIS> mainstem bundle branch> anterosuperior bundle> posterioinferior bundle> purkinje fibers > right bundle branch

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Which parts of conduction pathway represent pacemaker activity?

SA Node and AV node

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What factors affect conduction speed of the heart?

membrane excitability (funny sodium channels), size of tissue, CT around heart, and the connexins of gap junctions

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What allows for functional syncytium?

desmosomes and gap junctions

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Phase 4 in pacemakers

Rest stage pacemakers are unstable, decreased in K+ channel opening, increased Ca transient channels

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Phase 0 in pacemakers

open L type calcium channels

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Phase 1 in pacemakers

There is no repolarization

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Phase 2 in pacemakers

there is no plateu

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Phase 3 in pacemakers

L type Ca channels close and K+channels slowly open

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Ectopic focus

when purkinje fibers takes over heart activity

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Phase 4 in contractile cells

Stable (-90); leaky channels still open

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Phase 0 in contractile cells

Funny sodium channels open (fast voltage gated)

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Phase 1 in contractile cells

inactivation of Na+ channels and K+ voltage gate channels open

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Phase 2 in contractile cells

L type Ca channels open and voltage gated K+ close

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Phase 3 contractile cells

L type Ca channels close and leaky K+ channels open

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What are 3 effects of Ach on M2 receptors on heart?

decrease funny sodium channel activation to reduce steepness of phase 4
Increase potassium conductance to maximize diastolic potential (lets heart fill)
Decrease transient Ca channels activity reducing phase 4

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What are 2 effects of B1 receptors on heart?

Increases activity funny sodium channels increasing steepness of phase 4
increase of transient Ca activity which increases steepness of phase 4 and makes threshold more negative

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What are 2 adrenergic receptors of the heart?

B1 and B2 which are both Gs coupled which increase AC activity

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What is the cholinergic receptor on the heart?

M2 which is Gi and decreases AC activty

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period during which the cell membrane cannot be reexcited by an external stimulus, regardless of the level of external voltage applied

Absolute Refractory Period

Period during which only a local response can be produced by a larger than normal depolarizing stimulus. During this period, a propagated AP cannot be generated

Effective Refractory Period

It starts at the end of the ERP. Period during which a propagated AP can be generated with a depolarizing stimulus that is larger than normal

Relative Refractory Period

Short interval during which the cell is more excitable than normal, so a weaker than usual depolarizing stimulus can initiate a propagated AP

Supernormal Period

the period from the onset of the AP to the end of the supernormal period.

Full Recovery Time

How is excitation and contraction coupled?

Calcium does the membrane depolarization and the contraction via entry through L type Ca channels then tha CICR from SR

record obtained from the body surface that registers the differences in electrical potential generated by the heart

ECG (EKG)

P wave

atrial depolarization

QRS complex

ventricular depolarization

T wave

ventricular repolarization

PR interval

time from the beginning of the P wave to the beginning of the QRS complex

ST segment

time from the end of ventricular depolarization to the beginning of the T wave

where are lead attachments

Mean Electrical Axis

Average of all the instantaneous mean electrical vectors during depolarization of the ventricles

Right axis deviation

lead 1 is negative and aVF (lead 3) is positive

left axis deviation

positive lead 1 and negative aVf

What can't you see on ECG?

SA node, AV node, bundle his, bundle branches, and purkinje network

How do you calculate HR?

300/# of big boxes between two R waves

Rapid heart rate of >100 beats per minute P waves of successive beats are closer together

Tachycardia

Slow heart rate of <60 beats per minute P waves of successive beats are farther apart

Bradycardia

3 causes of arrhythmia

Conduction Blocks (aka Heart Blocks), Premature depolarizations, Fibrillations

Conduction to ventricles is slightly delayed, Prolonged P-R interval, No treatment necessary, May occur in those with some structural heart disease

First Degree Block

Conduction to ventricles is intermittently blocked Ratios from ECG = 3:1 or 2:1 (2Ps:1QRS), Block is above or below Bundle of His, some patients require artificial pacemaker

Second Degree Block

No impulses from atria reach the ventricles, No relationship between P waves and QRS, Bradycardia, Ventricle pumping is severely compromised, Artificial pacemaker required

Third Degree Block

What causes PAC and PVC

enhanced automaticity due to ectopic foci or extra systoles

When Cardiac muscle undergoes irregular contraction that is ineffectual in propelling blood Re-entry with multiple irregular loop circuits

Fibrillation

Atrial Fibrillation

Since atria don’t significantly help with ventricular filling… Compatible with life and full activity; may be seen in those with chronic heart disease No P waves; treat w/ β-blockers to drop HR and re-establish sinus rhythm

Ventricular fibrillation

Twitching of ventricular muscles >not pumping blood >loss of consciousness within seconds death unless immediate intervention (defibrillator)

What is function of defibrillator?

Applies a strong electrical current that will force the entire myocardium into a brief refractory state Depolarizes the entire heart at once (stops the heart!) This forced refractory state gives the SA node the chance to take over as boss again and establish sinus rhythm