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Physio > EKG 6 > Flashcards

EKG 6 Flashcards

1
Q

Causes of arrhymias

A

. Anatomical variation
. Altered ANS activity (altered sinus rhythms)
. Electrolyte disturbances (altered K or Ca)
. Drugs
. Myocardial ischemia

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2
Q

Myocardial ischemia consequences

A

. Infarcts

. Injured tissue (inadequate O2)

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3
Q

Depolarization in injured tissue

A

. Due to accumulation of K in the extracellular spaced

. Depolarized cells do not conduct as rapidly due to voltage inactivation of Na channels

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4
Q

Injury currents

A

. Currents flow btw depolarized and non-depolarized regions

. May result in ectopic foci developing

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5
Q

Ischemia in relation to dispersion of refractory periods

A

. Ischemia opens specific K channels leading to early repolarization in affected area
. Shorter AP duration is responsible for a shorter refractory period
. Regions w/ differing degrees of ischemia will have differing refractory periods

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6
Q

ATP-sensitive K channels (IKatp channels) in relation to ischemia

A

. Inhibited by physiological conc. Of intracellular ATP so they are largely closed
. Open during ischemia
. Shortens AP duration which results in reduced Ca entry during the plateau
. Contractility is reduced in ischemia region and ATP is spared
. Reduces likelihood of irreversible damage to the cardiac myocytes in the ischemic area
. Shortened APs lead to arrhythmias

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7
Q

Accumulation of toxic metabolites during ischemia

A

. Cell membranes breakdown during ischemia
. Causes accumulation of phospholipid metabolites
. Block many channels and open some
. Cause altered conduction
. Can also cause spontaneous depolarization which can lead to ectopic foci

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8
Q

Reentry

A

. Single incoming electrical impulse causes more than 1 depolarization of the same cell or region due to re-excitation
. Occurs due to shortening the refractory period or slowing conduction

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9
Q

Altered sinus rhythms

A

. Originating in SA node
. Tachycardia or bradycardia
. P waves, QRS complex, and T waves are all present and relatively normal

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10
Q

Sinus block

A

. 1+ sinus impulses fails to initiate cardiac cycle (P wave, QRS, and T wave are all missing)
. Atria fail to depolarize bc the SA node fails to depolarize it, the SA node depolarized but the wave fails to exit node, or the SA node depolarized but the impulse fails to stimulate atria bc impulse is weaker than normal or atria tissue doesn’t respond

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11
Q

Incomplete sinus block

A

. Occasional dysfunction in which one (common) or 2 cycles is missing
. Pause is a multiple of normal P-P period
. Causes: digitalis toxicity, carotid sinus massage, ischemia

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12
Q

Supraventricular Tachycardia

A

. Originates above ventricles in SA node, atrial, or AV node
. Lumped together as SVT bc it is hard to distinguish
. P waves not clearly seen at higher HRs

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13
Q

Paroxysmal SVT

A

. Appears suddenly and ends suddenly
. Precipitated by premature atrial complex which causes reentry
. Symptoms: lightheadedness and palpitations
. Well tolerated as long as rate is less than 190
. Older people can get angina and infarcts from it

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14
Q

Junctional tachycardias

A

. Subset of supraventiruclar tachycardias
. Arise from AV junction
. QS and T waves normal
. Other have no P wave or P wave can come after QRS
. Seen to be inverted in Lead II if present in normal space

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15
Q

Atrial flutter

A

. Originates from ectopic pacemaker or reentry circuit in atria
. Get saw tooth pattern
. Waves occur at 250-350/min
. Accompanying QRS complexes and T waves occurring at lower rate

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16
Q

Atrial fibrillation

A

. Similar to flutter but modified P waves are smaller in amplitude and occur at rates over 350/min
. Uncoordinated electrical activity at extremely high rates
. Leads to uncoordinated mechanical activity

17
Q

What are the most common atria-ventricular dysrhythmia?

A

. AV conduction block

18
Q

First degree AV block

A

. Prolonged PR interval
. 1 P wave for every QRS
. Looks relatively normally, need to measure PR interval to determine

19
Q

Second degree A block

A

. Partial dissociation of atria and ventricles
. Not every P wave is followed by QRS
. Wenckebach Phenomenon: gradually inc. PR interval until finally P wave isn’t followed by QRS, then cycle repeats
. Mobitz Type II: PR interval constant, some P waves not followed by QRS (2:1, 3:1)

20
Q

Third degree AV block

A

. Complete dissociation of atria and ventricles
.P and QRS are totally independent of one another
. Complete heart block
. Secondary pacemaker takes over
. Requires an artificial pacemaker

21
Q

Premature ventricular complexes

A

. Extra QRS dur to abnormal depolarization of ventricles primer to arrival of normal impulse
. Caused by ectopic focus or reentry in ventricles
. Extra QRS are accompanied by contraction (extrasystoles)
. Early contraction weaker than normal that’s followed by compensatory pause since cells are in refractory period when normal SA impulse arrives
. Leads to skipped beat
. Compensatory pause followed by stronger than normal contraction
. Occur at low frequency in normal person

22
Q

Wolff-Parkinson-White syndrome

A

. Caused by 2nd conduction pathway btw atria and ventricles
. known as Pre-excitation
. Conduction through pathway faster than AV node so ventricles depolarized sooner than normal
. Causes short PR interval and wide QRS w/ initial hump (delta wave)
. Occurs bc QRS complex is generated by 2 waves of depolarization (first through aberrant pathway, 2nd through normal pathway)

23
Q

Ventricular Tachycardias

A

. Abnormally high rate caused by ectopic focus or reentry in ventricles
. QRS complexes unusual
. P and T waves obscured
. Precede ventricular flutter and fibrillation bc ventricles don’t fill well and heart pumps less efficiently at high rate
. O2 requirement inc. due to inc. work causing myocardial ischemia

24
Q

Ectopic focus

A

. Pacemaker other than normal pacemaker
. One that fires occasionally may lead to individual complexes
. Ones that fire repeatedly and faster than rate of firing of SA node will drive other cells, result in tachycardias

25
Q

Torsades de Pointes

A

. Ventricular tachycardia w/ unique appearance

26
Q

Ventricular flutter

A

. Very rapid tachycardia which usually progressed to fibrillation due to ischemia
. QRS complexes themselves don’t inc. or dec. in amplitude to same degree as Torsades

27
Q

Ventricular fibrillation

A

. Uncoordinated electrical activity of ventricles at extremely high rate (350-500 bpm)
. Leads to uncoordinated mechanical activity
. Ventricles can’t pump and death ensues
. Due to firing of multiple ectopic foci

Physio (62 decks)

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