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Clin Med-Cardio pt 2 > ECG finishing touches lecture > Flashcards

ECG finishing touches lecture Flashcards

1
Q

Bundle of Kent that directly connects atrium to ventricles

A

Wolff-Parkinsons White

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2
Q

PR interval shortened to under 0.12 seconds
QRS widened to more than 0.10
***delta wave present

A

WPW

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3
Q

hallmark*** slurring of upstroke due to Kent bundle conduction (delta wave), wide QRS at base (between 2-2.5 boxes wide), narrow QRS at top

A

WPW

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4
Q

Arrhythmias associated with WPW

A 
PSVT
A fib (even faster than usual bc Kent Bundle conducts faster than AV node)

**can have vent rates up to 300 with a fib in WPW

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5
Q

Cannot read what in a WPW EKG?

A

Ischemia
Infarct
LVH

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6
Q
  • *Cannot interpret Q waves (if present) for MI in the presence of WPW abnormality on ECG.
  • *Cannot interpret LVH by voltage criteria (if present) in the presence of WPW abnormality.
  • *Cannot interpret ischemia via ST segment depression or T wave inversion in the presence of WPW abnormality.
A

WPW

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7
Q

99% of the time, irregularly irregular EKG means…

A

A fib

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8
Q

Bypass from atrium into Bundle of His

A

Lown-Ganong-Levine Syndrome

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9
Q

Very short PR interval

Associated w PSVT

A

Lown Ganong Levine Syndrome

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10
Q

This drug has a narrow therapeutic to toxic ration and is a potent stimulator of arrhythmias

A

Digoxin

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11
Q

ST segment scooping

A

Digoxin

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12
Q

Multiformed PVCs are most common EKG presentation of

A

Digoxin toxicity

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13
Q

Digoxin causes SA nodal suppression and…

A

AV block

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14
Q
  • Accelerated junctional rhythm

* Atrial tachycardia with AV block

A

seen with Digoxin

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15
Q

mild ST segment depression
Flattening of the T wave
Appearance of a U wave

A

HYPOkalemia

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16
Q

T waves across the entire 12 lead EKG begin to peak

A

HYPERkalemia

17
Q

PR interval become prolonged, and the P wave gradually flattens and then disappears

A

HYPERkalemia

18
Q

Ultimately, QRS complex widens until it merges with the T wave, forming a SINE WAVE** pattern. V fib may eventually develop

A

Hyperkalemia

19
Q

QT interval should not exceed ______ of the R-R interval

A

one half

20
Q 
tricyclic antidepressants
erythromycin (and other macrolides)
antifungals
myocardial ischemia
myocardial infarction

can cause…

A

QT prolongation

21
Q

Pt comes in with chest pain. EKG shows HUGE!!! T waves n V3-V5..whats going on?

A

Early MI!!! Anterolateral*

22
Q

Prolonged QT interval puts at risk for…

A

V fib

23
Q

OD of tricyclic antidepressants can cause…

A

ST depression

24
Q

Pt comes in with diffuse ST elevation..seen in all leads except aVL and aVR. What is it? And DOC?

A

Acute pericarditis

tx with NSAIDS

25
Q

EKG with LOW VOLTAGE…what could be going on?

A

Pericardial effusion

26
Q

EKG with narrow QRS and rate of 150. Can be 3 things….

A
  1. atrial flutter with 2:1 AV block
  2. PSVT
  3. sinus tachycardia
27
Q

Young healthy individual
Sinus bradycardia
Slight ST elevation

A

Early repolarization

28
Q

deep T wave inversions until proven otherwise mean…

A

ischemia or NSTEMI

29
Q

wide, bizarre QRS complexes

**small vertical line seen before every QRS

A

electronic ventricle pacemaker!

ventricles are conducting on a cell to cell basis, which is why there are wide QRS

30
Q

vertical line seen before every P wave

A

atrial pacemaker

31
Q

Causes SA nodal suppression and AV block

*can basically cause any arrhythmia

A

Digoxin

32
Q

Most common arrhythmia caused by Digoxin

A

Multifocal PVCs

33
Q

2 most specific arrhythmias caused by Digoxin

A

Accelerated junctional rhythm

Atrial tachycardia with AV block

34
Q

Diffuse peaked T waves
no P waves
QRS widens, merges with T waves
Sine wave forms

*V fib may eventually develop

A

HYPERkalemia

35
Q

Pt comes in with NVD

ECG shows BIG** T waves in precordial leads

A

HYPERkalemia

36
Q

class 1a, 1c, 3 anti-arrhythmic agents
erythromycin, non sedating anti histamines
macrolides, antifunals

can all cause…

A

QT prolongation

Clin Med-Cardio pt 2 (11 decks)

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