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DMS EKG > DMS EKG II > Flashcards

DMS EKG II Flashcards

1
Q

What is the accessory pathway for WPW?

A

Bundle of Kent

can be R/L sided

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2
Q

PSVT in WPW

A

PAC may go to normal AV node but bundle will be refractory then it will get the current from the other side & pass it back to the AV node
—narrow QRS, goes along normal pathway = orthodromic tachycardia …antegrade

may go opposite way - may look like Vtach
wide QRS - abnormal pathway = antidromic tachycardia …reciprocating

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3
Q

AV reciprocating tachycardia

A

PSVT seen in WPW b/c reentry loop btwn atria & ventricles

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4
Q

What is orthodromic tachycardia?

A

PSVT in tachycardia that goes through antegrade direction causing narrow QRS complex

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5
Q

What is antidromic tachycardia?

A

PSVT in WPW that goes through reciprocating direction causing wide QRS complex

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6
Q

What is the accessory pathway in Lown-Ganong-Levine syndrome?

A

James fiber…intranodal
in AV node but no delay

conduction occurs through normal pathways

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7
Q

LGL characteristics?

A

shortened PR interval

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8
Q

What arrhythmias can be seen w/ WPW?

A

Afib
Vfib
PSVT

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9
Q

EKG changes w/ MI

A

should be seen in 2 or more leads..don’t see all changes

  1. T wave peaking followed by T wave inversion
  2. ST segment elevation
  3. Appearance of new Q waves
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10
Q

What do T wave changes show?

A

ischemia - usually inverted symmetrically

if infarction occurs, T wave inversion will last for months to years

can be seen w/ MI, BBB, vent hypertrophy w/ repol abnormalities

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11
Q

What is pseudonormalization?

A

Pt may have inverted T waves, but having active MI so T waves go back making it seem normal

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12
Q

What does ST segment elevation show?

A

injury
reversible

reliable sign MI occurred & immediate Tx required

usually return to normal after a few hours

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13
Q

What does persistent ST segment elevation indicate?

A

formation of a vent. aneurysm

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14
Q

STEMI vs. J point elevation

A

S - bowed upward & merges w/ T wave

J - T wave maintains independent waveform
common in healthy people

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15
Q

What do Q waves indicate?

A

irreversible cell death - diagnostic of MI
appear w/in several hours-days & stay for lifetime
ST segment usually returns to baseline when Q waves appear

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16
Q

What causes reciprocal changes?

A

part of heart dies so electrical forces inc. elseware to show tall positive R waves
seen in distant leads
May show ST depression

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17
Q

Which lead can you not diagnose MI with?

A

aVR

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18
Q

Where are normal Q waves typically seen?

A

L lateral leads
(I, aVL, V5 & V6)

inferior leads sometimes - II & III

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19
Q

Pathologic Q waves

A
  1. > 0.04s in duration

2. Depth must be at least 1/3 the height of the R wave in the same complex

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20
Q

A block in the R coronary artery can cause???

A

AV block b/c feeds AV node

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21
Q

What does the L circumflex supply?

A

lateral wall of the L ventricle

I, aVL, V5 & V6

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22
Q

What is typically seen w/ an anterior infarct?

A

V1-V6

Q waves not always seen but a dec. in normal pattern of precordial R wave progression

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23
Q

When is poor R wave progression seen?

A
  1. Anterior infarct
  2. RVH
  3. Chronic lung disease
  4. Improper lead placement
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24
Q

Which artery is occluded w/ inferior infarct?

A

R coronary artery or its descending branch

II, III, aVF

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25
Q

Which artery is occluded w/ posterior infarcts?

A

R coronary artery

reciprocal changes in anterior leads - esp. V1
ST depression & tall R waves in anterior leads

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26
Q

RVH vs. posterior infarct

A

RVH - large R wave in V1 w/ R axis deviation

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27
Q

What is bad about non-Q wave MIs?

A

lower mortality rate initially but higher risk for later infarction & mortality later

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28
Q

What is apical ballooning syndrome?

A

Looks like MI w/ T wave inversion & ST segment elevation

seen mostly in elderly women
ballooning of LV
typically brought on by emotional stress
may have elevated Troponins but no blockage
may develop HF/shock but usually improve w/in a few wks

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29
Q

Angina

A

ST segment depression or T wave inversion that goes away after attack

30
Q

Prinzmetal’s angina

A

from coronary artery spasm
ST segment elevation = reversible transmural injury
return to baseline when given nitroglycerin

31
Q

How can you diagnose MI w/ LBBB?

A

ST-segment elevation at least 1 mm in any lead w/ a predominant R wave

32
Q

When do you stop a stress test?

A

Dx presence & severity of CAD

  1. Pt can’t continue
  2. Pts max. HR has been reached
  3. Sx occur
  4. Significant changes on EKG
33
Q

What is a positive stress test?

A

ST segment depression > 1mm that is horizontal or downsloping & lasts for >0.08s

34
Q

When are stress tests performed?

A
  1. CP w/ normal EKG
  2. Recent infarction to assess prognosis
  3. > 40 w/ diabetes, peripheral vascular disease, prior MI or FH of premature heart disease
  4. Suspicion of silent ischemia - dyspnea, fatigue, palpitations
  5. Pts >40 who want to start an exercise program
35
Q

Contraindications to stress testing

A
  1. Acute systemic illness
  2. Severe aortic stenosis
  3. Uncontrolled CHF
  4. Severe HTN
  5. Angina at rest
  6. Presence of significant arrhythmia
36
Q

What can hyperkalemia turn into?

A

Vfib
death

measure of clinically significant toxicity rather than serum K+ level

37
Q

EKG changes w/ hyperkalemia

A
  1. Peaked T waves in every lead
  2. Prolonged PR interval
  3. P wave gradually flattens then disappears
  4. QRS widens, merging w/ T wave, forming a sine wave pattern later going to Vfib

All the K+ is going to the T wave & stealing it from the P wave

38
Q

EKG changes w/ hypokalemia

A
  1. ST segment depression
  2. Flattening of the T wave
  3. Appearance of a U wave
    - usually has same axis as T wave, best seen in anterior leads
    - -may be seen w/ normal hearts
39
Q

What does hypocalcemia cause?

A

Prolonged QT interval

could lead to Torsades de Pointes

40
Q

What does hypercalcemia cause?

A

shortened QT interval

41
Q

What does hypomagnesemia cause?

A

usually due to GI/renal losses
may inc/exacerbate hypokalemia
may cause Vent arrhythmias w/ acute MI
may cause digoxin toxicity & foster hypocalcemia & Torsades de Pointes

42
Q

What does hypermagnesemia cause?

A

usually due to renal failure/excessive intake
Doesn’t really change EKG
Severe elevations may cause prolonged PR/QRS intervals or cardiac arrest

43
Q

EKG changes w/ hypothermia

A

<30 C
Everything slows - sinus bradycardia & prolonged segments & intervals
ST elevation - abrupt ascent at the J point then a sudden plunge to baseline = Osborn J wave
Arrhthmias - slow Afib most common
Muscle tremor artifact due to shivering - may look like Aflutter

44
Q

What is an Osborn J wave & when is it seen?

A

abrupt ascent at the J point then a sudden plunge to baseline

seen w/ hypothermia

45
Q

EKG w/ therapeutic levels of Digoxin

A
  1. ST segment depression - gradual downslope emerging from previous R wave
    best seen in V5&V6
  2. Flattening/inversion of T wave

most prominent in leads w/ tall R waves
may be difficult to differentiate from Vent hypertrophy w/ repol

46
Q

EKG w/ toxic levels of Digoxin

A
  1. Sinus node depression - sinus exit block or sinus node suppression
  2. Conduction blocks - 1/2/3rd degree AV block
  3. Tachyarrhythmias - PAT & PVCs most common
47
Q

What is the most common rhythm disturbance of Digoxin toxicity?

A

PAT w/ 2nd degree AV block

most common cause of PAT w/ block

48
Q

What is the most common cause of PAT w/ block?

A

Digoxin

49
Q

What drugs can prolong the QT interval?

A
  1. Antiarrhythmics - sotalol, quinidine, procainamide, disopyramide, amiodarone
  2. Tricyclic antidepresants, phenothiazines, erythromycin, quinolones, antifungals50
50
Q

What should the QTc stay under?

A

500 ms

550 ms if BBB

51
Q

What are ST segment elevations characteristic of?

A

Acute injury

may also be seen w/ vent. aneurysms, pericarditis, benign early repol

52
Q

EKG changes w/ pericarditis

A

Diffuse

  1. ST segment elevation
  2. T wave flattening/inversion
    - usually occur after ST segments normalize
  3. PR interval may be depressed
  4. Pericardial effusion may show electrical alternans
53
Q

Hypertrophic Obstructive Cardiomyopathy

A

May have LVH, L axis deviation, Q waves laterally & maybe inferiorly

54
Q

Myocarditis

A

may cause conduction blocks

especially BBBs & hemiblocks

55
Q

EKG changes w/ COPD

A
  1. Low voltage
  2. R axis dev
  3. Poor R wave progression in precordial leads

can lead to chronic cor pulmonale & R sided CHF
will show RA enlargement (P Pulmonale) & RVH w/ repolarization abnormalities

56
Q

S1Q3T3

A

Acute Pulmonary Embolism!!!

57
Q

Acute Pulmonary Embolism

A
  1. RVH w. repolarization changes due to acute RV dilation
  2. RBBB
  3. S1Q3T3
    - Q wave only in lead III

arrhythmias may be seen - most commonly sinus tachycardia & Afib

58
Q

CNS Disease

A

Subarachnoid bleed or cerebral infarction can cause diffuse T wave inversion & prominent U waves
T waves usually deep, wide & symmetrical
Sinus bradycardia may be seen

59
Q

Sudden Cardiac Death Causes

A
  1. ATHEROSCLEROSIS
  2. Hypertrophic cardiomyopathy
  3. Long QT interval syndrome
  4. Arrhythmogenic RV dysplasia
  5. WPW
  6. Viral myocarditis
  7. Infiltrative diseases of myocardium (amyloidosis & sarcoidosis)
  8. Valvular heart disease
  9. Drug abuse (cocaine & meth)
  10. Commotio cordis
  11. Anomalous origin of the coronary arteries
  12. Brugada syndrome
60
Q

What is commotio cordis?

A

blunt force to the chest causing Vfib

61
Q

Brugada syndrome

A

Autosomal dominant
More common in men in their 20-30 than women
Affects voltage dependent sodium channels during repol.
Can cause vent. arrhythmias that can cause sudden death, most commonly a fast polymorphic Vtach that looks like Torsades
SCD most likely to occur during sleep

62
Q

EKG changes w/ Brugada

A
  1. RBBB

2. ST segment elevation in V1-V3

63
Q

EKG changes w/ Athlete’s heart

A
  1. Resting sinus bradycardia
  2. Nonspecific ST segment elevation & T wave changes
    Usually ST elevation in precordial leads w/ T wave flattening/inversion
  3. Criteria for LVH & sometimes RVH
  4. Incomplete RBBB
  5. Arrhythmias, including junctional rhythms & a wandering atrial pacemaker
  6. 1st degree or Wenckebach AV block
64
Q

Which leads are Q waves normally seen in?

A

L lateral

I, aVL, V5 & V6

65
Q

What is seen w/ an anterolateral infarct?

A

L main artery occlusion

changes in V1-V6, I & aVL

reciprocal changes inferiorly

66
Q

What can cause ST segment depression?

A
  1. Non-Q wave infarcts >48hrs
  2. Angina
    • stress test
  4. Therapeutic levels of digoxin
  5. Hypokalemia
67
Q

What can cause ST segment elevation?

A
  1. MI
  2. Prinzmetal’s angina
  3. J point elevation
  4. Apical Ballooning syndrome
  5. Pericarditis
  6. Myocarditis
  7. Hyperkalemia
  8. Pulmonary Embolism
  9. Brugada syndrome
  10. Hypothermia
68
Q

Changes w/ WPW?

A

Short PR interval less than 0.12s
Wide QRS more than 0.1s
Delta waves

69
Q

What arrhythmia does Brugada syndrome most commonly cause?

A

fast polymorphic Vtach that looks like Torsades

70
Q

Which block is from below the AV node in the His bundle?

A

Type II 2nd degree AV block

DMS EKG (2 decks)

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