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DMS EKG > DMS EKG II > Flashcards

DMS EKG II Flashcards

(70 cards)

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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
Which artery is occluded w/ posterior infarcts?
R coronary artery reciprocal changes in anterior leads - esp. V1 ST depression & tall R waves in anterior leads
26
RVH vs. posterior infarct
RVH - large R wave in V1 w/ R axis deviation
27
What is bad about non-Q wave MIs?
lower mortality rate initially but higher risk for later infarction & mortality later
28
What is apical ballooning syndrome?
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
29
Angina
ST segment depression or T wave inversion that goes away after attack
30
Prinzmetal's angina
from coronary artery spasm ST segment elevation = reversible transmural injury return to baseline when given nitroglycerin
31
How can you diagnose MI w/ LBBB?
ST-segment elevation at least 1 mm in any lead w/ a predominant R wave
32
When do you stop a stress test?
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
What is a positive stress test?
ST segment depression > 1mm that is horizontal or downsloping & lasts for >0.08s
34
When are stress tests performed?
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
Contraindications to stress testing
1. Acute systemic illness 2. Severe aortic stenosis 3. Uncontrolled CHF 4. Severe HTN 5. Angina at rest 6. Presence of significant arrhythmia
36
What can hyperkalemia turn into?
Vfib death measure of clinically significant toxicity rather than serum K+ level
37
EKG changes w/ hyperkalemia
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
EKG changes w/ hypokalemia
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
What does hypocalcemia cause?
Prolonged QT interval could lead to Torsades de Pointes
40
What does hypercalcemia cause?
shortened QT interval
41
What does hypomagnesemia cause?
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
What does hypermagnesemia cause?
usually due to renal failure/excessive intake Doesn't really change EKG Severe elevations may cause prolonged PR/QRS intervals or cardiac arrest
43
EKG changes w/ hypothermia
<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
What is an Osborn J wave & when is it seen?
abrupt ascent at the J point then a sudden plunge to baseline seen w/ hypothermia
45
EKG w/ therapeutic levels of Digoxin
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
EKG w/ toxic levels of Digoxin
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
What is the most common rhythm disturbance of Digoxin toxicity?
PAT w/ 2nd degree AV block most common cause of PAT w/ block
48
What is the most common cause of PAT w/ block?
Digoxin
49
What drugs can prolong the QT interval?
1. Antiarrhythmics - sotalol, quinidine, procainamide, disopyramide, amiodarone 2. Tricyclic antidepresants, phenothiazines, erythromycin, quinolones, antifungals50
50
What should the QTc stay under?
500 ms 550 ms if BBB
51
What are ST segment elevations characteristic of?
Acute injury may also be seen w/ vent. aneurysms, pericarditis, benign early repol
52
EKG changes w/ pericarditis
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
Hypertrophic Obstructive Cardiomyopathy
May have LVH, L axis deviation, Q waves laterally & maybe inferiorly
54
Myocarditis
may cause conduction blocks | especially BBBs & hemiblocks
55
EKG changes w/ COPD
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
S1Q3T3
Acute Pulmonary Embolism!!!
57
Acute Pulmonary Embolism
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
CNS Disease
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
Sudden Cardiac Death Causes
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
What is commotio cordis?
blunt force to the chest causing Vfib
61
Brugada syndrome
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
EKG changes w/ Brugada
1. RBBB | 2. ST segment elevation in V1-V3
63
EKG changes w/ Athlete's heart
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
Which leads are Q waves normally seen in?
L lateral I, aVL, V5 & V6
65
What is seen w/ an anterolateral infarct?
L main artery occlusion changes in V1-V6, I & aVL reciprocal changes inferiorly
66
What can cause ST segment depression?
1. Non-Q wave infarcts >48hrs 2. Angina 3. + stress test 4. Therapeutic levels of digoxin 5. Hypokalemia
67
What can cause ST segment elevation?
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
Changes w/ WPW?
Short PR interval less than 0.12s Wide QRS more than 0.1s Delta waves
69
What arrhythmia does Brugada syndrome most commonly cause?
fast polymorphic Vtach that looks like Torsades
70
Which block is from below the AV node in the His bundle?
Type II 2nd degree AV block

DMS EKG (2 decks)

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