DMS EKG II Flashcards
What is the accessory pathway for WPW?
Bundle of Kent
can be R/L sided
PSVT in WPW
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
AV reciprocating tachycardia
PSVT seen in WPW b/c reentry loop btwn atria & ventricles
What is orthodromic tachycardia?
PSVT in tachycardia that goes through antegrade direction causing narrow QRS complex
What is antidromic tachycardia?
PSVT in WPW that goes through reciprocating direction causing wide QRS complex
What is the accessory pathway in Lown-Ganong-Levine syndrome?
James fiber…intranodal
in AV node but no delay
conduction occurs through normal pathways
LGL characteristics?
shortened PR interval
What arrhythmias can be seen w/ WPW?
Afib
Vfib
PSVT
EKG changes w/ MI
should be seen in 2 or more leads..don’t see all changes
- T wave peaking followed by T wave inversion
- ST segment elevation
- Appearance of new Q waves
What do T wave changes show?
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
What is pseudonormalization?
Pt may have inverted T waves, but having active MI so T waves go back making it seem normal
What does ST segment elevation show?
injury
reversible
reliable sign MI occurred & immediate Tx required
usually return to normal after a few hours
What does persistent ST segment elevation indicate?
formation of a vent. aneurysm
STEMI vs. J point elevation
S - bowed upward & merges w/ T wave
J - T wave maintains independent waveform
common in healthy people
What do Q waves indicate?
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
What causes reciprocal changes?
part of heart dies so electrical forces inc. elseware to show tall positive R waves
seen in distant leads
May show ST depression
Which lead can you not diagnose MI with?
aVR
Where are normal Q waves typically seen?
L lateral leads
(I, aVL, V5 & V6)
inferior leads sometimes - II & III
Pathologic Q waves
- > 0.04s in duration
2. Depth must be at least 1/3 the height of the R wave in the same complex
A block in the R coronary artery can cause???
AV block b/c feeds AV node
What does the L circumflex supply?
lateral wall of the L ventricle
I, aVL, V5 & V6
What is typically seen w/ an anterior infarct?
V1-V6
Q waves not always seen but a dec. in normal pattern of precordial R wave progression
When is poor R wave progression seen?
- Anterior infarct
- RVH
- Chronic lung disease
- Improper lead placement
Which artery is occluded w/ inferior infarct?
R coronary artery or its descending branch
II, III, aVF
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
RVH vs. posterior infarct
RVH - large R wave in V1 w/ R axis deviation
What is bad about non-Q wave MIs?
lower mortality rate initially but higher risk for later infarction & mortality later
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
Angina
ST segment depression or T wave inversion that goes away after attack
Prinzmetal’s angina
from coronary artery spasm
ST segment elevation = reversible transmural injury
return to baseline when given nitroglycerin
How can you diagnose MI w/ LBBB?
ST-segment elevation at least 1 mm in any lead w/ a predominant R wave
When do you stop a stress test?
Dx presence & severity of CAD
- Pt can’t continue
- Pts max. HR has been reached
- Sx occur
- Significant changes on EKG
What is a positive stress test?
ST segment depression > 1mm that is horizontal or downsloping & lasts for >0.08s
When are stress tests performed?
- CP w/ normal EKG
- Recent infarction to assess prognosis
- > 40 w/ diabetes, peripheral vascular disease, prior MI or FH of premature heart disease
- Suspicion of silent ischemia - dyspnea, fatigue, palpitations
- Pts >40 who want to start an exercise program
Contraindications to stress testing
- Acute systemic illness
- Severe aortic stenosis
- Uncontrolled CHF
- Severe HTN
- Angina at rest
- Presence of significant arrhythmia
What can hyperkalemia turn into?
Vfib
death
measure of clinically significant toxicity rather than serum K+ level
EKG changes w/ hyperkalemia
- Peaked T waves in every lead
- Prolonged PR interval
- P wave gradually flattens then disappears
- 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
EKG changes w/ hypokalemia
- ST segment depression
- Flattening of the T wave
- Appearance of a U wave
- usually has same axis as T wave, best seen in anterior leads
- -may be seen w/ normal hearts
What does hypocalcemia cause?
Prolonged QT interval
could lead to Torsades de Pointes
What does hypercalcemia cause?
shortened QT interval
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
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
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
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
EKG w/ therapeutic levels of Digoxin
- ST segment depression - gradual downslope emerging from previous R wave
best seen in V5&V6 - Flattening/inversion of T wave
most prominent in leads w/ tall R waves
may be difficult to differentiate from Vent hypertrophy w/ repol
EKG w/ toxic levels of Digoxin
- Sinus node depression - sinus exit block or sinus node suppression
- Conduction blocks - 1/2/3rd degree AV block
- Tachyarrhythmias - PAT & PVCs most common
What is the most common rhythm disturbance of Digoxin toxicity?
PAT w/ 2nd degree AV block
most common cause of PAT w/ block
What is the most common cause of PAT w/ block?
Digoxin
What drugs can prolong the QT interval?
- Antiarrhythmics - sotalol, quinidine, procainamide, disopyramide, amiodarone
- Tricyclic antidepresants, phenothiazines, erythromycin, quinolones, antifungals50
What should the QTc stay under?
500 ms
550 ms if BBB
What are ST segment elevations characteristic of?
Acute injury
may also be seen w/ vent. aneurysms, pericarditis, benign early repol
EKG changes w/ pericarditis
Diffuse
- ST segment elevation
- T wave flattening/inversion
- usually occur after ST segments normalize - PR interval may be depressed
- Pericardial effusion may show electrical alternans
Hypertrophic Obstructive Cardiomyopathy
May have LVH, L axis deviation, Q waves laterally & maybe inferiorly
Myocarditis
may cause conduction blocks
especially BBBs & hemiblocks
EKG changes w/ COPD
- Low voltage
- R axis dev
- 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
S1Q3T3
Acute Pulmonary Embolism!!!
Acute Pulmonary Embolism
- RVH w. repolarization changes due to acute RV dilation
- RBBB
- S1Q3T3
- Q wave only in lead III
arrhythmias may be seen - most commonly sinus tachycardia & Afib
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
Sudden Cardiac Death Causes
- ATHEROSCLEROSIS
- Hypertrophic cardiomyopathy
- Long QT interval syndrome
- Arrhythmogenic RV dysplasia
- WPW
- Viral myocarditis
- Infiltrative diseases of myocardium (amyloidosis & sarcoidosis)
- Valvular heart disease
- Drug abuse (cocaine & meth)
- Commotio cordis
- Anomalous origin of the coronary arteries
- Brugada syndrome
What is commotio cordis?
blunt force to the chest causing Vfib
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
EKG changes w/ Brugada
- RBBB
2. ST segment elevation in V1-V3
EKG changes w/ Athlete’s heart
- Resting sinus bradycardia
- Nonspecific ST segment elevation & T wave changes
Usually ST elevation in precordial leads w/ T wave flattening/inversion - Criteria for LVH & sometimes RVH
- Incomplete RBBB
- Arrhythmias, including junctional rhythms & a wandering atrial pacemaker
- 1st degree or Wenckebach AV block
Which leads are Q waves normally seen in?
L lateral
I, aVL, V5 & V6
What is seen w/ an anterolateral infarct?
L main artery occlusion
changes in V1-V6, I & aVL
reciprocal changes inferiorly
What can cause ST segment depression?
- Non-Q wave infarcts >48hrs
- Angina
- stress test
- Therapeutic levels of digoxin
- Hypokalemia
What can cause ST segment elevation?
- MI
- Prinzmetal’s angina
- J point elevation
- Apical Ballooning syndrome
- Pericarditis
- Myocarditis
- Hyperkalemia
- Pulmonary Embolism
- Brugada syndrome
- Hypothermia
Changes w/ WPW?
Short PR interval less than 0.12s
Wide QRS more than 0.1s
Delta waves
What arrhythmia does Brugada syndrome most commonly cause?
fast polymorphic Vtach that looks like Torsades
Which block is from below the AV node in the His bundle?
Type II 2nd degree AV block
