EKG II- Conduction Disorders, BBB, Pre Excitation, Myocardial Ischemia v. Infarction, Angina Flashcards
AV Block vs. Bundle Branch Block (BBB)
AV–> signal is blocked between the sinus node and terminal Purkinje fibers
BBB–> conduction blocked in ONE or BOTH ventricular branches
- fascicular/hemi block –> if blocked in only a portion of a branch
AV blocks- First degree
prolonged delay at the level of the AV node
- normal sinus held longer at the AV node
- PR interval >0.20 s (one big box)
every p wave gives a QRS, all beats conducted but delayed (prolonged PR)
What can cause a first degree AV block?
beta blocker, calcium channel blocker (diltiazem), or high vagal tone (vomiting, sleep apnea)
Av node is SLEEPY
AV blocks- Second degree and its types
not every impulse arrives to the ventricles
- mobitz type I second degree AV block (wenckebach block)
- mobitz type II second degree AV block
Mobitz Type I (Wenckebach) Second Degree AV block
block is within the Av node
- delay is increasing with each beat then DROP
(PR interval keeps increasing with each beat before the drop)
NO intervention needed
longer longer longer BLOCK, now i have a wenckebach
Mobitz Type II Second Degree AV Block
block BELOW the AV node in the His bundle
- no lengthening of PR interval, just QRS DROP
- evidence of progressive severe conduction system ds
REQUIRES PACEMAKER IMPLANT
AV Blocks- 2:1 block
do not have PR intervals to compare
- drop beats every other normal beat
is still a type II block since there is no prolonged PR interval
AV Blocks- Third Degree
no communication between atrial and ventricular conduction
- site at AV node OR below
- ATRIA- sinus rhythm 60-100 bpm
- VENTRICLES- escape rhythm 30-40 bpm
no P for every QRS, no pattern, no communication (P and Q don’t agree, now you have a third degree)
av dissociation
REQUIRES PACEMAKER if not reversibl (caused by meds)
Bundle Branch Blocks
conduction block in R or L bundle branch
- ventricular conduction should be <0.10 s with a leftward axis (0-90 degrees)
- width of QRS >0.12 s and configuration is changed–> BBB
R block- congenital/born with it
L block- pathological/smth occurred
pathological- procedure, MI, scar tissue
Right Bundle Branch Block
R depolarization is delayed
- QRS >0.12 s
- V1: initial R wave, second R wave as delayed R ventricle depols
- V6/left precordial leads: late deep S wave
R-S-R prime –> rabbit ears
Left Bundle Branch Block
Left depolarization is delayed
- QRS > 0.12s and WIDE
- V6/leads over LV –>broad or notched R wave
- V1/lead over RV–> broad deep S wave
L axis deviation may be present
V1- rS
V6- R
RBBB vs LBBB
which leads/what do you see:
- ST segment
- T waves
RBBB: R precordial leads with show ST segment depression and T wave inversions
LBBB: L lateral leads show ST segment depression and T wave inversion
Who gets a BBB? R and L
RBBB- diseased conduction or normal phenomenon
LBBB- rarely normal, seen in underlying cardiac ds, degenerative or ischemic
BBB- Critical Rate
BBB can be interm,ittent or fixed
- sometimes only appears at a faster “critical rate”
- so normal QRS at slow rate and wide (BBB) at faster rate – Rate related bundle
What disorders may require a titanium pacemaker?
sick sinus syndrome, mobitz II, 3rd degree AV block, Bifascicular block
Atrial Pace
paced impulse followed by p wave
- complete verticle line at start of p wave (only from electrical pulse, never naturally)
Atrial Ventricular Paced beat
atrial spike (vertical line) before and after the p wave
Ventricular Paced beat
sinus rhythm with ventricular pacing
- vertical line at start of QRS complex
Pre-excitation syndromes
Accesory pathway exists that conducts faster than the AV node
Wolf-Parkinson White (WPW) and Lown-Ganong-Levine
Pre-excitation: Wolff-Parkinson-White (WPW)
- bundle of kent
- SHORT PR interval < 0.12 s
- QRS > 0.10 s
P slopes into the QRS–> DELTA WAVE
Pre-excitation: Lown-Ganong-Levine
- James Fiber (intra-nodal)
- uses conduction system past AV node (NO DELTA WAVE)
- NORMAL QRS
- only short PR interval (<0.12s)
MI and Ischemia
Ischemia- MC narrowed coronary arteries lead to restriction and then no blood flow (infarction)
- superimposed thrombosis initiated by plaque rupture
- evolving changes on EKG while tropnin levels waiting from the lab
Ischemia - symptoms
substernal pressure, L shoulder pain, jaw radiating pain
- angina is typical chest pain assoc w CAD (coronary artery ds)
- ST segment depression or T wave inversions
- retun to baseline after relief of symptoms
Ischemia EKG
- T wave inversions
- can be normal variant in V3-V4 in young person
MI EKG changes
- T wave peaking followed by T wave inversion
- ST segment elevation
- apperance of new Q waves, >0.04 s (40ms) and depth at least 1/3 height of the R wave in the same complex (except aVR)
pathologic Q waves caused by the dead tissue walls
6 hrs till irreversible tissue death
Reciprocal changes in MI
- important to look for infarctions first
- not going to see ST elevation in ischemia
- if you do see ST elevation might also see reciprocal changes in other leads (depressions but NOT ischemia)
MI & Ischemia- Non Q wave infarction
- T wave inversion and ST segment DEPRESSIONS
- lower risk of initial mortality, but higher risk for further infarction
“small, incomplete infarction”
-prevent next MI w/aggressive management
Ischemia- Printzmetal Angina
- ST segment elevation
- can occur at anytime, coronary artery SPASM
- Return to baseline quickly w/ anti-anginal meds (NITROGLYCERIN)
infarction would not go away with nitro
NO CLOT, just spasm
