C: Ekg Abnormalities Ii

Front 1

If we see a negative p-wave, and a shortened PR (but normal QRS, QT, and T)... what should we think about?

Back 1

depolarization of the atria is heading in the opposite direction of normal, and it's getting to the ventricle sooner.
= junctional/ectopic rhythm.

Front 2

Describe first degree AV block.

Back 2

not really even a 'block' persay, it's just a large delay b/t p-wave and QRS.

Everything else is normal though, and every P has a QRS, etc.

Front 3

Second Degree AV block has two types, what are they? What is also called Wenckebach?

Which is more dangerous? Why?

Back 3

Mobitz type I, Mobitz type II

Type I

Type II - it is more likely to progress to complete block.

Front 4

Describe the Wenckebach irregularity.

Describe 2nd deg. AV Type II.

Back 4

Progressive prolongation of the PR interval, until you lose a beat. You will often see a pattern of "group beating"

fixed P to R relationship (consistent conduction), just suddenly dropped a beat. NO steady prolongation.

Front 5

What is seen in a high grade AV block?

Third Degree AV block?

Back 5

Basically a more severe Mobitz type II - this is a bridging term.

can be 3:1 or larger....

Complete dissociation of P waves from QRS

Front 6

What is a Supraventricular tachycardia? Another name?

Characteristics?

Back 6

rhythm process in which the ventricles are activated from the atria or AV node/His bundle region
- narrow QRS tachycardia

QRS typically narrow (w/o additional BBB)
Usually paroxysmal (starts and stops abruptly) = PSVT

Front 7

What are some causes of sinus tachycardia?

Back 7

Hypovolemia
Fever
Respiratory distress
Hyperthyroidism
Bronchodilators
exercise, excitement, etc.

Front 8

What is the typical direction for an atrial flutter circuit?

What is seen on ECG?
Most important leads to look at?

Back 8

counterclockwise.

P-wave vector changes, now looks away from your inferior leads, and is aiming more towards V1.
- sawtoothed P-waves in inferior leads w/ variable ventricular response
- positive in V1.
- ~300waves/min

inferior leads and V1

Front 9

What is a typical description of an a.fib rate?

Which lead is it best seen in?
What is actually keeping us alive?

Back 9

Chaotic, rapid atrial rate at 400-600 bpm

No well described circuit...

V1

The fact that most impulses are being blocked by the AV node.
- Irregular which ones get through!

Front 10

What are the 3 forms of a.fib? Which is unable to be restored to sinus rhythm by Tx?

Associated dz?

Back 10

Paroxysmal, Persistant, Permanent

Chronic/Permanent

Cardiac dz like HTN, CAD, etc.

Front 11

What can RF be used to treat? What does it do?

Back 11

a.flutter, afib, SVT

Compartmentalizes the atria

Front 12

What is ventricular tachycardia? (VT) Common rate range?

Can be either non-______ or ______. What do these categorizations mean?

Features? What is a specific sign (but not a sensitive one)?

Back 12

Focused firing from the ventricles
100-250bpm

non-sustained or sustained:
Non-sustained VT is defined as a run of tachycardia of less than 30 seconds duration; a longer duration is described as sustained VT.

Wide-complex tachycardia
P's aren't associated with V's.... look for them - they are specific but not very sensitive.

Front 13

What is the difference between a monomorphic and a polymorphic VT?

When you think something might be VT or PSVT, what do you do?

Back 13

VT may be monomorphic (typically regular rhythm originating from a single focus with identical or similar QRS complexes) or polymorphic (may be irregular rhythm, with beat to beat variation in QRS complexes).

Treat as if VT. some Tx for PSVT can kill VT pts.

Front 14

* Rate greater than 100 beats per minute (usually 150-200)
* Wide QRS complexes (>120 ms)
* Presence of atrioventricular (AV) dissociation
* Fusion beats

.... suggests?

Back 14

VT.

Front 15

Monomorphic VT implies ______, but sometimes be seen in structurally ______ hearts.

Polymorphic VT can result from ________ or conditions that prolong _______ _______.

Back 15

Heart Dz; normal

myocardial ischemia; ventricular repolarization

Front 16

Totally chaotic rapid ventricular rhythm; often precipitated by VT is called? Tx?

Order the following: Polymorphic VT, VF, Monomorphic VT

Back 16

VFibrillation

Fatal unless promptly terminated (DC Shock)

Mono --> poly --> VF

Front 17

What is a delta wave?

Back 17

preexcitation of the ventricle, obliterating QRS interval. Depending on how much preexcitation you get, you'll get more/less slurring.

Front 18

What are some characteristics of Wolff-Parkinson-White Syndrome?

Back 18

very short PR interval, slurred QRS (Delta waves). Very suspicious for preexcititation of the ventricles.

Front 19

(aVF, aVL, V1) = format of positivity of delta wave. Given these patterns, give probably WPW AP location:
+ + -
+ - +
- - +
- + +

Back 19

Left lateral
left posterior septal
Right post. septal
Right. Lateral/anterior

Front 20

What else can sort of cause the Sx of WPW?

Back 20

Atrioventricular re-entry tachycardia, if it is orthostatic.

Front 21

What defines a Long QT (LQT)? Autosomal dominant inhereited dz? Recesive? Is sporadic dz possible?

What are the three types of LQT and their pathophysiological mechanisms?

Where is each seen?

Back 21

QTc > .46s (fem) .44 (male)
Romano-Ward Syndrome
Jervelll-Lange-Nielsen Syndrome
Yes.

LQT 1 (exercise/swimming), 2 (emotion/auditory): decreased function of 2 potassium channels, prolong QT
LQT 3 (die in sleep/rest): gain of functon in NA channel, prolongs ST segment and thereby prolongs QT

Front 22

Of the LQTs the one that has Tall, wide-based T-waves?

T-valve alternans, low or not T-wave?

tall, wide based waves?

Back 22

LQT1

2

3

Front 23

The ST segment represents the current flow generated when myocardial cells repolarize
This is mediated by the opening of ________ channels on the cell membrane allowing ________ to flow out of the cell and return to a negative membrane potential

Back 23

potassium, potassium

Front 24

ST elevation in one region of the heart can yield __ ________ on the other side.

Back 24

ST depression.

Front 25

Please give the drug therapy or ion change (increase/decrease) associated with each of the following ECG changes.

Back 25

Front 26

Please fill in the blanks.

Back 26

Front 27

Plz fill in the blanks.

Back 27

Front 28

ST depression, T wave inversion, no Q waves

ST seg elevation, no Q waves

Abnormal Q waves, ST seg elevation or depression, T waves may be abnormal

please match these with MI, myocardial ischemia, and myocardial injury

Back 28

Ischemia: ST segment depression, T wave inversion, no Q waves
Injury: ST segment elevation, no Q waves
Infarct: abnormal Q waves, ST segment elevation or depression, T waves may be abnormal

Front 29

Leads __ and ___ are the most sensitive to look at for MI b/c they're over the most muscle.

Back 29

V5 and V6

Front 30

ST elevation that can signify an MI has what characteristics?

Back 30

>1-2mm in two or more contiguous leads

usually upwardly convex configuration

Front 31

When localizing an MI, tell me what location you think of when you see q's in:

V1-V3
V2-V4
V4-V6
I, avL
II, III, avF

Do these localizations hold true for RBBB? LBBB? Which leads can be assessed, if this doesn't hold true?

Back 31

anteroseptal
anterior
anterolateral
high lateral
inferior

(basically just the areas that they're over)

RBBB yes.
LBBB, no.
- have to assess only V5, V6, I, aVL

Front 32

R wave should be (smaller/larger) in leads over the infarcted tissue?

How many leads w/ Q are needed for true localization? How about for just calling the cath lab?

Back 32

smaller.

3 leads. 2 leads.

Front 33

What leads are opposite of the inferior leads?

Back 33

The anterior leads! V1-V3

Front 34

To Dx an Acute MI in LBBB, you need:

>/= ___mm STE concordant w/QRS
>/= ___mm STD in _____
>/= ____mm STE discordant w/ QRS

Back 34

1mm
1mm in V1-V3
5mm

Front 35

How can you Dx a posterior infarct?

Back 35

R in V1 or V2 >/= 0.04
R > S in V1 or V2
-- This is the 'mirror image' of a Q wave if we had a posterior lead. ***Understand?***
Acute STD & upright T in V1 or V2

Front 36

What is Cabrera's sign?

Does LBBB preclude Dx-ing MI?

Back 36

'notching' or the ascending S in the mid-left precordial leads.

No, but it can mask changes of prior or acute MI --> reducing sensitivity of ECG in those situations.

Front 37

When you see an ECG i/ someone w/ respiratory infection where the J-point (bt QRS and ST/T) is trying to reach back to baseline.... coupled with diffuse elevations.... what should you be suspicious of?

Back 37

pericarditis.

Front 38

ST elevation (all leads except aVR)
J point returns to baseline
T wave inversion
ECG resolution

ST/T changes
PR depression
Low voltage QRS
Electrical alternans
Sinus tachycardia


--- what should we be thinking of?

Back 38

Acute pericarditis

Front 39

Acute MI
Aneurysm
Pericarditis
Early repolarization
LV hypertrophy
LBBB/RBBB
Paced rhythms
Hyperkalemia
Assorted cardiomyopathies (HCM, WPW, Brugada, infiltrative disease, myocarditis)
Congenital heart disease
Pulmonary disease (chronic, PE)

.....all are on the diff Dx of ___ _______.

Back 39

ST elevation