EKG Flashcards

1
Q

sinus tach

A

> 100 bpm
if >140-150 (something else going on)

sinus denotes that there is a p-wave

junctional implies absence of p-wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

sinus brady

A

HR less than 60

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

atrial flutter

A

“saw tooth pattern”: flutter/f-waves

comes in specific HRs, (comes with a block)
300/150/75

300: 1:1
every 1 f-wave you are getting a QRS
-v. few things make a HR 300!

150: 2:1 (most common)
2 f-waves for a QRS
-consider a flutter along with sinus tach

75: 3:1
3 f-waves for a QRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

a flutter

A

rapid succession of identical back to back atrial depolarization waves

identical morphology –> “saw tooth”
tx same as a fib (rate control, anticoag., cardioversion)

definitive tx is catheter ablation: trying to destroy wire? (neural condition) that is causing the arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

know chart of AVL, V1 etc

A

on slide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

cheat

A

print out 2x as fast

spread out rhythm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

atrial fibrillation

A

irregularly irregular, Chaotic erratic baseline

no discernable p-waves, Irregularly spaced qrs complexes

usually in response to ventricular response (pulse, HR)

serious if RVR (rapid ventricular response)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

a fib slide

A

FA: HTN, CAD, rheumatic heart disease, *binge drinking (“holiday heart”), HF, valvular disease, *hyperthyroidism

can lead to atrial stasis, CVA, thromboembolisms

worse: in and out of a fib! –>atrial “kick”; feels like worms–>thrombus gets knocked out–>stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

a fib tx

A

rate control (B-blockers, β-blocker, non-dihydropyridine Ca2+ channel blocker, digoxin)

anticoagulation (coumadin/warfarin, pradaxa) (may not need based on RAD score)

rhythm control (class IC, III antiarrhythmics)

cardioversion (electrical or pharmaceutical)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the concern with a fib with RVR ??

A

the concern is decreased heart filling (i.e. HR 160)

hypotensive (BP dec.)

if use B-blocker to lower HR, problem: exacerbate hypotension (often still use with hope that lowering HR increases filling time, eventually inc. BP)

ST depression in lateral leads
oxygen delivery to heart is sacrificed: rate-related ischemia
-reversible, need to slow down HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

pericarditis

A

inflammation of heart sac
disease of younger ppl

EKG changes: diffuse ST segment elevation
looks like a “global MI”: systemic problem

KEY: PR depression
dips below baseline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Superventricular tachycardia: SVT

A

HR 160-170, can be as high as 210, 220

palpitations, SOB, syncope, lightheadedness, etc.

can’t make out p-waves

regular rate (vs. afib)

rate-related ischemia:
ST depression

when rhythm interrupted: adenosine was given, or other mechanisms to stop SVT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how do you stop SVT

A

bear down
or carotid massage 1 side

adenosine: will stop heart, unpleasant experience, CP, SOB
- warn them: will feel like you are going to die

if pressure of 80: shock him!
“edison medicine” (unstable pt)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how to tx hyperkalemia w/ EKG changes

A

**calcium: does NOT lower K+ BUT stabilizes cardiac membrane

second: lower K+ with insulin IV

then dextrose to avoid hypoglycemia

more K+ lowering drugs:

albuterol
bicarb 
Kayexelate (sucks!)
causes diarrhea, intenstinal ischemia, necrosis
(does not lower K+ much! dead drug)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

hyperkalemia on EKG

A

peaked T-waves
similar to early MI (hyperkalemia more common)

will increase if exacerbated/prolonged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

severe hyperkalemia

A

widened QRS (bad!!! always)

peaked T waves

PR prolongation

near sinusoidal pattern–>seconds to live

give Ca2+!!! can see QRS narrowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

if all drugs not working in hyperkalemia ??

why does this happen??

A

dialysis

stopped taking diuretic, still K+
noncompliant with dialysis, renal diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

V tach

A

varying presentation
AV dissociation

stable:
A/O, mild symptoms, stable vitals besides tachy, no resp distress, have time!
-tx: drogas

unstable:
hypotensive, confused, lethargic, dead
-tx: shock

tx differently!
can’t tell from EKG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

torsades de pointe

A

near death, very serious rhythm

polymorphic vtach
sinusoidal waveform

*long QT interval is huge risk factor

can lead to vfib: DEAD!

causes:
drugs, (that inc. QT: macrolides: azithromycin, erythromycin; zofran) (more to come)
low K+, low Mg+

tx: Mg sulfate

if K+ continually low even with tx, check Mg level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

which drugs cause long QT (can lead to torsades)

A

ABCDE

antiArrhythmics (class 1A, III)
antiBiotics (macrolides)
antiCychotics (haldol/haloperidol)
antiDepressants (TCA's: narrow window)
antiEmetic (zofran/ondansetron)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

congenital long QT syndrome: inherited

A

Romano-ward syndrome:

autosomal dominant, pure cardiac phenotype (no deafness)

Jervell and Lange Nielsen syndrome:

autosomal recessive and sensorineural deafness

22
Q

congenital long QT syndrome: others

A

repolarization abnormality (ion channel defects)

inc. risk of sudden cardiac death due to torsades de pointes

23
Q

1st degree AV block, sinus bradycardia

A

PR >200 msec (prolonged)

asymptomatic, benign

24
Q

2nd degree type 1

mobitz 1

A

usually asymp, regularly irregular

PR lengthens then QRS drops! :at least you saw it coming (less sev.)

25
Q

2nd degree type 2

mobitz 2

A

QRS drop without lengthening PR

tx: pacemaker

frequent, random dropping

present with syncope due to lack of cardiac output

FA: may progress to 3rd degree block

26
Q

3rd degree block

A

QRS: HR in 30s!
miscommunication btw SA and AV node (intrinsic, slower)

p-waves: all march out (i.e. HR 70)

ZERO relationship btw p waves and QRS
atrial rate faster than ventricular rate-bradycardic rhythm (not sinus bradycardic: p-waves not influencing QRS)

27
Q

3rd degree HB tx

can often be caused by ??

A

tx: pacemaker needed
often v. symptomatic

lyme disease can cause this

28
Q

RBBB

A

QRS > 100?
“bunny ears”: V1, V2, V3 (rSR’)

V4, V5, V6: wide S wave

typically asymptomatic
may be acute (rare)

from scar tissue from HA, infection, etc

29
Q

LBBB

A

more worrisome than RBBB

V6: broad R wave with deep S, inverted T-wave

V1, V2, V3: QS pattern

cannot dx acute MI in LBBB

QRS > 120 mS

need previous EKG to dx this over STEMI:
STEMI unless proven otherwise

page cardiologist

30
Q

STEMI

A

ST elevation MI

“tombstone”

some cardiologist require
reciprocal changes:

ST segment depressions
T-wave inversions:
further support MI

31
Q

inferior wall MI

A

II, III, aVF

reciprocal changes in 1, aVL, V2

32
Q

anterior wall MI

A

“the widow maker”

V2, V3, V4, V5

reciprocal changes: aVR ??

occlusion of LAD, supplies largest part of heart

the more proximal, the more damage

33
Q

why do ppl die of heart attack?

A

lethal arrhythmias

necrosis –>source of arrhythmias

34
Q

anterior wall MI: don’t confuse with ??

A

hyperkalemia!

35
Q

Brugada syndrome

A

autosomal dominant
asian, mostly male (8:1)
pseudo RBBB

ST elevation V1-V3 (all the time, not a STEMI)

inc. risk of ventricular tachyarrhythmias and sudden cardiac death

no known CAD or structural abnormality

36
Q

Brugada syndrome tx

A

implantable cardioverter-defibrillator (ICD)

about 75% increase in survival? (dec. in morb/mort)

37
Q

Vfib

A

completely erratic rhythm
no waves of any sort
fatal if no immediate CPR/defibrillation
(DEAD)

38
Q

rhythm you go into before death

reasoning behind ??? everywhere

A

Vfib and Vtach

AEDs

39
Q

inferiolateral ischemia

A

oxygen deficiency to inferiolateral area

analogous to penumbra in stroke (dead area is necrosis)
-is reversible, can save!

how to fix??:
find the source
i.e. unstable angina (CAD pre-MI)

40
Q

how to ID inferiolateral ischemia

A

ST segment depression (acute! typically) -dynamic

inferior: II, III, aVF
lateral: V5, V6

ddx from ST depression/T-wave inversion caused by from CAD (can be acute or old!)

41
Q

WPW: Wolff-Parkinson White

A

most common type of ventricular pre-excitation syndrome

abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) BYPASSES rate-slowing AV node

ventricles begin to partially depolarize earlier as seen via delta wave and wide QRS and short PR

may result in reentry circuit–>SVT (what kills!)

42
Q

WPW tx

A

NO DIGOXIN, NO B-BLOCKERS, NO CCBs

43
Q

T-wave inversion lateral leads (ischemia)

A

inversion: V2, V3, V4, V5, V6 ?

44
Q

slide 86: inferior MI, anything else??

what vessel occluded in inf. MI

A

RCA : may also lead to posterior MI

45
Q

posterior wall MI

A
  1. (often) in conjuction with inferior wall MI
  2. ST depression in V1 or V2 (back of heart)-OPPOSITE/RECIPROCAL of anterior wall MI (so depression vs elevation)
    * flip around and read thru back, will look elevated*
46
Q

LAD artery in MI

A

anterior wall MI (V1-V4)
anteroseptal (V1-V2)
anteroapical (V3-V4) (distal LAD)

47
Q

LCX (circumflex) or LAD in MI

A

anterolateral (V4-V6)

48
Q

LCX in MI

A

lateral wall (I, AVL)

49
Q

RCA in MI

A

inferior wall (II, III, AVF)

50
Q

inferior wall MI (RCA) will present with what type of symptoms ??

A

GI symptoms: epigastric pain, N/V

*don’t miss!

51
Q

how to tx MI

A

ASA
plavix (clopidogrel)
(both decrease morb/mort)

nitro? (does not dec. mort/morb) will make feel better
actually give first! works quickest to decrease preload

52
Q

don’t give nitro to pt w. ??

A

inferior wall MI

RV responsible for pre-load, if knocked out, exacerbates decreased pre-load, weakens pump

ECHO: of MI shows: wall motion abnormality, hypokinesis

give morphine