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Flashcards in EKG Deck (77)
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1
Q
Sinus tachycardia
A
-Rate is over 100; just a fast rate (may be 120-150 but NOT as high as 160)
-Regular rhythm
2
Q
Sinus bradycardia
A
-Rate is less than 60; SLOW rate (if getting into 30s, start to suspect an AV block, usually wont be THAT low)
-Regular rhythm
3
Q
Sinus vs. Junctional
A
Sinus- has a P wave
Junctional- absence of a P wave
4
Q
Atrial flutter
A
-Flutter waves (F waves)
-Saw tooth pattern
-Rapid succession of identical back to back atrial depolarization waves
5
Q
Atrial flutter treatment
A
Tx same as afib
Definitive treatment is catheter ablation
6
Q
Rule for measuring Atrial flutter on EKG
A
300/150/75 rule
300- 1:1 (For every QRS- you have 1 P wave)
**150- 2:1 block**
75- 3:1 block
7
Q
HR of _______ tells you its atrial flutter (count it out by QRS complex)
A
150

If you see HR of 150, you HAVE to consider atrial flutter
8
Q
Atrial fibrillation
A
*NO P WAVES*
-Irregularly irregular (classic!!!)
-Chaotic erratic baseline
-No p waves prior to qrs
-Irregularly spaced qrs complexes
9
Q
Causes of A-fib
A
-HTN
-CAD (coronary artery disease)
-rheumatic heart disease
-*binge etoh (holiday heart)*
-valvular heart disease
-*hyperthyroid*
-Atrial stasis
-CVA
-thromboemobolism
10
Q
Treatment (rate control vs rhythm control)
A
RATE CONTROL: B blockers, digoxin, Ca ch blockers, anticoagulation (coumadin, pradaxa)

RHYTHM CONTRO: class IC, III or cardioversion (electrical or pharmaceutical, last option)
11
Q
A fib with RVR (rapid ventricular response)
A
-seen in older patients, worry that ventricles aren't filling
-Looks like A Fib but with very irregular AVF, V1, V2, V3
-Atria aren’t filling properly (no time bc of high HR), ventricles can’t fill either, BP drops severely, hypotension
12
Q
What can't be used to treat A Fib with RVR?
A
**B blocker or Ca channel blocker- can’t use this bc it will drop BP even further**
13
Q
During A Fib with RVR lateral leads will show
A
ST depression (esp older patients, with high HR)

-Reason: heart is getting ischemic, low cardiac output; O2 delivery to heart is getting sacrificed; this is a RATE related change (rate related ischemia, NOT necrosis or MI, but ischemia)
14
Q
Pericarditis
A
*Most common EKG change- DIFFUSE ST SEGMENT ELEVATION*
(ALL ST segments will be elevated; Must see this on an anatomical lead)
-->LOOK FOR bump immediately following QRS

**PR DEPRESSION IS ALSO SEEN**
(also look for big dip right BEFORE QRS complex)
15
Q
Pericarditis is seen primarily in
A
younger people
-Inflammation of lining of heart
16
Q
SVT (Supraventricular tachycardia)
A
-HR more that 160, 170 but can be as high as 210-220
-Complaint is *palpitations*, light headedness, chest pain, etc.
17
Q
SVT shows what EKG changes
A
-Rate related ischemia (ST depression is seen)
**Look for dip immediately AFTER QRS complex**

-HR will be more than 160-170 (or higher)
-REGULAR rhythm
18
Q
If rhythm is regular (P-->QRS-->T) but rate is very fast, think ____
A
SVT
19
Q
For SVT treatment, may need to give
A
Adenosine (very unpleasant to give, heart stops, see flat line on EKG, but then you'll see P wave, then QRS and HR will resume)

Can try asking patient to bear down or carotid massage one side of neck at a time before giving adenosine
20
Q
Giving Adenosine during SVT will cause
A
the rate related ischemia to stop

(if adenosine doesn't work may beed to shock patient)
21
Q
Hyperkalemia
A
-peaked T waves
-look for another small peak/triangle right after QRS
22
Q
Most important treatment for Hyperkalemia
A
CALCIUM

(doesn’t lower K level, doesn’t do ANYTHING to K level, don't want to worry about this first, must first stabilize the cardiac membrane; ***Calcium- cardiac membrane stabilization***)
23
Q
Treatment order for Hyperkalemia
A
1. Calcium (stabilize membrane)
2. IV Insulin (to lower K) and Dextrose (need to counteract insulin to prevent hypoglycemia)
3. Albuterol and Bicarb- both lower K
24
Q
Kayexalate
A
is a drug but it isn’t good; give orally, causes diarrhea; doesn’t lower K very much, gives you intestinal necrosis and ischemia = BAD!!
25
Q
What will also show peaked T waves?
A
early MI
(but usually it's hyperkalemia!)
26
Q
Where to look for severe/uncontrolled hyperkalemia
A
V1, V2, V3 will show HUGE peaked T waves
27
Q
EKG changes seen when hyperkalemia goes untreated
A
*QRS widens (widened QRS is always BAD)
*Peaked T waves
*Prolonged PR interval
*Near sinusoidal pattern - see sine waves; patient has seconds left to live --> GIVE CALCIUM!!!!!!! (see immediate changes, will narrow/close QRS, etc.)
28
Q
If none if your drugs are working to lower K, must ______
A
use dialysis
29
Q
Causes of hyperkalemia
A
Patients taking K but not going to dialysis, eating K in their diet, non-compliant with dialysis, must figure out problem and prevent it or they will keep coming back
30
Q
V tach EKG changes
A
-all leads are irregular
-AV dissociation
31
Q
Clinical presentation of V tach
A
Stable vs Unstable (can't tell difference from EKG)

Stable- pt is alert, oriented and vitals are stable, not in resp distress; you have time with these pts (can treat with drugs)

Unstable- hypotensive, confused, lethargic (treatment= gets shocked)
32
Q
Treatment for stable vs unstable v tach
A
DIFFERENT!!
stable- drugs
unstable- shock
33
Q
Torsades de pointes
A
-Polymorphic vtach
-Sinusoidal waveform
**Long qt interval is huge risk factor**
34
Q
Torsades de pointes treatment
A
MAGNESIUM
35
Q
Causes of Torsades de pointes
A
Not from heart attack, usually a definitive cause: drugs, low k, low mg (electrolyte abnormalities), iatrogenic

Think drugs that increase QT interval: Macrolides (Arythromycin, azythromycin) and Zofran (for N/V)
36
Q
Drugs that can cause a long QT interval
A
-Antiarrhythmic (class 1A, III)
-Antibiotics (macrolides)
-Antipsychotics (haldol/haloperidol)
-Antidepressants (TCA’s)
-Antiemetic (zofran-brand/ ondansetron-generic)
37
Q
Congenital long qt syndrome
A
1. ROMANO-WARD SYNDROME
Autosomal dominant, pure cardiac phenotype (no deafness)
2. JERVELL & LANGE NIELSEN SYNDROME
Autosomal recessive, + sensorineural deafness

-Both are repolarization abnormalities, usually due to ion channel defects
-increased risk of sudden cardiac death due to torsades de pointes
38
Q
1st degree AV block
A
-Prolonged PR (PR > 200msec)
-sinus bradycardia
-benign, asymptomatic
39
Q
2nd degree AV block type 1 (mobitz 1)
A
-PR progressively gets longer, then drops a QRS
-usually asymptomatic
-P wave transmits without QRS
-Regularly Irregular (irregular, with pattern)
-QRS gets longer and longer and longer, then eventually drops
40
Q
2nd degree AV block type 2 (mobitz 2)
A
-PR remains constant, but occasionally drops a QRS
-More serious, QRS just drops out of nowhere
-Treated with pacemaker
41
Q
2nd degree AV block type II presents clinically with
A
Patients present with syncope and lightheadedness (because with QRS drops, no CO)
42
Q
3rd degree (complete heart block)
A
-P and QRS are independent of each other
-P-P equal; R-R equal; atrial rate faster than ventricular
-AV and SA nodes aren’t communicating
-QRS is doing what AV node is doing (HR WILL BE 30)
-P waves will march out; can predict where every single P wave will be
-NO RELATIONSHIP between P waves and QRS complexes
43
Q
Disease that can cause 3rd degree HB
A
Lyme Disease
44
Q
Treatment for 3rd degree HB
A
-Pacemaker needed
-Pt is often very symptomatic
45
Q
Important EKG findings for 3rd degree HB
A
1. P waves march out
2. QRS complexes are seen without any correlating P waves before them
46
Q
RBBB (Right Bundle Branch Block)
A
-Look for bunny ears in V1, V2, V3
-QRS must be more than 100
-Lead V5, V6- SEE A WIDE S WAVE
-Usually asymptomatic, may be acute (usually its not)
47
Q
Cause of RBBB
A
-Usually get BBB from scar tissue, previous damage from MI or infection
48
Q
LBBB
A
-Looks like a stmi but its NOT
-QS pattern (distinct) will be in V1, 2, and 3
-Broad R wave, deep S wave, and inverted T wave
-QRS is more than 120 (enlarged, wide QRS)
49
Q
Diagnosing LBBB
A
Can’t diagnose LBBB on its own, if you don’t have an old EKG to see a definite change, you call it a stmi (MI)
50
Q
MI will show up on EKG as
A
ST segment elevation
(HUGE hill after QRS, looks like tombstone)
51
Q
If ST elevation is seen in leads II, III or AVF, stmi is located in ___________
A
inferior wall
52
Q
Reciprocal changes are
A
ST segment depressions and T wave inversions that FURTHER SUPPORT an MI occurring on an EKG
(some doctors will not call it a stmi without seeing reciprocal changes; seem in upper left hand corner of EKG, leads I, II, aVL)
53
Q
Inferior wall MI
A
-ST elevation in leads II, III, aVF
-may see reciprocal changes in I, II and AVL
54
Q
Anterior wall MI
A
-“Widow maker”
-Occlusion of LAD  causes more damage than right or circumflex; more proximal lesion= more damage
-ST segment elevation in V2, V3, V4, V5 (V1-V5 possible)
55
Q
Why people die of MI they are actually dying of
A
lethal arrhythmias--> occur bc of necrosis (necrosis causes arrhythmias)
56
Q
STMI's may be confused with
A
hyperkalemia but its NOT

Need to think about patient presentation
(patient with this EKG will present with pain down arm, SOB, chest tightness, pain, etc)
57
Q
If ST elevation in V1-V5 think
A
Anterior wall MI
58
Q
Brugada syndrome
A
-Autosomal dominant
-Asian, males mostly
-Pseudo right bundle branch block
-ST elevation V1-V3 (NOT A STMI)
-Increased risk of ventricular tachyarrhythmias and sudden cardiac death (die of v-tach or v-fib)
-No known CAD or structural abnormality
59
Q
Treatment for Brugada Syndrome
A
implantable defibrillator (huge decrease in morbidity and mortality)
60
Q
V fib
A
-completely irregular, squiggly line; no waves of any sort
-Pt comes in dead, pulseless
-must use defibrillator/AED
61
Q
When people die they usually have
A
v-fib or v-tach (lethal arrhythmias)
62
Q
Inferiolateral ischemia description/causes
A
Ischemia- oxygen deficiency to an area (similar to penumbra in stroke)
Ischemia is reversible; you must find the source in order to fix this

Could be unstable angina, coronary artery disease to high decree, causing ischemia but not yet an MI (very close, similar to a TIA)
63
Q
Inferiolateral ischemia EKG findings
A
***SEE ST SEGMENT DEPRESSION (dip right after QRS, usually ALWAYS an acute, VERY RARELY is it old/chronic)***
ST segment depression is active/dynamic; something is happening in the body (ISCHEMIA)

***SEE T WAVE INVERSTION; can be OLD (need an old EKG to compare)***
64
Q
WPW (wolff parkinson white)
A
-Most common type of ventricular preexcitaion syndrome
-Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses the rate-slowing AV node
-May result in reentry circuit, causing SVT
65
Q
WPW (wolff parkinson white) EKG findings
A
-Delta wave (ventricles begin to partially depolarize earlier as seen via delta wave)

-wide QRS
-short PR
66
Q
WPW (wolff parkinson white) treatment
A
***NO DIGOXIN, B-BLOCKERS, CA CH BLOCKERS (will kill patient)***
67
Q
Inferior MI is most likely due to
A
-Vessel occluded is most likely RCA (right coronary artery)
-This can also lead to posterior MI (RCA occlusion)

-If someone is having posterior MI, its in conjunction with an inferior wall MI, displayed with ST depression in VI or VII
-Can get posterior MI in absence of inferior MI, but not very common
68
Q
Anterior wall MI (V1-V4), MI in which artery?
A
LAD (left anterior descending)
69
Q
Anteroseptal (V1-V2), MI in which artery?
A
LAD
70
Q
Anteroapical (V3-V4), MI in which artery?
A
distal LAD
71
Q
Anterolateral (V4-V6), MI in which artery?
A
LCX (left circumflex) or LAD
72
Q
Lateral wall (I, AVL), MI in which artery?
A
Left circumflex
73
Q
Inferior wall (II,III,AVF), MI in which artery?
A
RCA
74
Q
What symptoms are most commonly seen with inferior wall MI compared to all other MIs?
A
WILL SEE GI SYMPTOMS; Epigastric pain, nausea, vomiting***
75
Q
Order of drugs for MI treatment
A
With any MI:
1. Aspirin first
2. Plavix (or clopridogel) second
3. then debate about Nitro third
(Aspirin and Plavix will decrease morbidity and mortality, Nitro will NOT, but helps s/s, pain)
76
Q
Inferior wall MI you WILL NOT GIVE
A
NITRO**- may cause R sided heart failure, R vent (responsible for preload), it will decrease, R vent isn’t pumping blood correctly; nitro decreases preload, BP will drop even further, very dangerous; use morphine instead, NOT NITRO!!
77
Q
What will you see on echocardiogram with MI?
A
Wall motion abnormality (hypokenesis)