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EKG Flashcards

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
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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
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3
Q

Sinus vs. Junctional

A

Sinus- has a P wave

Junctional- absence of a P wave

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4
Q

Atrial flutter

A
  • Flutter waves (F waves)
  • Saw tooth pattern
  • Rapid succession of identical back to back atrial depolarization waves
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5
Q

Atrial flutter treatment

A

Tx same as afib

Definitive treatment is catheter ablation

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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

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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

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8
Q

Atrial fibrillation

A
  • NO P WAVES*
  • Irregularly irregular (classic!!!)
  • Chaotic erratic baseline
  • No p waves prior to qrs
  • Irregularly spaced qrs complexes
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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
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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)

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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
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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

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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)

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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)

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15
Q

Pericarditis is seen primarily in

A

younger people

-Inflammation of lining of heart

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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.

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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
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18
Q

If rhythm is regular (P–>QRS–>T) but rate is very fast, think ____

A

SVT

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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

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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

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21
Q

Hyperkalemia

A
  • peaked T waves

- look for another small peak/triangle right after QRS

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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)

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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
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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!!

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25
What will also show peaked T waves?
early MI | but usually it's hyperkalemia!
26
Where to look for severe/uncontrolled hyperkalemia
V1, V2, V3 will show HUGE peaked T waves
27
EKG changes seen when hyperkalemia goes untreated
* 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
If none if your drugs are working to lower K, must ______
use dialysis
29
Causes of hyperkalemia
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
V tach EKG changes
- all leads are irregular | - AV dissociation
31
Clinical presentation of V tach
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
Treatment for stable vs unstable v tach
DIFFERENT!! stable- drugs unstable- shock
33
Torsades de pointes
- Polymorphic vtach - Sinusoidal waveform * *Long qt interval is huge risk factor**
34
Torsades de pointes treatment
MAGNESIUM
35
Causes of Torsades de pointes
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
Drugs that can cause a long QT interval
- Antiarrhythmic (class 1A, III) - Antibiotics (macrolides) - Antipsychotics (haldol/haloperidol) - Antidepressants (TCA’s) - Antiemetic (zofran-brand/ ondansetron-generic)
37
Congenital long qt syndrome
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
1st degree AV block
- Prolonged PR (PR > 200msec) - sinus bradycardia - benign, asymptomatic
39
2nd degree AV block type 1 (mobitz 1)
- 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
2nd degree AV block type 2 (mobitz 2)
- PR remains constant, but occasionally drops a QRS - More serious, QRS just drops out of nowhere - Treated with pacemaker
41
2nd degree AV block type II presents clinically with
Patients present with syncope and lightheadedness (because with QRS drops, no CO)
42
3rd degree (complete heart block)
- 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
Disease that can cause 3rd degree HB
Lyme Disease
44
Treatment for 3rd degree HB
- Pacemaker needed | - Pt is often very symptomatic
45
Important EKG findings for 3rd degree HB
1. P waves march out | 2. QRS complexes are seen without any correlating P waves before them
46
RBBB (Right Bundle Branch Block)
- 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
Cause of RBBB
-Usually get BBB from scar tissue, previous damage from MI or infection
48
LBBB
- 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
Diagnosing LBBB
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
MI will show up on EKG as
ST segment elevation | HUGE hill after QRS, looks like tombstone
51
If ST elevation is seen in leads II, III or AVF, stmi is located in ___________
inferior wall
52
Reciprocal changes are
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
Inferior wall MI
- ST elevation in leads II, III, aVF | - may see reciprocal changes in I, II and AVL
54
Anterior wall MI
- “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
Why people die of MI they are actually dying of
lethal arrhythmias--> occur bc of necrosis (necrosis causes arrhythmias)
56
STMI's may be confused with
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
If ST elevation in V1-V5 think
Anterior wall MI
58
Brugada syndrome
- 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
Treatment for Brugada Syndrome
implantable defibrillator (huge decrease in morbidity and mortality)
60
V fib
- completely irregular, squiggly line; no waves of any sort - Pt comes in dead, pulseless - must use defibrillator/AED
61
When people die they usually have
v-fib or v-tach (lethal arrhythmias)
62
Inferiolateral ischemia description/causes
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
Inferiolateral ischemia EKG findings
***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
WPW (wolff parkinson white)
- 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
WPW (wolff parkinson white) EKG findings
-Delta wave (ventricles begin to partially depolarize earlier as seen via delta wave) - wide QRS - short PR
66
WPW (wolff parkinson white) treatment
***NO DIGOXIN, B-BLOCKERS, CA CH BLOCKERS (will kill patient)***
67
Inferior MI is most likely due to
- 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
Anterior wall MI (V1-V4), MI in which artery?
LAD (left anterior descending)
69
Anteroseptal (V1-V2), MI in which artery?
LAD
70
Anteroapical (V3-V4), MI in which artery?
distal LAD
71
Anterolateral (V4-V6), MI in which artery?
LCX (left circumflex) or LAD
72
Lateral wall (I, AVL), MI in which artery?
Left circumflex
73
Inferior wall (II,III,AVF), MI in which artery?
RCA
74
What symptoms are most commonly seen with inferior wall MI compared to all other MIs?
WILL SEE GI SYMPTOMS; Epigastric pain, nausea, vomiting***
75
Order of drugs for MI treatment
``` 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
Inferior wall MI you WILL NOT GIVE
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
What will you see on echocardiogram with MI?
Wall motion abnormality (hypokenesis)

CSI- Winter (44 decks)

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