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Intern Month Lectures > Cards/EKGs > Flashcards

Cards/EKGs Flashcards

1
Q

Causes of LBBB

A 
Aortic stenosis
Ischaemic heart disease
Hypertension
Dilated cardiomyopathy
Anterior MI (2/2 LCx or RCA blockage + LAD doesn't supply LPost fascicle)
Primary degenerative disease (fibrosis) of the conducting system (Lenegre disease)
Hyperkalaemia
Digoxin toxicity
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2
Q

Causes of RBBB

A

Right ventricular hypertrophy / cor pulmonale
Pulmonary embolus
Ischaemic heart disease
Rheumatic heart disease
Myocarditis or cardiomyopathy
Degenerative disease of the conduction system
Congenital heart disease (e.g. atrial septal defect)

2/2 RCA MI or LCx MI

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3
Q

RBBB features

A

Broad QRS > 120 ms
RSR’ pattern in V1-3 (‘M-shaped’ QRS complex)
Wide, slurred S wave in the lateral leads (I, aVL, V5-6)

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4
Q

Sodium-channel blocking agent — e.g. tricyclic antidepressant ECG features

A

patient presenting with seizures and hypotension, the combination of…

QRS broadening > 100 ms
R’ wave in aVR > 3 mm

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5
Q

Name the 8 Steps involved in reading an ECG

A 
Rate: fast, slow, normal?
Wide QRS or narrow?
Reg or irreg?
Ps or not? Connected to QRS?
Mean QRS axis/other intervals
Ischemic/Infarct
Hypertrophy
Special Situations
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6
Q

300 bpm

A

Artifact

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7
Q

200 bpm

A

Likely a bypass tract (WPW)

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8
Q

160+ bpm

A

AVNRT, AVRT

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9
Q

150 bpm

A

atrial flutter

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10
Q

140 bpm

A

Be careful with calling this or anything above this SINUS

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11
Q

100 bpm

A

Sinus tach

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12
Q

60 bpm

A

Lower limit of NSR

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13
Q

50 bpm

A

Bradycardia, but look at the P waves to make sure its actually sinus before you call it sinus brady

AV node rate

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14
Q

40 bpm

A

Ventricular escape rhythm

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15
Q

Right Axis Deviation

A

Likely pathology on R side of heart

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16
Q

Left Axis Deviation

A

Likely path on L side of heart

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17
Q

Isoelectric point on ECGs

A

TP segment

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18
Q

What causes diffuse ST elevation?

A

Pericarditis

Benign Early Repolarization

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19
Q

Normal ECG findings in children

A

Heart rate >100 beats/min

Rightward QRS axis > +90°

T wave inversions in V1-3 (“juvenile T-wave pattern”)

Dominant R wave in V1
RSR’ pattern in V1
Marked sinus arrhythmia
Short PR interval (< 120ms) and QRS duration (<80ms)
Slightly peaked P waves (< 3mm in height is normal if ≤ 6 months)
Slightly long QTc (≤ 490ms in infants ≤ 6 months)
Q waves in the inferior and left precordial leads.

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20
Q

PR Interval

A

Time from the onset of the P wave to the start of the QRS complex.

It reflects conduction through the AV node.

Normal 120 – 200 ms duration (three to five small squares).

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21
Q

PR segment abnormalities (2)

A

Pericarditis (PR depression, widespread STE)

Atrial ischaemia

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22
Q

1 ECG big and little box width (ms)

A

Big 200 ms

Little 40 ms

23
Q

Broad QRS causes (and their patterns)

A

Right bundle branch block produces an RSR’ pattern in V1 and deep slurred S waves in the lateral leads.

Left bundle branch block produces a dominant S wave in V1 with broad, notched R waves and absent Q waves in the lateral leads.

Hyperkalaemia is associated with a range of abnormalities including peaked T waves

TCA poisoning is associated with sinus tachycardia and tall R’ wave in aVR

Wolff-Parkinson White syndrome is characterised by a short PR interval and delta waves

Ventricular pacing will usually have visible pacing spikes

Hypothermia is associated with bradycardia, long QT, Osborn waves and shivering artefact

24
Q

aVR abnormalities (3)

A

Late R wave in aVR - Na channel blocker (TCA) use

PR elevations in AVR signifies pericarditis

Isolated STE in aVR but diffuse STD (>6 leads) elsewhere → R heart STEMI

25
Q

STEMI Definition

A

New ST segment elevation at the J point in at least two contiguous leads of

≥ 2 mm (0.2 mV) in men
≥ 1.5 mm (0.15 mV) in women
in leads V2-V3

or

≥ 1 mm (0.1 mV) in other contiguous chest leads or the limb leads

This means 1 mm in any two contiguous leads except leads V2 or V3, where the elevation must be 2 mm in men or 1.5 mm in women.

26
Q

Posterior MI findings

A

ST depression V1 to V4.
R > S in V1-V2 (upside-down Q wave)
ST elevation in the posterior leads of a posterior ECG (V7-V9).

27
Q

What does A New Left Bundle Branch Block signify?

A

Equivalent to a STEMI!

28
Q

Sgarbossa Criteria

A

In patients with left bundle branch block (LBBB) infarct diagnosis based on the ECG is difficult.
The baseline ST segments and T waves tend to be shifted in a discordant direction (“appropriate discordance”), which can mask or mimic acute myocardial infarction.
However, serial ECGs may show dynamic ST segment changes during ischemia.

The original three criteria used to diagnose infarction in patients with LBBB are:

  1. Concordant ST elevation > 1mm in leads with a positive QRS complex (score 5)
  2. Concordant ST depression > 1 mm in V1-V3 (score 3)
  3. Excessively discordant ST elevation > 5 mm in leads with a -ve QRS complex (score 2).
29
Q

Inverted T waves are seen in the following conditions

A 
Normal finding in children
Persistent juvenile T wave pattern
Myocardial ischaemia and infarction
Bundle branch block
Ventricular hypertrophy (‘strain’ patterns)
Pulmonary embolism
Hypertrophic cardiomyopathy
Raised intracranial pressure
30
Q

How to treat a R sided MI (inferior/posterior)

A

NO NITRO, they are preload dependent, give them FLUIDS instead

31
Q

Inferior MI reciprocal leads

A

I, aVL

32
Q

Posterior MI reciprocal

A

V1, V2, V3, V4

33
Q

Lateral MI reciprocal leads

A

Reciprocal II, III, aVF

Lateral leads 1, aVL, V5, V6

34
Q

7 Life Threatening Causes of Chest Pain

A 
ACS
Aortic Dissection
Cardiac Tamponate
PE
PTX
PNA
Esophageal Rupture (Boerhaave's)
35
Q

Chest Pain Tests (8)

A

ECG!!!

CBC
BMP
Troponin
BNP
UA - why?
CXR
Cardiac u/s?
36
Q

ACS Treatment (7)

A
  1. Nitrates (unless R sided or EDysf meds)
  2. ASA (aspirin) - nonentiric coated, chew, decr. mortality
  3. P2Y inhibitor (plavix-clopidogrel), decr. mortality
  4. Heparin/Anticoagulant (UFH —OR– enoxaparin-lovenox)
  5. IIb/IIIa Inhibitor - tirofiban-aggrostat OR integrillin
  6. Beta Blockers (to decrease myocardial demand, dont give 2 asthmatics)
  7. Thrombolytics vs Cath lab (but you’d stop Plavix!!!)
37
Q

HEART Score Components

A 
History (suspicious or not?)
ECG (changes?)
Age (<45, >65?)
Risk factors (how many?)
Troponin (nl or elevated?)
38
Q

HEART Score meaning….MACE

A

Chance of Major Adverse Cardiac Events (MACE)
0-3 points - 2% in 6 weeks
4-6 points - 13% in 6 weeks
7-10 points - 50% in 6 weeks

39
Q

Dosing nitrates in ACS

A

Reduces pain, does not reduce mortality

Sublingual: 0.3-0.4 mg q5 min up to 3 doses
IV nitroglycerin: 10-15 mcg/min and titrate up slowly
Paste? not used much here

Don’t give in EDysf patients within 24h (viagara, levitra) or 48h (cialis)

40
Q

Plavix-clopidogrel dosing

A

600 mg PO, followed by 300 mg PO qd.

If pt already on plavix, an addl. 300 mg is given.

Must not have had plavix in 1 week? if getting surgery.

41
Q

Role of beta blockers in ACS and dosing

A

Decrease myocardial O2 demand
Increase long term survival (not short)
Don’t give 2: CHFers, heart block, asthmatics (can cause bronchospasm)

Dosing
Metoprolol or atenolol

Metoprolol
50 mg PO q6h x2d,
then 100 mg PO q12h

42
Q

Door to balloon time (ACS)

A

90 min in PCI capable hospital

120 min for a transfer

43
Q

Nicardipine (used for, doses, drip)

A

Calcium-channel blocker

Used for hemorrhagic stroke to achieve BP control SBP<185, MAP<110. Can also use labetalol

44
Q

Epinephrine MOA for

  1. ACLS
  2. anaphylaxis
  3. asthma
  4. croup
  5. hypoglycemia
A

Non-selective alpha and beta agonist produced by adrenal glands.

  1. ACLS:
    ↑ perfusion pressure to the brain and heart. b1-aderenergic: ↑HR, ↑contractility, ↑ AVN conductivity
  2. anaphylaxis
    - bronchodilatation
    - Down-regulates the release of histamine, tryptase, and other inflammatory mediators from mast cells and basophils
  3. asthma
    bronchodilatation
  4. croup
    decreased laryngeal edema
    bronchodilatation
  5. hypoglycemia?
    Liver: Stimulates glycogenolysis (↑ glucose)
45
Q

Lidocaines role in ACLS

A

Lidocaine and amiodarone show benefit in witnessed arrest

1-1.5 mg/kg over 15 secs (max total 3mg/kg)

Either works or doesn’t
CNS side effects, perioral numbness/tingling, can cause seizures

Try to give 1 dose over 15 seconds so that it’ll dramatically and precipitously ↓ likelihood of seizures

46
Q

2 options for shock resistant VT/VF (after 3-4 shocks and amiod/lido)

A

Change position of the pads—put posterolateral.

Beta blockade – Esmolol 0.5mg/kg

  • give 30mg IV push then start drip at 3 mg/min
  • 5–10 min to effect
47
Q

What should lead 1 look like?

A

Everything upright

48
Q

STE definition

A

> 1 mm STE in everything but V1 and V2 IN TWO ANATOMICALLY contiguous leads

49
Q

What causes diffuse ST elevation? (2)

A
  1. Pericarditis

2. Benign Early Repolarization

50
Q

4 antiarrhythmic meds to use to cardiovert stable wide complex VT

A

MONOMORPHIC VT
Amiodarone (150 mg over 10 minutes)
Lidocaine (100 mg over 15 seconds)
Procainamide (35-100 mg/min)

POLYMORPHIC VT (Torsades)
Magnesium!!!!! 2g (can drop BP, slow push over ƒ30 seconds)
51
Q

Stable SVT Tx

A

Adenosine 12 mg IV push, then 18 mg IV push (slows conduction in AV node)

1/2 dose in central line (6, 12 mg)

52
Q

Unstable SVT Tx

A

DC cardioversion (100J), remember to sedate with etomidate

53
Q

Risk of giving adenosine in SVT?

A

If it’s WPW, you decrease AVN conduction will increase conduction in bypass tract –> more instability

54
Q

Symptomatic bradycardia Rx

A
  1. atropine 0.5 mg.
  2. If doesn’t work –> can give 1 mg
  3. If doesn’t work –> epi drip at 1 cc/min (1 mcg/min epi
  4. pace

Intern Month Lectures (13 decks)

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