Flashcards in Cards/EKGs Deck (54):
Causes of LBBB
Ischaemic heart disease
Anterior MI (2/2 LCx or RCA blockage + LAD doesn't supply LPost fascicle)
Primary degenerative disease (fibrosis) of the conducting system (Lenegre disease)
Causes of RBBB
Right ventricular hypertrophy / cor pulmonale
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
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)
Sodium-channel blocking agent — e.g. tricyclic antidepressant ECG features
patient presenting with seizures and hypotension, the combination of…
QRS broadening > 100 ms
R’ wave in aVR > 3 mm
Name the 8 Steps involved in reading an ECG
Rate: fast, slow, normal?
Wide QRS or narrow?
Reg or irreg?
Ps or not? Connected to QRS?
Mean QRS axis/other intervals
Likely a bypass tract (WPW)
Be careful with calling this or anything above this SINUS
Lower limit of NSR
Bradycardia, but look at the P waves to make sure its actually sinus before you call it sinus brady
AV node rate
Ventricular escape rhythm
Right Axis Deviation
Likely pathology on R side of heart
Left Axis Deviation
Likely path on L side of heart
Isoelectric point on ECGs
What causes diffuse ST elevation?
Benign Early Repolarization
Normal ECG findings in children
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.
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).
PR segment abnormalities (2)
Pericarditis (PR depression, widespread STE)
1 ECG big and little box width (ms)
Big 200 ms
Little 40 ms
Broad QRS causes (and their patterns)
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
aVR abnormalities (3)
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
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
≥ 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.
Posterior MI findings
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).
What does A New Left Bundle Branch Block signify?
Equivalent to a STEMI!
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).
Inverted T waves are seen in the following conditions
Normal finding in children
Persistent juvenile T wave pattern
Myocardial ischaemia and infarction
Bundle branch block
Ventricular hypertrophy (‘strain’ patterns)
Raised intracranial pressure
How to treat a R sided MI (inferior/posterior)
NO NITRO, they are preload dependent, give them FLUIDS instead
Inferior MI reciprocal leads
Posterior MI reciprocal
V1, V2, V3, V4
Lateral MI reciprocal leads
Reciprocal II, III, aVF
(Lateral leads 1, aVL, V5, V6)
7 Life Threatening Causes of Chest Pain
Esophageal Rupture (Boerhaave's)
Chest Pain Tests (8)
UA - why?
ACS Treatment (7)
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
5. Beta Blockers (to decrease myocardial demand, dont give 2 asthmatics)
6. Thrombolytics vs Cath lab (but you'd stop Plavix!!!)
HEART Score Components
History (suspicious or not?)
Age (<45, >65?)
Risk factors (how many?)
Troponin (nl or elevated?)
HEART Score meaning....MACE
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
Dosing nitrates in ACS
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)
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.
Role of beta blockers in ACS and dosing
Decrease myocardial O2 demand
Increase long term survival (not short)
Don't give 2: CHFers, heart block, asthmatics (can cause bronchospasm)
Metoprolol or atenolol
50 mg PO q6h x2d,
then 100 mg PO q12h
Door to balloon time (ACS)
90 min in PCI capable hospital
120 min for a transfer
Nicardipine (used for, doses, drip)
Used for hemorrhagic stroke to achieve BP control SBP<185, MAP<110. Can also use labetalol
Epinephrine MOA for
Non-selective alpha and beta agonist produced by adrenal glands.
↑ perfusion pressure to the brain and heart. b1-aderenergic: ↑HR, ↑contractility, ↑ AVN conductivity
-Down-regulates the release of histamine, tryptase, and other inflammatory mediators from mast cells and basophils
decreased laryngeal edema
Liver: Stimulates glycogenolysis (↑ glucose)
Lidocaines role in ACLS
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
2 options for shock resistant VT/VF (after 3-4 shocks and amiod/lido)
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
What should lead 1 look like?
>1 mm STE in everything but V1 and V2 IN TWO ANATOMICALLY contiguous leads
What causes diffuse ST elevation? (2)
2. Benign Early Repolarization
4 antiarrhythmic meds to use to cardiovert stable wide complex 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)
Stable SVT Tx
Adenosine 12 mg IV push, then 18 mg IV push (slows conduction in AV node)
1/2 dose in central line (6, 12 mg)
Unstable SVT Tx
DC cardioversion (100J), remember to sedate with etomidate
Risk of giving adenosine in SVT?
If it's WPW, you decrease AVN conduction will increase conduction in bypass tract --> more instability