HIS DEBS as arrythmogenic factors
H=Hypoxia—->COPD, PE
I=Ischemia and Irritability—->infarction, inflammation, infection
S=Sympathetic stimulation—->hyperthyroidism, CHF, nervousness, exercise
D=Drugs—->quinidine
E=Electrolyte disturbances—->Ca, Mg
B=Bradycardia—-> sick sinus syndrome
S=Stretch—-> enlargement and hypertrophy
Normal biphasic wave of P in which leads?
Lead III and V1
Normal septal Q wave in which leads?
Lead I, aVL, V5, V6 (rarely in inferior leads + V3, V4)
Normal QT interval over RR interval ratio?
40%
2 steps checking axis of QRS
1) Lead I and aVF (if both positive=normal range)
2) Lead with most equal biphasic QRS (perpendicular)
2 common causes for sustained ectopic rhythm
Digitalis toxicity, beta-agonists from inhaler therapies
4 Qs for arrhythmias
Q1: Are normal P wave present? including right axis
Q2: QRS wide or narrow? (3格界定)
* Q1 and Q2 decide the arrhythmia is ventricular or supraventricular (atrial or junctional).
Q3: What’s the relationship b/t P and QRS? (one-to-one=atrial origin)
Q4: Is the rhythm regular or irregular?
5 types of sustained supraventricular arrythmias
- PSVT=AVNRT (AV nodal reentranttachycardia)
- A flutter
- A fibrillation
- MAT (multifocal atrial tachycardia)
- PAT (paroxysmal atrial tachycardia)=ectopic atrial tachycardia
PSVT HR
150-250 bpm
3 leads to check the retrograde P wave in PSVT
Lead II, III, V1 (pseudo-R’)
Common causes of A fib
- Mitral valve disease
- CAD
- Hyperthyroidism
- PE
- Pericarditis
- Long-lasting HTN
2 irregular rhythm of supraventricular arrhythmia
A-fib, MAT
Define MAT (multifocal atrial tachycardia) and when is it commonly seen
> 3 different P wave morphologies
Severe lung disease
Pattern of PAT (paroxysmal atrial tachycardia). Can it be slowed down by carotid message as in PSVT?
a warm-up or cool-down period
No or mild slowing.
Rules of malignancies that PVCs may cause life-threatening arrhythmias
- Frequent PVCs
- > 3 PVCs in a row
- Multi form PVCs
- R-on-T phenomenon
- Any PVC occurring in the setting of an AMI
2 common conditions that accelerated idoventricular rhythm seen
- AMI
2. Early hours following reperfusion
How does Torsades de pointes occur?
A PVC falling during the elongated T wave
Electrolytes that cause TdP?
Hypo-Ca, hypo-Mg, hypo-K
ABX that cause TdP?
Erythromycin, quinolones, levofloxacin
Can supraventricular beat have a wide QRS?
Yes.
An early PAC occurs–> run through LBB (RBB still in refractory period)–> RBB receives conduction from LBB–> wide, bizarre QRS that looks like a PVC. (aberrant conduction)
Clinical clues to ddx VT and PSVT:
- Which is more common in a diseased heart?
- Which can be terminated by carotid massage?
- Which is commonly a/w AV dissociation?
- Cannon A wave may be seen?
- VT
- PSVT
- VT
- VT
What happen to AV node in AV dissociation?
Constantly refractory by impulses from above and below
EKG clues to ddx VT and PSVT:
- P always followed by QRS?
- Fusion beats may be seen?
- Initial deflection may in opposite direction of the normal QRS?
- PSVT
- VT
- VT
When does Ashman phenomenon occur?
It’s a wide, aberrant conduction of supraventricular beat after a QRS complex that is preceded by a long pause.
Bundle branches anticipate another long pause following this beat and repolarize slowly–> before completion of repolarization, another supraventricular impulse passes through AV node, but the conduction is blocked along the normal pathways–> wide, bizarre QRS (looks like a PVC)
Which arrhythmia is the best setting for Ashman phenomenon?
A Fib
How to check AV block?
Relationship of P and QRS
Def of first-degree AV block
PR> 0.2 sec (5小格)
Does first-degree AV block a block?
No, only a delay
Def of Mobitz type I second-degree AV block (or Wenchebach block)
Progressive lengthening of each successive PR until one P fails to conduct through AV node (漸行漸遠)
* Block in AV node, usually transient and benign
Def of Mobitz type II second-degree AV block
Conduction is an all-or-nothing phenomenon w/o progressive lengthening of PR
* Block in His bundle, usually serious
Which rhythm can be suppressed: PVC or ventricular escape rhythm?
PVC
Which rhythm can be life-saving: PVC or ventricular escape rhythm?
Ventricular escape rhythm
Def of third-degree AV block
Presence of AV dissociation in which ventricular rate is slower than sinus or atrial rate
Leading cause of third-degree AV block
Degenerative disease of conduction system
A common cause of reversible complete heart block
Lyme disease: block located in AV node, narrow-QRS junctional escape rhythm
Which AV block(s) requires permanent pacemaker?
Mobitz type II heart block and third-degree
Can different degrees of AV block coexist?
Yes
Why QRS is wide in BBB? (>3格)
Delayed depolarization
What does ST and T look like in BBB?
Similar change as in secondary repolarization abnormalities in ventricular hypertrophy (ST: depression, T: inversion)
What’s ‘critical rate’ in BBB?
The ventricles conduct normally at slow HR, but above a certain rate, BBB develops. This certain HR is critical rate.
When doesn’t criteria of ventricular hypertrophy apply?
Presence of BBB
What does hemiblock change on EKG
Axis dev
Left anterior hemiblock axis and vector direction
-30 to -90 degrees
Depolarization: inferior-to-superior, R-to-L
Left posterior hemiblock axis and vector direction
+90 to +180 degrees
Depolarization: superior-to-inferior, L-to-R
What’s incomplete BBB?
Morphologies of LBBB or RBBB but QRS normal
What’s the bypass pathway name in WPW syndrome?
Bundle of Kent (can be L or R sided b/t atrium and ventricle)
Why QRS is wide in WPW syndrome?
Premature activation–> a fusion beat (small region of myocardium depolarize first)
2 most common tachyarrhythmias seen in WPW syndrome
PSVT, A fib
Route of narrow-QRS of PSVT in WPW syndrome
PAC down AV node–> ventricle–> bundle of Kent–> atrium–> ventricle
Route of wide-QRS of PSVT in WPW syndrome
Atrium–> bundle of Kent–> ventricle–> AV node–> atrium
What’s the worst scenario A fib causes in WPW syndrome
VF
3 stages of MI
- Peaks and inverts–> hyperacute T wave
- STE and merges with T
- New Q
Difference of T in MI and hypertrophy
Symmetric T in MI, asymmetric T in hypertrophy
What does a changing T mean
Ischemia
What does a changing ST mean
Injury
What does it mean if the STE persists after MI?
Formation of a ventricular aneurysm
What does a pathologic Q mean?
Irreversible myocardial cell death–> unable to conduct an electrical current–> electrical forces direct away from the area
Which lead normally has a deep Q?
aVR (thus, not helpful in assessing MI)
Which supplies the AV node mostly: RCA or LCX?
RCA
Leads for inferior infarct and artery
II, III, aVF, RCA
Lateral infarct and artery
I, aVL, V5, V6, LCX
Anterior infarct and artery
V1-V6, LAD
Posterior infarct and artery
Reciprocal changes in anterior leads esp V1, RCA
Anterolateral infarct artery
LCA
When does poor R wave progression occur?
- Anterior infarction
- RVH
- Chronic lung disease
Why check posterior MI in case of inferior MI confirmed?
Same blood supply
How to differentiate tall R in V1 in RVH and posterior MI?
R axis dev
Conditions that result in STE
- MI (mostly transmural)
- Prinzmetal’s angina
- J point elevation (benign early repolarization, esp V4)
- Acute pericarditis
- Acute myocarditis
- Hyper-K
- PE
- Brugada syndrome
- Hypothermia
Conditions that result in STD
- Typical angina
2. Non-Q wave infarction
When does ‘rule of appropriate discordance’ apply?
Normal LBBB (QRS and J point are in different directions)= if they’re in same direction, something wrong!
What is ‘modified Sgarbossa criteria’ for?
Dx AMI in the setting of LBBB (new/old)
CIs to stress testing
- Any acute systemic illness
- Severe aortic stenosis
- Uncontrolled CHF
- Severe HTN
- Angina at rest
- Presence of a significant arrhythmia
Drugs that prolong QT (6)
- Anti-arrhythmic Class IC and III
- TCAs
- Phenothiazines (ex. methylene blue, anti-psychotics)
- Erythromycin
- Quinolone ABX
- Antifungals
How to treat inherited long QT (3)
- Beta-blockers
- Implantable defibrillator
- Restricted from competitive sports (adrenalin bursts)
EKG change in acute pericarditis (in large effusion)
Diffuse STE and flattened/inverted T (low voltage, electrical alternans)
Why electrical alternans occur
Large effusion allows the heart to rotate freely w/in the sac that changes the axis every time it beats
EKG change in a nonmassive PE
Normal or sinus tachycardia
Definitive Rx for Brugada syndrome
ICD
Most common ventricular arrhythmia in Brugada syndrome
Polymorphic ventricular tachycardia (resembles TdP)