S3C22 - Cardiac Rhythm Disturbances Flashcards
1
Q
Cardiac pacemaker physiology
A
- three types of cardiac cells: pacemaker cells, purkinje cells (that conduct the electrical wave faster than normal cardiac cells) and contractile cells
- AV band of fibrous connective tissue b/w atria and ventricles prevents electrical messages from getting through so that signal only goes through AV node
- SA supplied by sinus node artery that arises from RCA in 55% of cases and L circumflex in 45%
- AV node blood supply is from RCA in 90% of people and L circumflex in 10%
2
Q
Normal ECG
A
- runs at 25mm/s
- potential difference that points towards a recording electrode is assigned a positive deflection and vice versa
- P wave = atrial depolarization (atrial repolarization is obscured by the QRS)
- normal P wave is <0.1sec with <0.3millivolt (3mm)
- PR interval =0.12-0.2 sec (3-5mm)
- QRS = ventricular depolarization
- 0.06-0.10 sec
- delay in ventricular conduction results in wide QRS or if impulse arises from elsewhere
- depolarization starts on septum and begins by going right before everything suddenly depolarizes to the left, this initial right movement is detected as a downward deflection in the recording electrode (eg. V6) = q wave
- ST segment - plateau phase of ventricular depolarizaiton
- usually isoelectric (1mm may be normal)
- T wave = ventricular repolarization
- QT = ventricular depolarization and repolarization
- 0.33-0.42 sec
- QTc = QT/square root(R-R)
- QTc <470msec is normal
3
Q
Bradyarrhythmias
A
- atropine 0.5mg IV q5min up to 3mg
- if pacing and atropine unsuccesful, may consider epi 2-10mcg/min IV or dopamine 2-10mcg/kg/min IV
4
Q
Synchronized cardioversion
A
- applies electrical current about 10msec after peak of R wave to reduce chance of inducing v fib
- risk of CV: myocardial damage, induced arrhythmias, thrombus, hypotension
- in an unstable chronic a fib pt there is a 1.2-1.5% risk of embolizing a thrombus
5
Q
Arhythmia - questions to ask on history
A
- caffeine intake
- symptoms of hyperthyroid
- family history of sudden death
- recreational drug use
- meds - antipsycotics, TCA
- palpitations assoc with dizziness, syncope, presycnope are very concerning for v tach
- electrolytes should be checked
6
Q
Sinus Arrhythmia Definition
A
- normal P waves and PR intervals
- 1:1 AV conduction
- variation of at least 0.12s b/w the shortest and longest P-P interval
- normal finding in children and young adults, normal to change with respiration
7
Q
PAC - premature atrial contractions
A
- originate from pacemaker cells in the atrium outside of the sinus node
- usually do not indicate heart disease although if they are frequent it may be a sign of chronic lung dz, IHD, or dig toxicity, or stress, smoking, caffeine use
- may precipiatate atrial tachy, flutter, fib
- ECG:
- ectopic P wave appears sooner than the expected beat
- P wave has a different shape and axis
- may or may not be conducted thorugh the AV node therefore QRS may be narrow but might not be if conducted aberrantly thru the infranodal system
8
Q
Bradycardia
A
- sinus brady = <60 beats/min
- causes: physiologic, pharmacologic, pathologic (MI - inferior - increased ICP, hypothyroidism, carotid sinus hypersensitivity)
9
Q
Sick Sinus Syndrome
A
- abnormality of the supraventricular impulse generation and conduction that produces a wide variety of intermittent SVT and bradyarrhythmias
- the SVT rhythms are usually AF, junctional tachy, reentrant SVT, and a flutter
- bradyarrhythmias are usually sinus and SA block often with assoc AV nodal conduction abnormalities and inadequate AV jxnal escape rhythm
- cardiac dz associated with SSS: IHD, rheumatic d/o, myo-/pericarditis, rheumatolocial d/o, tumors, sugical damage, cardiomyopathies
- dx: usually requires ambulatory holter or EP studies
- tx: pacemaker first line, not drugs
10
Q
SVT
A
-approach: wide or narrow QRS?
- wide:
- regular: v tach, antidromic AVRT, SVT with abherrancy
- irregular: polymorphic VT, SVT with abherr.
- narrow:
- regular: sinus tach (not technically an SVT), atrial tach, AVRT, AVNRT, junctional tach, atrial flutter
- irregular: a fib, MAT, a flutter with variable block
11
Q
AVnRT
A
-AVnRT: re-entry of an impulse w/in the AV node, usually occurs from an ectopic beat that encounters the AV node during the partial refractory period
- ECG:
- p wave burried w/in the QRS complex (not visible)
- 1:1 conduction
- normal QRS
- can be associated with rheumatic heart dz, acute pericarditis, ACS, mitral prolapse
- Tx: increase vagal tone (20% success) (strain for 10sec then release and it is after you release that conversion may happen), adenosine (90% effective)
- 2nd line: CCB, BB
- verapamil may decrease contractility and hence CO (do not give CCB in CHF pts)
- verapamil also causes hypotension - may use CaCl for prevention or tx of verapamil-induced hypotension
- BB - propranolol IV has 80% success rate, SE of hypotension and decreased CO
- adenosine is safe in pregnancy and unstable pts (it is not contraindicated in WPW if QRS is narrow!)
12
Q
AVRT
A
- reentry usually occurs retrograde through a bypass tract thus producing a narrow QRS (orthodromic)
- antegrade conduction through the accessory bundle (antidromic) produces a wide QRS that is difficult ot differentiate from v-tach
- Lown-ganong-Levine syndrome - condition where the circuit goes through the James fibers that insert directly into the infranodal conducting system thereby passing by the AV node (and it’s delay)
- ECG: short PR, normal QRS
- Mahaim bundles allow impulse to travel a different pathway after it has already travelled through the AV node, the different pathway is slower and causes a delta wave b/c the ventricles are being triggered differently
- WPW - uses bundle of kent, bypasses AV node, causes a delta wave as ventricles start depolarizing before trigger gets to the normal conducting system
- type of WPW depends on direction of initial delta wave, which is determined by where the bundle of kent inserts into the ventricles
- rates >300 bpm should raise suspicion for preexciation syndrome
- ECG: short PR, delta wave
-tx WPW:
- any wide-complex antidromic tachy should be treated as v.tach b/c of a risk of rapid ventricular rates and degeneration to v. fib
- ** avoid BB, CCG, adenosine – using these can force the circuit to go down the accessory pathway and cause v. fib
- Procainamide 17mg/kg IV over 30min
- cardioversion
13
Q
WPW
A
-85% are narrow complex
14
Q
Atrial Flutter
A
ECG:
- regular atrial rate of 250-350bpm
- sawtooth flutter waves (especially inferior leads)
- AV block usually 2:1
- usually associated with heart disease or AMI
- other causes: CHF, PE, myocarditis, trauma, dig tox
- treat as in a fib
15
Q
Atrial Fibrillation
A
ECG: fibrillatory waves in V1,2,3 and aVF, irregular rhythm
- associated with 4 major d/o: rheumatic heart dz, HTN, IHD, thyrotoxicosis
- other causes: lung dz, pericarditis, acute EtOH, PE, septal defect
- tx:
- stable: BB or CCB first-line - diltiazem will work in ~5 mins, amiodarone is 2nd line
- do not use BB/CCB if heart failure or accessory pathway - use amio or dig instead
- unstable: cardiovert DC
-tx meds:
- diltiazem 15-20mg IV over 2 min followed by an infusion 5mg/h (may titrate up to 20mg/h)
- metoprolol 5mg IV q5min up to 15mg
- AC:
- pts with chronic a fib and pts with planned DC CV should be AC for 3w
31
Q
Fascicular Blocks
A
- 3 infranodal pathways: RBBB, LASF, LPIF
- LBBB takes out the LASF and the LPIF
- Bifascicular block = RBB+LASF / RBB + LPIF / LBBB
- Trifascicular block =
- RBB + LASF +1st deg AV block
- RBB + LPIF + 1st deg AV block
- LBB + 1st deg AV vlock
- alternating RBBB and LBBB
- causes of blocks: ischemia, cardiomyopathy, valvular, myocarditis, surgery, congenital
- bifasc/trifascicular blocks indicate advanced organic dz
34
Q
Brugada
A
- genetic condition affecting phase 0 sodium channels
- present with syncope/sudden death
- ECG:
- j-point elevation V1 and V3
- RBBB
- in pt with syncope and family hx of sudden death the pt should be sent for provocative tests even if ECG normal
- can be unmasked with procainamide, flecainide, ajmaline
- tx: implanted defibrillator
