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
16
Q
MAT - multi-focal tachycardia
A
-irregular rhythm with >3 sites of atrial ectopy
ECG: P waves with different shapes and direction
- usually inverted in the inferior leads
- ectopic P may occur before or after QRS
- shortened PR
- normal QRS
- associated d/o: lung dz, CHF, sepsis, methylxanthine toxicity
- tx: treat the underlying d/o
- cardioversion has no effect
17
Q
Junctional Arrhythmias
A
- defn: impulse arises from the AV node or the bundle of His above the bifurcation
- signal travels retrograde to atria and antegrade to ventricles (atria may contract before, during or after ventricles depending on site of ectopy)
18
Q
Juntional Arrhythmias
-Junctional Premature Contractions
A
ECG:
- ectopic p wave has a different shape and direction (inverted in leads II, III, aVF)
- p wave may occur before or after QRS
- shorter then normal PR interval
- premature QRS
- normal-shaped QRS
- may be isolated, multiple (bigeminy/trigeminy) or multifocal
- usually occur in disease states: CHF, dig tox, IHD, AMI
- treat underlying d/o
19
Q
Junctional Arrhythmia
-Junctional Rhythm
A
- occurs when SA node fires too slowly or doesn’t reach the AV… jxnal excape beats occur at rates 40-60bpm
- generally do not conduct retrograde to atria therefore no p wave
- however can get an AV node that takes over with enhanced automaticity and rates of 60-100bpm occur or if it is jxnal tachy then rates >100pbm
- in this case it will get atrial capture
- occurs in CHF, myocarditis, hypokalemia, dig tox
- accelerated or junctional tachy occur in dig tox, acute rheum fever, inferior MI
- if pt on digoxin for a fib and now seeing a regular QRS rhythm consider dig tox
- tx: atropine can be used if symptomatic in order to get the SA node going again
20
Q
Ventricular Arrhythmias
-PVC
A
- cause by an ectopic ventricular impulse
- ECG:
- p waves do not proceed QRS
- retrograde P waves present
- QRS is premature and wide
- ST and T wave are directed opposite to major QRS deflection
- occur in normal pts, IHD, ACS, dig tox, CHF, hypokalemia, alkalosis, hypoxia, sympathomimetics
- tx:
- treat underlying d/o
- if >3 PVCs in a row then treat as nonsustained v tach
21
Q
Ventricular Arrhythmias
-Ventricular Parasystole
A
ECG: variation in coupling b/w preceding sinus beat and ectopic beat, fusion beats, common relation b/w interectopic beat intervals
22
Q
Ventricular Arrhythmias
-Accelerated Idioventricular Rhythm
A
-ectopic rhythm of ventricular origin
ECG: wide, regular QRS, rate 40-100, runs of 3-30 beats, begins with a fusion beat
- seen in ACS, or after thrombolysis of an MI
- associated with VT but not VF
- tx:
- if leading to a decreased CO then may need atrial pacing
23
Q
Ventricular Arrhythmias
-Ventricular Tachycardia
A
-defn: >3 beats of ectopic ventricular source at rate >100bpm
ECG: wide QRS, >100bpm (often 150-200), constant QRS axis
- can be a narrow QRS 5% of the time
- 2 types: monomorphic and polymorphic
- polymorphic: torsades de pointe
- QRS axis goes from + to - in a single lead
- occurs with prolonged and uneven ventricular repolarizaiton (long QT)
- drugs responsible: quinidine, procainamide, TCA
- RF: >65yo, F, renal dz, electrolyte disturbance, genetic predispostion, drugs
- very rare in pts w/o heart dz
- RF: ACS, IHD, HOCM, MVP, drugs, hypoxia, alkalosis, lytes
- tx:
- NEVER use CCB
- unstable: DC cardioversion
- stable, monomorphic:
- amiodarone 150mg over 10mins, may repeat q10min for total of 2g (good for ACS, LV dysfxn)
- procainamide 50mg/min IV up to 17mg/g (12mg/kg if CHF)(do not use if ACS or LV dysfxn)
- 2nd line: lidocaine
- polymorphic - torsades:
- MgSO4 1-2g IV over 60-90sec then infusion at 1-2g/h
- correct lytes, stop drugs, pace (if TDP secondary to brady from heart block)
- polymorphic VT
- treat urgently, consider urgent revascularization b/c high incidence of IHD
24
Q
Ventricular Arrhythmias
-Ventricular fibrillation (V. fib)
A
- totally disorganized depolarization and contraction of small areas of the vetnricles, no effective pumping
- ECG: fine to coarse zigzag pattern w/o P or QRS
- no pulse, no BP
- causes: MI, dig tox, quinidine, hypothermia, trauma, electrolyte abnormality
- Tx:
- immediate defib with 200J (biphasic)
- followed by 5 cycles of CPR then check pulse
- if it persists consider amiodarone 300mg IV bolus
25
Q
First degree SA block
A
- delay is in conduction of the signal out of the sinus node into the atria
- can not be seen on ECG
26
Q
Second degree SA Block
A
- occurs whenever an expected P wave and corresponding QRS are absent
- wenckebach SA block missing P wave appears after a period of progressive prolongation of the conduction time from the SA node to the atrium (not detectable on ECG)
- however, may see a progressive shortening of the PR interval on ECG before a missing P wave
- constant type of 2nd SA block is when SA conduction time remains the same before and after blocked impulses
- SA conduction time remains constant before and after blocked impulses
27
Q
Third degree SA block
A
- p 147
- no P wave from sinus node is seen, transmission completely blocked
28
Q
Sinus Arrest / Pause
A
- failure of impulse formation w/in sinus node
- same conditions that produce SA block cause sinus arrest: dig tox, OD of BB/CCB/ASA/quinidine, rheum fever, MI, myocarditis
- brief periods may occur nomrally in young pts with increased vagal tone
- tx: atropine or pacing
29
Q
AV heart block
A
- First-degree: delay in AV conduction (at node or lower) manifested by a prolonged PR interval (>0.2sec)
- can occur normally, if no structural heart abnormality then same mortality as general population
- Second degree: intermittent AV conduction
- Mobitz 1 = Wenckebach: progressive prolongation of PR until beat is dropped
- usually occurs at level of AV node
- Tx: not necessary unless evidence of hypoperfusion
- atropine 0.5mg IV, rpt q5min up to 2mg
- pacing (confirm hypoperfusion due to rate and not other cause - MI)
- Mobitz 2: PR remains the same with random dropped beats
- usually in infranodal system with coexistent fascicular or BBB and wide QRS
- cause: usually structural damage, permanent and may rapidly progress to complete block
- 60% of pts will respond to atropine
-Third degree: complete interruption of AV conduction
- no AV conduction, block may occur at node or infranodal
- if block at AV node then a junctional rhythm may ensue at 40-60bpm with narrow QRS (b/c rhythm originates above the bifurcation of the bundle of his)
- correlations can be made b/w the clinical ECG, approximate location of the block and risk of progression
- AV nodal block: block of AH area, usually reversible, self-limited, good prognosis
- Infranodal block: block of HV area, caused by dz of His bundle or branches, usually irreversible, may have serious prognosis
30
Q
AV dissociation
A
- separate and independent pacemakers drive the atria and ventricles
- 2 types: passive or active
- passive AV diss: impulse fails to reach the AV node b/c of sinus node failure/block, escape rhythm takes over, paces the ventricles, then when sinus node recovers the atrial activity resumes
- active AV diss: slower PM acclerates to usurp the sinus node and captures the ventricles (v-tach is an example)
- fusion beats are common
- Tx: if symptomatic treat as in an AV block
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
32
Q
LBBB
A
ECG
- QRS >120msec
- large and wide R wave - I, aVL, V5, V6
- small R wave followed by deep S wave - II, III, aVF, V1-V3
- no q waves in leads I, V5, V6
33
Q
RBBB
A
ECG
- prolonged QRS >120msec
- triphasic QRS complexes (RSR) - V1
- wide S wave - lateral leads I, V5, V6
- normal onset ventricular activation in lead V6
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
35
Q
Long QT
A
-prolonged QTc from derangement in cardiac myocytes
- >470 in men
- >480 in women
- increased risk of ventricular arrhythmias and torsades
- congenital or acquired
- pts present with syncope
36
Q
Preterminal Rhythms
A
-PEA: electrical complexes without mechanical contraction of the heart - cardiac arrest
- causes: Hs and Ts
- acidosis, hypoglycemia, toxins (TCA, dig, CCB, BB), ventricular wall rupture
-Idioventricular rhythm: escape rhythm with wide QRS >160msec and rate <40, with fairly ineffective contractions
- occur due to complete infranodal block, MI, tamponade, hemorrhage
- tx: CPR, epinephrine
- agonal ventricular rhythm: very broad irregular ventricular complexes at slow rate usually without contractions
- asystole: no cardiac electrical activity
- tx: CPR, epi
37
Q
Pacemakers
A
-potential problems:
- problems with the pocket (infection)
- problems with leads (most common)
- failure to pace
- failure to sense
- malfunction causing overpacing/runaway pacing
- battery problems
