65. Dysrhythmias Flashcards
1
Q
What is a dysrhythmia?
A
Abnormality in cardiac rhythm
2
Q
How does normal depolarisation work in non pacemaker cells?
A
Depol when membrane potential becomes less neg (ie moved from -90 to -70) due to na channel open and influx of positive charge
Augmented at 30-40mv by ca slow ch
Then begins relative refractory period by fast channels
3
Q
How do pacemaker cells differ from non impulse generating cells?
A
Spontaneous depol via slow sodium influx
4
Q
What 2 vessels supply the SA node?
A
RCA
Lcx
5
Q
SA node rate
A
60-90
6
Q
AV node base rhythm and blood supply
A
45-60
RCA primarily, Lcx otherwise
7
Q
Bundle of his/purkinje five base rate
A
30-45
8
Q
Preexcitation defn
A
Early ventricular depol via accessory pathway (outside av node between atria and ventricle)
9
Q
What are the 3 bundle branch fasicles
A
Left anterior superior
Left posterior inferior
Right bundle
10
Q
What artery typically supplies the LASB and rbb?
A
LAD
11
Q
Which artery typically supplies LPIB?
A
RCA or Lcx
12
Q
What is enhanced automaticity
A
Spontaneous depolarization in nonpacemaker cells or depol at abn threshold (low) for pm cells
13
Q
Early vs delayed afterdepolarizations
A
Another depol just before full resting potential reached
Vs
After full rp reached
14
Q
What is a reentry dysrhythmia?
A
Repetitive condition of impulses through self sustaining circuit
15
Q
Class I agents dysrhymia - effect?
A
Fast sodium channels
A, b and c altering RMP
16
Q
Class I antidysrthymic agents: how do they work and example?
A
Slow conduction atria, av node and his
Suppress conduction through accessory pathway
Slow depol and repol
Anticholinergic and mild ino
Procainammde - vt and svt
17
Q
Preferred agent in treating wpw dysrhythmia?
A
Procainamide
18
Q
Class 1b dysrhythmia agents - how do they work and ex?
A
Slow conduction and depol less than class I
Also SHORTEN qtc
Little effect on accessory pathway Slow depol
Lidocaine - also suppress SA and av
Can cause asystole if used in AMI
No use in SVT
19
Q
4 phases of nonpacemaker cell depol
A
4 - RMP with normal na/k
0 depol with na in and overshoot
1- relaxation of fast na to come down to plateau from overshoot
2- plate day - ca in
3- repol ph with k out
20
Q
Class ic agents compared to ia and b, examples meds
A
Profoundly slow depol and conduction
Can also create new arrh
Flecainaide: paroxysmal act and certain vt. NOT for pt with structural heart disease
Propafenone: same as 1a, 1c with some beta adrenergic, ccb
For afib and vt.
NOT for structural heart disease
21
Q
Class Ii antidysrhmic agents - what are thee and what do they do?
A
Beta blockers
Suppress SA node and slow av node conduction
- good for atria dysr like AVNRT
22
Q
CI to beta blocker use
A
Adv HF
pregnancy
Asthma and copd unless cardioselective
Preexisting brady, beyond first deg heart block
23
Q
Class 3 antidys- what do they do and how?
Ex amio
A
Block k channels, various qt effects
Tx many vent and atrial dys
- Amiodarone - first line acute VT. has some ia, ii and iv actions
- half life 9-36d after one IV dose
- se: hypot, Brady, HF
24
Q
What two organs can amiodarone effect other than heart?
A
Thyroid
Lung
25
What is ibutilide?
Class 3
Induced slower na current, prolongs refractory period
For afib and flutter
Can prolong qt and polymorphic vt
26
what does sotalol do? (Mech)
Beta blocker and class iii
27
Adverse effects of amiodarone: acute effects x3
Hypotension
Slowing of HR
decreased contractility
28
Adverse effects of amiodarone- common 3
Corneal deposits
Photosensitive
GI intolerance
29
Adverse effects of amiodarone- less common longer term effects - name 5
Hyperthyroidism or hypo
Heart failure
Pulmonary fibrosis
Bradycardia
Blue green skin changes
30
Adverse effects of amiodarone: increases levels of what 5 drugs?
Phenytoin
Procainamide
Warfarin
Digoxin
Flexainaide
31
Class iv antiarrh agents: what do they do
Block slow ca to slow conduction in the av node and suppress SA node less so
Used in svt
Concern for vasodilation, in heart block can cause even worse bradycardia
32
What is adenosine?
Purine nuceloside
Terminated regular nonatrial barrow complex tachydys
NOT for heart transplant
6mg then 12 then 12 again if no go, r/a rhythm
33
How does digoxin work?
Inhibit ATP dep Na-K pump to increase Ic na concentration and decrease intracellular k
34
When may digoxin be useful for dys?
Not first line
Svt if in cs or HF
35
Which rhythms is magnesium helpful for?
ventricular tachycardia
particularly torsades
36
What is isoproterenol and when is it used?
nonsel beta agonist to speed conduction sa and av node
Administration is via IV bolus if needed (1 to 2 mcg), but more commonly by IV infusion (2 to 10 mcg/minute titrated to effect).
37
What basic parts of ECG to look at when considering dysrhythmia analysis?
ventricular rate
rhythm
QRS width
P wave presence and relation to QRS
rhythm changes
multiple lead presence of changes
previous ecg
38
Vagal manuevers effect on AVNRT vs afib/flutter
A nodal reentrant tachycardia may terminate abruptly with vagal maneuvers, whereas it often temporarily slows the ventricular rate in those with atrial fibrillation or atrial flut- ter; ventricular tachycardia patients rarely have any change after vagal maneuvers.
39
Sinus bradycardia ddx of causes
healthy /N
inferior wall MI
hypothermia, hypoxia, drug effects (especially β-adrenergic blockers and calcium channel blockers), and intrinsic sinus node disease (i.e., sick sinus syndrome)
40
Why use isoproterenol instead of atropine?
In the post-heart transplant patient, use an iso- proterenol infusion (2 to 10 mcg/min titrated to effect) as atropine is ineffective.
due to loss Parasymp NS
41
Defn sinus brady
P wave assuming normal mor- phology, a fixed P-P interval equal to the R-R interval, and a ventric- ular rate below 60 beats/min
42
Defn sinus dysrthymia
manifestation of the natural variation in heart rate that occurs during the respiratory cycle, manifested on the surface ECG as normally conducted P waves with a variable P-P interval
43
Sick sinus syndrome - cause in eldelry?
fibrotic degeneration. It is associated with cardiomyopathies, con- nective tissue diseases, and certain drug
44
LT mangement SSS
pm
45
AV block - where is impaired conduction?
atria, AV node, or proximal His-Purkinje system
46
Defn first deg AVB
prolonged conduction at the level of the atria, AV node (most common), or His-Purkinje system. On the ECG, first-degree AV block shows a prolonged PR interval (>0.20 second), typically with a narrow-QRS complex
47
Defn second degree AVB (overall)
Second-degree AV block is when one or more (but not all) atrial impulses fail to reach the ventricles. The conduction ratio is the num- ber of P waves to the number of QRS complexes over a period (e.g., 3 : 2, 2 : 1). When the atrial rate is unusually fast, such as with atrial flut- ter, a conduction ratio of 2:1 may be physiologic, reflecting the normal refractory period of the AV node
48
Defn second deg AVB type 1
Wenckebach or Mobitz I AV block, is associated with progressive impairment of conduction within the AV node
49
Tx 2nd deg AVB type II?
not necessarily
50
Defn type II second deg AVB
is a conduction block just below the level of the AV node
random drop no prolongation
51
Second deg AVB type I vs II: clinical
type I ac, inferior MI, rheumatic fever, dig or beta blocker
II: chr, anteroseptal, Lenegre dis cardiomyopathy
52
Second deg AVB type I vs II: electrophysiology
av node, inc relative def, decremental conducton
vs
II: infranodal, no rel fractory period, all or none conduction
53
Second deg AVB type I vs II: response to atropine and exercise vs carotid massage/
type I: better; worse
type II: worse,better
54
Pacemakers above the His bundle often have a narrow-QRS complex at a rate of __ to __ beats/min, whereas pace- makers at or below the His bundle produce a wide-QRS complex at a rate of _ --_ beats/min.
45-60
30-45
55
This specific dysrhythmia is classically associated with digoxin toxicity.
When a complete heart block occurs in the presence of atrial fibrillation, the fibrillatory atrial waves are accompanied by a slow and regular ventricular response (so-called regularized atrial fibrillation).
56
ecg hallmark of chb
V dissociation (i.e., no electrocardiographic relationship between P waves and QRS com- plexes), with an R-R interval longer than the P-P interval. Conversely, the presence of AV dissociation with an R-R interval shorter than the P-P interval (e.g., as occurs with accelerated
57
bigeminy defn
extrasystole (pac or pvc) after every other native beat
58
Name 5 causes of grouped impulses
Wenckebach mechanism (usually at atrioventricular node, but can occur else- where)
Sinoatrial exit block
Atrial tachycardia or flutter with alternating conduction Frequent extrasystoles
Nonconducted atrial trigemini
Concealed or interpolated extrasystoles
59
PVC ddx of causes
catecholamine excess, such as pain, anxiety, and use of stimulants (e.g., caffeine, nicotine, cocaine, amphetamines). Pathologic conditions associated with frequent PVCs include myocardial infarc- tion, potassium or magnesium disturbances, and medication toxicity (notably any with sodium channel-blocking or sympathetic enhancing activity)
60
ECG features that help distinguish between different narrow- complex tachycardias include:
appearance of P waves and the regularity or irregularity of the R-R interval
61
Two ways to distinguish sinus tach from atrial flutter or junctional rhthm
adenosine
vagal manuevers
62
PAC vs PVC - name 6 ways to distinguish
PAC:
No compensatory pause
Preceding P wave (different from sinus P wave; occasionally buried in T wave)
Usually classic right bundle branch block pattern (especially if long- short cycle sequence appears) identical to sinus QRS
QRS axis normal or near-normal QRS rarely > 0.14 s
PVC:
Fully compensatory pause (unless interpolated)
No preceding P waves (although retrograde atrial conduction can cause inverted P wave after QRS)
Left bundle branch block, right bundle branch block, or hybrid pattern
Frequently bizarre QRS axis QRS often > 0.14 s
63
DDX name 8 causes of PVC and ventr tachycardia
Acute or previous myocardial infarction or ischemia Hypokalemia
Hypoxemia
Ischemic heart disease
Valvular disease
Catecholamine excessa
Other drug intoxications (especially cyclic antidepressants) Idiopathic causesb
Digoxin toxicity
Hypomagnesemia
Hypercapnia
Class I antidysrhythmic agents
Ethanol
Myocardial contusion
Cardiomyopathy
Acidosis
Alkalosis
Methylxanthine toxicity
64
sinus tach max adult rate vs kids (typical max)
In adults, sinus tachycardia rarely exceeds a rate of 170 beats/min; in infants and young children, it is not unusual to see rates above 200 to 225 beats/min.
65
Multifocal at defn
MAT) is a form of AT with three or more distinct P wave morphologies, and varying PR and P-P intervals from the multiple ectopic atrial foci
66
name 5 irregular rhytms (ddx)
Atrial fibrillation
Atrial tachycardia or flutter with varying conduction Multifocal atrial tachycardia
Multiple extrasystoles
Wandering pacemaker (usually atrial)
Parasystole
67
Afib: atrial amount per min?
300 to 600 atrial impulses/min
68
Paroxysmal afib defn
spont converts
69
Persistent afib defn
rq cardioversion to convert
70
permanent afib
no further efforts to restore sinus rhythm
71
classic ventricular rate in afib
150-170
if >200 - look for accessory pathway
72
DDX - name 8 causes of afib
Hypertensive heart disease Cardiomyopathy
Ischemic heart disease
Valvular disease (especially mitral) Congestive heart failure Pericarditis
Hyperthyroidism
Sick sinus syndrome
Myocardial contusion
Acute ethanol intoxication (holiday heart syndrome) Idiopathic
Cardiac surgery
Catecholamine excess
Pulmonary embolism
Accessory pathway (Wolff-Parkinson-White) syndrome
73
what is ashman phenomenon in afib?
aberrant ventricular conduc- tion of an early-arriving atrial impulse following a relatively long R-R interval, the result of a partially refractory His bundle.
74
when not to use nodal agents in afib?
if wide!!
75
Name 5 drugs and routes for pharm conversion of afib/flutter
IV procainamide, 30–50 mg/min, up to a total dose of 18–20 mg/kg (12 mg/kg in patients with congestive heart failure) or until conversion or side effects occur
or
Amiodarone, 150 mg IV over 10{en dash}15 minutes, followed by 1 mcg/min IV infusion for 6 hours then 0.5 mcg/min IV for 18 hours (or switch to oral)
or
Ibutilide, 0.015–0.02 mg/kg IV, over 10–15 min (conversion usually occurs within 20 min if successful)
or
Oral propafenone, 600 mg (contraindicated in the setting of structural heart disease or ischemia)
or
Oral flecainide, 300 mg (contraindicated in the setting of structural heart disease or ischemia)
76
Aflutter classic rate
regular rate of 250 to 350 beats/min (300 beats/min is classic)
77
AVNRT defn
regular, narrow-complex rhythm with a ventricular rate of 130 beats/ min or greater, commonly more than 160 beats/min
78
tx avnrt
If vagal maneuvers fail to restore sinus rhythm, first-line therapy for AVNRT is adenosine (6 mg rapid, large-bore IV bolus followed by a flush; repeat with 12 mg if no effect on rate). This approach is success- ful in 85% to 90% of cases and is safe. In refractory cases, diltiazem, esmolol, or metoprolol are options. Rarely needed, synchronized car- dioversion (at 100 to 200 J, biphasic preferred) can terminate AVNRT refractory to pharmacologic therapy or in a patient with hemodynamic instability.
79
Junctional tachycardia - seen with what 3 categories of disesase?
struct heart disease
metabolic disturbance
drug tox
80
Preexcit defn
depolarization of the ventricular myocardium via an accessory pathway (or bypass tract) linking the atria to the ven- tricles, circumventing the normal AV node
81
WPW syndrome accessory pathway - 3 characteristic ecg findings
* Short PR interval (<0.12 second)
* QRS duration longer than 0.10 second
* Slurred upstroke to the QRS complex, referred to as a delta wave
82
ortho vs antidromic
ortho - regular electrical down n pathway, up accessory vs anti starts down accessory pathway (wide, unstable, worry about vfib)
83
Lown Ganong Levine syndrome
paroxysmal narrow complex vtach, short PR, normal QRS similar tx to wpw
84
SVT with aberrancy - how does this occur?
bbb
accessory pathway
85
Brugada ECG criteria for VT
If any + = VT, all neg = svt
needs to be regular
1. absence of any RS complexes in precordial leads
2. RS duration >100msc (from beginning R to deepest S)
3. AV dissoc (particularly look limb leads inferior and V1-2)
4. sp VT morphology
86
Name 5 diseases associated with WPW
Idiopathica
Cardiomyopathy (especially hypertrophic) Transposition of great vessels Endocardial fibroelastosis
Mitral valve prolapse
Tricuspid atresia
Ebstein disease
87
Unstable pt with wide complex tachy - what do?
shock - tx as vt
88
Vtach vs svt with aberrancy: clinical features
vt: age >50
hx mi/hf/cabg/AS heart dis, previous vt
age
89
Vtach vs svt with aberrancy: PE differences
vt: cannon a waves
variations arterial pulse
variable first heart sound
svt has none of above
90
Vtach vs svt with aberrancy: ecg
vt: fusion beats, av dissoc, qrs >0.14, LAD
no response vagal manuevers
vs
p waves with qrs, usualy qrs <0.14, axis N/close, slow/terminate with vagal manuevers
91
Vtach vs svt with aberrancy: qrs typical pattern
vt: R, qR or RS in V1 vs V6: S, rS, or qR
concordance + or negative
--
svt: v1: rSR'
V6: qRs
92
Griffith approach for VT
BBB sought in V1 and V6
then look for AV dissoc
if no bbb and remainder leads av dissoc = vt dx
93
MC cause VT
reentry mechanisms
94
NSVT vs sustained
<30s reverting spont vs sustained = prolonged
95
Monomorphic VT classic pattern
regular pattern
rate 150-200 beats/min
96
Stable pt with VT tx
amiodarone 3-5mg/kg IV over 20 min - terminates 90%
2nd line:
procainamide 30-50mg/min IV up to 18mg/kg or until vt terminated
alt procain: lidocaine 1-1.5mg/kg IV bolus up to 3mg/kg max then infusion
97
Unstable pt with vt tx?
synchronized cardioversion
98
Torsades criteria
1. Ventricular rate greater than 200 beats/min
2. Undulating QRS axis, with the polarity of the complexes appearing to shift about the baseline
3. Paroxysms of less than 90 seconds
99
Verecki criteria for VT
1. initial R wave lead aVR - yes = VT
2. initial R or Q wave in aVR >40msec
3. neg directed notch and mostly negative QRS in aVR
4. initial aVR ventricular activation velocity dived by terminal velocity 17 or less
if any yes vt
if all no = svt
100
Torsades tx
Mag 1-2g push
incr HR VR 100-120b/min - overdrive pasing or isoproterenol
101
In contrast to acquired, how is congenital torsades tx?
beta blockers
102
Brugada: what is this?
ventricular dysrhythmia triggering syncope or sudden cardiac death in the absence of structural heart disease.
linked to inherited disease of na channel blockers
103
Brugada ecg pattern
downward coved or humped (saddleback) ST segment elevation in leads V1 to V3
--> needs adm for consideration icd
104
Acquired causes of prolonged qtc
Pause-Dependent (Acquired)
Drug-induced—class IA and IC antidysrhythmics; many phenothiazines and butyrophenones (notably haloperidol and droperidol), cyclic antidepressants, antibiotics (especially macrolides), organophosphates, antihistamines, anti- fungals, antiseizure and antiemetic agents
Electrolyte abnormalities—hypokalemia, hypomagnesemia, hypocalcemia (rarely)
Diet-related—starvation, low protein
Severe bradycardia or atrioventricular block Hypothyroidism
Contrast injection
Cerebrovascular accident (especially intraparenchymal) Myocardial ischemia
Acquired (Rare)
Cerebrovascular disease (especially subarachnoid hemorrhage)
Autonomic surgery: radical neck dissection, carotid endarterectomy, truncal
vagotomy
105
Congenital causes of prolonged QTC
Jervell and Lange-Nielsen syndrome (deafness, autosomal recessive) Romano–Ward syndrome (normal hearing, autosomal dominant) Sporadic (normal hearing, no familial tendency)
Mitral valve prolapse
106
What is the primary electrochemical difference between pace- maker and nonpacemaker cells?
a. Lack of a plateau phase 3 in nonpacemaker cells
b. Rapid phase 0 upstroke in nonpacemaker cells after stimulus c. Slow calcium ion influx during phase 2 for pacemaker cells d. Slow phase 4 spontaneous depolarization in pacemaker cells e. Transient membrane repolarization by potassium channel
closure during phase 1 for pacemaker cells
d
107
For a reentrant tachydysrhythmia to occur, what three condi-
tions exist?
a. Electrolyte disturbance, ischemia, and altered conduction in
an endogenous atrioventricular pathway
b. Electrolyte disturbance, two conduction pathways, with one
of the pathways being slower
c. Ischemia, two conduction pathways, with one of the path-
ways being slower
d. Two conduction pathways, one path being slower, and differ-
ing responsiveness
e. Two conduction pathways with equal responsiveness
d
108
Classic antifibrillatory effects are seen with which class of anti- dysrhythmic?
a. IA b. IB c. IC d. II e. III
e
109
The most frequent proarrhythmic effects are seen with which class of antidysrhythmic?
a. IA
b. IB
c. IC d. II
e. III
c
110
A 49-year-old woman presents with a sudden onset of palpita-
tions and shortness of breath. This has happened once before. She has no past history and takes no medications. Vital signs are temperature, 36.0°C (96.8°F) oral, blood pressure, 115/69 mm Hg, heart rate 156 beats/min, respiratory rate 24 breaths/min, and oxygen (O2) saturation, 98%. Her electrocardiogram (ECG) is shown in Fig. 65.28. What is the most appropriate interven- tion?
a
