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Rosens > 65. Dysrhythmias > Flashcards

65. Dysrhythmias Flashcards

1
Q

What is a dysrhythmia?

A

Abnormality in cardiac rhythm

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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

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3
Q

How do pacemaker cells differ from non impulse generating cells?

A

Spontaneous depol via slow sodium influx

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4
Q

What 2 vessels supply the SA node?

A

RCA
Lcx

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5
Q

SA node rate

A

60-90

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6
Q

AV node base rhythm and blood supply

A

45-60
RCA primarily, Lcx otherwise

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7
Q

Bundle of his/purkinje five base rate

A

30-45

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8
Q

Preexcitation defn

A

Early ventricular depol via accessory pathway (outside av node between atria and ventricle)

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9
Q

What are the 3 bundle branch fasicles

A

Left anterior superior
Left posterior inferior
Right bundle

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10
Q

What artery typically supplies the LASB and rbb?

A

LAD

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11
Q

Which artery typically supplies LPIB?

A

RCA or Lcx

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12
Q

What is enhanced automaticity

A

Spontaneous depolarization in nonpacemaker cells or depol at abn threshold (low) for pm cells

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13
Q

Early vs delayed afterdepolarizations

A

Another depol just before full resting potential reached
Vs
After full rp reached

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14
Q

What is a reentry dysrhythmia?

A

Repetitive condition of impulses through self sustaining circuit

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15
Q

Class I agents dysrhymia - effect?

A

Fast sodium channels
A, b and c altering RMP

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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

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17
Q

Preferred agent in treating wpw dysrhythmia?

A

Procainamide

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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

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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

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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

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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

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22
Q

CI to beta blocker use

A

Adv HF
pregnancy
Asthma and copd unless cardioselective
Preexisting brady, beyond first deg heart block

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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

  1. Amiodarone - first line acute VT. has some ia, ii and iv actions
    - half life 9-36d after one IV dose
    - se: hypot, Brady, HF
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24
Q

What two organs can amiodarone effect other than heart?

A

Thyroid
Lung

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25
Q

What is ibutilide?

A

Class 3
Induced slower na current, prolongs refractory period
For afib and flutter
Can prolong qt and polymorphic vt

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26
Q

what does sotalol do? (Mech)

A

Beta blocker and class iii

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27
Q

Adverse effects of amiodarone: acute effects x3

A

Hypotension
Slowing of HR
decreased contractility

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28
Q

Adverse effects of amiodarone- common 3

A

Corneal deposits
Photosensitive
GI intolerance

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29
Q

Adverse effects of amiodarone- less common longer term effects - name 5

A

Hyperthyroidism or hypo
Heart failure
Pulmonary fibrosis
Bradycardia
Blue green skin changes

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30
Q

Adverse effects of amiodarone: increases levels of what 5 drugs?

A

Phenytoin
Procainamide
Warfarin
Digoxin
Flexainaide

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31
Q

Class iv antiarrh agents: what do they do

A

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

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32
Q

What is adenosine?

A

Purine nuceloside
Terminated regular nonatrial barrow complex tachydys

NOT for heart transplant

6mg then 12 then 12 again if no go, r/a rhythm

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33
Q

How does digoxin work?

A

Inhibit ATP dep Na-K pump to increase Ic na concentration and decrease intracellular k

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34
Q

When may digoxin be useful for dys?

A

Not first line
Svt if in cs or HF

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35
Q

Which rhythms is magnesium helpful for?

A

ventricular tachycardia
particularly torsades

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36
Q

What is isoproterenol and when is it used?

A

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).

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37
Q

What basic parts of ECG to look at when considering dysrhythmia analysis?

A

ventricular rate
rhythm
QRS width
P wave presence and relation to QRS
rhythm changes
multiple lead presence of changes
previous ecg

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38
Q

Vagal manuevers effect on AVNRT vs afib/flutter

A

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.

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39
Q

Sinus bradycardia ddx of causes

A

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)

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40
Q

Why use isoproterenol instead of atropine?

A

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

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41
Q

Defn sinus brady

A

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

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42
Q

Defn sinus dysrthymia

A

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

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43
Q

Sick sinus syndrome - cause in eldelry?

A

fibrotic degeneration. It is associated with cardiomyopathies, con- nective tissue diseases, and certain drug

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44
Q

LT mangement SSS

A

pm

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45
Q

AV block - where is impaired conduction?

A

atria, AV node, or proximal His-Purkinje system

46
Q

Defn first deg AVB

A

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
Q

Defn second degree AVB (overall)

A

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
Q

Defn second deg AVB type 1

A

Wenckebach or Mobitz I AV block, is associated with progressive impairment of conduction within the AV node

49
Q

Tx 2nd deg AVB type II?

A

not necessarily

50
Q

Defn type II second deg AVB

A

is a conduction block just below the level of the AV node
random drop no prolongation

51
Q

Second deg AVB type I vs II: clinical

A

type I ac, inferior MI, rheumatic fever, dig or beta blocker

II: chr, anteroseptal, Lenegre dis cardiomyopathy

52
Q

Second deg AVB type I vs II: electrophysiology

A

av node, inc relative def, decremental conducton
vs

II: infranodal, no rel fractory period, all or none conduction

53
Q

Second deg AVB type I vs II: response to atropine and exercise vs carotid massage/

A

type I: better; worse

type II: worse,better

54
Q

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.

A

45-60

30-45

55
Q

This specific dysrhythmia is classically associated with digoxin toxicity.

A

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
Q

ecg hallmark of chb

A

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
Q

bigeminy defn

A

extrasystole (pac or pvc) after every other native beat

58
Q

Name 5 causes of grouped impulses

A

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
Q

PVC ddx of causes

A

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
Q

ECG features that help distinguish between different narrow- complex tachycardias include:

A

appearance of P waves and the regularity or irregularity of the R-R interval

61
Q

Two ways to distinguish sinus tach from atrial flutter or junctional rhthm

A

adenosine
vagal manuevers

62
Q

PAC vs PVC - name 6 ways to distinguish

A

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
Q

DDX name 8 causes of PVC and ventr tachycardia

A

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
Q

sinus tach max adult rate vs kids (typical max)

A

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
Q

Multifocal at defn

A

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
Q

name 5 irregular rhytms (ddx)

A

Atrial fibrillation
Atrial tachycardia or flutter with varying conduction Multifocal atrial tachycardia
Multiple extrasystoles
Wandering pacemaker (usually atrial)
Parasystole

67
Q

Afib: atrial amount per min?

A

300 to 600 atrial impulses/min

68
Q

Paroxysmal afib defn

A

spont converts

69
Q

Persistent afib defn

A

rq cardioversion to convert

70
Q

permanent afib

A

no further efforts to restore sinus rhythm

71
Q

classic ventricular rate in afib

A

150-170

if >200 - look for accessory pathway

72
Q

DDX - name 8 causes of afib

A

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
Q

what is ashman phenomenon in afib?

A

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
Q

when not to use nodal agents in afib?

A

if wide!!

75
Q

Name 5 drugs and routes for pharm conversion of afib/flutter

A

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
Q

Aflutter classic rate

A

regular rate of 250 to 350 beats/min (300 beats/min is classic)

77
Q

AVNRT defn

A

regular, narrow-complex rhythm with a ventricular rate of 130 beats/ min or greater, commonly more than 160 beats/min

78
Q

tx avnrt

A

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
Q

Junctional tachycardia - seen with what 3 categories of disesase?

A

struct heart disease
metabolic disturbance
drug tox

80
Q

Preexcit defn

A

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
Q

WPW syndrome accessory pathway - 3 characteristic ecg findings

A
  • 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
Q

ortho vs antidromic

A

ortho - regular electrical down n pathway, up accessory vs anti starts down accessory pathway (wide, unstable, worry about vfib)

83
Q

Lown Ganong Levine syndrome

A

paroxysmal narrow complex vtach, short PR, normal QRS similar tx to wpw

84
Q

SVT with aberrancy - how does this occur?

A

bbb
accessory pathway

85
Q

Brugada ECG criteria for VT

A

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
Q

Name 5 diseases associated with WPW

A

Idiopathica
Cardiomyopathy (especially hypertrophic) Transposition of great vessels Endocardial fibroelastosis
Mitral valve prolapse
Tricuspid atresia
Ebstein disease

87
Q

Unstable pt with wide complex tachy - what do?

A

shock - tx as vt

88
Q

Vtach vs svt with aberrancy: clinical features

A

vt: age >50
hx mi/hf/cabg/AS heart dis, previous vt

age </=35
no hx heart ids
previous svt

89
Q

Vtach vs svt with aberrancy: PE differences

A

vt: cannon a waves
variations arterial pulse
variable first heart sound

svt has none of above

90
Q

Vtach vs svt with aberrancy: ecg

A

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
Q

Vtach vs svt with aberrancy: qrs typical pattern

A

vt: R, qR or RS in V1 vs V6: S, rS, or qR
concordance + or negative
–
svt: v1: rSR’
V6: qRs

92
Q

Griffith approach for VT

A

BBB sought in V1 and V6
then look for AV dissoc

if no bbb and remainder leads av dissoc = vt dx

93
Q

MC cause VT

A

reentry mechanisms

94
Q

NSVT vs sustained

A

<30s reverting spont vs sustained = prolonged

95
Q

Monomorphic VT classic pattern

A

regular pattern
rate 150-200 beats/min

96
Q

Stable pt with VT tx

A

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
Q

Unstable pt with vt tx?

A

synchronized cardioversion

98
Q

Torsades criteria

A
  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
Q

Verecki criteria for VT

A
  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
Q

Torsades tx

A

Mag 1-2g push
incr HR VR 100-120b/min - overdrive pasing or isoproterenol

101
Q

In contrast to acquired, how is congenital torsades tx?

A

beta blockers

102
Q

Brugada: what is this?

A

ventricular dysrhythmia triggering syncope or sudden cardiac death in the absence of structural heart disease.

linked to inherited disease of na channel blockers

103
Q

Brugada ecg pattern

A

downward coved or humped (saddleback) ST segment elevation in leads V1 to V3

–> needs adm for consideration icd

104
Q

Acquired causes of prolonged qtc

A

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
Q

Congenital causes of prolonged QTC

A

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
Q

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

A

d

107
Q

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

A

d

108
Q

Classic antifibrillatory effects are seen with which class of anti- dysrhythmic?
a. IA b. IB c. IC d. II e. III

A

e

109
Q

The most frequent proarrhythmic effects are seen with which class of antidysrhythmic?
a. IA
b. IB
c. IC d. II
e. III

A

c

110
Q

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

a

Rosens (48 decks)

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