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Arrhythemias Flashcards

0
Q

What is susceptibility to an arrhythmia based on?

A

genetic abnormalities and acquired structural heart disease

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1
Q

What does how dangerous an arrhythmia is depend on?

A

how much it impairs cardiac output or how likely it is to deteriorate into a more serious disturbance

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2
Q

What increases susceptibility?

A 
electrolyte abnormalities
hormonal imbalances
hypoxia
drug effects
myocardial ischemia
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3
Q

Classification of arrhythmias includes what?

A

those caused by

  1. disorders of impulse formation or automaticity
  2. abnormalities of conduction
  3. reentry
  4. triggered activity
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4
Q

heart rate under 60

A

sinus bradycardia

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5
Q

who is sinus bradycardia normal in? why?

A

athletes ; increase in vagal tone

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6
Q

what is sinus bradycardia assocaited with an increased risk for?

A

ectopic rhythms

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7
Q

heart rate >100 is _____ and occurs with what?

A

sinus tachycardia

occurs with fever, exercise, pain, emotion, shock, thyrotoxicosis, anemia, heart failure, and use of many drugs.

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8
Q

what beats are found in normal hearts, and do not alone constitute heart disease?

A

atrial premature beats

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9
Q

what is the most common paroxysmal tachycardia?

what persons does this occur in?

A

paroxysmal supraventricular tachycardia (PSVT)

usually occurs in persions without structural problems

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10
Q

what is the most common chronic arrhythmia?

A

atrial fibrillation

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11
Q

T/F incidence and prevalence of A-fib increases with age.

A

true

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12
Q

Who does atrial flutter usually occur in?

A

COPD (chronic obstructive pulmonary disorder)
CHF
Atrial Septal Defect
CAD (coronary artery disease)

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13
Q

Who do junctional rhythms occur in?

A

patients with normal hearts or those with myocarditis, CAD, or digitalis toxicity

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14
Q

transient failure of impulse formation into the sinus node

A

sinus pause

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15
Q

name 5 drugs that cause sinus bradycardia

A

digitalis
Bblockers
clacium channel blockers
antiarrhythmic agents such as sotalol and amiodarone

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16
Q

which causes sinus bradycardia?
hyperkalemia hypokalemia?
hyperthyroidism hypothyroidism
hyperthermia hypothermia?

A

hyperkalemia
hypothyroidism
hypothermia

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17
Q

when sinus pause (inactivity) is prolonged it is called?

A

sinus arrest

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18
Q

the result of abnormal transmission between the sinus node and the atrium

A

sinoatrial exit block

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19
Q

PR interval longer than .20

A

First degree AV Block

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20
Q

is p married to Q in first degree heart block?

A

yes

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21
Q

p-r interval >.2 with a narrow QRS

A

first degree AV block

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22
Q

progressive lengthening of the PR interval until a P wave is blocked

A

Second degree AV block Type 1
“starts out normal fast and then gets slower and slower until it decides it needs a break (dropped QRS)”
Wenckebach
-series of cycles with phrogressive blocking of AV Node conduction until the final P wave is totally blocked in the AV NOde, eliminating the QRS response.
-Each repeating Wenckebach series has a consistent P:QRS ratio like 3:2, 4:3, 5:4, etc. (one less QRS than P waves in the series)

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23
Q

P-R interval .12 - .2
series of cycles consisting of ONE normal PQRST cycle preceeded by a series of paced P waves that fail to conduct through the AV node (no QRS) response

A

Second Degree Heart Block Type 2 “Mobitz”
-Each repeating Mobitz series has a consistent P:QRS ratio
like 3:1 , 4:1, 5:1

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24
Q

type 2 av block with narrow QRS

A

site of block is usually in the His bundle above the bifercation but may occasionally be in the AV node

25
Q

what are the finding that favor infrandoal AV block?

A

a history of near syncope or syncope
a QRS duration above .12
improved AV conduction during with carotid sinus massage
worsening AV conduction with atropine and exercise

26
Q

Why is it important to know the site of the AV block in teh ASYMPTOMATIC patient with 2:1 AV block?

A

because infranodal block is assoc w/ worse prognosis and mandates the implantation of a pacemaker

27
Q

T/F Mobitz 2:1 is less severe than Mobitz 3:1 & 4:1.

A

true
when mobitz blocks three atrial depolarizaitons (pwaves) producing a single ventricular response (QRS) this is written “3:1 block” , which describes the mechanism of conduction
these extremely slow ventricular rates may produce loss of consciousness (syncope)

28
Q

how do you determine the difference between 2:1 AV block of Wenckebach and Mobitz?

A

Parasympathetic Vagal Maneuvers

  • Wenchebach increases cycles/series to produce 3:2 or 4:3
  • Mobitz - vagal maneuverse either eliminate the block, producing a 1:1 AV conduction, or they have no effect.
  • *Explanation: av node is richly supplied with parasympathetic innervation, so vagal maneuvers inhibit the AV Node, making it more refractory
  • Therefore, vagal maneuvers increase paraysmpathetic inhibition of the AV node, increasing the number of cylces/series to produce 3:2 or 4:3 Wenchkebach
  • But if the 2:1 block is Mobitz (th eblock in the ventricular conduction system), vagal maneuvers either eliminate teh block, producing 1:1 AV conduction or they have no effect
29
Q

name the dz: PR interval

  1. increased consistently
  2. progressively increases in each series of cycles
  3. totally variable
  4. decreased
A
  1. primary AV block
  2. Wenchebach
  3. tertiary AV block
  4. WPW and LGL syndrome
30
Q

What has P without QRS response

A

Wenckebach and Mobitz secondary AV blocks

Tertiary AV block - independent atrial and ventricular rates

31
Q

conduction of supraventricular depolarizations to the ventricles is TOTALLY BLOCKED… an automaticity focus ESCAPES to PACE the ventricles at its INHERENT rate.

A

Complete 3 degree block
-atrial conductions are NOT conducted to the ventricles
**ATRIOVENTRICULAR DISSOCIATION and an atrial rate that is faster than the ventricular rate
RR and PP intervals are usually constant
PR interval will vary because the P is independent of the QRS

32
Q

joined QRS aka “rabbit ears”
prolonged QRS > .12 (3 boxes or more)
what leads do u look at?

A

Bundle Branch Block
R and R prime
look at V1 and V2 and V5 and V6

33
Q

the presence of a full compensatory pause suggests =
aberrant APCs or VPCs
atrial vs ventricular premature complexes

A

VPC’s
full compensatory pause (RR interval surround the APC = twice teh sinus cycle length) suggests lack of sinus node resetiing, thus favoring a ventricular rather than an atrial site of origin

34
Q

which bundle branch block are u more likely to see an atrial premature complex?

A

right b/c it has a longer refractory period

35
Q

describe prevalence of APC’s

A
  1. increases with age
  2. freq. with structural ht dz such as chronic renal failure and chronic pulmonary dz
  3. increased in teh early stages of an MI with a subsequent decrease in frequency after 10 days (this characteristic may be related to atrial ischemia, increased filling pressures, or the increased catecholamine state often seen during MI.)
  4. appear to be freqent in PERICARDITIS
36
Q

what are the symtpoms of APC

A

palpitations, or the sensations of skipped beats
dizziness and heart failure like symptoms might occurin the setting of ATRIAL BIGEMINY with nonconducted atrial premature beats
bigeminy = abnormal beats occur every other concurrent beat

37
Q

what is the treatment for a pt with APC’s with no symptoms?

with if they have symptoms?

A 
with no symptoms treat by removing underlying fators that are known to cause ectopic beats such as alcohol and caffeine intake.
pt with symptoms = BETA BLOCKERS... followed by CCB and class IC agents such as flecainide and propafernone
38
Q

P wave buried in QRS

describe the 3 locations

A

JPC - junctional premature complexes
1. perinodal = retrogradal atrial activation preceeds ventricular activation
2. His Bundle = retrograde atrial activation ALWAYS follows ventricular activation (P wave that follows the QRS)
3.

39
Q

if a JPC impulse does not conduct in either antegrade nor retrograde activation, the result is what?

A

AV BLOCK

** CONCEALED JPC’S

40
Q

What are the common settings of JPC

A

digitalis toxicity
high catecholamine states
hypokalemia
MI

41
Q

wide QRS with a compensatory pause

A

VPC = ventricular premature complex

42
Q

T/F VPCs have NO prognostic significance in patients with a normal heart, their presence in paitents with heart dz is often associated with poor outcome. in patients with a history of MI the presence of VPC’s increases MORTALITY.

A

true

43
Q

what is the treatment of VPC’s in symptomatic patient

A

BetaBlocker 1st
if beta blocker therapy fails then amiodarone or catheter ablation should be considered.
when catheter ablation is performed, the VPC site of origin is identified and radiofrequency energy is applied to eleminate it

44
Q

what is the rate of atrial tachycardia
what causes this
how do u read it on an EKG

A

100-250
caused by an ectopic atrial focus discharging at a rate faster than the sinus rate
different p-wave morphology
most commonly AV conduction is 1:1, however variable AV block might be seen

45
Q

When atrial tachycardia occurs WITH Av BLOCK then what is expected?

A

digoxin toxicity

46
Q

what is the treatment for atrial tachycardia?

A

when not a result of digoxin toxicity…. BB and CCB are the mainstays o ftherapy
-catheter ablation can eliminate this arrhythmia in 75-90% of pt

47
Q

what is defined by the presence of three or more p wave morphologies and a rate greater than 100 beats/min

A

Multifocal atrial tachycardia

48
Q

when do you commonly see MAT?

A

in pt with underlying lung dz; it is seen in the setting of an acute MI, hypokalemia, hypomagnesemia, and it may be precursor of a-fib
-Aminophylline use may also be a contributing factor

49
Q

what is the treatment for MAT

A

rate control of this arrhythmia may be difficult but Verapamil is frequently effective
-treatment is directed at underlying dz

50
Q

re-enterent tachycardial localized in the right atrium with passive activation of the left atrium

A

atrial flutter

51
Q

if propagation of the impulse in atrial flutter is in what direction will it produce a negative p wave in the inferior leads with a sawtooth pattern?

A

counter clockwise

52
Q

what is the rate of atrial flutter

A

250-350

53
Q

what is the usual ventricular rate with a-flutter

A

usually 2:1 AV conduction with Ventricular rate of 150

54
Q

AFL can result in the presence of an accessory pathway, teh ventricular rate can be rapid, resulting in hemodynamic compromise and V-fib.
when AFL is assoicated with hemodynamic compromise or angina, what is the treatment of choice?

A

IMMEDIATE CARDIOVERSION

55
Q

Pt with A-Flutter who is hemodynamically stable, but remains symptomatic despite rate control drugs, what should be attempted?

A 
rhythm control with drugs or catheter ablation
when class IA anti-arrhythmic agents are used to convert AFL to sinus rhythm, the ventricular rate MUST first be controlled with digoxin, BB, or CCB.
56
Q

most common sustained supraventricular tachycardia

A

atrial fibrillation

57
Q

what is the rate of ventricle in Atrial Fib

A

irregularly irregular at rates between 120-170

58
Q

EKG findings for A-fib

A

NO P WAVES

59
Q

what is the physical examination of a pt with A-FIb

A

variation in the intensity of S1, an irregular cardiac rhythm, and absence of waves in the jugular venous pulsations

60
Q

at the very short RR intervals tha toccur intermittently during rapid heart rates, the minimal diastolic filling time and subsequent low stroke volume fail to do what?

A

produce a palpable pulse
-a discrepancy may therefore exist between the ausculated heart rate and the palpable pulse rate, with the ausculated rate being more accurate reflection of the true ventricular rate

61
Q

Treatment of A-Fib

A

warfarin to prevent thromboembolic event
digoxin, BB, or CCB for control of heart rate
if AF is assoc with hemodynamic compromise = CARDIOCONVERSION

:) (11 decks)

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