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SA DX & TX I > Exam 4 - Cardiac Arrhythmias > Flashcards

Exam 4 - Cardiac Arrhythmias Flashcards

1
Q

what does the p wave, pr interval, qrs complex, & t wave represent in an ecg?

A

p wave - atrial depolarization

pr interval - av nodal conduction

qrs complex - ventricular depolarization

t wave - atrial repolarization

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2
Q

what is the autonomic control over the SA node in regards to sympathetic & parasympathetic?

A

sympathetic - increases rate

parasympathetic - decreases rate

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3
Q

where is the location of the SA node?

A

located in the upper right atrium close to the cranial vena cava

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4
Q

what rate do the pacemakers set in the SA node?

A

70-160 bpm

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5
Q

what is the physiology of the SA node?

A

pacemaker cells spontaneously depolarize

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6
Q

where is the AV node located?

A

endocardial - interatrial septum near the junction of the atria and ventricles

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7
Q

what is the physiology the AV node is responsible for?

A

propagated depolarization from atrial myocardium with:
- pacemaker capability
- slows conduction: allows the atria to expel blood into the ventricles & protects ventricles from pathologic arrhythmias
- autonomic control: same as SA node

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8
Q

what on the ecg represents the av node?

A

pr segment

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9
Q

what is the action of the bundle of HIS & purkinje fibers?

A

bundle of HIS - conduct rapidly between the AV node & its branches

fascicular branches divide into left & right bundles

purkinje fibers - conduct rapidly through the ventricular endocardium

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10
Q

what on ecg represents the bundle of HIS/purkinje fibers?

A

QRS complex

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11
Q

what are the intrinsic pacing rates of the SA node, AV node, & bundle of HIS/purkinje fibers?

A

sa node: 70-160 bpm

av node: 40-60

bundle of HIS/purkinje fibers: 20-40

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12
Q

what pathologic conditions can affect conduction in the heart?

A

inflammation, infection/parasites, fibrosis, & infarction

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13
Q

what are the major differences between the effect of increased sympathetic & increased parasympathetic tone in regards to the cardiovascular system?

A

sympathetic:
- increases rate of SA node discharge
- increases speed of AV nodal conduction
- increased risk of ventricular arrhythmias

parasympathetic:
- decreases rate of SA node discharge
- decreased speed of AV nodal conduction
- ‘vagal maneuver’

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14
Q

why can a rapid heart rate result in a decreased cardiac output?

A

decreased diastolic filling will cause decreased stroke volume

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15
Q

why can a slow heart rate decrease cardiac output?

A

there is adequate but decreased overall output

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16
Q

what are some cardiac origins of arrhythmias?

A

structural - cardiomyopathy, valve disease, infectious (chagas, endocarditis), or inflammatory

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17
Q

what are the 3 big non-cardiac origins of arrhythmias?

A

hypoxia, pain, & electrolyte abnormalities (hyperthyroidism, hyperkalemia, medications, toxins)

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18
Q

why are cardiac arrhythmias of clinical importance?

A

can result in clinical decompensation through:

-decreased cardiac function, blood pressure, reduced tissue perfusion, limits exercise capacity, syncope, myocardial fibrillation, asystole, & sudden death

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19
Q

when would you treat cardiac arrhythmias?

A

clinical signs - weakness, collapse, cough, breathing difficulty

if the rhythm carries a risk of sudden death

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20
Q

what are the advantages & disadvantages of using an ecg for a patient with a cardiac arrhythmia?

A

advantages: immediate rate & rhythm diagnosis

disadvantages: short duration represents a fraction of the animal’s day & some arrhythmias are intermittent

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21
Q

when would you want to use a holter monitor for a patient with an arrhythmia?

A

ideal if you suspect an intermittent arrhythmia, screening for boxer ARVC & doberman DCM, & to assess the animal’s response to therapy

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22
Q

what are some indications for performing an ECG?

A
  • suspect arrhythmia: abnormal auscultation or pulses, patient has a history of weakness/collapse
  • screening: breed predisposition
  • pre-anesthetic work up
  • monitoring a sick patient with trauma or metabolic disease or one that is on anti-arrhythmic drug therapy
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23
Q

why would you run cardiac troponin I for a patient with an arrhythmia?

A

it is an indicator of myocardial damage

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24
Q

where can conduction go wrong?

A

-abnormal rate: too fast/slow

  • abnormal conduction: SA node, AV node, bundles of HIS
  • abnormal tissue generating beats: supraventricular or ventricular
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25
Q

what is the normal mechanism for initiating systole?

A

normal sinus rhythm - beats originate from the sinus node with a normal heart rate range

exercise may increase the rate & vagal stimulation may decrease the rate

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26
Q

what are some clinical signs of bradyarrhytmias?

A

weakness, collapse, signs of heart failure (ascites, pulmonary edema)

27
Q

what are 3 common cardiac causes of bradyarrhythmias?

A
  1. sinus node dysfunction - sinus arrest, sick sinus syndrome
  2. av block
  3. atrial standstill - hyperkalemia
28
Q

what are some non-cardiac causes of bradyarrhythmias?

A

hyperkalemia, excessive vagal tone (gi disease, pancreatitis, CNS), hypothermia, & medications such as opioids, beta/calcium blockers

29
Q

what is the treatment for bradyarrhythmias?

A

atropine response test & treat the underlying cause

30
Q

what breeds are predisposed to developing sick sinus syndrome?

A

mini schnauzer, cocker spaniel, & westies

31
Q

what is sick sinus syndrome?

A

sinus node dysfunction +/- av nodal involvement with inappropriate bradycardia/tachycardia/sinus arrest

32
Q

what is the treatment for sick sinus syndrome?

A

is tachycardia/bradycardia causing clinical signs - consider holter

pacemaker +/- anti-arrhythmics

33
Q

what is sinus arrest?

A

no sinus node activity > 2 r-r intervals

34
Q

what is seen on this ecg?

A

sinus arrest

35
Q

what conditions can result in hyperkalemia causing atrial standstill?

A

urinary blockage/rupture, iatrogenic, addisonian crisis

36
Q

what is the treatment for atrial standstill caused by hyperkalemia?

A

manage the hyperkalemia

37
Q

what does this ecg show?

A

atrial standstill - no p wave & slow rate

38
Q

what breed is associated with muscular dystrophy causing atrial standstill?

A

english springer spaniel

39
Q

what is the treatment for muscular dystrophy causing atrial standstill?

A

pacemaker

40
Q

what do av blocks affect on ecg?

A

the p-r interval

41
Q

what are the 3 types of av block?

A
  1. 1st degree: slow av conduction
  2. 2nd degree: interrupted AV conduction
  3. 3rd degree: incomplete AV conduction
42
Q

what is 1st degree av block caused by?

A

increased vagal tone, drugs, & av nodal disease

43
Q

how is 1st degree av block diagnosed?

A

ecg

44
Q

what is seen on this ecg?

A

1st degree av block - prolonged p-r interval characteristic of slow av conduction

45
Q

what is the characteristic finding of type I 2nd degree av block?

A

prolongation of p-r interval until p wave isn’t conducted

46
Q

what causes 2nd degree av block?

A

increased vagal tone, drugs, & av nodal disease

47
Q

what is seen on this ecg?

A

type I 2nd degree av block

48
Q

what is the characteristic finding of type II 2nd degree av block?

A

some p waves conduct & others don’t & sometimes there is a pattern

49
Q

what causes type II 2nd degree av block?

A

increased vagal tone, drugs, & av nodal disease

50
Q

what is seen on this ecg?

A

type II 2nd degree av block

51
Q

what is seen on this ecg?

A

3rd degree av block

52
Q

what characteristics are seen on ecg of 3rd degree av block?

A

complete failure of av node to conduct, some portion of the conduction system must take over & you see escape complexes with a slow heart rate, & no associated between p waves & qrs complex

53
Q

what are the clinical signs associated with av block?

A

collapse or fainting, heart failure, forward failure: weakness/lethargy

54
Q

what diagnostics are run for av block?

A

atropine response test

55
Q

what is the treatment for av block?

A

address the underlying cause & pacemaker if clinical signs & there isn’t a response to atropine

56
Q

how is the atropine response test performed?

A

give 0.04 mg/kg atropine IV & wait for the anticipated response in 5-10 minutes

  1. heart rate increases to > 160 bpm without further block = secondary to high vagal tone
  2. heart rate doesn’t increase or only slightly does & block persists = av nodal disease
57
Q

what is supraventricular tachycardia?

A

intermittent or continuous impulses originating from the atrial myocardium or av node

58
Q

what are some examples of supraventricular tachycardias?

A

atrial fibrillation, atrial flutter, atrial tachycardia, & av nodal reentrant

59
Q

what are the ecg characteristics of atrial fibrillation?

A

no p waves & irregular rhythm

60
Q

what are the causes of atrial fibrillation?

A

primary, lone atrial fibrillation in giant breeds

secondary to significant structural heart disease

61
Q

what is ventricular tachycardia?

A

intermittent or continuous impulses originating from the ventricular myocardium

62
Q

what is seen on this ecg?

A

ventricular tachycardia - PVC, wide & bizarre qrs

63
Q

when do you treat ventricular tachycardia?

A

heart rate is > 180, can lead to decompensation

hemodynamically unstable

complex: multiform, sustained, r on t

SA DX & TX I (59 decks)

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