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Applied Clinical Veterinary Nursing > ECG Equipment and Monitoring > Flashcards

ECG Equipment and Monitoring Flashcards

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1
Q

how is the heart rate controlled?

A

2 branches of the autonomic NVS -
sympathetic and parasympathetic branches

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2
Q

how is the heart rate accelerated?

A

sympathetic nervous system releases hormones to accelerate heart rate

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3
Q

what is released by the sympathetic nervous system to accelerate heart rate?

A

catecholamines - adrenaline and noradrenaline

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4
Q

how is the heart rate decelerated?

A

parasympathetic nervous system releases acetylcholine to slow heart rate

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5
Q

what are the 2 types of cardiac cells?

A

electrical cells

myocardial cells

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6
Q

what is the function of the electrical cells

A

spontaneously generate electrical impulses and respond to impulses

transmit an electrical pulse from one cell to the next

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7
Q

how are electrical cells distributed?

A

in an orderly fashion

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8
Q

which type of cells make up the conduction system of the heart?

A

electrical cells

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9
Q

where are the myocardial cells found?

A

make up the walls of the atrium and ventricles of the heart

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10
Q

which type of cells make up the atrial and ventricular walls?

A

myocardial cells

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11
Q

what cardiac functions are the myocardial cells responsible for?

A

contraction and ability to stretch

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12
Q

which cells make the heart able to contract and stretch?

A

myocardial cells

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13
Q

what is required for cardiac muscle cells to contract?

A

an electrical stimulus

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14
Q

what state are the cardiac cells at rest?

A

polarised (relaxed)

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15
Q

when happens to the cardiac cells when there is an electrical stimulus?

A

cells start to depolarise

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16
Q

what allows the heart time to refill ready for the next stimulation and contraction?

A

heart must repolarise and return to its resting potential between beats

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17
Q

which parts of the heart are involved in contraction?

A

SA node

AV node

Bundle of His

Purkinje fibres

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18
Q

what is the SA node?

A

a small area of modified cardiac cells (specialised fibres)

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19
Q

where is the SA node located?

A

right atrium wall

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20
Q

which cells act as the pacemaker for the heart?

A

cells making up the SA node

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21
Q

how does autonomic tone affect heart rate?

A

sympathetic increases rate
parasympathetic decreases rate

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22
Q

what is the AV node?

A

specialised group of cardiac muscle cells

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23
Q

where is the AV node located?

A

top if the interventricular septum

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24
Q

how quickly does the electrical impulse from the SA node pass through the AV node?

A

passes through AV slower than SA

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25
Q

why is the electrical impulse through the ANV node slower than the SA node?

A

is it deliberately slow, so that ventricular contraction will be correctly coordinated following atrial contraction

(allows atria time to fully contract before the ventricles do)

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26
Q

what is the Bundle of His?

A

specialised bundle of nerve tissue fibres

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27
Q

why is the bundle of His necessary?

A

myocardium of the atrium walls is not in electrical continuity with myocardium of the ventricular walls

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28
Q

how does conduction pass through the AV ring?

A

through the Bundle of His

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29
Q

what does the AV ring connect?

A

the atria to the ventricles

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30
Q

where is the bundle of His located?

A

a narrow pathway which runs down the interventricular septum

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31
Q

how does the bundle of His divide?

A

divides in the interventricular septum into left and right bundle branches - these branches then spread into the right and left ventricles

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32
Q

what happens to the left bundle branch of the bundle of His?

A

divides further into anterior and posterior fascicles

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33
Q

what are the Purkinje fibres?

A

a network of specialised neurones, which are organised in very fine branches

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34
Q

what does the bundle of His go on to connect with?

A

the Purkinje fibres

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35
Q

where are the Purkinje fibres located?

A

spread out through the myocardium of the right and left ventricles

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36
Q

where does the wave of ventricular contraction begin?

A

in the myocardium at the apex of the heart (bottom of ventricles)

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37
Q

what is the stage where the ventricles contract called?

A

ventricular systole

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38
Q

what happens after the heart cells repolarise?

A

the SA node fires another impulse and the cycle begins again

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39
Q

what is electrocardiography?

A

a continuous measurement of the changing potential differences in the electrical activity of the heart

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40
Q

what does an ECG machine detect?

A

the depolarisation wave travelling across the heart

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41
Q

how does the ECG machine records the depolarisation wave?

A

as deflection

-ive deflections = downwards
+ive deflections = upwards

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42
Q

when are ECGs used?

A

diagnostic - arrhythmias

triage

anaesthesia

monitoring patients with known arrhythmias

newly identified pulse deficits

during CPR

metabolic or electrolyte abnormalities

blood transfusions

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43
Q

which type of surgery heavily relies on ECG for monitoring?

A

during pericardiocentesis and central line catheter placement (arrhythmias can arise during procedure)

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44
Q

what are the 2 types of commonly used ECG electrodes?

A

crocodile clips - directly onto patients skin with spirit

ECG pads - onto paws with tape/thorax

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45
Q

what are the general considerations for obtaining a good ECG trace?

A

patient in right lateral recumbency

remove sources of interference e.g. mobiles

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46
Q

why might a paper trace ECG recording machine be used?

A

has high diagnostic value

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47
Q

why might a patient be attached to a Holter monitor?

A

for monitoring over a longer period - patient can go home and any abnormal activity reviewed at recheck

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48
Q

what is telemetry?

A

monitoring patients with ECG from a distance

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49
Q

what is the advantage of telemetry?

A

less machines attached directly to patient

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50
Q

what should you consider when troubleshooting an ECG?

A

check setting on machine, batteries, charge

are leads still attached and on correct legs

minimise patient movement as interferes with trace, ideally have in right lateral recumbency
panting/purring can also affect trace

check contact of crocodile clips to skin, reapply spirit
change pads if dry/dislodged/not sticking well

clip fur for better contact

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51
Q

what does the P wave represent?

A

atrial depolarisation

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52
Q

why is the P wave small compared to the QRS wave?

A

muscle mass of atria is relatively small, therefore electrical changes associated with the depolarisation are also small

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53
Q

what does the P-R interval represent?

A

the time between atrial depolarisation and ventricular depolarisation

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54
Q

how is the P-R interval measured?

A

as the onset of the P wave to the onset of the R wave

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55
Q

what is indicated by a normal P-R interval?

A

the electrical impulse is travelling between the atria and ventricles correctly

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56
Q

what is indicated by the Q wave?

A

depolarisation of the ventricular septum

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57
Q

which part of the ventricles is the first to depolarise?

A

ventricular septum

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58
Q

why is the Q wave shown as a downward deflection on an ECG trace?

A

travels in a direction away from the positive electrode

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59
Q

what does the R wave indicate?

A

depolarisation of the majority of the ventricular myocardium

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60
Q

why is the R wave so large?

A

the ventricular myocardium is a large mass of muscle tissue - creates a large positive deflection

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61
Q

what does the S wave respresent?

A

final depolarisation of a small mass of tissue at the base of the heart

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62
Q

what does the QRS complex represent?

A

depolarisation (activation) of the ventricles, followed by ventricular muscle contraction

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63
Q

where do we see baseline ECG trace?

A

the P-R segment and the S-T segment

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64
Q

what is the s-T segment?

A

the interval between ventricular depolarisation and ventricular repolarisation

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65
Q

what does the T wave represent?

A

repolarisation of the ventricles - marks the beginning of ventricular relaxation

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66
Q

why does the T wave occur?

A

there is a potential difference across the myocardium here, until is completely repolarised - usually results in a small positive deflection from the baseline

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67
Q

why can the T wave vary?

A

repolarisation of the myocardium can be random in cats and dogs - can be positive, negative or both

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68
Q

what are our main considerations when interpreting an ECG?

A

heart rate

presence/absence of expected waves

presence/absence of arrhythmias

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69
Q

what is a bradyarrhythmia?

A

slow arrythmia

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70
Q

what is a tachyarrhythmia?

A

fast arrhythmia

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71
Q

what do we need to consider in terms of arrhythmia source?

A

sinus arrhythmia vs ventricular arrhythmia vs supraventricular arrhythmia

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72
Q

what type of issues can cause arrhythmias?

A

abnormalities in rate, electrical impulse conduction and abnormalities associated with ectopia

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73
Q

what are the types of sinus rhythms?

A

normal sinus rhythm

sinus arrhythmia

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74
Q

what are the types of bradyarrhythmias?

A

sinus bradycardia

sick sinus syndrome

AV blocks

escape beats

hyperkalaemia

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75
Q

what are the types of tachyarrhythmias?

A

sinus tachycardia

supraventricular tachycardia

atrial fibrillation

ectopic beats

accelerated idioventricular rhythm

ventricular tachycardia

R-on-T phenomenon

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76
Q

what are the cardiac arrest rhythms?

A

ventricular fibrillation

pulseless ventricular tachycardia

pulseless electrical activity

asystole

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77
Q

what is sinus rhythm?

A

normal rhythm

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78
Q

what does an ECG trace look like for sinus rhythm>?

A

P wave, QRS complex and T wave present

P wave present for every QRS complex

all complexes identical

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79
Q

what does sinus rhythm sound like on auscultation?

A

regular heart sounds

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80
Q

where does the electrical impulse originate from in sinus arrhythmia?

A

SA node

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81
Q

what does sinus arrhythmia look like on ECG?

A

normal P wave for every QRS wave

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82
Q

what is sinus arrhythmia?

A

commonly a regular variation in HR, which co-insides with respiration (respiratory sinus arrhythmia)

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83
Q

what is sinus arrhythmia associated with?

A

an increase in parasympathetic activity (vagal tone) on the SA node

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84
Q

what heart rhythm can be seen due to increased parasympathetic activity on the SA node?

A

sinus arrhythmia

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85
Q

do cats dispay sinus arrhythmia?

A

rarely

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86
Q

what type of rhythm is sinus arrhythmia?

A

regularly irregular

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87
Q

what causes sinus bradycardia?

A

SA node impulse and corresponding depolarisation occurs slower than normal

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88
Q

what does sinus bradycardia look like on ECG?

A

P wave for every QRS wave

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89
Q

what happens to the heart rate in sinus bradycardia?

A

heart rate may be inappropriately slow for age/breed/species

pulse for every heart beat

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90
Q

what type of rhythm is sinus bradycardia?

A

regularly regular

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91
Q

what are the broad causes of sinus bradycardia?

A

normal in some breeds

can be due to issue with SA node

often secondary to another disease process which increases vagal tone

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92
Q

what are the other causes of sinus bradycardia?

A

hyperadrenocorticism and associated electrolyte abnormalities

BOAS

raised ICP

vaso-vagal reaction (nerve stimulation)

hypocalcaemia/hypothermia/hypoglycaemia

hypothyroidism

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93
Q

how is sinus bradycardia treated?

A

dictated by underlying cause - depends if patient has clinical signs of arrhythmia

temporary management via an anticholinergic to increase HR

positive inotrope if anticholinergic unsuccessful

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94
Q

what is sick sinus syndrome?

A

problem with SA node function - failure to discharge electrical impulse

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95
Q

how does sick sinus syndrome present?

A

severe bradycardia occurs due to decreased SA node input (<30bpm)

periods of asystole can be present for several seconds without escape beats (sinus arrest)

96
Q

which animals are affected by sick sinus syndrome?

A

older animals (6-10 years)

WHWT, cocker spaniels, cairn terriers and miniature schnauzers

rare in cats

97
Q

what type of condition is sick sinus syndrome?

A

degenerative condition

98
Q

how is sick sinus syndrome treated?

A

responds poorly to medical management

requires pacemaker

99
Q

what are the potential risks of pacemaker placement?

A

infection

lead dislodgement

failure to place correctly

venous thrombosis

100
Q

what are the nursing considerations after pacemaker placement?

A

no walking for 48 hours post-placement

harness walks only

care with neck restraint

no jugular samples

101
Q

what is heart block?

A

problem with the electrical conduction system of the heart

102
Q

how does AV block occur?

A

electrical impulses from the SA node are delayed, or completely blocked, going through the AV node - electrical signals may not reach the ventricles

103
Q

what causes AV block?

A

can be due to a disease process or drug-related effect at the AV node

104
Q

which blocks affect the AV node?

A

AV bock or AV nodal block

105
Q

which blocks affect the left or right bundle branches?

A

bundle branch blocks

106
Q

what is first degree AV block?

A

delayed conduction through the AV node

107
Q

what does first degree AV block look like on ECG?

A

normal P wave and QRS complex

longer interval between the P wave and corresponding QRS complex (prolonged P-R interval)

108
Q

how does second degree AV block differ from first degree?

A

longer conduction delay, some beats dropped

109
Q

what does second degree AV block look like on ECG?

A

some P waves will not have a corresponding QRS

QRS complexes are normal in morphology

110
Q

how do the QRS complexes in AV block have a normal shape?

A

there is conduction through the AV node

111
Q

what are the 2 types of second degree AV block?

A

mobitz type I
mobitz type II

112
Q

what happens in mobitz type I?

A

P-QRS gap becomes longer and longer, then there is a P wave without a corresponding QRS complex

once QRS complex missed, snaps back to normal

113
Q

what is mobitz type I also known as?

A

wenkebach

114
Q

what happens in mobitz type II?

A

P-QRS complex normal (P-R interval same each time)

occasionalP with with no corresponding QRS complex

115
Q

what is 3rd degree AV block?

A

complete lack of conduction through the AV node

116
Q

what does 3rd degree AV block look like on ECG?

A

multiple P waves without QRS complexes

P waves occur faster, sometimes followed by a tall QRS-T complex

117
Q

why do ventricular ‘escape beats’ occur in 3rd degree AV block?

A

they are ectopic beats which act as a rescue for the heart, permitting a heart beat

animal would die without them

118
Q

how do ventricular escape beats occur?

A

an electrical impulse occurs from random cardiac cells, before cardiac standstill occurs

119
Q

what do ventricular escape beats look like?

A

wide and bizarre, with an absent P wave

120
Q

what is the heart rate during AV block?

A

rate of ventricular escape beats is typically 20-40bpm

121
Q

what are the clinical signs of AV block?

A

if severe block is present, signs of decreased cardiac output e.g. lethargy, syncope, collapse

122
Q

how can AV block be treated?

A

management of underlying condition e.g. hypoadrenocorticism

vagolytic drugs e.g. atropine, glyocpyrrulate

severe 2nd and 3rd degree blocks require pacemaker implantation

123
Q

what is hyperkalaemia?

A

increased serum potassium levels

124
Q

what is the normal range for serum potassium?

A

3.5-5.0 mmol/l

125
Q

what effect does increased potassium have on heart function?

A

severity of arrhythmia progresses as K+ increases

126
Q

what type of arrhythmia does hyperkalaemia typically induce?

A

bradyarrhythmias

127
Q

how do arrhythmias due to hyperkalaemia present on ECG?

A

reduced/absent P waves

spiked T waves

shortened QT interval

prolonged QRS complex

128
Q

how does severe hyperkalaemia affect the heart?

A

progresses to atrial standstill, sine wave pattern, ventricular fibrillation and eventual asystole

129
Q

what are some of the causes if hyperkalaemia?

A

urethral obstruction e.g. blocked bladder

AKI e.g. toxin

hypoadrenocorticism e.g. Addisonian crisis

130
Q

arrhythmias due to hyperkalaemia be treated?

A

calcium gluconate bolus

neutral insulin infusion

dextrose infusion

131
Q

how can a calcium gluconate bolus treat arrhythmias due to hyperkalaemia?

A

reduces risk of ventricular fibrillation and protects cardiac myocytes from effect of elevated K+

(doesn’t actually reduce K+ levels)

132
Q

how can a neutral insulin infusion help treat hyperkalaemia?

A

causes movement of potassium into cells

133
Q

how can a dextrose infusion help treat hyperkalaemia?

A

cells uptake glucose, intracellular shift of K+ into cells prevents hypoglycaemia due to insulin infusion

134
Q

what happens in sinus tachycardia?

A

SA node generates an impulse and depolarisation at a rate faster than normal

135
Q

what does sinus tachycardia look like on ECG?

A

normal sinus rhythm, with normal P-QRS-T complexes

136
Q

what type of rhythm is sinus tachycardia?

A

regularly regular rhythm

137
Q

can pulses still be felt in sinus tachycardia?

A

pule should be present for every heartbeat, with very fast rates pulses may become weaker

138
Q

when does sinus tachycardia occur?

A

can be normal e.g. after exercise

occurs with pain, stress, hypovolaemia, anaemia

139
Q

where do supraventricular tachyarrhythmias originate?

A

atrial in origin (occurs in atrium)

140
Q

where do supraventricular tachyarrhythmias occur?

A

occur at a point other than the SA node, then conduct via the AV node to the ventricles

141
Q

what does a supraventricular arrhythmia typically look like on ECG?

A

QRS complexes relatively normal in appearance

often taller and narrower than normal

142
Q

where do ventricular arrhythmias originate?

A

ventricular in origin

143
Q

what happens in ventricular arrhythmias?

A

normal conduction pathway is not followed

144
Q

how do ventricular arrhythmias appear on ECG?

A

QRS complexes appear wide and bizarre

145
Q

how can we tell if a cardiac impulse has arisen from an ectopic location?

A

if the P-QRS-T complex looks different to normal

146
Q

if a P-QRS-T complex in a trace looks abnormal, what does this mean?

A

the impulse has arisen from an ectopic location

147
Q

what does ectopic mean?

A

out of place (electrical impulse did not originate from the SA node)

148
Q

when do ectopic beats occur?

A

prematurely

149
Q

why do ectopic beats look abnormal?

A

they interrupt the normal rhythm, before the SA node is ready to initiate another impulse

150
Q

where do ectopic beats originate?

A

can originate from the atria or ventricles

151
Q

how are ectopic beats classified?

A

by their point of origin

152
Q

what an atrial premature complex?

A

an ectopic beat that is atrial in origin

153
Q

what is an ectopic beat that is atrial in origin called?

A

atrial premature complex

154
Q

what is an ectopic beat that is junctional in origin called?

A

junctional premature complex

155
Q

what is a junctional premature complex?

A

an ectopic beat that is junctional in origin

156
Q

what is an ectopic beat that is ventricular in origin called?

A

ventricular premature complex

157
Q

what is a ventricular premature complex?

A

an ectopic beat which is ventricular in origin

158
Q

give an example of some arrhythmias which have ectopic beats

A

supraventricular tachycardia

escape beats (e.g. 3rd degree AV block)

159
Q

what is a supraventricular arrhythmia?

A

an abnormal electrical impulse which occurs at an ectopic site in the atria (not the SA node)

160
Q

what does a supraventricular arrhythmia look like on ECG?

A

often an abnormal P wave (as it is not initiated by the SA node) followed by a QRS complex

161
Q

what type of rhythm is a superventricular arrhythmia?

A

often irregularly irregular

162
Q

what are the alternative terms for a superventricular arrhythmia?

A

atrial premature complex (APC)

premature atrial contraction (PAC)

atrial premature beat (APB)

163
Q

how many APCs are considered supraventricular tachycardia?

A

three or more APCs in a row

164
Q

what is the heart rate during supraventricular tachycardia?

A

rapid - can be 170-350bpm

165
Q

what does supraventricular tachycardia look like on ECG?

A

QRS complexes are almost like normal, however they are narrower and more upright

may or may not be an associated P wave

166
Q

what type of rhythm is supraventricular tachycardia?

A

regularly irregular

167
Q

what are the clinical signs associated with supraventricular tachycardia?

A

slow SVT = often no signs

fast SVT (>250bpm) = weakness/collapse, poor pulse quality, poor peripheral perfusion, pale MMs, prolonged CRT

168
Q

why do clinical signs of supraventricular tachycardia occur?

A

due to inadequate diastolic filling

169
Q

what causes supraventricular tachycardia?

A

usually associated with underlying cardiac disease e.g. DCM

sometimes associated with systemic disease e.g. toxicity, hypovolaemia, electrolyte imbalance, ischaemia

170
Q

how can supraventricular tachycardia be treated?

A

treatment of any underlying causes

beta-blockers

calcium channel blockers

171
Q

what type of arrhythmia is atrial fibrillation?

A

supraventricular tachyarrhythmia

172
Q

what is atrial fibrillation?

A

characterised by rapid and irregular contractions of the atria (‘quivering’)

173
Q

which species gets atrial fibrillation more commonly?

A

relatively common in dogs, rare in cats

174
Q

what might we find on examination of a patient in atrial fibrillation?

A

pulse deficits common

irregular pulse (ventricles may contract before they have filled sufficiently)

rapid HR (>200bpm), irregular beating with no obvious pattern

175
Q

what does atrial fibrillation look like on ECG?

A

fibrillating baseline

QRS complex tall and narrow

no visible P waves

176
Q

why is there no visible P waves with atrial fibrillation?

A

impulse not from the SA node

177
Q

what type of rhythm is atrial fibrillation?

A

irregularly irregular

178
Q

how can atrial fibrillation be treated?

A

calcium channel blockers

beta-blockers

digoxin

amiodarone

179
Q

what are the goals of atrial fibrillation treatment?

A

decrease heart rate and increase cardiac output

180
Q

what is a junctional premature complex?

A

ectopic beats that arise from an area within the atrioventricular junction, therefore ventricles are usually activated normally

181
Q

what is the atrioventricular junction?

A

region of the AV node

182
Q

what do junction premature complexes look like on ECG?

A

QRS complexes are premature, with morphology very similar to sinus complexes but narrower

usually without a preceding P wave, but this may be hidden, abnormal or premature

183
Q

what are junctional premature complexed also called?

A

premature junctional complex

junctional premature beat

184
Q

where does the impulse come from in ventricular arrhythmias?

A

abnormal electrical impulse starts at an ectopic site below the AV node

185
Q

what acts as the pacemaker in ventricular arrhythmias?

A

another area in the ventricles

186
Q

what do complexes look like in ventricular arrhythmias?

A

wide and bizarre as normal electrical pathway is not followed

187
Q

what cause ventricular arrhythmias?

A

underlying primary cardiac disease

as a complication due to another condition e.g. GDV, pyometra, splenectomy, pancreatitis, anaemia

188
Q

what is a ventricular premature complex?

A

an ectopic beat that occurs prior to normal SA node depolarisation

189
Q

where do VPCs start?

A

an unusual location in the ventricles

190
Q

what do VPCs look like on ECG?

A

no preceding P wave (except by coincidence)

wide and bizarre QRS complex

191
Q

how do VPCs affect pulses?

A

pulse quality may feel weak with certain beats

pulse deficits present

192
Q

what can ventricular premature complexes also be called?

A

premature ventricular contractions

193
Q

what does AIVR stand for?

A

accelerated idioventricular rhythm

194
Q

what is AIVR?

A

3 or more VPCs together

195
Q

what is the heart rate during AIVR?

A

not very elevated - 140-180bpm

196
Q

does AIVR affect cardiac function significantly?

A

generally considered benign rhythm at lower rates, unlikely to be causing decreased cardiac output, haemodynamic compromise or hypotension

197
Q

what is the treatment for AIVR?

A

treatment not usually required

198
Q

when is AIVR sometimes seen?

A

in patient recovering from abdominal surgery

199
Q

what can AIVR develop into?

A

ventricular tachycardia

200
Q

what is the difference between AIVR and ventricular tachycardia?

A

traces look similar but AIVR is at a slower HR (140-180bpm)

201
Q

how are VPCs identified as V-tach?

A

3 or more VPCs occurring in a row with heart rate >180bpm

202
Q

what does V-tach look like on ECG?

A

QRS complexes wide and bizarre, with absent P waves and large T waves

203
Q

what clinical findings would you expect to see in a patient with V-tach?

A

pulses weak, rapid and irregular, with pulse deficits

hypotension/collapse due to reduced cardiac output

signs of haemodynamic compromise

204
Q

what signs of haemodynamic compromise might be seen in a patient with V-tach?

A

altered mentation

signs of hypoperfusion (pale mm’s prolonged CRT, hypothermia, weak/absent peripheral pulses)

205
Q

what are some of the causes of V-tach?

A

primary cardiac disease e.g. DCM/HCM

significant abdominal pathology e.g. GDV

inflammation/inflammatory mediators e.g. septic abdomen, trauma

severe anaemia

abnormal autonomic activity e.g. pain

electrolyte disturbances

drug toxicities e.g. caffeine, cocaine

neoplasia e.g. haemangiosarcoma

206
Q

what are the consequences of sustained V-tach?

A

decreased systemic tissue perfusion (cardiogenic shock)

decreased cardiac perfusion

development of myocardial failure

development of malignant arrhythmia (v-fib)

sudden death

207
Q

what is the aim of treatment for V-tach?

A

convert to sinus rhythm and low HR down to allow better cardiac output and peripheral perfusion

208
Q

what does treatment for V-tach depend on?

A

degree of haemodynamic compromise and underlying cause

209
Q

which patients in V-tach are more likely to require immediate drug intervention?

A

patients with underlying heart disease - risk of cardiac arrest

210
Q

what is V-tach called if there is no associated pulse?

A

pulseless ventricular tachycardia (PVT)

211
Q

which drug is the most commonly used for treating V-tach?

A

lidocaine - sodium channel blocker

212
Q

how is lidocaine given for treatment of V-tach?

A

boluses then CRI

213
Q

which other drugs might be used in management of V-tach?

A

beta-blockers

amiodarone

procainamide

magnesium

214
Q

how does the R-on-T phenomenon occur?

A

VPC is so premature, it is superimposed on the T wave of the preceding complex - can be a sinus beat or ectopic beat

215
Q

why is R-on-T phenomenon potentially very serious?

A

the end of the T wave is a ‘vulnerable period’

anything abnormal during this period can preclude the occurrence of V-tach and V-fib

216
Q

what happens to the ventricles during R-on-T phenomenon?

A

ventricles have not had time to completely repolarise from the previous contraction before they are depolarised again

217
Q

what is the aim of using a defibrillator?

A

to reset the electrical state of the heart, thereby converting from a shockable arrhythmia to normal sinus rhythm

218
Q

why do we need to take car with which rhythms we defibrillate?

A

shockable rhythms seen less frequently - defibrillating a non-shockable rhythm can be detrimental to survival

219
Q

what are the shockable rhythms?

A

ventricular fibrillation

pulseless ventricular tachycardia

220
Q

what are the non-shockable rhythms?

A

asystole

pulseless electrical activity (PEA)

221
Q

what is ventricular fibrillation?

A

no effective ventricular contractions (all chaotic)

222
Q

how serious is V-fib?

A

pre-terminal condition - results in patient death unless instantly recognised and treated

223
Q

what does v-fib look like on ECG?

A

rapid, irregular, wavy baseline with no recognisable normal complexes

224
Q

what are the 2 types of v-fib?

A

fine or coarse

225
Q

how will a patient in v-fib present?

A

collapsed - no cardiac output, therefore no palpable pulses

226
Q

what is the treatment for v-fib?

A

immediately start CPR

v-fib is a shockable rhythm - defib required

227
Q

what is PEA?

A

electrical impulses within the heart, but no corresponding myocardial contractions

228
Q

what does PEA look like on ECG?

A

may show slow, normal or fast HR

often normal P-QRS-T complex, which may become increasingly wide and bizarre

229
Q

what will be found upon clinical exam of a patient with PEA?

A

no audible heart beats, no palpable pulses, no cardiac output

230
Q

what is the treatment for PEA?

A

CPR, adrenaline, atropine

only defibrillate if converts to a shockable rhythm

231
Q

what is the most common arrest arrhythmia in dogs and cats?

A

asystole

232
Q

what does asystole look like on ECG?

A

straight, flat-line ECG

no complexes

233
Q

what does asystole mean?

A

patient in CPA - no cardiac movement, no pulses or cardiac output

234
Q

what is the treatment for asystole?

A

start CPR immediately

non-shockable rhythm

235
Q
A

Applied Clinical Veterinary Nursing (31 decks)

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