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ACVN - MEDICAL NURSING > ECG Equipment and Monitoring > Flashcards

ECG Equipment and Monitoring Flashcards

1
Q

What is the action of the heart?

A

to pump the blood around the body and lungs

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2
Q

What is the myocardium composed of?

A

cardiac muscle which Contracts rhythmically and automatically without nervous input which is controlled by electrical impulses

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3
Q

How is heart rate controlled?

A

by the two branches of the autonomic (involuntary) nervous system which consists of sympathetic nerveous system and parasympathetic nervous system

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4
Q

What does the smpathetic nervous system release?

A

releases hormones (catecholamines – e.g. adrenaline and noradrenaline) to accelerate
heart rate

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5
Q

What does the parasympathetic nervous system release?

A

the hormone acetylcholine to slow heart rate

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6
Q

What is the function of the electrical cells?

A
  • Conduction system of the heart
  • Distributed in an orderly fashion
  • Spontaneously generate electrical impulses and respond to impulses
  • Transmit an electrical pulse from one cell to the next
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7
Q

What is the function of the myocarial cells?

A
  • Make up the walls of the atrium and ventricles of the heart
  • They are responsible for contraction and ability to stretch
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8
Q

What is a co-ordinated artrioventricular contraction?

A
  • Make up the walls of the atrium and ventricles of the heart
  • They are responsible for contraction and ability to stretch
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9
Q

What must the cardiac muscles recieve in order to be able to contrat?

A

an electrical stimulus

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10
Q

What are cardiac cells at rest?

A

polarized (relaxed)

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11
Q

What happens when cardiac cells are stimulated by an electrical impulse?

A

they start to depolarize

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12
Q

What is the heart conduction system?

A
  • Electrical stimulus must first depolarise the two atria, causing them to contract
  • After an appropriate time interval, it must depolarise the two ventricles,
    stimulating them to contract
  • Heart must repolarise (relax) and return back to its resting potential between beats
  • Allows heart time to refill ready for the next stimulation and contraction
  • Cycle begins again
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13
Q

What is the sinoatrial node (SA node)?

A

Small area of modified cardiac muscle cells (specialised fibres)

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14
Q

Where is the SA node located?

A

right atrium wall

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15
Q

What does the SA node do?

A

initiates the heart beat, controls heart rate

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16
Q

What is the SA node influened by?

A

balance in autonomic tone

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17
Q

What is the autonomic tone?

A

Sympathetic increases rate, parasympathetic decreases rate

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18
Q

What does the SA node to to cause depolarization?

A

fires electrical impulse which causes depolarization to spread through the atrial muscle cells

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19
Q

What is artial systole?

A

when the impulse spreads across the atria and causes both artria to contract

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20
Q

Which direction does blood move from due to the SA node?

A

right atrium into the right ventricle and left atrium into the left ventricle

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21
Q

What is the function of the artioventricular node (AV node)?

A

nerve impulse passes throught the AV node and is another specialised group of cardiac muscle celsl

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22
Q

What is the location of the AV node?

A

top of the interventricular spectrum

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23
Q

What do electrical impulses do in the AV node?

A

they spread from the SA node at a slower pace

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24
Q

Why is the speed of electrical depolarization slow through the AV node?

A

so ventricular contraction with be correctly coordinated following artial contraction which allows the atria time to fully contract before the ventricles do

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25
Q

What is the Bundle of His?

A

Specialised bundle of nerve tissue fibres that is a narrow pathway that runs down the interventricular
septum. It divides in the ventricular septum into right and left bundle branches and branches spread into the right and left ventricles. The left bundle branch divides further into anterior and posterior fascicles

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26
Q

Where does conduction pass through the Bundle of His?

A

passes through the AV ring (from the atria into the
ventricles) through the bundle of His

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27
Q

What does the Purkinje Fibres connect to?

A

the Bundle of His

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28
Q

What are Purkinje fibres?

A

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

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29
Q

Where do the conduction fibres spread through?

A

the myocardium of the left and right ventricles

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30
Q

What is it called when the ventircles contract?

A

ventricular systole

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31
Q

What does the SA node do when the heart cells repolarize?

A

fires another impulse and the heart conduction cycle starts over

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32
Q

What happens when an electrical impulse is conducted along the hearts pathways?

A

depolarization of the cells spreads down the spetum towards the ventricles which is depolarization of the myocardium

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33
Q

Where does the wave of ventricular contraction begin?

A

in the myocardium at the apex of the heart and contraction spreads upwards through the muscle of the ventricles

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34
Q

What is an ECG?

A

an electrocardiograpth is a voltmeter

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35
Q

What does an ECG measure and record?

A

the changing electrical activity of the heart, by using positive and negative electrodes

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35
Q

When are ECGs used?

A
  • Diagnostic: arrhythmias
  • Triage
  • Anaesthesia (during/recovery)
  • Monitoring inpatients with known arrhythmias
  • Critical patients
  • Newly identified pulse deficits
  • Cardiopulmonary resuscitation (CPR) determines shockable rhythms
  • Metabolic or electrolyte abnormalities (Ca+ / K+)
  • During pericardiocentesis and central line catheter
    placement (arrhythmias can arise during procedure)
  • Used as part of a hands off method of monitoring
    (e.g. blood transfusions)
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36
Q

When is an electrical potential created?

A

when parts of the atria nearest the SA node are depolarized

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37
Q

What does an ECG detect?

A

the depolarization wave travelling across the heart

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38
Q

How are ECGs recorded?

A

as a wave of deflection, –ve deflections are displayed as downwards and +ve deflections are displayed as upwards

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39
Q

How are crocodile clips used to obtain an ECG?

A
  • Clipped directly onto patient’s skin
  • Check contact with skin and apply spirit to aid contact
  • Be gentle with patient and placing electrodes
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40
Q

How are ECG pads used to obtain an ECG?

A
  • Adhesive pad
  • Applied directly to patient’s paws with tape to secure or onto thorax
  • Electrode must have good contact with paw pads or thorax (clip fur
    from chest)
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41
Q

What are the general considerations for obtaining an ECG?

A
  • Patient in right lateral recumbency
  • Remove sources of interference e.g. mobiles etc.
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42
Q

What is a multiparameter machine?

A

continuous monitoring of a patient

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43
Q

What are the benefits of holter monitoring?

A
  • can monitor over a long period
  • patient can go home for ECG monitoring
  • Any abnormal activity can be reviewed at recheck
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44
Q

What are the benefits of using paper-trace recording machines?

A

high diagnostic value

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45
Q

Wha are the benefits of using telemetry?

A
  • can monitor patients from a distance
  • less machines attached directly to the patient
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46
Q

If something doesn’t look right on the ECG, how would you troubleshoot?

A
  • Check settings on machine, batteries, charge machine if low battery etc.
  • Are the leads still attached
  • Are the leads on the correct legs
  • Minimise movement of patient
  • Ideally in right lateral, a lot of movement interferes with trace
  • Panting or purring
  • Check contact of crocodile clips to skin, reapply spirit
  • Change ECG electrodes if dislodged, dry or not sticking well
  • Clip more fur for better contact of electrodes or clips
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47
Q

What does the P wave represent?

A

atrial electrical activity

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48
Q

Why are electrical changed associated with depolarization small on the P wave?

A

because the muscle mass of the atria is small

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49
Q

What does the atrial depolarisation wave look like on ECG?

A

a small upward excursion (+ve deflection)

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50
Q

What does the P-R wave represent?

A

time between atrial depolarisation and ventricular depolarisation

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51
Q

How is the P-R wave measured?

A

the distance between the onset of the P wave to the onset of the R wave

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52
Q

What does a normal P-R interval mean?

A

the electrical impulse is travelling between the atria and ventricles correctly so not too fast and not too slow

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53
Q

What is the Q wave?

A

a small depolarisation wave that travels in a direction away from the postive electrode

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54
Q

What is the first part of the ventricles to depolarise?

A

the ventricular septum

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55
Q

What happens once the depolarisation wave passes through the AV node?

A

it travels rapidly through conduction tissue to the ventricles via the purkinje fibres and Bundle of His

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56
Q

What does the Q wave look like on ECG?

A

small downward wave (-ve deflection)

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57
Q

When does the R wave occur?

A

when the majority of the centricular myocardium is depolarised

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58
Q

What does depolarisation of the ventricular myocardium do?

A

creates a depolarisation wave that travels towards the _ve electrode

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59
Q

Which wave on the ECG is the largest?

A

the R wave

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60
Q

Where does final depolarisation occur?

A

at the base of the heart

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61
Q

What does the S wave look like on ECG?

A

a small -ve deflection

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62
Q

What is the QRS complex?

A

the waveform that represents the depolarisation of the ventricles followed by ventricular muscle contraction

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63
Q

When is there no longer an electrical potential difference?

A

when all the atria has been depolarisaed

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64
Q

What is the PR segment?

A

the distance between the p wave and the q wave

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65
Q

Where is the ST segment situated?

A

between the s wave and the t wave

66
Q

What is the T wave?

A

represented repolarisation of the ventricles

67
Q

What do T waves mark?

A

beginning of ventricular relaxation

68
Q

What is bradyarrhythmia?

A

slow arrythmia

69
Q

What is tachyarrythmia?

A

fast arrythmia

70
Q

What do arrythmias include?

A

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

71
Q

What are sinus rhythms?

A

Normal sinus rhythm
- Sinus arrhythmia

72
Q

What are Bradyarrhythmias?

A
  • Sinus bradycardia
  • Sick sinus syndrome
  • Atrioventricular blocks
  • Escape beats
  • Hyperkalaemia
73
Q

What are Tachyarrhythmias examples?

A
  • Sinus tachycardia
  • Supraventricular tachycardia
  • Atrial fibrillation
  • Ectopic beats
  • Accelerated idioventricular
    rhythm
  • Ventricular tachycardia
  • R-on-T Phenomenon
74
Q

What are examples of cardiac arrest rhythms?

A
  • Ventricular fibrillation
  • Pulseless ventricular
    tachycardia
  • Pulseless electrical
    activity
  • Asystole
75
Q

Which is present in sinus rhythm?

A
  • P wave, QRS complex and T wave present
  • P wave present for every QRS complex
  • All complexes identical
  • Regular heart sounds on auscultation
  • Pulse for every heart beat
  • Heart rate within normal range for age,
    breed and species
76
Q

What type of rhyth is sinus rhythm?

A

Regularly regular rhythm

77
Q

Where does the electrical impulse originate from with sinus arrhythmia?

A

SA node

78
Q

Wat is present in sinus arrythmia?

A
  • Normal P wave for every QRS-T wave
  • Pulse present for every heart beat
  • Commonly a regular variation in HR (speeds up and slows down), which co-insides with respiration
  • Respiratory sinus arrhythmia
  • Associated with an increase in parasympathetic activity (vagal tone) on the SA node
  • Normal and common rhythm in dogs (is HR within normal range for age/breed of dog)
79
Q

What type of rhythm is sinus arrythmia?

A

regularly irregular rhythm

80
Q

What is sinus bradycardia?

A

the SA node impulse and corresponding depolarisation occurs slower than normal

81
Q

What is present in sinus bradycardia?

A
  • Normal sinus rhythm
  • P wave for every QRS-T wave
  • Heart rate may be inappropriately slow for age, breed and species (usually < 60 bpm)
  • Pulse present for every heart beat
82
Q

What type of rhythm is sinus bradycardia?

A

regularly regular rhythm

83
Q

what causes sinus bradycardia?

A
  • Normal in some breeds, e.g. giant breed dogs and athletically fit dogs
  • Can be due to a problem with the SA node
  • Often secondary to another disease process which increases vagal tone (rather than primary cardiac disease)
84
Q

What other causes are there with sinus bradycardia?

A
  • Hypoadrenocorticism and associated electrolyte abnormalities e.g.
    hyperkalaemia
  • Brachycephalic obstructive airway disease (BOAS) e.g. French bulldogs
  • Increased intracranial pressure (ICP) e.g. Cushing’s reflex
  • Vaso-vagal reaction (vagal nerve stimulation)
  • Hypocalcaemia
  • Hypothermia
  • Hypoglycaemia
  • Hypothyroidism
85
Q

How can you treat sinus bradycardia?

A
  • temporary such at anticholinergic
  • positive inotrope if anticholingeric unsuccessful such as dopamine or dobutamide
86
Q

What causes sick sinus syndrome?

A

problem with the SA node function so failure to discharge an electrical impulse

87
Q

What happens with sick sinus syndrome?

A

decrease SA node ouput, severe bradycardia with periods of asytoleswithout escape beats

88
Q

How do you treat sick sinus sydrome?

A

surgery to fit pacemaker as they respond poorly to atropine

88
Q

What is sick sinus sydrome?

A

degenerative condition

89
Q

What are the risks associated with pacemakers?

A

infection, lead dislodgement,
failure to pace correctly, venous thrombosis

90
Q

What are the nursing considerations for patients with pacemakers?

A

no walking for 48 hours post
surgery, harness walks only, care with neck restraint,
no jugular samples

91
Q

What is a heart block?

A

= problem with the electrical conduction
system of the heart

92
Q

What is atrioventricular block?

A

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

93
Q

Which blocks affect the AV node?

A

atrioventricular block (AV block) or AV nodal block

94
Q

What blocks affect either the left or right bundle branches?

A

bundle branch blocks

95
Q

What is first degree AV block?

A
  • Delayed conduction through the AV node
  • Normal P wave and QRS complex
  • Longer interval between the P wave and the corresponding QRS complex (prolonged P-R interval)
96
Q

What is second degree AV block?

A
  • Longer conduction delay
  • Some P waves will not have a corresponding QRS i.e. there are dropped beats
  • QRS complexes are normal in morphology (there has been conduction through the AV node, therefore QRS has a normal shape)
97
Q

Wha is mobitz type 1 second degree AV block?

A
  • P-QRS gap becomes longer and longer (P-R interval)
  • Then P wave without corresponding QRS complex
  • Once QRS complex missed, snaps back to normal
98
Q

What is mobitz type II second degree AV block?

A
  • P-QRS complex normal (P-R interval
    the same each time)
  • Occasional P wave without a corresponding QRS complex
99
Q

What is third degree AV block?

A
  • Complete lack of conduction through the AV node
  • Multiple P waves without QRS complexes, P waves
    occur faster, sometimes followed by a tall QRS-T
    complex
  • Ventricular ‘escape beats’ occur
  • These are ectopic beats, acting as a rescue for the
    heart, permitting a heart beat
  • An electrical impulse occurs from random cardiac cells, before cardiac standstill occurs
100
Q

What are escape beats?

A

wide and bizzare with an absent p wave

101
Q

What are the clinical signs of 3rd degree AV block?

A

decreased cardiac output e.g lethargy, syncope, collapse

102
Q

How do you treat atrioventricular block?

A
  • Management of underlying condition e.g. hypoadrenocorticism
  • Vagolytic drugs e.g. atropine or glycopyrrolate
  • Severe 2º and 3º A-V blocks require pacemaker implantation
103
Q

What is hyperkalaemia?

A

increased serum potassium levels

104
Q

What will you see on ECG with hyperkalaemia?

A
  • Bradycardia
  • Reduced/absent P waves
  • Spiked T waves
  • Shortened QT interval
  • Prolonged QRS complex
105
Q

What can cause hyperkalaemia?

A
  • Urethral obstruction e.g. blocked bladder
  • Acute kidney injury e.g. toxin
  • Hypoadrenocorticism e.g. Addisonian crisis
106
Q

How do you treat hyperkalaemia?

A
  • Calcium gluconate bolus: reduces risk of ventricular fibrillation and protects
    cardiac myocytes from affect of elevated K+ (doesn’t actually decrease K+
    levels)
  • Neutral insulin infusion: causes movement of potassium into cells
  • Dextrose infusion: cells uptake glucose, intracellular shift of K+, prevents
    hypoglycaemia due to insulin infusion
107
Q

What is sinus tachycardia?

A

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

108
Q

What do you see present with sinus tachycardia?

A
  • Normal sinus rhythm, with normal P-QRS-T complexes
  • Heart rate is faster than normal for age, breed and species
  • Pulse present for every heart beat (with very fast rates pulses may become
    weaker)
  • Can be normal e.g. after exercise
  • Occurs with pain, stress, hypovolaemia, anaemia etc.
109
Q

What type of rhythm is sinus tachycardia?

A

Regularly regular rhythm

110
Q

What is supraventricular arrhthmias?

A
  • Atrial in origin (occurs in atrium)
  • Occur at a point other than the SA node, then
    conduct via the AV node to the ventricles
  • QRS complexes relatively normal in appearance
  • Often taller and narrower than normal
111
Q

What are ventricular arryhtmias?

A
  • Ventricular in origin (occurs in ventricles)
  • Normal conduction pathway is not followed
  • QRS complexes appear wide and bizarre
112
Q

What are artial ectopic beats called?

A

atrial premature complex (APC)

113
Q

What are junctional ectopic beats called?

A

= junctional premature complex (JPC)

114
Q

What are ventricular ectopic beats called?

A

ventricular premature complex (VPC)

115
Q

What is a supraventricular arryhthmia?

A

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

116
Q

What is a supraventricular ectopic beat?

A

above the AV node

117
Q

What does a suptraventricular ectopic beat cause?

A
  • a premature heartbeat (occurs earlier than expected after the last
    complex, prior to the next SA node impulse)
  • Often an abnormal P wave (as it’s not initiated by the SA node), followed by a QRS complex
118
Q

What type of rhythm is a supraventricular arrhythmia?

A

irregularly irregular rhythm

119
Q

What else is a Supraventricular Arrhythmia called?

A

atrial premature complex (APC), premature atrial contraction (PAC), or atrial premature
beat (APB)

120
Q

what is supraventricular tachycardia?

A

Three or more APCs in a row

121
Q

How does Supraventricular Tachycardia present?

A
  • Rapid heart rate (can be 170 – 350 bpm)
  • QRS complexes are almost like normal however they are narrower and more upright
  • May or may not be an associated P wave
122
Q

what type of rhythm is Supraventricular Tachycardia?

A

regularly irregular rhythm

123
Q

What clinical signs do you see wih fast Supraventricular Tachycardia?

A

weakness/collapse, poor pulse quality, poor peripheral
perfusion, pale MM’s and prolonged CRT

124
Q

what causes Supraventricular Tachycardia?

A
  • Usually associated with underlying cardiac disease e.g. dogs with dilated
    cardiomyopathy (DCM)
  • Sometimes associated with systemic disease e.g. toxicity, hypovolaemia,
    electrolyte imbalances, ischaemia
125
Q

What does treatment do for Supraventricular Tachycardia?

A

decrease heart rate

126
Q

How do you treat Supraventricular Tachycardia?

A
  • Treat any underlying systemic causes
  • Beta-blockers e.g. sotalol, atenolol
  • Calcium channel blockers e.g. diltiazem
  • Some available as IV preparations
127
Q

what is atria fibrilation?

A

a Supraventricular tachyarrhythmia

128
Q

How is artial fibrilation characterised?

A

rapid and irregular contractions of atria (‘quivering’)

129
Q

What is commonly seen with artial fibrilation?

A
  • Pulse deficits, irregular pulse (ventricles may contract before they have filled sufficiently)
  • Rapid HR (often >200 bpm), irregular beating with no obvious pattern
  • Fibrillating baseline
  • Supraventricular QRS complex (normal but taller and narrower)
  • No visible P-waves (impulse not from SA node)
130
Q

What type of rhythm is artial fibrilation?

A

irregularly irregular rhythm

131
Q

How do you treat artial fibrilation?

A
  • Decrease HR
  • Increase cardiac output
  • Calcium channel blockers e.g. diltiazem
  • Beta-blockers e.g. sotalol, atenolol
  • Digoxin
  • Amiodarone
  • Some available as IV preparations
132
Q

What are junctional premature complexes?

A

Ectopic beats that arise from an area within the atrioventricular junction
(region of the AV node), therefore ventricles are usually activated normally

133
Q

What are ventricular arrythmias?

A

SA nodeno longer controls the ventricular contractions
- Abnormal electrical impulse starts at an ectopic site below the AV node
- Another area in the ventricles takes over the pacemaker role
- Complex is wide and bizarre as normal electrical pathway not followed

134
Q

What causes ventricular arrhythmias?

A
  • Underlying primary cardiac disease e.g. dogs with DCM
  • As a complication due to another condition e.g. gastric dilatation and volvulus
    (GDV), pyometra, splenectomy, pancreatitis, anaemia
135
Q

WHAT IS A VENTRICULAR PREMATURE COMPLEX?

A

Ectopic beat that occurs prior to normal SA node depolarisation

136
Q

how do PVCs present?

A
  • VPC starts at an unusual location in the ventricles
  • No preceding P wave, except by coincidence (impulse does not follow normal conduction
    pathway)
  • Wide and bizarre QRS complex (it takes longer for the conduction to occur)
  • Pulse quality may feel weak with certain beats
  • Pulse deficits present (not always a pulse for every heart beat)
137
Q

What is accelerated idoventricular rhythm?

A

3 or more vpcs together

138
Q

how do AIVRs present?

A
  • Heart rate is not very elevated (140-180 bpm)
  • Generally considered benign rhythm at this
    rate, unlikely to be causing decreased cardiac output, haemodynamic compromise or hypotension
  • Treatment not usually required
  • For example seen in patients recovering from
    extensive abdominal surgery
  • Monitor ECG closely for progression to ventricular tachycardia
139
Q

what is ventricular tachyycardia?

A

3 or more vpcs occurring in a row with a heart rate >180 bpm (can be >300 bpm!)

140
Q

how does v-tach present?

A

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

141
Q

What are the clinical findings of v-tach?

A
  • Pulse weak, rapid and irregular, with pulse deficits
  • Likely to be decreased cardiac output: hypotension, collapse
  • Signs of haemodynamic compromise
  • Altered mentation
  • Signs of hypoperfusion (pale mm’s, prolonged CRT, hypothermia, weak or absent peripheral pulses)
142
Q

what are the causes of v-tach?

A
  • Primary cardiac disease e.g. dogs with DCM, or cats with hypertrophic
    cardiomyopathy (HCM)
  • Significant abdominal pathology e.g. GDV, acute pancreatitis, or a haemoabdomen e.g. due to a ruptured spleen
  • Inflammation/inflammatory mediators e.g. septic abdomen, significant trauma
  • Severe anaemia
  • Abnormal autonomic activity (high sympathetic tone) e.g. pain
  • Electrolyte disturbances e.g. hypercalcaemia, hypokalaemia
  • Drug toxicities e.g. caffeine, cocaine
  • Neoplasia e.g. haemangiosarcoma
143
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 (ventricular fibrillation)
  • Sudden death
144
Q

how do you treat v-tach?

A
  • Aim = convert to sinus rhythm and slow HR down to allow better cardiac output and peripheral perfusion
  • Depends on degree of haemodynamic compromise and underlying cause
  • Patients with underlying heart disease more likely to require immediate drug intervention (risk of cardiac arrest)
  • Priority to also manage underlying disease process e.g. blood transfusion for anaemic patients, surgery for septic focus
  • If there is no associated pulse = pulseless ventricular
    tachycardia (PVT)
  • EMERGENCY: start CPR immediately
  • PVT is a shockable rhythm (using a defibrillator)
145
Q

what medication can you give to treat v-tach?

A
  • Lidocaine
  • Most commonly used drug, rapid onset of action
  • Sodium channel blocker
  • Boluses then constant rate infusion (CRI)
  • Beta-blockers e.g. sotalol
  • Amiodarone
  • Procainamide
  • Magnesium
146
Q

what is r-on-t phenomenom?

A

VPC is so premature, it is superimposed on
the T wave of the preceding complex (close to, or on top of, a preceding T-wave)
- Can be on a sinus beat or an ectopic beat

147
Q

what causes r-n-t phenomenom?

A

Ventricles have not had time to completely repolarise from previous contraction, before they are depolarised again

148
Q

What is the aim for using a defibrilator?

A
  • Send a high energy electric shock to the heart (called
    a defibrillation)
  • Aims to reset the electrical state of the heart, thereby
    converting from a shockable arrhythmia to normal
    sinus rhythm
  • May require more than one defibrillation
  • Shockable rhythms seen less frequently
  • Defibrillating a non-shockable rhythm can be
    detrimental to survival
149
Q

What are shockable rhythms?

A

ventricular fibrillation
and pulseless ventricular tachycardia

150
Q

what are non-shockable rhythms?

A

asystole and pulseless
electrical activity (PEA)

151
Q

what is pulseless v-tach?

A

If there is no pulse present with ventricular tachycardia, this is called pulseless ventricular tachycardia (PVT)

152
Q

what is v-fib?

A

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

153
Q

what is fine v-fib?

A

smaller hinner trace

154
Q

what is coarse v-fib?

A

larger more erratic trace

155
Q

how does v-fib present?

A
  • No effective ventricular contractions (all chaotic)
  • ECG has rapid, irregular, wavy baseline with no recognisable normal complexes
  • No cardiac output, therefore no palpable pulses, patient will be collapsed
156
Q

how do you treat v-fib?

A
  • Immediately start CPR
  • Shockable rhythm
  • Electrical defibrillation required
157
Q

what is pulseless electrical activity?

A

Electrical impulses within the heart, but no corresponding myocardial contractions

158
Q

how does PEA present?

A
  • ECG may show slow, normal or fast heart rate
  • Often normal P-QRS-T complex, which may become
    increasingly wide and bizarre
  • Physical exam: no audible heart beats, no palpable
    pulses, no cardiac output
159
Q

how do you treat PEA?

A
  • CPR, adrenaline, atropine
  • Continue CPR with 2 minute cycle breaks to check ECG rhythm
  • Check pulse concurrently
  • Non-shockable rhythm
  • Only defibrillate if converts to a shockable rhythm
160
Q

what is asytole?

A
  • Most common arrest arrhythmia in dogs and cats
  • Straight, flat-line ECG
  • Patient in cardiopulmonary arrest (CPA): no cardiac movement, no pulses or cardiac output
161
Q

IS ASYTOLE A SHOCKABLE RHYTHM?

A

NO

ACVN - MEDICAL NURSING (22 decks)

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