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Applied Clinical Veterinary Nursing > ECGs > Flashcards

ECGs Flashcards

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1
Q

Describe the role of the sympathetic and parasympathetic nervous system in control of heart rate.

A

SNS releases hormones (catecholamines e.g. adrenaline/noradrenaline) to accelerate HR
PNS releases hormone acetylcholine to slow HR

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2
Q

Describe the two types of cardiac cells.

A

Electrical cells - conduction system of heart, distributed in orderly fashion. Spontaneously generate electrical impulses and respond to impulses, transmit an electrical pulse from one cell to the next
Myocardial cells - make up walls of atrium and ventricles, responsible for contraction and ability to stretch

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3
Q

Describe the sinoatrial node.

A

Small area of modified cardiac muscle cells (specialised fibres)
Located in right atrium wall
Initiates heartbeat, ‘pacemaker’, controls HR

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4
Q

Describe how the SA node works.

A

SA node fires electrical impulse which causes depolarisation to spread through atrial muscle cells
Impulse spreads across atria, causing both atria to contract (atrial systole)
Blood moves from right atrium to right ventricle and left atrium to left ventricle

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5
Q

Describe the atrioventricular node.

A

Specialised group of muscle cells
Located at top of interventricular septum
Speed of electrical depolarisation wave through AV node is deliberately slow so that ventricular contraction will be correctly coordinated following atrial contraction - allows atria time to fully contract before ventricles do

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6
Q

Describe how the AV node works.

A

Electrical impulse from SA node spreads through AV node at a slower pace
Acts like a gate to slow impulse before it enters the ventricles

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7
Q

Describe the Bundle of His.

A

Specialised bundle of nerve tissue fibres
Narrow pathway that runs down interventricular septum
Divided into right and left bundle branches, which spread into right and left ventricles
Left bundle branch divides further into anterior and posterior fascicles

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8
Q

Describe how the Bundle of His works.

A

Myocardium of atrium walls not in electrical continuity with myocardium of ventricular walls
Conduction passes through AV ring (from atria to ventricles) through Bundle of His

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9
Q

Describe the Purkinje fibres.

A

Bundle of His connects with Purkinje fibres
Network of specialised neurones, organised in very fine branches
Conduction fibres spread out though myocardium of right and left ventricles

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10
Q

Describe ventricular systole.

A

Electrical impulse spreads down Purkinje fibres, depolarisation of myocardium down septum towards ventricles
Wave of ventricular contraction begins at apex of heart (bottom of ventricles) and spreads upwards through muscle of ventricles
Blood pushed upwards out of heart - R ventricle to pulmonary artery (to lungs) / L ventricle to aorta (to body)
After heart cells repolarise, SA node fires another impulse and cycle begins again

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11
Q

How does an ECG machine work?

A

-ve and +ve electrodes placed either side of heart, detects depolarisation wave travelling across heart
Records the wave as deflection (-ve downwards, +ve upwards)

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12
Q

When are ECGs used?

A

Arrhythmias - diagnosis/monitoring
Triage
Anaesthesia and recovery
Critical patients
Newly identified pulse deficits
CPR for shockable rhythms
Metabolic/electrolyte abnormalities e.g. Ca+/K+)
Pericardiocentesis and central line catheter placement
Hands-off monitoring e.g. blood transfusions

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13
Q

What four types of ECG equipment can be used?

A

Multi-parameter monitors - continuous
Paper-trace recording machine - high diagnostic value
Holter monitoring - monitoring over longer period, at home
Telemetry - from a distance

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14
Q

What is the P wave?

A

Atrial depolarisation

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15
Q

What is the P-R interval?

A

Time between atrial depolarisation and ventricular depolarisation

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16
Q

What is the Q wave?

A

Depolarisation of ventricular septum

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17
Q

What is the R wave?

A

Depolarisation of majority of ventricular myocardium

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18
Q

What is the S wave?

A

Final depolarisation at base of heart

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19
Q

What is the QRS complex?

A

Depolarisation of ventricles, followed by ventricular muscle contraction

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20
Q

What is the T wave?

A

Repolarisation of ventricles

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21
Q

What are the types of arrhythmia?

A

Regularly regular, irregularly irregular, regularly irregular
Bradyarrhythmia / tachyarrhythmia
Sinus / ventricular / supraventricular

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22
Q

Describe a sinus rhythm.

A

Normal!
P wave, QRS complex, T wave
All complexes identical, pulses for every heartbeat
Regular heart sounds and HR
Regularly regular rhythm

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23
Q

Describe sinus arrhythmia.

A

Regular variation in HR commonly associated with respiration
Associated with increased parasympathetic activity on SA node
Normal P wave, QRS complex, T wave
Pulse present for every heartbeat
Regularly irregular rhythm

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24
Q

Describe sinus bradycardia.

A

Normal sinus rhythm, P wave, QRS complex, T wave
SA node impulse and corresponding depolarisation slower than normal
HR inappropriately slow (usually <60bpm)
Pulse present for every heartbeat
Regularly regular rhythm

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25
Q

What are some causes of sinus bradycardia?

A

Normal in some breeds e.g. giant/athletically fit
Due to problem with SA node
Often secondary to another disease process that increases vagal tone (rather than primary cardiac disease)
Hypoadrenocorticism, hyperkalaemia
BOAS
Increased ICP e.g. Cushing’s reflex
Vaso-vagal reaction
Hypocalcaemia, hypothermia, hypoglycaemia, hypothyroidism

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26
Q

How can we treat sinus bradycardia?

A

Dictated by underlying cause
Clinical signs? - treating hyperkalaemia, raised ICP
Temporary management with anticholinergic to increase HR e.g. atropine/glycopyrrolate
OR positive inotrope e.g. dopamine/dobutamine

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27
Q

What is sick sinus syndrome?

A

Problem with SA node function - failure to discharge electrical impulse
Severe bradycardia occurs (often <30bpm)
Periods of asystole (sinus arrest) without escape/rescue beats
SA node normally starts again, but sinus arrest recurrent

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28
Q

How can we treat sick sinus syndrome?

A

Responds poorly to medical management - requires surgery to place pacemaker
Potential risks = infection, lead dislodgement, failure to place correctly, venous thrombosis

29
Q

What is atrioventricular block?

A

Electrical impulses from SA node delayed/blocked
Therefore electrical signal may not reach ventricles

30
Q

What is first degree AV block?

A

Delayed conduction through AV node
Normal P wave and QRS complex, but longer interval between (prolonged P-R interval)

31
Q

What is second degree AV block?

A

Longer conduction delay
Some P waves will not have corresponding QRS complex i.e. there are dropped beats
QRS has normal shape as has been conduction through AV node
Two types - Mobitz type I and Mobitz type II

32
Q

What is Mobitz type I second degree AV block?

A

P-QRS gap becomes longer and longer
Then P wave without QRS complex
Once QRS complex missed, snaps back to normal

33
Q

What is Mobitz type II AV block?

A

P-QRS complex normal, intervals same each time
Occasional P wave without corresponding QRS complex

34
Q

What is third degree AV block?

A

Complete lack of conduction through AV node
Multiple P waves without QRS complexes
Ventricular escape beats occur, generated from random cardiac cells - without which animal would die
HR slow, typically 20-40bpm

35
Q

What are the clinical signs of third degree AV block?

A

Signs of decreased cardiac output e.g. lethargy, syncope, collapse

36
Q

How can we treat third degree AV block?

A

Management of underlying condition e.g. hypoadrenocorticism
Vagolytic drugs e.g. atropine/glycopyrrolate
Pacemaker implantation

37
Q

Describe hyperkalaemic arrhythmias.

A

Severity of arrhythmia progresses as K+ increases
Bradycardia
Reduced/absent P waves, spiked T waves, shortened QT interval, prolonged QRS complex
Progresses to atrial standstill, sine wave pattern, ventricular fibrillation and eventual asystole

38
Q

What are some causes of hyperkalaemic arrhythmias?

A

Urethral obstruction e.g. blocked bladder
Acute kidney injury e.g. toxin
Hypoadrenocorticism e.g. Addisonian crisis

39
Q

How can we treat hyperkalaemic arrhythmias?

A

Calcium gluconate bolus - reduces risk of Vfib and protects cardiac myocytes from effects of elevated K+
Neutral insulin infusion - causes movement of K+ into cells
Dextrose infusion - cells uptake glucose, intracellular shift of K+, prevents hypoglycaemia due to insulin infusion

40
Q

What is sinus tachycardia?

A

SA node generates impulse and depolarisation at rate faster than normal
Normal sinus rhythm, normal P-QRS-T complexes
Regularly regular rhythm
Heart rate faster than normal for age/breed/species
Pulse present for every heartbeat (but may be weaker)

41
Q

What can cause sinus tachycardia?

A

Pain
Stress
Hypovolaemia
Anaemia etc.

42
Q

Describe supraventricular arrhythmias.

A

Atrial in origin
Occur at point other than SA node, then conduct via AV node to ventricles
QRS complexes relatively normal in appearance
Often taller and narrower than normal

43
Q

Describe ventricular arrhythmias.

A

Ventricular in origin
Normal conduction pathway not followed
QRS complexes appear wide and bizarre

44
Q

What are ectopic beats?

A

Electrical impulse did not originate from SA node, rather from elsewhere (not pacemaker cells)
Occur prematurely and interrupt normal rhythm, before SA node ready to initiate another impulse
P-QRS-T complex looks different to normal

45
Q

What are the different types of ectopic beats?

A

Atrial premature complex (APC)
Junctional premature complex (JPC)
Ventricular premature complex (VPC)
Supraventricular tachycardia
Escape beats

46
Q

What are supraventricular arrhythmias?

A

Abnormal electrical impulse which occurs at ectopic site in atria
Above the AV node
Causes premature heartbeat
Often abnormal P wave, followed by QRS complex
Often irregularly irregular rhythm
Called atrial premature complex / premature atrial contraction / atrial premature beat

47
Q

What is supraventricular tachycardia?

A

Three or more APCs in a row
Rapid heartbeat (170-350bpm)
QRS complexes almost normal but narrower and more upright
May or may not be an associated P wave
Regularly irregular rhythm

48
Q

What are the clinical signs of a fast supraventricular tachycardia?

A

Weakness/collapse
Poor pulse quality
Poor peripheral perfusion
Pale MMs and prolonged CRT
Due to inadequate diastolic filling

49
Q

What are the causes of supraventricular tachycardia?

A

Usually associated with underlying cardiac disease e.g. DCM
Sometimes associated with systemic disease e.g. toxicity, hypovolaemia, electrolyte imbalances, ischaemia

50
Q

How can we treat supraventricular tachycardia?

A

Decrease HR and treat any underlying causes
Beta blockers e.g. sotalol/atenolol
Calcium channel blockers e.g. diltiazem

51
Q

What is atrial fibrillation?

A

Rapid and irregular contractions of atria (quivering)
Pulse deficits common, irregular pulse
Rapid HR (>200bpm), irregular beating with no obvious pattern
Fibrillating baseline
QRS complex normal but taller and narrower
No visible P-waves (impulse not from SA node)
Irregularly irregular rhythm

52
Q

How do we treat atrial fibrillation?

A

Decrease HR and increase cardiac output
Calcium channel blockers e.g. diltiazem
Beta-blockers e.g. sotalol/atenolol
Digoxin
Amiodarone

53
Q

What are junctional premature complexes?

A

Ectopic beats that arise from region from AV node, so ventricles are activated normally
QRS complexes premature, sinus complexes but narrower
Usually without associated P wave

54
Q

What are ventricular arrhythmias?

A

SA node no longer controls ventricular contractions
Abnormal electrical impulse starts at ectopic site below AV node
Another area in ventricles takes over pacemaker role
Complex wide and bizarre

55
Q

What are some causes of ventricular arrhythmias?

A

Underlying primary cardiac disease e.g. DCM
As a complication of another condition e.g. GDV, pyometra, splenectomy, pancreatitis, anaemia

56
Q

What are ventricular premature complexes?

A

Ectopic beat that occurs prior to normal SA node depolarisation
VPC starts at unusual location in ventricles
No associated P wave, wide and bizarre QRS complex
Pulse quality may be weak, pulse deficits present

57
Q

What is accelerated idioventricular rhythm?

A

3 or more VPCs together
HR not very elevated (140-180bpm)
Unlikely to be causing decreased CO, haemodynamic compromise or hypotension
Treatment not usually required
Can progress to Vtach

58
Q

What is ventricular tachycardia?

A

3 or more VPCs in a row with heart rate >180bpm
QRS complexes wide and bizarre, absent P wave and large T wave

59
Q

What clinical findings do we see with ventricular tachycardia?

A

Pulse weak, rapid and irregular with deficits
Decreased CO - hypotension, collapse
Haemodynamic compromise - altered mentation, hypoperfusion (pale MMs and prolonged CRT, hypothermia, weak or absent peripheral pulses)

60
Q

What are some causes of ventricular tachycardia?

A

Primary cardiac disease e.g. DCM/HCM
Significant abdo pathology e.g. GDV, acute pancreatitis, haemoabdomen (ruptured spleen)
Inflammation e.g. septic abdomen, trauma
Severe anaemia
Pain
Electrolyte disturbances e.g. hypercalcaemia, hypokalaemia
Drug toxicities e.g. caffeine, cocaine
Neoplasia e.g. haemangiosarcoma

61
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

62
Q

What is the aim of treatment of V-tach?

A

Convert to sinus rhythm, slow HR down to allow better cardiac output and peripheral perfusion

63
Q

What is pulseless ventricular tachycardia?

A

V-tach with no associated pulse
Emergency! - start CPR immediately
This is a shockable rhythm

64
Q

What medications can be used to treat ventricular tachycardia?

A

Lidocaine - sodium channel blocker, boluses then CRI
Beta-blockers e.g. sotalol
Amiodarone
Procainamide
Magnesium

65
Q

Which rhythms are shockable?

A

Ventricular fibrillation
Pulseless ventricular tachycardia

66
Q

Which rhythms are non-shockable?

A

Asystole
Pulseless electrical activity

67
Q

What is pulseless electrical activity?

A

Electrical impulses within heart but no corresponding myocardial contractions
ECG may show slow, normal or fast HR
Often normal P-QRS-T complex becoming increasingly wide and bizarre
No audible heartbeats, no palpable pulses, no cardiac output

68
Q

How can we treat pulseless electrical activity?

A

CPR, adrenaline, atropine

69
Q
A

Applied Clinical Veterinary Nursing (40 decks)

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