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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
What are some causes of sinus bradycardia?
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
26
How can we treat sinus bradycardia?
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
27
What is sick sinus syndrome?
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
28
How can we treat sick sinus syndrome?
Responds poorly to medical management - requires surgery to place pacemaker Potential risks = infection, lead dislodgement, failure to place correctly, venous thrombosis
29
What is atrioventricular block?
Electrical impulses from SA node delayed/blocked Therefore electrical signal may not reach ventricles
30
What is first degree AV block?
Delayed conduction through AV node Normal P wave and QRS complex, but longer interval between (prolonged P-R interval)
31
What is second degree AV block?
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
What is Mobitz type I second degree AV block?
P-QRS gap becomes longer and longer Then P wave without QRS complex Once QRS complex missed, snaps back to normal
33
What is Mobitz type II AV block?
P-QRS complex normal, intervals same each time Occasional P wave without corresponding QRS complex
34
What is third degree AV block?
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
What are the clinical signs of third degree AV block?
Signs of decreased cardiac output e.g. lethargy, syncope, collapse
36
How can we treat third degree AV block?
Management of underlying condition e.g. hypoadrenocorticism Vagolytic drugs e.g. atropine/glycopyrrolate Pacemaker implantation
37
Describe hyperkalaemic arrhythmias.
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
What are some causes of hyperkalaemic arrhythmias?
Urethral obstruction e.g. blocked bladder Acute kidney injury e.g. toxin Hypoadrenocorticism e.g. Addisonian crisis
39
How can we treat hyperkalaemic arrhythmias?
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
What is sinus tachycardia?
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
What can cause sinus tachycardia?
Pain Stress Hypovolaemia Anaemia etc.
42
Describe supraventricular arrhythmias.
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
Describe ventricular arrhythmias.
Ventricular in origin Normal conduction pathway not followed QRS complexes appear wide and bizarre
44
What are ectopic beats?
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
What are the different types of ectopic beats?
Atrial premature complex (APC) Junctional premature complex (JPC) Ventricular premature complex (VPC) Supraventricular tachycardia Escape beats
46
What are supraventricular arrhythmias?
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
What is supraventricular tachycardia?
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
What are the clinical signs of a fast supraventricular tachycardia?
Weakness/collapse Poor pulse quality Poor peripheral perfusion Pale MMs and prolonged CRT Due to inadequate diastolic filling
49
What are the causes of supraventricular tachycardia?
Usually associated with underlying cardiac disease e.g. DCM Sometimes associated with systemic disease e.g. toxicity, hypovolaemia, electrolyte imbalances, ischaemia
50
How can we treat supraventricular tachycardia?
Decrease HR and treat any underlying causes Beta blockers e.g. sotalol/atenolol Calcium channel blockers e.g. diltiazem
51
What is atrial fibrillation?
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
How do we treat atrial fibrillation?
Decrease HR and increase cardiac output Calcium channel blockers e.g. diltiazem Beta-blockers e.g. sotalol/atenolol Digoxin Amiodarone
53
What are junctional premature complexes?
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
What are ventricular arrhythmias?
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
What are some causes of ventricular arrhythmias?
Underlying primary cardiac disease e.g. DCM As a complication of another condition e.g. GDV, pyometra, splenectomy, pancreatitis, anaemia
56
What are ventricular premature complexes?
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
What is accelerated idioventricular rhythm?
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
What is ventricular tachycardia?
3 or more VPCs in a row with heart rate >180bpm QRS complexes wide and bizarre, absent P wave and large T wave
59
What clinical findings do we see with ventricular tachycardia?
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
What are some causes of ventricular tachycardia?
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
What are the consequences of sustained V-tach?
Decreased systemic tissue perfusion (cardiogenic shock) Decreased cardiac perfusion Development of myocardial failure Development of malignant arrhythmia (V-fib) Sudden death
62
What is the aim of treatment of V-tach?
Convert to sinus rhythm, slow HR down to allow better cardiac output and peripheral perfusion
63
What is pulseless ventricular tachycardia?
V-tach with no associated pulse Emergency! - start CPR immediately This is a shockable rhythm
64
What medications can be used to treat ventricular tachycardia?
Lidocaine - sodium channel blocker, boluses then CRI Beta-blockers e.g. sotalol Amiodarone Procainamide Magnesium
65
Which rhythms are shockable?
Ventricular fibrillation Pulseless ventricular tachycardia
66
Which rhythms are non-shockable?
Asystole Pulseless electrical activity
67
What is pulseless electrical activity?
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
How can we treat pulseless electrical activity?
CPR, adrenaline, atropine
69

Applied Clinical Veterinary Nursing (40 decks)

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