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Y4 SA - Collapse, weakness & exercise intolerance > Dysrhythmias > Flashcards

Dysrhythmias Flashcards

(60 cards)

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1
Q

Where do electrical impulses in the heart originate from?

A
  • the SA node
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2
Q

Steps of the conduction system in the heart

A

▪Impulse originates from SA node
▪Spreads across atria to cause atrial contraction
▪Can only pass through AVN to reach ventricular myocardium
▪AVN delays impulse to allow for ventricular filling
▪Spreads rapidly through bundle of His, bundle branches and Purkinje network to cause ventricular contraction

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3
Q

What does an ECG do?

A
  • records cardiac electrical activity by measuring the amplitude and direction of flow of electricity between a positive and negative electrode
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4
Q

Steps to take an ECG

A
  • Patient placed in right lateral recumbency and electrodes attached to limbs
  • By using one electrode as a positive pole and another one as a negative pole we can measure the overall direction and magnitude of the electrical current
  • Most commonly use hexaxial system which uses 3 electrodes to produce 6 ‘leads’ by using different electrodes as the positive and negative poles
  • In practice we mostly concentrate on lead II as this is most useful for assessing the rhythm
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5
Q

Why might you need a Holder monitor to identify arrhythmias?

A
  • they may be intermittent
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6
Q

Genesis of electrocardiogram in lead II (i.e. how each of the PQRST waves are produced)

A
  1. Impulse starts at SA node and travels across atria towards +ve electrode (P-wave)
  2. Pause as reaches AV node and usually small –ve deflection as overall direction of impulse sl towards right ventricle (away from +ve electrode) when first crosses AV node; (Q-wave).
  3. Impulse moves rapidly across ventricular myocardium mostly in direction of +ve electrode leading to large +ve deflection(R-wave)
  4. then spreads up myocardium towards atria and away from +ve electrode leading to –ve deflection (S-wave).
  5. Ventricular repolarisation is seen and this results in small +ve deflection; (T-wave)
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7
Q

What are sinus rhythms / where do they originate from?

A

▪Rhythms originating from the Sino-atrial node and following the correct conduction pathways

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8
Q

Dysrhythmia Definition

A

An abnormal heart rhythm caused by a disturbance in the heart’s electrical conduction system

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9
Q

Presenting signs of dysrhythmias - history

A

▪ Syncope
▪ Lethargy/weakness
▪Exercise Intolerance
▪ ‘Funny turns’
▪Known cardiac disease

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10
Q

Presenting signs of dysrhythmias - PE

A

▪Abnormal heart rate
▪Audible irregular rhythm
▪Pulse deficits
▪Evidence of underlying cardiac disease (e.g. murmur)

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11
Q

Causes of Dysrhythmias

A

▪Structural cardiac disease
▪ Drugs
▪ Toxins
▪Metabolic diseases/electrolyte imbalance
▪Systemic disease – sepsis, neoplasia
▪Primary issue with the heart’s inherent conduction system

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12
Q

When to tx dysrhythmias

A

medication indicated if will improve patient survival or the patient is showing clinical signs related to the occurrence of a dysrhythmia

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13
Q

Treatment Options

A

▪Anti-dysrhythmic drugs
▪ Pacemaker
▪Ablation with catheters
▪Implantable cardiovertors

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14
Q

Steps to interpret an ECG

A

▪What is the heart rate?
- Count number of beats in 3 seconds (check paper speed) and multiply by 20; Assess different parts of the ECG;
▪Is the rhythm regular or irregular?
- This is not synonymous with normal/abnormal
▪Do the ECG waves appear normal?
▪Is each P wave followed by a QRS?
▪Is there a P wave before each QRS?
▪ECG measurements
- focus on measurements that are clinically relevant

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15
Q

Types of Dysrhythmia

A

▪Bradyarrhythmia
▪ Tachyarrhythmia

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16
Q

What does bradyarrhythmia lead to? (re HR)

A
  • Leads to a reduction in heart
    rate
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17
Q

What does tachyarrhythmia lead to? (re HR)

A
  • Leads to an elevation in heart rate when present
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18
Q

Types of tachyarrhythmias & where they originate from

A

▪Supraventricular
- Originating from above the
ventricles
▪ Ventricular
- Originates from the ventricles

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19
Q

What can cause a Bradyarrhythmia?

A
  • Markedly increased vagal tone – sinus bradycardia; consider giving atropine (parasympatholytic) and check for resolution
  • Abnormal generation of an impulse at the Sino-atrial node
  • Abnormal conduction of the impulse at the AV node
  • ALSO consider underlying primary causes: electrolyte imbalances (esp hyperkalaemia), primary cardiomyopathy/valvular disease, drug toxicity/effect
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20
Q

2 types of sinus node disease

A
  • sinus arrest
  • persistent atrial standstill
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21
Q

Sinus Arrest

A
  • SAN fails to discharge
  • Pause noted on ECG with no P- QRS-T complex
  • Pause can be terminated by either a sinus complex (sinus pause)
  • If SAN doesn’t fire then next fastest pacemaker takes over
  • AV node then ventricular cells
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22
Q

Persistent Atrial Standstill

A
  • SAN not working at all
  • Complete absence of p-waves
  • Next fastest pacemaker takes over
  • HR is usually slower but regular
  • QRST usually appears normal if AVN takes over
  • Wide/bizarre QRS if ventricular myocardial cells take over
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23
Q

Sick Sinus Syndrome

A
  • term commonly used to describe sinus node dysfunction with clinical signs
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24
Q

Type 1 Atrioventricular Block

A
  • delay in the transmission of the impulse
  • prolonged P-R interval
  • p-waves always eventually conducted
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25
Type 2 Atrioventricular Block
- occasional block; p-wave not conducted ▪Mobitz type I: conduction through the AVN progressively slower and then leads to a blocked beat – progressively longer P-R intervals until non-conducted P-wave ▪Mobitz type II: occasional blocked beats but P-R interval constant
26
Type 3 Atrioventricular Block
- complete block – p-waves and QRS complexes not related to each other
27
Bradyarrhythmia Treatment
▪Underlying cause should be treated – eg correction of hyperkalaemia ▪If no or limited clinical signs treatment likely not required - Sinus node dysfunction may not have associated clinical signs and sudden death is very rare. - Type 1 and most type 2 AV blocks often a response to increased vagal tone – often noted under GA ▪In cases of sick sinus syndrome, advanced type 2 AV block and type 3 AV block, an artificial pacemaker is often the only effective treatment ▪Parasympatholytic or sympathomimetic drugs such as atropine or terbutaline may be attempted but are largely ineffective
28
Appearance of supraventricular tachycardia (SVT) on ECG
- ventricular impulse conduction normal and QRS normal in appearance – tall and narrow
29
Appearance of ventricular tachycardia (VT) on ECG
▪Ventricular conduction abnormal leading to wide and bizarre QRS complexes
30
What is a premature beat?
- any beat that occurs before it is expected
31
Why is a premature beat an ectopic beat?
- because it doesn't originate from the sinus node
32
When can premature beats occur?
▪Can occur when normal myocardial cells develop ability to become a pacemaker cell (ischaemic damage) or a short-circuit is created in the myocardium ▪Common example of this is secondary to atrial enlargement in dogs with mitral valve disease
33
Do premature beats need tx?
▪On their own very unlikely to require treatment but can give clue to myocardial damage/remodelling/other systemic illness
34
Will premature beats originating from the atrial/AVN and ventricular myocardium appear the same?
- no
35
What can premature beats lead to?
- sustained firing from this ectopic focus resulting in tachyarrhythmias
36
Types of Supraventricular Tachyarrhythmia
▪Atrial tachycardia ▪Accessory pathway (AP) mediated tachycardia ▪Atrial flutter ▪Atrial Fibrillation
37
When does atrial tachycardia occur?
- when there is an ectopic pacemaker in atria that is able to fire at a high rate
38
Accessory pathway (AP) mediated tachycardia
- rare - very high heart rates - gap in insulation between atria and ventricles: -- Impulse can bypass the AVN -- Or ventricular impulse can retro-conduct back into atrium
39
Is atrial flutter common?
- no
40
Is atrial fibrillation common?
- yes - esp in conditions that cause significant left atrial enlargement
41
Treatment of supraventricular tachyarrhythmia
- try and stop ectopic focus from firing (eg Sotalol) or slow conduction through AVN node (eg Diltiazem) with anti-arrhythmic drugs - some cases with an accessory pathway can be treated with radio-catheter ablation
42
What is the most common SVT?
- atrial fibrillation
43
What is atrial fibrillation a result of?
- concurrent activation of different areas of atrial myocardium, likely atrial enlargement
44
ECG characteristics of A Fib
- HR: normal (lone AF) to tachycardia - Rhythm: irregular - f-waves: P waves not seen instead fluctuations of baseline - QRS: normal as ventricular activation via normal pathways (can have concurrent ventricular issues in some cases)
45
Treatment of A Fib
- if high rate then slow conduction through AVN -- combination treatment with Diltiazem and Digoxin often effective
46
Types of Ventricular Tachyarrythmia
▪Ventricular Premature Beat ▪Ventricular Tachycardia (VTAC) ▪Ventricular Flutter
47
Ventricular premature beats on ECG
- wide and bizarre QRS - can occur in couplets and triplets
48
VTAC ECG
- sequence of or >4 ventricular beats with a rate > 160bpm - often a fast and unstable rhythm
49
Ventricular flutter ECG
- a very rapid VTAC in which T waves and QRS are no longer distinguishable
50
What is the danger with ventricular flutter?
- often precedes death
51
Ventricular tachyarrhythmia tx
Is anti-arrhythmia treatment required? – Base decision on clinical signs and nature of ECG findings (rate, changing appearance to QRS complex, indistinguishable T-waves), consider Holter monitor, look for underlying cause VTAC: acute setting consider lidocaine IV (constant rate infusion); oral long-term meds: mexiletine, sotalol* (1st choice), amiodarone
52
Problem with Antiarrhythmic Drugs
- not benign and they can promote other arrythmias, reduce cardiac output etc
53
Treating dysrhythmias
▪Treat underlying causes if present: eg: correction of electrolyte abnormalities, systemic illness/neoplasia, withdrawal of medication, in some cases treating congestive heart failure can improve rhythm ▪Ensure if arrhythmia present that treatment will likely lead to a reduction of clinical signs/improve quality of life or reduce risk of sudden death – not all arrythmias require treatment if having minimal impact on patient ▪If in doubt contact cardiologist for advice and consult drug formulary ▪Ensure owners informed of potential risks of medications
54
Class 1b drug most commonly used for ventricular arrhythmias (& its mode of action)
- lidocaine -- Block Na+ channels, enhance repolarisation
55
Class II drug most commonly used for ventricular arrhythmias & SVT (& its mode of action)
- atenolol -- beta-blocker -- redues myocardial oxygen demand -- beware if underlying myocardial dz as will reduce CO -> generally contraindicated if CHF present
56
Class III drug most commonly used for ventricular arrhythmias (& its mode of action)
- sotalol -- beta-blocker -- blocks K+ channels -- less cardiac depression cf class II so often used if concurrent myocardial dz
57
Class IV drug most commonly used for heart rate control of SVT (& its mode of action)
- diltiazem -- calcium channel blocker -- reduces conduction through AV node -- some reduction in myocardial contractility
58
Class V drug most commonly used for atrial fibrillation (& its mode of action) Best results when combined with... What should you NOT use if for?
- digoxin -- narrow therapeutic index -- adverse effects common -- measure serum level -- blocks Na+/K+ ATPase -> leads to slower AVN conduction and mild increase in contractility - used with diltiazem (although digoxin is going out of favour and diltiazem commonly used alone) - don't use for ventricular arrhythmias
59
What do anti-arhythmic drugs acting by altering ion flow reduce the risk of?
- an ectopic impulse being generated or slowing impulse generation/conduction
60
How do you treat a clinically significant bradyarhythmia?
- pacemaker

Y4 SA - Collapse, weakness & exercise intolerance (7 decks)

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