16.3 Dysrhythmia for dentists Flashcards

1
Q

What is a dysrhythmia?

A

An abnormality in the rate, rhythm, conduction or site of origin of the cardiac action potential.

A dysrhythmia can involve more than one of these e.g. 3rd degree heart block causes an abnormality of the heart rate, rhythm, conduction and site of origin.

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2
Q

Describe the polarity of cardaic mycoytes.

A

-Cardiac tissue is excitable tissue
- Cells can alter their polarity from -80/-90mV to+30mV
- Changes in voltage are mediated by voltage-gated ion channels

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3
Q

Explain the phases of cardiac action potential.

A

Phase 0 = initiation of cardiac AP, voltage gated Na channels open, sodium influx causes rapid depolarisation

Phase 1 = Na channels close, voltage gated K channels open, efflux of potassium ions, rapid repolarisation

Phase 2 = voltage gated Ca channels open and Ca influx into cells, slows the rate of repolarisation

Phase 3 = excess potassium release, calcium channels close, rapid repolarisation

Phase 4 = return to resting potential

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4
Q

Describe the electrophysiology of the heart.

A
  • Myocardium has its own intrinsic myogenic acitvity
  • Sinoatrial node is where the primary pacemaker cells of the heart are found
  • SA node causes atria to depolarise (right then left)
  • The intrinsic rate of the SA node is approx. 70bpm
  • Wave of excitation spreads across the atria causing them to contract, and reaches the AV node
  • Atrioventricular node beats approx. 50bpm
  • AV node contraction travels through the Bundle of His (typically beats at 40bpm) and into the Purkinje fibres (can beat at 30-40bpm )which causes the ventricles to contract
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5
Q

What does an ECG measure?

A

ECG measures resultant changes in electric potential over time (dmV/dt) at the skin surface.

  • A positive voltage (AP) moving towards the electrode = upstroke on ECG trace
  • An ECG shows the pattern of a resultant net effect of all the different action potentials recorded in that lead, e.g. 100mV travelling towards electrode, and 30mV moving away = overall change by 70mV
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6
Q

How is an ECG recorded?

A
  • Electrodes are placed on the chest and limbs
  • An ECG lead is a graphical representation of the heart’s electrical activity which is calculated by analysing data from several ECG electrodes
  • Different leads provide different views of the heart
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7
Q

Describe the ECG wave form.

A
  • P wave: atrial depolarisation in response to SA node triggering (atria contract)
  • PR interval: delay of AV node to allow filling of ventricles
  • QRS complex: ventricular depolarisation (ventricles contract) shape of wave depends on where the dominant block of muscle is relating to the positive lead of the ECG
  • ST segment: should be flat, beginning of ventricle repolarisation
  • T wave: ventricular repolarisation
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8
Q

What is sinus rhythm?

A

Normal/healthy rhythm of the heart.
Each P wave is followed by a QRS complex, and each PR interval is 120-200ms.

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9
Q

What are the clinical features of dysrhythmias/arrythmias?

A
  • Palpitations
  • Dyspnoea (breathlessness)
  • Angina, caused by excessive workload for tachydysrhythmias, or by a relatively reduced perfusion of the coronary arteries for bradycardic individuals
  • Syncope, fainting episode
  • Sudden adult death
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10
Q

How are dysrhythmias classified?

A

By rate:
- Greater than 100bpm = tachydysrhythmia
- Less than 50bpm = bradydysrhythmia

By rhythm:
- Ectopic: abnormal site of pacemaker activity
- Atrial fibrillation
- Atrial flutter
- Asytole/ventricular fibrillation = flatline, death

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11
Q

How are tachydysrhythmias classified?

A

Classified accoridng to QRS complex width:
- Narrow complex tachycardia = 3 small squares or less (<120ms). Could be sinus tachycardia, atrial tachycardia, atrial fibrillation, atrial flutter
- Broad complex tachycardia = wider than 3 small squares (>120ms)

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12
Q

Name the aetiologies of arrhythmias.

A
  • Conduction system abnormalities: conduction system block, accessory pathways
  • Abnormal pacemaker activity: electrophysiology abnormalities
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13
Q

What is a conduction system block?

A

Issue with the conduction of the heart causing an arrhythmia.
- Can be congenital
- Can be due to cariac myopathies
- Valvular heart disease: stretches and damages conduction system
- Myocardial fibrosis

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14
Q

What are accessory pathways?

A
  • People can be born with abnormal or excessive accessory pathways which cause excessive short circuits in the conduction system
  • E.g. Wolf-Parkinson-White syndrome, bundle of Kent, micro short-circuits
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15
Q

What are electrophysiological abnormalities?

A

Conditions where the cardiac myocytes depolarise at the wrong time of the cardiac cycle, variety of causes:
- Electrolyte disturbances e.g. sodium, potassium, calcium, magnesium
- Ion channel abnormalities
- Acid/base disturbances
- Endocrine conditions e.g. thyroid disorders

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16
Q

What system is used to classify anti-arryhthmic drugs?

A

Vaughan Williams Classification
- Class I
- Class II
- Class III
- Class IV

17
Q

What are class I drugs?

A
  • Act on phase 0 of the cardiac cycle
  • Block voltage gated sodium channels
  • Use-dependent drug, meaning it is more likely to act on a channel in an active state (open) than an inactive channel
18
Q

How are class I drugs sub-classified?

A
  • Type 1a: drugs dissociate at an intermediate rate, historic
  • Type 1b: fast dissociation, used to treatment ventricular tachycardias and ventricular fibrillation e.g. Lidocaine binds to voltage gated sodium channels, risk of causing dysrhythmia
  • Type1c: slow dissociation, main drug used in practice. E.g. flecainide to treat atrial fibrillation and Wolf-Parkinson-White syndrome
18
Q

What are class II drugs?

A
  • Beta blockers
  • Act on phases 2 and 4
  • Mainly used to reduce tachydysrhythmias
  • E.g. propanolol, bisoprolol, atenolol
  • Side effects: bronchospasm, peripheral vasoconstriction, erectile dysfunciton
19
Q

What are class III drugs?

A
  • Potassium channel blockers
  • Delay repolarisation
  • Act on phase 3
  • Amiodarone and Sotalol
20
Q

What are the side effects of potassium channel blockers/Amiodarone?

A
  • Thyroid abnormalities
  • Skin discolouration
  • Pulmonary fibrosis
  • Prolonged QT interval
21
Q

What is QT prolongation?

A
  • QT interval is very long, poses a risk of a long repolarisation period
  • Creates risk of developing polymorphic ventricular tachycardia
22
Q

Which 2 drugs pose a risk of QT prolongation?

A
  • Amiodarone
  • Sotalol

Both pose risk of dysrhythmia as a result

23
Q

What are class IV drugs?

A
  • Calcium channel blockers
  • Slow the heart and weaken the strength of the heart’s contraction
  • Can exacerbate heart failure
  • E.g. diltiazem and verapamil
  • Adverse effects: gingival hypertrophy, flushing, constipation, perivenual oedema
24
Q

Provide examples of antidysrhythmic drugs outside of the Vaughan Williams classification system.

A
  • Atropine
  • Catecholamines: adrenaline, isoprenaline, noradrenaline
  • Adenosine
  • Calcium chloride
  • Magnesium chloride
  • Digoxin
25
Q

What is digoxin?

A
  • A cardiac glycoside
  • Strutu
  • Derived from digitalis plant
  • Used to treat atrial fibrillation and heart failure with atrial fibrillation
26
Q

What is a chronotrope?

A
  • Positive chronotropes increase heart rate
  • Negative chronotropes decrease heart rate
27
Q

Explain the positive chronotropic action of digoxin.

A
  • Inhibits sodium/potassium ATPase pump of cardiac myocytes
  • Increases intracellular sodium
  • Increased intracellular calcium

Increases strength of contraction of the heart

28
Q

Explain the negative chronotropic action of digoxin.

A
  • Increases vagus nerve stimulation
  • Increases atrioventricular node block

Decreases heart rate

29
Q

What are the side effects of digoxin?

A
  • Nausea and vomiting
  • Yellow tinged vision
  • Dysrhythmia: usually bradydysrhythmia, ventricular dysrhythmia, AV block