16.3 Dysrhythmia for dentists Flashcards
What is a dysrhythmia?
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.
Describe the polarity of cardaic mycoytes.
-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
Explain the phases of cardiac action potential.
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
Describe the electrophysiology of the heart.
- 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
What does an ECG measure?
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
How is an ECG recorded?
- 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
Describe the ECG wave form.
- 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
What is sinus rhythm?
Normal/healthy rhythm of the heart.
Each P wave is followed by a QRS complex, and each PR interval is 120-200ms.
What are the clinical features of dysrhythmias/arrythmias?
- 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
How are dysrhythmias classified?
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
How are tachydysrhythmias classified?
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)
Name the aetiologies of arrhythmias.
- Conduction system abnormalities: conduction system block, accessory pathways
- Abnormal pacemaker activity: electrophysiology abnormalities
What is a conduction system block?
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
What are accessory pathways?
- 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
What are electrophysiological abnormalities?
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
What system is used to classify anti-arryhthmic drugs?
Vaughan Williams Classification
- Class I
- Class II
- Class III
- Class IV
What are class I drugs?
- 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
How are class I drugs sub-classified?
- 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
What are class II drugs?
- 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
What are class III drugs?
- Potassium channel blockers
- Delay repolarisation
- Act on phase 3
- Amiodarone and Sotalol
What are the side effects of potassium channel blockers/Amiodarone?
- Thyroid abnormalities
- Skin discolouration
- Pulmonary fibrosis
- Prolonged QT interval
What is QT prolongation?
- QT interval is very long, poses a risk of a long repolarisation period
- Creates risk of developing polymorphic ventricular tachycardia
Which 2 drugs pose a risk of QT prolongation?
- Amiodarone
- Sotalol
Both pose risk of dysrhythmia as a result
What are class IV drugs?
- 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
Provide examples of antidysrhythmic drugs outside of the Vaughan Williams classification system.
- Atropine
- Catecholamines: adrenaline, isoprenaline, noradrenaline
- Adenosine
- Calcium chloride
- Magnesium chloride
- Digoxin
What is digoxin?
- A cardiac glycoside
- Strutu
- Derived from digitalis plant
- Used to treat atrial fibrillation and heart failure with atrial fibrillation
What is a chronotrope?
- Positive chronotropes increase heart rate
- Negative chronotropes decrease heart rate
Explain the positive chronotropic action of digoxin.
- Inhibits sodium/potassium ATPase pump of cardiac myocytes
- Increases intracellular sodium
- Increased intracellular calcium
Increases strength of contraction of the heart
Explain the negative chronotropic action of digoxin.
- Increases vagus nerve stimulation
- Increases atrioventricular node block
Decreases heart rate
What are the side effects of digoxin?
- Nausea and vomiting
- Yellow tinged vision
- Dysrhythmia: usually bradydysrhythmia, ventricular dysrhythmia, AV block
