Term
|
Definition
| a disturbance of normal cardiac rhythm |
|
|
Term
|
Definition
|
|
Term
| How are dysrhythmias classified? |
|
Definition
- the site of origin of the abnormality - atrial, junctional or ventricular
- whether the HR is increases or decreased
- whether the hear beating is regular or irregular |
|
|
Term
| What types of regular atria dysrhythmias are there? |
|
Definition
- atrial tachycardia (150-240bpm)
- atrial flutter (240-350bpm) |
|
|
Term
| What types of irregular atria dysrhythmias are there? |
|
Definition
atrial fibrillation
1% incidence
symptoms: palpations, chest pain, dizziness or occasionally asymptomatic |
|
|
Term
| What types of ventricular dysrhythmias are there? |
|
Definition
ventricular tachycardia (120-300bpm, regular)
ventricular fibrillation (irregular) |
|
|
Term
| Is atrial or ventricular dysrhythmias more serious? |
|
Definition
| Ventricular, however atrial can lead to ventricular |
|
|
Term
|
Definition
| a dysrhythmia that arises above the levels of the ventricle, it excludes dysrhythmias arising from the SAN, atria or AVN. |
|
|
Term
| What are cardiac dysrhythmias due to? |
|
Definition
| change in the generation or conduction of electrical impulses. |
|
|
Term
| What are the 4 basic phenomena that underlie disturbances of cardiac rhythm? |
|
Definition
abnormal pulse generation:
- automaticity
- triggered activity (delayed after-depolarisation)
abnormal impulse conduction:
- heart block
- reentry |
|
|
Term
| What causes automaticity (ectopic pacemaker activity)? |
|
Definition
increased phase 4 depolarisation in subsidiary pacemakers
induction of pacemaker activity in quiscent tissue |
|
|
Term
| What encourages automaticity? (4) |
|
Definition
1. catecholaimnes actine on b1-adrenoceptors increase the rate of depolarisation during phase 4 and can cause normally quiescent parts of the heart to take on a spontaneous rhythm.
2. increased sympathetic activity increase If
3. pain increases sympathetic discharge and increases adrenaline
4. partial ischaemic damage also causes abnormal pacemaker activity due to rise in extracellular K+ |
|
|
Term
| Which is the most common mean of initiating dysrhythmia in HF? |
|
Definition
|
|
Term
| When do early after depolarisations occur? |
|
Definition
abnormal depolarisation during phase 2 or 3
extra AP arises before the membrane potential has returned to its stable resting level |
|
|
Term
| What would cause a phase 2 disruption? |
|
Definition
augmented opening of L-type ca2+ channels
MAIN ONE |
|
|
Term
| What would cause a phase 3 disruption? |
|
Definition
|
|
Term
| What do early after depolarisations result from? |
|
Definition
sympathetic stimulation
heart failure |
|
|
Term
| When are delayed after depolarisations seen? |
|
Definition
| after the membrane has returned to its resting membrane potential |
|
|
Term
| Why do delayed after depolarisations occur? |
|
Definition
| abnormally raised intracellular calcium (via the transcient inward current) which triggers inward current and hence a train of abnormal APs. |
|
|
Term
| What is the effect or raised intracellular calcium concs? |
|
Definition
1. activates NCX which results in net influx of one positive charge and hence membrane depolarisation
2. opens non-selective cation channels in membrane causing depolarisations |
|
|
Term
| What do delayed after depolarisations result from? |
|
Definition
sympathetic stimulation
heart failure
cardiac glycosides |
|
|
Term
| What is a re-entry dysrhythmia? |
|
Definition
- electrical impulses re-excite regions of the myocardium after the refractory period has passed
- this propagates impulses to trigger APs outside normal SAN control |
|
|
Term
| What can a re-entry dysrhythmia result from? |
|
Definition
| anatomical abnormalities or more commonly myocardial damage |
|
|
Term
| List the classes of antidysrhythmic drugs |
|
Definition
I - Sodium channel blockers
II - beta-adrenoceptor antagonists
III - potassium channel blockers
IV - calcium channel blockers (calcium antagonists)
Other - cardiac glycosides (digitalis) |
|
|
Term
| Which class is further divided and how? give one example for each |
|
Definition
Class I - sodium channel blockers
1a) intermediate dissociation - quinidine
1b) fast dissociation - lidocaine
1c) slow dissociation - flecainide |
|
|
Term
| Describe Class I mechanism and how this affects the AP |
|
Definition
| Block Na+ channels by binding to the site on the alpha-subunit. The characteristic effect on the AP (of non-pacemaker cells) is to reduce the max rate of depolarisation in phase 0. |
|
|
Term
| What 3 states are Ca2+ channels able to exist in? |
|
Definition
1. resting (closed but capable of opening)
2. open (activated)
3. refractory (closed and incapable of opening; inactivated) |
|
|
Term
| Explain use dependence in Class 1 antidysrhythmic drugs |
|
Definition
| The faster the heart beats, the more effective the drugs work (blocks tachycardia, not normal heart rate). The more frequently the channels are activated, the greater the degree of block produced. |
|
|
Term
| Explain the mechanism of use dependence in Class 1 antidysrhythmic drugs |
|
Definition
| Class I drugs bind to channels most strongly when they are either in open or refractory state, therefore the channel has to be open to work, the more channels that are open, the greater the effect of binding and greater effect. |
|
|
Term
| Why are beta blockers used? |
|
Definition
| Ventricular dysrhythmias seen with MI are due to increased sympathetic activity. B-AR stimulation increases SAN frequency (If) and AVN conduction and Ca2+ entry. |
|
|
Term
| What are the effects of beta blockers (antagonists) |
|
Definition
- increase refractory period of the AVN by blocking the adrenoreceptors so adrenaline cannot bind, thus inhibiting the G-protein signalling cascade.
- APs will be generated at a reduced frequency. |
|
|
Term
| What effect do beta blockers have on the AP? |
|
Definition
- Phase 0 and 4 of the SA/AVN AP and phase 2 of the ventricular AP will be slowed.
- Both increase in duration. |
|
|
Term
|
Definition
- prolong the cardiac AP and the QT interval by delaying the slow outward K+ current
- block the delayed K+ channels |
|
|
Term
| What effect do class III drugs have on the AP? |
|
Definition
- by blocking delayed K+ channels, phase 3 of AV/SAN/Ventricular AP are prolonged.
- heart takes longer to repolarise, so frequency of AP generation is decreased. |
|
|
Term
| What does it mean when we say Class III exhibit reverse use dependent prolongation of the AP duration? |
|
Definition
| the less frequent the channels are activated, the greater the degree of block produced |
|
|
Term
|
Definition
| block L-type Ca2+ channels, slowing conduction in the SA and AV nodes and hence prolong depolarisation |
|
|
Term
| What effect do class IV drugs have on the AP? |
|
Definition
| prolongation of phase 0 of the SA/AVN potential and phase 2 (plateau) of ventricular AP. |
|
|
Term
| In the SA/AVN AP, the upstroke (0) is carried by the... |
|
Definition
|
|
Term
| In the SA/AVN AP, repolarisation (3) is due to the... |
|
Definition
| delayed potassium current |
|
|
Term
| In the SA/AVN AP, small depolarisaiton (4) is due to the... |
|
Definition
| net inward current (principally the funny current) |
|
|
Term
| In the atria/ventricles, the upstroke (0) is carried by the... |
|
Definition
|
|
Term
| In the atria/ventricles, the plateau (2) is due to the... |
|
Definition
|
|
Term
| In the atria/ventricles, repolarisation (3) is carried by the... |
|
Definition
| delayed potassium current |
|
|
Term
| List the four main mechanisms by which anti-dysrhythmias work |
|
Definition
1. reduced frequency (If)
2. slowed conduction (ICa and INa)
3. increased refractory period (IK)
4. reduced intracellular Ca2+ (ICa) |
|
|
Term
| What are the AP effects of class Ia? |
|
Definition
- slows conduction (INa)
- increases refractory perid (IK) - Class III |
|
|
Term
| What are the uses and side effects of class Ia? |
|
Definition
U: ventricular and supraventricular dysrhythmias
SE: torases de pointes (Q), anticholinergic (D), lupus (P) |
|
|
Term
| What are the AP effects of class Ib? |
|
Definition
- little effect on conduction (INa)
- prevent immature beats |
|
|
Term
| What are the uses and side effects of class Ib? |
|
Definition
U: ventricular dysrhythmia following MI
SE: bolus lidocaine (i.v. or i.m.): seizures, coma |
|
|
Term
| What are the AP effects of class Ic? |
|
Definition
|
|
Term
| What are the uses and side effects of class Ic? |
|
Definition
U: ventricular and supraventricular tachycardias
SE: well-tolerated DO NOT GIVE TO ISCHAEMICS |
|
|
Term
| When are beta blockers used and give an example |
|
Definition
propranolol
- ctronols ventricular rate in supraventricular tachyacardias
- supress non-sustained ventricular arrhythmias
- reduce ectopic pacemaker activity and delayed after-depolarisations |
|
|
Term
| What are the class II adverse effects |
|
Definition
exacerbate HF
fatigue
nightmares |
|
|
Term
| When are class III used and give an example |
|
Definition
sotalol
- control SA and ventricular rate in atrial fibrillation and atrial flutter |
|
|
Term
| What are the class III adverse effects |
|
Definition
| irregular rhythm of atria diagnosed by absence of P waves and an irregular ventricular rate |
|
|
Term
| When are class IV used and give an example |
|
Definition
verapamil
- supraventricular arrhythmias to slow ventricular rate |
|
|
Term
| What are the class IV adverse effects |
|
Definition
HF
Wolff-Parkinson-White
cannot be used in patients with heart block |
|
|
Term
| What is Wolff-Parkinson-White? |
|
Definition
| a pre-excitation syndrome caused by a rapidly conducting pathway between atria and ventricles |
|
|
Term
| What is a pre-excitation syndrome? |
|
Definition
| a condition where the ventricles of the heart become depolarised too early, which leads to their partial premature contraction. |
|
|
Term
| What are the main actions of glycosides on the heart? |
|
Definition
- cardiac slowing and reduced rate of conduction through AVN
- increased force of contraction
- disturbances of rhythm (block of AV conduction, increased ectopic pacemaker activity) |
|
|
Term
| What are the adverse effects of cardiac glycosides? |
|
Definition
|
|
