Dysrhythmias Flashcards

Question

What type of receptor mediates the effect of the vagus nerve on the SA node?

Answer 1

M2 mAChR ## Footnote M2 muscarinic acetylcholine receptors are involved in heart rate regulation.

Answer 2

* Constipation * Blurred vision * Dry mouth * Higher doses: confusion, delirium ## Footnote Atropine acts as a non-selective mAChR antagonist (can cross blood-brain barrier)

Answer 3

Signal in its own right Adenosine interacts with specific receptors A1, A2A, A2B, A3 (GPCRs) A1 is important in the AV node = coupled to Gi

Answer 4

A1 receptor ## Footnote The A1 receptor plays a crucial role in regulating heart rhythm at the AV node.

Answer 5

20-30 seconds ## Footnote Adenosine has a very short plasma half-life, making it effective for rapid interventions.

Answer 6

- Very short plasma half-life due to uptake (10 seconds) - Given as an IV bolus into a central vein = 20-30 seconds duration of action - Useful for quickly terminating dysrhythmias (PSVT & AV node dependent tachycardia in WPW) - Has replaced verapamil for this purpose

Answer 7

* Bradycardia * Worsening heart block * Facial flushing as it’s a vasodilator * Chest pain (usually transient and not a major concern) * Bronchospasm = should be used in caution with patients with bronchial asthma or COPD * Interacts with caffeine and theophylline = both are adenosine receptor antagonists so can reduce the efficiency of adenosine

Answer 8

* Bergamottin * Dihydroxybergamottin * Citrus furanocoumarins ## Footnote These compounds can irreversibly inhibit CYP3A4, leading to drug interactions.

Answer 9

90% + Second-line treatment for various dysrhythmias when medications fail.

Answer 10

Quickly restore heart to natural rhythm under the control of the SA node - Can be done pharmacologically using medicines such as adenosine - Can be done electrically = typically used when the patient has a pulse (e.g. Supraventricular tachycardia or AF) - Shock is delivered in synch with the R wave = minimises the risk of inducing a more dangerous dysrhythmia (e.g. VF) - Antidysrhythmic drugs and anticoagulants often given prior to procedure - May administer amiodarone after procedure to help maintain the heart in sinus rhythm and prevent reoccurrence of dysrhythmia

Answer 11

Defibrillation is non-synchronized; cardioversion is synchronized ## Footnote Defibrillation is used for pulseless ventricular tachycardia or ventricular fibrillation.

Answer 12

Device placed inside the patient that monitors heart and delivers shocks if a dysrhythmia is detected

Answer 13

- supplements/ replaces function of the SA node and/or AV node (lasts up to 10 years) - Most commonly used to treat bradycardias, especially in conditions like heart block - Used after AV node ablation - Pacemaker leads are inserted through a catheter via the subclavian vein and the device’s main circuitry is implanted just below the collarbone Arne Larsson was the first person to have an implanted pacemaker = survived an extra 41 years

Answer 14

EAG and hERG interactions ## Footnote Long QT syndrome can be drug-induced and is linked to hERG mutations.

Answer 15

hERG interactions ## Footnote Many drugs have been withdrawn due to long QT syndrome linked to hERG.

Answer 16

Koller and Halsted ## Footnote Cocaine was used in dental surgery and as a safer alternative to ether and chloroform.

Answer 17

19th ## Footnote Cocaine had significant medical applications during this period.

Answer 18

Delays the electrical impulse from the atria to the ventricles, ensuring they don’t contract simultaneously

Answer 19

- An abnormal accessory pathway seen in Wolff-Parkinson-White syndrome that allows electrical signals to bypass the AV node, leading to tachycardia - Creates a global re-entry circuit that sends impulses looping around both the atria and ventricles - Lack of gatekeeper function (typically regulates the speed at which electrical impulses pass from the atria to the ventricles) so impulses from the atria can pa through unchecked at a high rate - High ventricular rates reduces the efficiency of heart’s pumping function so ventricles don’t have enough time to fill with blood between beats, causing decreased cardiac output and O2 delivery to tissues. The workload is increased = myocardial ischaemia

Answer 20

Represents atrial depolarisation or the electrical activity that causes atria to contract

Answer 21

Represents ventricular depolarisation or the electrical activity that causes ventricles to contract

Answer 22

Represents ventricular repolarisaton or the electrical recovery of the ventricles after contraction

Answer 23

- SA node is the primary pacemaker located in the right atrium = initiates heartbeats - AV node is located at the junction between the atria & ventricles and slows down conduction to allow the ventricles time to contract AFTER the atria - Bundle of His takes the signal to the base of the ventricles then, via purkinje fibres, into ventricular muscle - It uses the right and left bundle branches to do this

Answer 24

Phase 0 = a sharp spike, opening of Na+ channels Phase 1 = Na+ channels inactivate rapidly whilst K+ channels begin to open, brief repolarisation Phase 2 = long plateau phase where L-type Ca2+ channels open and Ca2+ ions balance the outward flow of K+ ions, stable membrane potential Phase 3 = activation of K+ channels is more prominent and Ca2+ channels close, rapid depolarisation Phase 4 = cell returns to its resting membrane potential, maintained by inward rectifier K+ channels

Answer 25

Phase 0 and 4 is referred to as the ‘funny current’ Phase 0 = T-type Ca2+ channels open and contribute to the pacemaker potential. Once the membrane potential reaches -40 mV, L-type Ca2+ channels will open and cause depolarisation Phase 4 = the pacemaker potential where HCN channels activate and spontaneous depolarisation occurs due to Na+ influx through these channels (this is the funny current) Phase 3 = Ca2+ channels inactivate and K+ channels open, repolarisation

Answer 26

Used to determine if someone has a dysthymia by measuring cardiac electrical activity Process requires 6 electrodes to be placed across the chest and one on each limb = 10 in total. Once in place, signals from the electrodes are amplified & recorded for about 10 seconds

Answer 27

Divided into several key waves, intervals and segments that correspond to different phases of the heart’s electrical activity during each cardiac cycle

Answer 28

Section between the end of the QRS complex and the T wave This is elevated in myocardial infarction

Answer 29

- In healthy cardiac tissue, the electrical signal is forced to split and travel down 2 separate pathways, around the non--conducting tissue. When the signal meets point B, it cannot travel back up the alternate branch as the tissue is in a refractory state = cannot conduct signals again immediately - When there is a unidirectional in one pathway, the AP can only travel downbeat one branch due to the damaged tissue impairing normal forward conduction = can only conduct signals in a retrograde (backwards) direction - In retrograde transmission, when the signal reaches point B, it is able to travel back up through the branch with the damaged tissue as it is no longer in a refractory state = cannot conduct signals conduct - The final condition is that the timing of the retrograde signal must be so that by the time it reaches point A again, the tissue in the undamaged branch is no longer in its refractory state. If this condition is met, the signal will be able to travel back down this branch and cause a self-perpetuating loop of electrical activity

Answer 30

- There are 2 pathways through the AV node: the slow pathway (recovers faster from the refractory period) and the fast pathway (has a longer refractory period) - Under normal conditions, when the signal travels down both pathways, the slow pathway is unable to propagate its signal because the fast pathway depolarises the shared tissue first = no re-entry circuit is formed - When there is an extra atrial AP (e.g. premature atrial contraction), the extra AP will travel down the slow pathway as it has recovered quickly from its refractory period BUT the fast pathway is still in the refractory state so cannot conduct the impulse. Once the signal reaches the point where the 2 pathways rejoin, it can trigger ventricular contraction and an extra atrial AP = NO RE-ENTRY CIRCUIT FORMED - With correct timing of the slow circuit, the timing of conduction is just right and the slow pathway signal can encounter the fast pathway after it’s recovered from its refractory period so the fast pathway allows the impulse to travel back up the pathway in a retrograde manner. When the signal reaches the atria, it can re-enter the slow pathway which has also recovered = CREATES A RE-ENTRY CIRCUIT = self-perpetuating tachycardia

Answer 31

Congenital, abnormal conduction paths that allow inappropriate signals to pass from one part the heart to another Are very rare but can lead to serious dysrhythmias

Answer 32

- Affects 0.2% of the population (starts at young age, teens-50) - Most commonly a re-entry circuits through the AV node - Ventricular rate goes up to 250 bpm - Palpitations, shortness of breath & chest pains - Cause unknown but triggered by anxiety, stress, caffeine and smoking - Attacks can be halted by Valsalva Manoeuvre (forced exhalation against a closed airway) - ECG shows a rapid but regular heart rate = difficult to see P waves

Answer 33

- Drugs - Surgery - Electrical approaches

Answer 34

- Na+ channel blocker - Acts on phase 0 - Block Na+ channels that are crucial in phase 0 of the cardiac muscle AP where rapid depolarisation occurs - By slowing influx of Na+, the drugs reduce the speed of conduction in the heart’s electrical system

Answer 35

- Beta blockers - Inhibit the effects of sympathetic activity at phases 2 and 4 - SNS activation increases the slope of the pacemaker potential in the SA node = reaches threshold faster and increases heart rate - It also prolongs the plateau phase which enhances contractility - The drugs block both these effects - Thus reducing HR and contractility

Answer 36

- K+ channel blockers - Prolong the action potential - Drugs prolong phase 3 by inhibiting the K+ influx and thus delaying repolarisation - This extends the duration of the AP and increases the refractory period - Thus preventing premature impulses and reducing HR

Answer 37

- Ca2+ channel blockers - Exert their primary effect on the SA and AV nodes where Ca2+ plays a key role in phase 0 depolarisation - They inhibit Ca2+ influx by slowing the firing rate of the SA node and delaying conduction through the AV node = slower HR - Also impact phase 2 (plateau phase) which relies on L-type calcium channels = reduction in force of contraction

Answer 38

- Many drugs are unclassified such as adenosine (works on muscarinic ACh receptors) and atropine - Many drugs have multiple sites of action —> amiodarone could be class I, II, III or IV - Sites of action may be different in disease state vs healthy tissue - Individual dysrhythmias can be treated with drugs from more than one class - Alternative is to prioritise clinical utility over the mechanism

Answer 39

Lidocaine (Ib) and Flecainide (Ic) Primarily act on non-nodal tissues i.e. atrial and ventricular muscle where Na+ channels play a key role in rapid depolarisation (phase 0)

Answer 40

- Used to treat ventricular dysrhythmias (e.g. ventricular tachycardia/fibrillation) in acute settings - Not used routinely after a heart attack any longer = replaced by amiodarone which acts on a wider range of dysrhythmias - Selectively targets inactivated channels, more commonly in ischeamic tissues - Serious systemic side effects such as seizures, comas and death at higher doses - Makes heart block worse

Answer 41

Lidocaine is injected near the nerves of a pain sensing neuron This blocks Na+ channels that are essential for generating action potentials in these neurons Stops transmission of pain signals to the CNS = localised pain relief

Answer 42

- Not used as a local anaesthetic - Binds to the open state of a channel (longer duration) - Good for Supraventricular tachycardias e.g. atrial fibrillation - Available in tablet form - Fewer CNS side effects than Lidocaine but can still lead to dizziness, visual disturbances, fatigue and mild GI side effects - Dangerous in patients who have structural heart damage as it can trigger ventricular tachycardia/fibrillation

Answer 43

All antidysrhythmic drugs have the potential to to cause dysrhythmias

Answer 44

Have sympathetic effects - Influences the pacemaker potential (phase 4), the depolarisation (phase 0) and the plateau phase (phase 2) - Actions on the plateau phase increases the force of contraction = a positive inotropic effect - Effects on phases 4 and 0 are key to antidysrhythmic actions of these drugs Beta blockers reduce the pacemaker slope meaning there is a slower HR = negative chronotropic effect (useful in treating sinus tachycardia) Also slow the conduction of the AV node and prolong the refractory period

Answer 45

- worsen heart block and cause bradycardia - can precipitate heart failure

Answer 46

- Blocks K+ channels to delay repolarisation - Causes prolonged action potential and refractory period - Decreases AV node conduction velocity so regulates heart rhythm and reduced the heart rate - Decreases re-entry tendency

Answer 47

Useful in a wide range of dysrhythmias E.g. Atrial fibrillation/flutter, ventricular & Supraventricular tachycardias and cardioversion of ventricular fibrillation

Answer 48

The study of a drug’s absorption, distribution, metabolism and excretion

Answer 49

- Can be administered orally or by IV - Has difficult pharmacokinetics - Very fat soluble so difficult to establish a stable plasma concentration - Given as an IV bolus (large dose administered by IV over a short period of time) in emergency situations - 100 day half life = takes 3 months for plasma levels to decrease by 50% after stopping the drug - Metabolised by CYP3A4 = metabolises over 30% of all drugs and certain dietary components can inhibit this enzyme so has a high potential for drug interactions as other drugs can be metabolised

Answer 50

- SA node is down-regulated by the vagus nerve to 70 bpm from 100 bpm = negative chronotropic effect - M2 mAChR in the SA node mediates this effect (activated by ACh release by the vagal nerve)

Answer 51

- The M2 mAChR is coupled to Gi which inhibits adenylyl cyclase - Upon receptor activation, the beta-gamma subunits open a potassium channel = KACh - This allows K+ efflux from the SA node cells - K+ outflow makes the resting membrane potential more negative - So it takes longer for the pacemaker potential to bring the cell to the threshold needed to activate VGCC - VGCC is a voltage gated calcium channel that is responsible for phase 0 of the SA node action potential Net result = reduction in HR

Answer 52

- Atropine binds to the M2 mAChR = a muscarinic receptor antagonist - Administration of this drug blocks KACh channel activation by M2 receptors - The resting membrane potential becomes less negative so the pacemaker potential reaches threshold quicker and can activate VGCC - Leads to increased HR

Answer 53

- Lowers heart rate through activation of KACh channels - Adenosine is continuously produced at low levels by heart muscle cells - Target AV node tissue, specifically the Adenosine A1 receptor - Lowers RMP - Increases in ischaemia by increasing KACh activation = reduction in HR

Answer 54

Found in all citrus fruits but particularly concentrated in grapefruit

Answer 55

- Cytochrome P450 enzymes found in the liver and GI tract = protect the body by breaking down foreign substances - Oxidise foreign molecules - Responsible for >50% of drug metabolism - Irreversibly inhibited by furanocoumarins (can significantly reduce enzyme’s activity) - As little as one fruit/glass of juice can cause the effect - Effects can occur over 3 days after consuming the fruit - Can cause overdose of prescription drugs (reduced metabolism)

Answer 56

- Involves inserting catheters through a large blood vessel and then the catheter is guided to the heart - This is minimally invasive and has a low risk —> high success rate (>90% for WPW) - Diagnostic catheters have electrodes on their tips that are used to pinpoint the exact area of tissue responsible for the dysrhythmia - Ablation catheter is used once the area is located to send radiofrequency energy to destroy the abnormal tissue and restore normal electrical conduction in the heart

Answer 57

The basic principle is to depolarise a large block of cardiac muscle It is a non-synchronised shock used in pulseless ventricular tachycardias/VF

Answer 58

Designed so that it will not deliver a defibrillation shock unless the patient actually needs it

Dysrhythmias Flashcards

(82 cards)