Antidysrhythmics

Question 1

Give the 3 common clinical indications for the use of adrenaline.

Answer 1

1) Cardiac arrest - routinely administered as part of the advanced life support algorithm.
2) Anaphylaxis - vital part of immediate management.
3) To induce local vasoconstriction - can be injected to control mucosal bleeding. Sometimes mixed with local anaesthetic drugs such as lidocaine to prolong local anaesthesia.

Question 2

1) Which receptors is adrenaline a potent agonist of?
2) Give the main sympathetic effects of adrenaline and state which receptor is agonised to cause these.
3) What physiological effects underpin the use of adrenaline in anaphylaxis?

Answer 2

1) alpha 1 and 2 and beta 1 and 2.
2) vasoconstriction of vessels supplying skin, mucosa and abdominal viscera (a1). Increases in heart rate, force of contraction and myocardial excitability (B1). Vasodilation of vessels supplying heart and muscles (B2)
3) The vascular effects described above and the additional effects mediated by B2 agonism - bronchodilation and suppression of inflammatory mediator release from mast cells.

Question 3

1) What are the risks of the use of adrenaline balanced against?
2) In cardiac arrest, what is restoration of output often followed by?
3) When given to conscious patients for anaphylaxis, what are some of the adverse effects?
4) Give 3 other important adverse effects in the use of adrenaline.

Answer 3

1) Risks are balanced against the severity of the condition that is being treated.
2) Adrenaline induced hypertension.
3) Anxiety, tremor, headache and palpitations.
4) Angina, myocardial infarction, arrhythmias.

Question 4

1) What 2 conditions are there no contraindications to the use of adrenaline in?
2) When should adrenaline be used with caution?
3) Where should combination adrenaline-anaesthetic preparations not be used and why?

Answer 4

1) Cardiac arrest and anaphylaxis
2) When given to induce local vasoconstriction in patients with heart disease.
3) areas supplied by an end artery such as fingers and toes as vasoconstriction can cause tissue necrosis.

Question 5

1) Give the main important interaction of adrenaline.

2) Describe the interaction.

Answer 5

1) Beta blockers.
2) in patients on beta blockers, adrenaline may cause widespread vasoconstriction as the alpha 1 vasoconstriction effect is not opposed by beta 2 vasodilation.

Question 6

1) Describe how adrenaline is prescribed in cardiac arrest.
2) Describe how adrenaline is prescribed in anaphylaxis.
3) Describe the prescription of adrenaline when used in an adrenaline-anaesthetic preparation.

Answer 6

1) With a shockable rhythm, administer 1mg adrenaline IV after 3rd shock and then every 3-5 minutes thereafter. With a non-shockable rhythm give adrenaline 1mg IV ASAP and then repeat every 3-5 minutes.
2) 500mcg IM, and repeat after 5 minutes.
3) adrenaline at a concentration of 1:200000 (5mcg/mL) along with anaesthetic.

Question 7

Give the common clinical indication for the use of Amiodarone and state when it would be used.

Answer 7

Management of a wide range of tachyarrhythmias - AF, A. Flutter, SVT, VT, refractory ventricular fibrillation.

Generally only used when other therapeutic options (drugs or DC cardioversion) are ineffective or inappropriate.

Question 8

1) List the 2 effects of Amiodarone on myocardial cells.
2) What do these effects cause?
3) How does Amiodarone reduce ventricular rate in AF and A. Flutter?
4) What does use of Amiodarone increase chances of conversion to throng its other effects?

Answer 8

1) blockade or Sodium, calcium and potassium channels and antagonism of alpha and beta adrenergic receptors.
2) Reduce spontaneous depolarisation (automaticity), slow conduction velocity and increase resistance to depolarisation (refractoriness), including in AVN.
3) Through interference with AV node conduction.
4) Increases chances of conversion to and maintenance of sinus rhythm.

Question 9

1) Why is Amiodarone useful in SVT?

2) What makes Amiodarone an option for treatment and prevention of VT/ refractory VF?

Answer 9

1) Amiodarone can break the self-perpetuating re-entry circuit that might include the AV node and restore sinus rhythm.
2) Because it can suppress spontaneous depolarisations.

Question 10

1) What can Amiodarone cause when administered through IV infusion in an acute setting?
2) Give the 4 major organs systems affected and specific adverse effects that can occur when Amiodarone is used chronically.
3) Why can Amiodarone cause thyroid abnormalities?

Answer 10

1) Hypotension.
2) Lungs (pneumonitis), heart (bradycardia/ AV block), liver (hepatitis), skin (photosensitivity and grey discolouration).
3) Due to its Iodine content and structural similarities to thyroid hormone.

Question 11

1) What are the 3 circumstances where you should not use Amiodarone?
2) Amiodarone increases plasma concentration of which 3 drugs, and what might this cause?
3) What should you do to the doses of the above mentioned drugs if Amiodarone is started?

Answer 11

1) Severe hypotension, heart block, active thyroid disease.
2) Digoxin, Verapamil, Diltiazem.
3) Half the doses of them.

Question 12

1) What is the exception to the rule that means that Amiodarone use can be initiated by a junior doctor?
2) How is the drug administered in this situation?
3) Outside of this one scenario, how is Amiodarone usually administered? Why is this?

Answer 12

1) in Cardiac arrest where Amiodarone is routinely given for VF or pulseless VT immediately after the third shock in the ALS algorithm.
2) 300mg IV (as bolus injection) followed by 20mL of 0.9% sodium chloride or 5% glucose as a flush.
3) Via a central line if continuous or repeated IV infusions are anticipated. This is because IV administration can cause significant phlebitis.

Question 13

When a patient is starting long term use of Amiodarone, what 3 pieces of advice should they be given?

Answer 13

1) Tell HCP if they get breathlessness, persistent cough, jaundice, restlessness, weight loss, tiredness or weight gain.
2) Advise not to drink grapefruit juice as this can increase risk of side effects.
3) Advise to avoid exposure to direct sunlight due to photosensitivity risk.

Question 14

1) How is Amiodarone monitored in a patient having an IV infusion?
2) How are patients taking long term Amiodarone monitored?

Answer 14

1) Monitoring heart rate and rhythm, and continuous cardiac monitoring.
2) Baseline tests: renal, liver and thyroid profiles. CXR. Then 6 monthly liver and thyroid profiles.

Question 15

Give the common clinical indication for the use of Atropine.

Answer 15

1) First line in the management of severe or symptomatic bradycardia to increase heart rate.

Question 16

Give the 2 common clinical indications for the use of antimuscarinics (hyoscine butylbromide).

Answer 16

1) First line pharmacological treatment for IBS, where they are used for their antispasmodic effect.
2) In palliative care to reduce copious respiratory secretions.

Question 17

1) What does stimulation of a muscarinic receptor do?
2) Give a brief description of the mechanism of action of antimuscarinics.
3) What can antimuscarinics do to the eye?

Answer 17

1) A wide range of parasympathetic effects (rest and digest).
2) Competitive inhibitor of acetylcholine > increase heart rate and conduction, reduce smooth muscle tone and peristaltic contraction (gut and urinary tract) and reduce respiratory secretions.
3) Relaxation of the pupillary constrictor and cilliary muscles, causing pupillary dilation and preventing accommodation, respectively.

Question 18

1) What are 3 adverse effects of antimuscarinics, considering their muscarinic antagonist property?
2) How might antimuscarinics cause urinary retention in patients with BPH?
3) Give 3 other adverse effects of a antimuscarinics.

Answer 18

1) Tachycardia, dry mouth, constipation.
2) By reducing detrusor muscle activity.
3) Blurred vision, drowsiness, confusion.

Question 19

1) Which patients should antimuscarinic use be avoided in?

2) Which patients should antimuscarinics be used with caution in?

Answer 19

1) Patients at risk of arrhythmias (Those with significant cardiac disease), unless the indication for use is bradycardia.
2) Use with caution in patients at risk of angle closure glaucoma, as they can precipitate a dangerous rise in intraocular pressure.

Question 20

1) What is the only important interaction for antimuscarinics?
2) Name 2 commonly used antimuscarinics.

Answer 20

1) Adverse effects are more pronounced when they are combined with other drugs that have antimuscarinic effects, such as tricyclics antidepressants.
2) Atropine and hyoscine butylbromide.

Question 21

1) Describe how atropine is prescribed for bradycardia.
2) What can be used as an alternative to atropine - What are the positives and negatives of this?
3) How is hyoscine butylbromide (buscopan) prescribed for IBS?

Answer 21

1) Atropine 300-600mcg every 1-2 minutes IV until the heart rate stabilises.
2) Glycopyronium - does not penetrate the brain so causes less drowsiness, but is not readily available on general wards.
3) 10mg 8 hourly - can be available without prescription.

Question 22

Why has it been suggested that for bradycardia the first dose of atropine should be no less than 600mcg?

Answer 22

Because paradoxically, low dose atropine could transiently slow the heart rate before the chronotropic heart rate effect begins.

Question 23

List the Vaughn Williams classes of Antidysrhythmic drugs and give examples of them.

Answer 23

Class 1: Sodium channel blockers (1a: Quinidine, 1b) Lidocaine, 1c) Flecainide)

Class 2: Beta blockers (Bisoprolol)

Class 3: Potassium channel blockers (Amiodarone and Sotalol)

Class 4: Calcium channel blockers (Verapamil and Diltiazem)

Question 24

Give the 2 Antidysrhythmic drugs unclassified in the Vaughn Williams system.

Answer 24

Adenosine and Digoxin.

Question 25

1) What is the common clinical indication for the use of Adenosine?
2) How do many forms of SVT arise?
3) What class is Adenosine?

Answer 25

1) First line diagnostic and therapeutic agent in SVT.
2) From a self-perpetuating electrical (re-entry) circuit that takes in the AV node.
3) Class 5 antidysrhythmic.

Question 26

1) Describe the basic mechanism of action of adenosine.
2) Give the main therapeutic effects of Adenosine on the heart.
3) What is the overall effect of Adenosine in treating SVT with a re-entry circuit involving the AVN?

Answer 26

1) Agonist of adenosine receptors on cell surfaces in the heart = activation of these G protein coupled receptors induces therapeutic effects.

2) Reduces frequency of spontaneous depolarisations (automaticity)
Increases resistance to depolarisation (refractoriness)
These 2 effects cause a slow in SAN conduction, rate abundant velocity, and increases AVN refractoriness.

3) Overall increased refractoriness of the AVN breaks the re-entry circuit which allows normal depolarisations of the SAN to resume control of heart rate (cardioversion).

Question 27

1) Why will adenosine not induce cardioversion In atrial flutter?
2) Give 4 main adverse effects to the use of adenosine.
3) Give 4 complete contraindications to the use of Adenosine.
4) Give 2 cautions when using Adenosine.

Answer 27

1) Because the re-entry circuits in atrial flutter do not involve the AVN.
2) Bradycardia and possibly asystole leading to a sinking feeling in the chest. Can be accompanied by breathlessness and a sense of impending doom.
3) Patients who will not tolerate transient bradycardic effects: Hypotension, coronary ischaemia, decompensated heart failure. Also completely contraindicated in asthma as may induce bronchospasm.
4) COPD and patients who have had a heart transplant (these are very susceptible to the effects of Adenosine).

Question 28

1) When should the dose of adenosine be halved?

2) Which drugs might cause the dose of adenosine required to be increased?

Answer 28

1) If the patient is also taking dipyridamole, as this blocks the cellular uptake of adenosine, prolonging and potentiating it’s effects.
2) Theophylline, Aminophylline and caffeine - they are competitive antagonists of adenosine receptors and reduce its effect causing a port response to adenosine.

Question 29

1) How should adenosine always be administered?
2) How should adenosine be prescribed?
3) When should lower doses of adenosine be used?

Answer 29

1) Always IV.
2) Prescribe in the once only section of the drug chart. Initial dose is adenosine 6mg IV. If this is ineffective, a 12mg dose should be given. Higher doses can be given in selected cases.
3) If administering via a central line.

Question 30

1) What should be done to ensure that the adenosine dose reaches the heart quickly to minimise cellular uptake en route?
2) How should adenosine be administered?

Answer 30

1) A large bore cannula (18 gauge -green - or bigger) should be used, sited as proximally as possible (e.g. antecubitcal fossa).
2) As a rapid injection and immediately followed with a flush - 20mL of 0.9% Sodium chloride.

Question 31

1) Give the common clinical indication for the use of Lidocaine.
2) Give the uncommon clinical indication for the use of Lidocaine.

Answer 31

1) First choice local anaesthetic, for example, urinary catheterisation and minor procedures.
2) Antiarrhythmic drug in VT and VF refractory to DC cardioversion (Amiodarone preferred in latter indication).

Question 32

Describe the mechanism of action of Lidocaine as an anaesthetic.

Answer 32

Enters cells in uncharged form > accepts proton to become positively charged > enters and blocks voltage gated Sodium channels from inside cell > prevents initiation and propagation of action potentials in nerves and muscles > induce local anaesthesia.

Question 33

Describe the mechanism of action of Lidocaine as an antidysrhythmic.

Answer 33

Reduces the duration of action potentials > slows conduction velocity > increases refractory period > terminates VT and improves chances of treating VF.

Question 34

1) What is the most common side effect of using Lidocaine?
2) Give the 4 adverse effects of Lidocaine on the neurological system.
3) Give the 2 adverse effects on the CVS if present in overdose quantities.

Answer 34

1) Stinging sensation during local administration.
2) Drowsiness, restlessness, tremor and fits.
3) Hypotension and arrhythmias.

Question 35

1) When should a reduced dose of Lidocaine be used?
2) What does Lidocaine rely on for elimination?
3) How can a desirable interaction between Lidocaine and Adrenaline be useful in practice?

Answer 35

1) In patients with reduced cardiac output.
2) Hepatic blood flow.
3) Co-administration of adrenaline and Lidocaine produces a desirable interaction that may prolong the local anaesthetic effect.

Question 36

1) For minor procedures, what dose of Lidocaine should be used?

Answer 36

1) 1% Lidocaine ( 10mg/ mL) solution of Lidocaine hydrochloride.

Question 37

Give 5 situations when Sotalol might be used.

Answer 37

1) Symptomatic non-sustained VT
2) Prophylaxis of paroxysmal atrial tachycardia or atrial fibrillation
3) paroxysmal AV re-entrant tachycardia
4) paroxysmal SVT after cardiac surgery
5) maintenance of sinus rhythm following cardioversion of atrial fibrillation or flutter.

Question 38

What 2 situations might you use Flecainide in?

Answer 38

1) Supraventricular arrhythmias

2) Ventriculae arrhythmias (initiated under direction of hospital consultant)

Question 39

Name the 3 preparations that might be used to treat electrolyte imbalances or metabolic disturbances of Calcium, Magnesium and Sodium.

Answer 39

1) Sodium - Sodium bicarbonate (8.4/4.2/1.26%)
2) Calcium - Calcium gluconate (10%) or Calcium chloride
3) Magnesium Sulphate

Question 40

1) Name the 2 electrolyte imbalance situations where calcium will be required.
2) Name the 3 other common clinical indications for the use of calcium and vitamin D.

Answer 40

1) Used in severe hyperkalaemia (as Calcium gluconate) to prevent life threatening arrhythmias.
Used for hypocalcaemia that is symptomatic (parasthesia, tetany, seizures) or severe (<1.9mmol/L).

2) Osteoporosis - calcium and vitamin D given to ensure positive calcium balance.
CKD - to treat and prevent secondary hyperparathyroidism and renal osteodystrophy.
Vitamin D deficiency - Vitamin D used in prevention and treatment, including for Rickets and osteomalacia.

Question 41

1) Give a very basic description of calcium homeostasis.
2) How do hyperphosphataemia and hypocalcaemia occur in CKD?
3) How does renal osteodystrophy then happen?

Answer 41

1) PTH and vitamin D increase serum calcium levels and bone mineralisation. Calcitonin reduces serum calcium levels.
2) Caused by impaired phosphate excretion and reduced activation of vitamin D.
3) These imbalances stimulate secondary hyperparathyroidism, leading to bony changes including renal osteodystrophy.

Question 42

1) What is the rationale behind using Calcium gluconate for severe hyperkalaemia?

Answer 42

1) Calcium raises the myocardial threshold potential, reducing excitability and the risk of arrhythmias. It does not have any effect on serum potassium level.

Question 43

1) Give 2 adverse effects of oral calcium.

2) Give 2 adverse effects of IV calcium and why these may occur.

Answer 43

1) Dyspepsia and constipation.
2) cardiovascular collapse (if administered too fast) and local tissue damage (if accidentally given into subcutaneous tissue).

Question 44

1) What is the one circumstance where calcium and vitamin D should be avoided?
2) Name 4 drugs that oral calcium reduces absorption of.
3) Why must Calcium not be allowed to mix with sodium bicarbonate if administered IV?

Answer 44

1) Hypercalcaemia
2) Iron, bisohosphonates, tetracyclines, levothyroxine.
3) Due to the risk of precipitation.

Question 45

1) How should Calcium be prescribed for severe hyperkalaemia?
2) How should Calcium gluconate be administered?
3) What monitoring is required for patients being given calcium gluconate for severe hyperkalaemia?

Answer 45

1) 10mL Calcium gluconate 10% for administration by slow IV injection.
2) Slow IV injection over 5-10 minutes into a large vein.
3) Continuous cardiac monitoring and repeat 12 lead ECG after administration of Calcium gluconate to confirm resolution of ECG abnormalities.