What anti arrhythmic drugs can be used in the management of atrial fibrillation?

Beta-antagonists (class 2); calcium-antagonists (class 4); flecainide (class 1c); amiodarone (class 3); digoxin (unclassified); magnesium

Pass: 3/5

What are the mechanisms of action of amiodarone?

Blocks Na, K, Ca channels; blocks beta adrenoreceptors; prolongs AV conduction; decreases automaticity; decreases automaticity of purkinje fibres

Prompt: what are the cellular mechanisms

Has actions on both rate and rhythm!

Pass: Bold

What are some important drug interactions with amiodarone?

warfarin (increased anticoagulant effect by inhibiting metabolism); digoxin ( increases plasma concentration leading to toxicity); increased cardiac effects of other antiarrhythmic agents; phenytoin ( increased plasma concentration)

Pass: at least 2


Describe the mechanism of action of lignocaine on the heart.

Blocks activated & inactivated Na channels; greater effect on ischaemic tissue; no vagal effects. Class 1 B antiarraythmic action.

Pass: Na channel block and Class 1B

Describe the adverse effects of lignocaine.

CNS: dizzy, anorexia, N&V, tinnitus, tremor, visual disturbance, paraesthesia, slurred speech seizure, resp depression

CVS: bradycardia, CVS collapse, uncommon proarrhythmia; can get SA arrest, impaired conduction may worsen/ precipitate pre existing CCF; decreased BP from myocardial depression


GI as above

Pass: CNS & Cardiac with at least x 3 example total


What are the features of digoxin toxicity?

G-I: anorexia, nausea, vomiting diarrhoea

CNS: visual disturbances, confusion, nightmares, agitation, drowsiness

Cardiac: features of bradycardia (progressing AV block, slow AF) and increased automaticity (VEBS and bigeminy, SVT with AV block, VT/VF)

Needs to recognise GI/CNS/Cardiac, as well as examples of bradycardia and inc. automaticity to pass

What factors might predispose patients towards digoxin toxicity?
Prompt: are there any interactions?

Electrolyte imbalance

Hypokalaemia, hypercalcaemia, hypomagnesaemia

Organ disease

Renal impairment, hypothyroidism, Other drugs

Amiodarone, calcium channel blockers, potassium depleting drugs

Bold (with at least one example of each) to pass



What are the principal effects of adenosine on cardiac conduction?

Inhibits AV nodal conduction

Pass: Bold

Describe the pharmacokinetics of adenosine.

Rapidly metabolised. By red cells and endothelial cells

Very short elimination half-life (seconds)

Pass: Bold

What are the clinical implications of this pharmacokinetic profile?

Therefore must be given by rapid IV bolus. Side effects are short lived. No prolonged action to keep patient out of the arrhythmia. (Proximal IV site as preference).

Pass: Bold

Name some indications and contraindications to its use.

Indication: supraventricular tachycardia; diagnostic Contraindications: AV block, sick sinus, acute asthma, lack of consent

Pass: SVT and 1 CI.


List some drugs used in hypertensive emergencies.

GTN , nifedipine , diazoxide , hydrallazine , nitroprusside , esmolol , labetalol

Pass: At least 3

Tell us about the pharmacokinetics of Na nitroprusside.

IV administration, onset minutes, peak effect minutes,

1/2 life 2 minutes (thiocyanate 3 days), duration of action 1-

10 minutes, elimination-RBC’s to cyanide, liver to thiocyanate, renally excreted

Pass: Drugs 2/4 Bold

What are the potential toxicities of Na nitroprusside?

Cyanide toxicity – hypotension , metabolic acidosis , pink skin , tachypnoea decreased reflexes , dilated pupils , coma

Thiocyanate toxicity – ataxia , blurred vision , headache , nausea , vomiting , tinnitus, SOB, delirium, unconsciousness

Pass: Both bolded categories and 1 example of each.


What are the effects of Ca channel blockers on smooth muscle?
(Prompt: tissue level)

Relax smooth muscle esp vascular smooth muscle

Arterioles more sensitive than veins

Does effect bronchiolar GIT and uterine

Pass: Bold

By what mechanisms do Ca channel blockers control angina?

Decrease myocardial contractility

Decrease oxygen demand

Decrease afterload by relaxing vascular smooth muscle

Verapamil/ diltiazem have a non-specific antiadrenergic effect and decrease heart rate

Relieve and prevent coronary artery spasm

Pass: Bold

Why is verapamil more efficacious than dihydropyridines in the treatment of arrhythmias?

Blockade of L-channels more marked in tissues that fire frequently

More marked effects on tissues that depend on Ca channels for activation, SA & AV nodes

More marked on tissues with tissues less polarised at rest



What is the adrenoreceptor selectivity of noradrenaline?
Prompt: What receptors does it act on?

alpha1 = alpha2; Beta1 >> Beta2

alpha 1: post-synaptic effector cells, especially smooth muscle

alpha 2: presynaptic nerve terminals, platelets, lipocytes, smooth muscle

beta 1: post synaptic effector cells, especially heart, lipocytes, brain

Pass: All 3 bold

Describe the cardiovascular effects of infused noradrenaline.

Increases peripheral vascular resistance

Increases SBP and DBP

Little chronotropy

Positive inotropy

Pass: 2 of 3 bolded


What are the mechanisms of action of FRUSEMIDE?

inhibits NKCC2 = a luminal Na+/K+/2Cl co-transporter of thick ascending limb of Loop of Henle

=> decreased reabsorption of NaCl

=> diuresis

increased prostaglandin synthesis

=> a)      inhibition of salt transport in thick ascending limb

=> b)     increased renal blood flow, decreased pulmonary congestion, decreased LV filling pressures

Pass: Bold

What are the toxic effects of FRUSEMIDE?

•             decreased K metabolic alkalosis

•             ototoxicity

•             hyperuricaemia

•             hypomagnesaemia

•             Allergy – rash, eosinophilia, interstitial nephritis

•             dehydration

•             hyponatraemia

4+ to pass – must include decr K & one non-electrolyte


Describe the pharmacokinetics of metoprolol.

PROMPT – What is its bioavailability and why?

  • Oral or IV
  • Volume of distribution – large
  • Half life – 3-4 hours
  • Metabolised in liver
  • Bioavailability 50% due to 1st pass effect

Pass Criteria:

  • Oral & IV & 1st pass
  • OR 3/5

How does metoprolol differ from propanolol in its action at beta receptors?

  • Beta 1 – full agonist
  • Beta 2 – 50-100 fold less potent

Pass Criteria:

  • Beta 1 selective

How do Beta blockers control hypertension?

  • Negative inotropic and chronotropic effects
  • Slow AV node conduction
  • Anatagonises release of renin/not fully understood

Pass Criteria:

  • Negative inotropic & chronotropic effect


How does heparin act?

  • Heparin binds endogenous antithrombin and enhances its activity.
  • Antithrombin inhibits factors IIa, IXa and Xa by complexing with them and inducing a conformational change.

Pass Criteria:

  • Bold to pass

How may heparin be administered?

  • IV vs SC
  • Continuously (following bolus) vs intermittent
  • Therapeutic vs prophylactically

Pass Criteria:

  • Bold to pass

What are the potential adverse effects of heparin?

  • Bleeding
  • Allergy
  • Alopecia
  • Osteoporosis
  • Heparin-induced thrombocytopaenia 
  • Mineralocorticoid deficiency

Pass Criteria:

  • Bold +1 to pass

What are the advantages of low molecular weight heparins compared to unfractionated heparin?

  • Have equal efficacy
  • Increased SC bioavailability
  • Require less frequent dosing
  • Less monitoring
  • Shorter chain heparin with less effect on thrombin (IIa)

Pass Criteria:

  • Demonstrates understanding

Questions 31 to 40
              GO ON TO
Questions 51 to 60