Lidocaine is a tertiary amide local anaesthetic and also a class IV antiarrhythmic.

Like other local anaesthetics, lidocaine works on the voltage-gated sodium ion channel on the nerve cell membranes. It works in the following steps:
1. diffuses through neural sheaths and the axonal membrane into the axoplasm
2. binds fast voltage-gated Na+ channels in the neuronal cell membrane and inactivates them
3. With sufficient blockage, the membrane of the postsynaptic neuron will not depolarise and will be unable to transmit an action potential, thereby preventing the transmission of pain signals

The same principle applies to Lidocaine’s actions in the heart as it blocks the sodium channels in the conduction system and the myocardium. This raises the threshold for depolarizing, making it less likely for the heart to initiate or conduct any action potential that can cause arrhythmia.

Angina pectoris is the most common symptom of ischemic heart disease and presents with chest pain relieved by rest and nitro-glycerine.

Nitrates are the first-line treatment to relieve chest pain caused by angina. The commonly used nitrates are:
1. Nitro-glycerine (NTG) – angina pectoris (treatment/prophylaxis), acute coronary syndrome, heart failure, hypertension
2. Isosorbide mononitrate (ISMN) – chronic angina pectoris (treatment)
3. Isosorbide dinitrate (ISDN) – angina pectoris (treatment/prophylaxis)

The nitrate drugs cause vasodilation via the action of nitric oxide.

The contraindications to the use of nitrate are the following:
1. Allergy to nitrates
2. Concomitant use of phosphodiesterases (PDE) inhibitors such as tadalafil and sildenafil
3. Right ventricular infarction
4. Hypertrophic cardiomyopathy
5. Cardiac tamponade
6. Constrictive pericarditis
7. Hypotensive conditions
8. Hypovolaemia
9. Marked anaemia
10. Mitral stenosis
11. Raised intracranial pressure due to cerebral haemorrhage or head trauma
12. Toxic pulmonary oedema

A study published in the Cochrane Database of Systematic Reviews in 2010 found that a single 1000-mg dose of aspirin is effective in treating acute migraine. It was discovered that 24 percent of aspirin users were pain-free after two hours, compared to 11 percent of placebo users. Because the BNF recommends a maximum dose of 900 mg for analgesia and most non-proprietary aspirin comes in a dose of 300 mg, a dose of 900 mg is frequently prescribed in the UK.

Because aspirin is not recommended for children under the age of 16 due to the risk of Reye’s syndrome, it would be inappropriate to give it to the 12-year-old with the viral URTI.

For uncomplicated dental pain, aspirin is an acceptable option, but not for patients who are taking warfarin. The combination of aspirin’s antiplatelet action and warfarin’s anticoagulation properties puts the patient at high risk of bleeding. Furthermore, aspirin can deplete the therapeutic levels of warfarin by displacing it from plasma proteins. It would be better to use another NSAID or analgesic.

In gout, aspirin should be avoided because it reduces urate clearance in the urine and interferes with the action of uricosuric agents. Naproxen, diclofenac, and indomethacin are better options.

Although aspirin is useful for inflammatory pains, the dose of aspirin required for an adequate analgesic effect in severe pain is associated with significant side effects. Naproxen would be a better first-line treatment option.

At muscarinic receptors, atropine blocks the action of the parasympathetic neurotransmitter acetylcholine. As a result, it inhibits the vagus nerve’s effects on both the SA and AV nodes, increasing sinus automaticity and facilitating AV node conduction.

At muscarinic receptors, atropine blocks the action of the parasympathetic neurotransmitter acetylcholine. As a result, it inhibits the vagus nerve’s effects on both the SA and AV nodes, increasing sinus automaticity and facilitating AV node conduction.

The most common cause of asystole during cardiac arrest is primary myocardial pathology, not excessive vagal tone, and there is no evidence that atropine is helpful in the treatment of asystole or PEA. As a result, it is no longer included in the ALS algorithm’s non-shockable section. Atropine is most commonly used in the peri-arrest period. It is used to treat bradycardia (sinus, atrial, or nodal) or AV block when the patient’s haemodynamic condition is compromised by the bradycardia.

If any of the following adverse features are present, the ALS bradycardia algorithm recommends a dose of 500 mcg IV:
Shock
Syncope
Myocardial ischaemia
Heart failure

Atropine is also used for the following purposes:
Topically as a cycloplegic and mydriatic to the eyes
To cut down on secretions (e.g. in anaesthesia)
Organophosphate poisoning is treated with
Atropine’s side effects are dose-dependent and include:
Mouth is parched
Vomiting and nausea
Vision is hazy
Retention of urine
Tachyarrhythmias
It can also cause severe confusion and hallucinations in patients, especially the elderly.

Paroxysmal supraventricular tachycardia is an intermittent tachycardia (HR > 100 bpm) and has the following characteristics:
1. Sudden onset/offset (Contrast with sinus tachycardia)
2. Electrical activity originates above the ventricle (Contrast with ventricular tachycardia)
3. Produces narrow QRS complex (<120ms) The most common cause of PSVT is Atrioventricular nodal re-entrant tachycardia (AVNRT), most common in young women with a mean age onset of 32 years old. There are recurrent episodes of palpitations, and most of the episodes spontaneously. Sometimes, some vagal manoeuvres are required:
1. Valsalva manoeuvre
2. immersing the face in ice-cold water
3. carotid sinus massage.

If PSVT keeps persisting or is causing severe symptoms, the treatment of choice is intravenous adenosine. The patient’s ECG should be continuously monitored throughout the treatment.

The recommended doses in adults are as follows:
– Initial dose of adenosine is 6 mg by rapid IV bolus
– If unsuccessful, give another dose of adenosine 12 mg by rapid IV bolus
– If unsuccessful, give a further dose of adenosine 12 mg by rapid IV bolus
The latest ALS guidelines advocate 18 mg for the third dose, whereas the BNF/NICE guidelines advocate 12 mg.

If adenosine fails or is contraindicated, intravenous verapamil can be used as an alternative, but it should be avoided in patients recently treated with beta-blockers.

Synchronized electrical cardioversion will be necessary with signs of hemodynamic instability or if drug treatment has failed to restore sinus rhythm.
Recurrent episodes of paroxysmal supraventricular tachycardia can be treated by catheter ablation or prevented with drugs such as flecainide, sotalol, diltiazem, or verapamil.

Abciximab (ReoPro) is a glycoprotein IIb/IIIa receptor antagonist that is a chimeric monoclonal antibody. It is primarily used during and after coronary artery procedures such as angioplasty to inhibit platelet aggregation.

The use of abciximab is contraindicated in the following situations:
Internal bleeding is present.
Within the last two months, you’ve had major surgery, intracranial surgery, or trauma.
Stroke in the previous two years
Intracranial tumour
Aneurysm or arteriovenous malformation
Haemorrhagic diathesis is a type of haemorrhagic diathesis.
Vasculitis
Retinopathy caused by hypertension

Enoxaparin is a low molecular weight heparin (LMWH) that works in the same way as heparin by binding to and activating the enzyme inhibitor antithrombin III. Antithrombin III inactivates thrombin by forming a 1:1 complex with it. Factor Xa and a few other clotting proteases are also inhibited by the heparin-antithrombin III complex.

Atropine is used to treat bradycardia (sinus, atrial, or nodal) or AV block when the patient’s haemodynamic condition is compromised by the bradycardia.

If any of the following adverse features are present, the ALS bradycardia algorithm recommends a dose of atropine 500 mcg IV:
Shock
Syncope
Myocardial ischemia
Insufficiency of the heart

If this does not work, give additional 500 mcg doses at 3-5 minute intervals until a maximum dose of 3 mg is reached. The heart rate can be slowed paradoxically if the dose is higher than 3 mg.

The ALS bradycardia algorithm also suggests the following interim measures:
Transcutaneous pacing
Isoprenaline infusion 5 mcg/min
Adrenaline infusion 2-10 mcg/minutes
Alternative drugs (aminophylline, dopamine, glucagon, glycopyrrolate)

Abciximab (ReoPro) is a glycoprotein IIb/IIIa receptor antagonist that is a chimeric monoclonal antibody. It is primarily used during and after coronary artery procedures such as angioplasty to inhibit platelet aggregation.

It’s approved for use as a supplement to heparin and aspirin in high-risk patients undergoing percutaneous transluminal coronary intervention to prevent ischaemic complications. Only one dose of abciximab should be given (to avoid additional risk of thrombocytopenia).

Before using, it is recommended that baseline prothrombin time, activated clotting time, activated partial thromboplastin time, platelet count, haemoglobin, and haematocrit be measured. 12 and 24 hours after starting treatment, haemoglobin and haematocrit should be measured again, as should platelet count 2-4 hours and 24 hours after starting treatment.
When used for high-risk patients undergoing angioplasty, the EPIC trial(link is external)found that abciximab reduced the risk of death, myocardial infarction, repeat angioplasty, bypass surgery, and balloon pump insertion.

The use of abciximab is contraindicated in the following situations:
Internal bleeding is present.
Within the last two months, you’ve had major surgery, intracranial surgery, or trauma.
Stroke in the previous two years
Intracranial tumour
Aneurysm or arteriovenous malformation
Haemorrhagic diathesis is a type of haemorrhagic diathesis.
Vasculitis
Retinopathy caused by hypertension

The following are some of the most common abciximab side effects:
Manifestations of bleeding
Bradycardia
Back ache
Pain in the chest
Vomiting and nausea
Pain at the puncture site
Thrombocytopenia

Bumetanide is a loop diuretic that inhibits sodium, chloride, and potassium reabsorption by acting on the Na.K.2Cl co-transporter in the ascending loop of Henlé. This reduces the osmotic gradient that forces water out of the collecting duct system and prevents the formation of a hypertonic renal medulla. This has a strong diuretic effect on the body.

It’s primarily used in patients with heart failure who aren’t responding to high doses of furosemide. Bumetanide and furosemide differ primarily in terms of bioavailability and pharmacodynamic potency.

In the intestine, furosemide is only partially absorbed, with a bioavailability of 40-50 percent. Bumetanide, on the other hand, is almost completely absorbed in the intestine and has a bioavailability of about 80%. Bumetanide is 40 times more potent than furosemide, and one milligram is roughly equivalent to 40 milligrams of furosemide.

Bumetanide also lowers the concentration of neuronal chloride, making GABA’s action more depolarizing. In the neonatal period, it is being studied as an antiepileptic.