Calcium-channel blockers, also known as calcium antagonists, stop calcium from entering cells through the L-type calcium channel. This causes vascular smooth muscle in vessel walls to relax, resulting in a decrease in peripheral vascular resistance.
They can be used for a variety of things, including:
Hypertension
Angina
Atrial fibrillation
Migraine

Calcium-channel blockers can be divided into two categories: dihydropyridines and non-dihydropyridines. The basic chemical structure of these two classes differs, as does their relative selectivity for cardiac versus vascular L-type calcium channels.

Dihydropyridines have a high vascular selectivity and lower systemic vascular resistance and blood pressure. As a result, they’re frequently used to treat hypertension. Modified release formulations are also used to treat angina, but their powerful systemic vasodilator and pressure-lowering effects can cause reflex cardiac stimulation, resulting in increased inotropy and tachycardia, which can counteract the beneficial effects of reduced afterload on myocardial oxygen demand.

The suffix -dpine distinguishes dihydropyridines from other pyridines. Examples of dihydropyridines that are commonly prescribed include:
Amlodipine
Felodipine
Nifedipine
Nimodipine

The phenylalkylamine class and the benzothiazepine class are two subgroups of non-dihydropyridines.

Phenylalkylamines are less effective as systemic vasodilators because they are relatively selective for the myocardium. This group of drugs lowers myocardial oxygen demand and reverses coronary vasospasm, making them useful in the treatment of angina. They are also occasionally used to treat arrhythmias. A phenylalkylamine calcium-channel blocker like verapamil is an example.

In terms of selectivity for vascular calcium channels, benzothiazepines fall somewhere between dihydropyridines and phenylalkylamines. They can lower arterial pressure without producing the same level of reflex cardiac stimulation as dihydropyridines because they have both cardiac depressant and vasodilator effects. Diltiazem is the only benzothiazepine currently in clinical use.

The purine nucleoside adenosine is used to diagnose and treat paroxysmal supraventricular tachycardia. Adenosine works by stimulating A1-adenosine receptors and opening potassium channels that are sensitive to acetylcholine. This causes the atrioventricular (AV) node’s cell membrane to become hyperpolarized, slowing conduction by inhibiting calcium channels.

Patients who have had a heart transplant are extremely sensitive to the effects of adenosine and should start with a lower dose of 3 mg, then 6 mg, and finally 12 mg. Dipyridamole potentiates the effects of adenosine, so it should be used with caution in patients who are taking it.

The use of adenosine is contraindicated in the following situations:
Asthma
COPD (chronic obstructive pulmonary disease)
Decompensated heart failure 
Long QT syndrome
AV block in the second or third degree
Sinusitis is a condition in which the sinuses become (unless pacemaker fitted)
Hypotension that is severe

It has a half-life of less than 10 seconds and acts quickly within that time frame. The actions last between 10 and 20 seconds.
Because of the short half-life of the drug, any side effects are usually only temporary. These are some of them:
a feeling of impending doom
Flushing of the face
Dyspnoea
Uncomfortable chest
Tastes metallic

Acetazolamide is a non-competitive, reversible inhibitor of carbonic anhydrase found in the cytosol of cells and on the brush border of the proximal convoluted tubule. Bicarbonate and hydrogen ions are converted to carbonic acid by carbonic anhydrase, which then converts carbonic acid to carbon dioxide and water. As a result, acetazolamide reduces the availability of hydrogen ions, causing sodium and bicarbonate ions to accumulate in the renal tubule, resulting in diuresis.
The mechanism of action of the various types of diuretics is summarised below:

1) Loop diuretics, e.g. furosemide, bumetanide
Act on the Na.K.2Cl co-transporters in the ascending loop of Henlé to inhibit sodium, chloride and potassium reabsorption.

2) Thiazide diuretics, e.g. Bendroflumethiazide, hydrochlorothiazide
Act on the Na.Cl co-transporter in the distal convoluted tubule to inhibit sodium and chloride reabsorption.

3) Osmotic diuretics, e.g. mannitol
Increases the osmolality of the glomerular filtrate and tubular fluid, increasing urinary volume by an osmotic effect.

4) Aldosterone antagonists, e.g. spironolactone
Acts in the distal convoluted tubule as a competitive aldosterone antagonist resulting in inhibition of sodium reabsorption and increasing potassium reabsorption.

5) Carbonic anhydrase inhibitors, e.g. acetazolamide
Inhibit the enzyme carbonic anhydrase preventing the conversion of bicarbonate and hydrogen ions into carbonic acid.

Clopidogrel, a thienopyridine derivative, prevents platelet aggregation and cross-linking by the protein fibrin by inhibiting the ADP receptor on platelet cell membranes (inhibits binding of ADP to its platelet receptor (P2Y12 ADP-receptor).

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.

The beta-adrenoceptors in the heart, peripheral vasculature, bronchi, pancreas, and liver are blocked by beta-adrenoceptor blocking drugs (beta blockers).

Beta blockers come in a wide range of strengths, with the choice largely determined by the disease being treated and the patient’s unique circumstances. The intrinsic sympathomimetic activity, lipid solubility, duration of action, and cardioselectivity of beta blockers all differ.

Some beta blockers are lipid (lipophilic) soluble, while others are water soluble (hydrophilic). Drugs that are more lipid-soluble are absorbed faster from the gut, undergo more first-pass metabolism, and are eliminated faster. They’re also more likely to get into the brain and cause central effects like insomnia and nightmares. Propranolol, pindolol, labetalol, and metoprolol are examples of lipid-soluble beta blockers. Beta blockers that are water-soluble are less likely to enter the brain and are more resistant to first-pass metabolism. They are excreted by the kidneys, and in renal impairment, dosage reduction is frequently required. Atenolol, nadolol, celiprolol, and sotalol are examples of water-soluble beta blockers.

Mannitol is the most widely used osmotic diuretic that is most commonly used to reduce cerebral oedema and intracranial pressure.
Mannitol has four FDA approved uses clinically:
1. Reduction of intracranial pressure and brain mass
2. reduce intraocular pressure if this is not achievable by other means
3. promote diuresis for acute renal failure to prevent or treat the oliguric phase before irreversible damage
4. promote diuresis to promote the excretion of toxic substances, materials, and metabolites

It can be used in rhabdomyolysis-induced renal failure, especially in crush injuries. Mannitol reduces osmotic swelling and oedema in the injured muscle cells and helps restore skeletal muscle function.

It is a low molecular weight compound and can be freely filtered at the glomerulus and not reabsorbed. This way increases the osmolality of the glomerular filtrate and tubular fluid, increasing urinary volume by an osmotic effect. It also does not cross the blood-brain barrier (BBB).

Mannitol causes an expansion of the extracellular fluid space, which may worsen congestive cardiac failure. Contraindications to the use of mannitol include:

1. Anuria due to renal disease
2. Acute intracranial bleeding (except during craniotomy)
3. Severe cardiac failure
4. Severe dehydration
5. Severe pulmonary oedema or congestion
6. Known hypersensitivity to mannitol

Amiodarone has a chemical structure that is similar to that of thyroxine and can bind to the nuclear thyroid receptor. It can cause both hypothyroidism and hyperthyroidism, though hypothyroidism is far more common, with 5-10% of patients suffering from it.

Mannitol is the most widely used osmotic diuretic that is most commonly used to reduce cerebral oedema and intracranial pressure.
It is recommended to use mannitol for the reduction of CSF pressure/cerebral oedema in a dose of 0.25-2 g/kg as an intravenous infusion over 30-60 minutes. This can be repeated 1-2 times after 4-8 hours if needed.

Mannitol has several contraindications and some of them are listed below:
1. Anuria due to renal disease
2. Acute intracranial bleeding (except during craniotomy)
3. Severe cardiac failure
4. Severe dehydration
5. Severe pulmonary oedema or congestion
6. Known hypersensitivity to mannitol

Dobutamine is a synthetic isoprenaline derivative that is used to provide inotropic support to patients with low cardiac output caused by septic shock, myocardial infarction, or other cardiac conditions.

Dobutamine is a sympathomimetic drug that stimulates beta-1 adrenergic receptors in the heart to produce its primary effect. As a result, it has inotropic properties that increase cardiac contractility and output. It also has a small amount of alpha1- and beta-2-adrenergic activity.

A summary of the mechanism and effects of different inotropic agents is shown below:
Inotrope
Mechanism
Effects
Adrenaline (epinephrine)
Beta-1 and -2 agonist at increasing doses;
Alpha-agonist at high doses
Increased cardiac output;
Vasoconstriction at higher doses
Noradrenaline (norepinephrine)
Mainly alpha-agonist;
Beta-1 and -2 agonist at increasing doses
Vasoconstriction;
Some increased cardiac output
Dopamine
Dopamine agonist at low doses;
Beta-1 and -2 agonist at increasing doses;
Alpha-agonist at high doses
Increased cardiac output;
Vasoconstriction at higher doses
Dobutamine
Mainly beta-1 agonist
Increased cardiac output