Heparin is a polymer of glycosaminoglycan. It occurs naturally and is found in mast cells. Clinically, it is used in two forms:
1. Unfractionated: widely varying polymer chain lengths
2. Low molecular weight: Smaller polymers only

Heparin works by binding to and activating the enzyme inhibitor antithrombin III. Antithrombin III inactivates thrombin (factor IIa) by forming a 1:1 complex with thrombin. The heparin-antithrombin III complex also inhibits factor Xa and some other proteases involved with clotting. The heparin-ATIII complex can also inactivate IX, XI, XII, and plasmin.

Heparin is not thrombolytic or fibrinolytic. It prevents the progression of existing clots by inhibiting further clotting. The lysis of existing clots relies on endogenous thrombolytics.

Heparin is used for:
1. Prevention and treatment of venous thromboembolism
2. Treatment of disseminated intravascular coagulation
3. Treatment of fat embolism
4. Priming of haemodialysis and cardiopulmonary bypass machines

There is no evidence that heparin is superior to low-molecular-weight heparins in preventing mortality from thrombosis.

Vitamin K is used to reverse the effects of warfarin but not heparin. For heparin, protamine sulphate is used to counteract its effects.

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

Amiodarone has a lot of potential toxic side effects, so it’s important to get a full clinical evaluation before starting treatment with it.

The following are some of the most common amiodarone side effects:

Arrhythmias
Corneal microdeposits
Hepatic disorders
Hyperthyroidism
Hypothyroidism
Hepatic disorders and jaundice
Nausea
Peripheral neuropathy
Respiratory disorders (including lung fibrosis)
Sleep disturbance
Skin reactions
QT prolongation

Amiodarone can cause optic neuritis, which is a very rare side effect. If this happens, the amiodarone should be stopped right away because it poses a risk of blindness.

Most people who take amiodarone develop corneal microdeposits, which go away once the medication is stopped and rarely cause vision problems.

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.

Amlodipine is a calcium-channel blocker that is frequently used to treat hypertension. Ankle swelling is a very common side effect of calcium-channel blockers, and it occurs quite frequently.

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.

Antiarrhythmic drug amiodarone is used to treat both ventricular and atrial arrhythmias. It’s a class III antiarrhythmic that works by prolonging the repolarization phase of the cardiac action potential, where potassium permeability is normally high and calcium permeability is low.

Dronedarone is sometimes used instead of amiodarone in certain situations. Although amiodarone is more effective than dronedarone, dronedarone has fewer side effects.

Grapefruit juice inhibits the metabolism of amiodarone.

The plasma half-life of amiodarone is very long, ranging from 2 weeks to 5 months. The half-life is about 2 months on average.
Because amiodarone is excreted in breast milk, it should be avoided by breastfeeding mothers.

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.

Because digoxin has a narrow therapeutic index, it can cause toxicity both during long-term therapy and after an overdose. Even when the serum digoxin concentration is within the therapeutic range, it can happen.

Acute digoxin toxicity usually manifests itself within 2-4 hours of an overdose, with serum levels peaking around 6 hours after ingestion and life-threatening cardiovascular complications following 8-12 hours.

Chronic digoxin toxicity is most common in the elderly or those with impaired renal function, and it is often caused by a coexisting illness. The clinical signs and symptoms usually appear gradually over days to weeks.

The following are characteristics of digoxin toxicity:
Nausea and vomiting
Diarrhoea
Abdominal pain
Confusion
Tachyarrhythmias or bradyarrhythmias
Xanthopsia (yellow-green vision)
Hyperkalaemia (early sign of significant toxicity)

Some precipitating factors are as follows:
Elderly patients
Renal failure
Myocardial ischaemia
Hypokalaemia
Hypomagnesaemia
Hypercalcaemia
Hypernatraemia
Acidosis
Hypothyroidism
Spironolactone
Amiodarone
Quinidine
Verapamil
Diltiazem

A rapid IV bolus of adenosine is given, followed by a saline flush. The standard adult dose is 6 mg, followed by 12 mg if necessary, and then another 12 mg bolus every 1-2 minutes until an effect is seen.

Patients who have had a heart transplant, on the other hand, 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.

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.