Corneal microdeposits are almost universally present (over 90%) in people who have been taking amiodarone for more than six months, especially at doses above 400 mg/day. Although these deposits usually cause no symptoms, about 10% of patients report seeing a ‘bluish halo.’ This goes away once the treatment is stopped, and it rarely causes vision problems.

Other effects of amiodarone on the eye are much rarer, occurring in only 1-2 percent of patients:
Optic neuropathy is a condition that affects the eyes.
Non-arteritic anterior ischaemic optic neuropathy (N-AION)
Swelling of the optic disc

Overdosing on calcium-channel blockers should always be taken seriously and regarded as potentially fatal. Verapamil and diltiazem are the two most lethal calcium channel blockers in overdose. These work by binding the alpha-1 subunit of L-type calcium channels, preventing calcium from entering the cell. In cardiac myocytes, vascular smooth muscle cells, and islet beta-cells, these channels play an important role.

>10 tablets of verapamil (160 mg or 240 mg immediate or sustained-release capsules) or diltiazem can cause serious toxicity (180 mg, 240 mg or 360 mg immediate or sustained-release capsules)

In children, 1-2 tablets of verapamil or diltiazem (immediate or sustained-release)

Symptoms usually appear within 1-2 hours of ingestion with standard preparations. However, with slow-release preparations, significant toxicity may take 12-16 hours to manifest, with peak effects occurring after 24 hours.

The following are the main clinical features of calcium-channel blocker overdose:
Nausea and vomiting
Hypotension
Bradycardia and first-degree heart block
Myocardial ischaemia and stroke
Renal failure
Pulmonary oedema
Hyperglycaemia

The following are some of the most important bedside investigations to conduct:
Blood glucose
ECG
Arterial blood gas
Other investigations that can be helpful include
Urea & electrolytes
Chest X-ray (pulmonary oedema)
Echocardiography

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. Glyceryl trinitrate
2. Isosorbide dinitrate

The nitrate drugs are metabolized in the following steps:
1. Release Nitrite ions (NO2-), which are then converted to nitric oxide (NO) within cells.
2. NO activates guanylyl cyclase, which causes an increase in the intracellular concentration of cyclic guanosine-monophosphate (cGMP) in vascular smooth muscle cells.
3. Relaxation of vascular smooth muscle.

Although nitrates are potent coronary vasodilators, their principal benefit in the management of angina results from a predominant mechanism of venous dilation:
– Bigger veins hold more blood
– Takes blood away from the left ventricle
– Lowers LVEDV (preload), LA pressure
– Less pulmonary oedema → improved dyspnoea

Flecainide is an antiarrhythmic drug of class Ic that works by blocking the Nav1.5 sodium channel in the heart, prolonging the cardiac action potential and slowing cardiac impulse conduction. It has a significant impact on accessory pathway conduction, particularly retrograde conduction, and significantly reduces ventricular ectopic foci.

Many different arrhythmias can be treated with flecainide, including:
Pre-excitation syndromes (e.g. Wolff-Parkinson-White)
Acute atrial arrhythmias
Ventricular arrhythmias
Chronic neuropathic pain

The use of flecainide is contraindicated in the following situations:
Abnormal left ventricular function
Atrial conduction defects (unless pacing rescue available)
Bundle branch block (unless pacing rescue available)
Distal block (unless pacing rescue available)
Haemodynamically significant valvular heart disease
Heart failure
History of myocardial infarction
Long-standing atrial fibrillation where conversion to sinus rhythm not attempted
Second-degree or greater AV block (unless pacing rescue available)
Sinus node dysfunction (unless pacing rescue available)

Flecainide should only be used in people who don’t have a structural heart problem. The CAST trial found a significant increase in sudden cardiac death and all-cause mortality in patients with an ejection fraction of less than 40% after a myocardial infarction, where it tended to be pro-arrhythmic.

Anti-arrhythmic drugs have a limited and ineffective role in the treatment of atrial flutter. It’s important to keep in mind that flecainide shouldn’t be used by itself to treat atrial flutter. When used alone, there is a risk of inducing 1:1 atrioventricular conduction, which results in an increase in ventricular rate that is paradoxical. As a result, it should be used in conjunction with a beta-blocker or a calcium channel blocker with a rate-limiting effect.

In atrial flutter, ventricular rate control is usually used as a stopgap measure until sinus rhythm can be restored. A beta-blocker (such as bisoprolol), diltiazem, or verapamil can be used to lower the heart rate.

Electrical cardioversion, pharmacological cardioversion, or catheter ablation can all be used to restore sinus rhythm. Cardioversion should not be attempted until the patient has been fully anticoagulated for at least three weeks if the duration of atrial flutter is unknown or has lasted for more than 48 hours. Emergency electrical cardioversion is the treatment of choice when there is an acute presentation with haemodynamic compromise. For the treatment of recurrent atrial flutter, catheter ablation is preferred.

Mannitol is an osmotic diuretic that stops the absorption of water throughout the tubule, thus increasing the osmolality of both glomerular and tubular fluid. It is used to:
1. decrease intraocular pressure in glaucoma
2. decrease intracerebral pressure
3. oliguria.

Furosemide is a loop diuretic that inhibits the Na/K/2Cl transported in the ascending limb of the Loop of Henle.

Bendroflumethiazide is a thiazide diuretic which inhibits the Na/Cl transporter.

Spironolactone is a potassium-sparing diuretic that acts as an aldosterone receptor antagonist.

Acetazolamide is a carbonic anhydrase inhibitor.

In most cases of atrial flutter, ventricular rate control is used as a stopgap measure until sinus rhythm is restored. A beta-blocker (e.g. bisoprolol), diltiazem, or verapamil can be used to reduce the rate of contractions in the heart.
Electrical cardioversion, pharmacological cardioversion, and catheter ablation can all be used to return the heart to a normal rhythm. Cardioversion should not be attempted until the patient has been fully anticoagulated for at least three weeks if the duration of atrial flutter is unknown or it has lasted longer than 48 hours. Emergency electrical cardioversion is the treatment of choice when there is a sudden onset of symptoms and haemodynamic compromise. For recurrent atrial flutter, catheter ablation is preferred.

Verapamil is a calcium-channel blocker that is non-dihydropyridine phenylalkylamine and can be used to treat supraventricular arrhythmias. It’s a calcium channel blocker with a high negative inotropic effect that lowers cardiac output, slows the heart rate, and may impair atrioventricular conduction. At high doses, it can cause heart failure, exacerbate conduction disorders, and cause hypotension.

Adults should take 240-480 mg of verapamil in 2-3 divided doses. 5-10 mg IV over 30 seconds is the corresponding intravenous (IV) dose. After an IV injection, the peak effect lasts 3-5 minutes, and the action lasts 10-20 minutes.

Verapamil should not be taken with beta-blockers like atenolol or quinidine because the combination of their negatively inotropic and negatively chronotropic effects can result in severe hypotension, bradycardia, impaired atrioventricular conduction, heart failure (due to impaired cardiac contractility), and sinus arrest.
The use of verapamil is contraindicated in the following situations:
Acute porphyrias are a type of porphyria that occurs suddenly.
Accessory conducting pathways are linked to atrial flutter or fibrillation (e.g. Wolff-Parkinson-White-syndrome)
Bradycardia
Shock caused by the heart
Insufficiency of the heart (with reduced ejection fraction)
Left ventricular function has been significantly harmed in the past (even if controlled by therapy)
Hypotension (blood pressure less than 90 mmHg)
AV block in the second and third degrees
Sinusitis is a condition in which the sinuses become
Sino-atrial occlusion

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.

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

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