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.

An ambulatory blood pressure reading of >150/95 is classified as stage 2 hypertension, according to the NICE care pathway for hypertension, and the patient should be treated with an antihypertensive drug.

A calcium-channel blocker, such as amlodipine, would be the most appropriate medication for a 59-year-old Caucasian man.

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.

The standard ABC approach should be used to resuscitate all patients as needed. If life-threatening toxicity is expected, intubation and ventilation should be considered early on. If hypotension and shock are developing, early invasive blood pressure monitoring is recommended.

The primary goal of specific treatments is to support the cardiovascular system. These are some of them:

1. Fluid resuscitation: Give up to 20 mL of crystalloid per kilogramme of body weight.

2. Calcium supplementation
This can be a good way to raise blood pressure and heart rate temporarily.
via central venous access: 10% calcium gluconate 60 mL IV (0.6-1.0 mL/kg in children) or 10% calcium chloride 20 mL IV (0.2 mL/kg in children)
Boluses can be given up to three times in a row.
To keep serum calcium >2.0 mEq/L, consider a calcium infusion.

3. Atropine: 0.6 mg every 2 minutes up to 1.8 mg is an option, but it is often ineffective.

4. HIET (high-dose insulin-euglycemic therapy):
The role of HIET in the step-by-step management of cardiovascular toxicity has changed.

5. Vasoactive infusions:
This was once thought to be a last-ditch measure, but it is now widely recommended that it be used sooner rather than later.
Insulin with a short half-life 50 mL of 50 percent glucose IV bolus plus 1 U/kg bolus (unless marked hyperglycaemia present)
Short-acting insulin/dextrose infusions should be continued.
Glucose should be checked every 20 minutes for the first hour, then hourly after that.
Regularly check potassium levels and replace if they fall below 2.5 mmol/L.
Titrate catecholamines to effect (inotropy and chronotropy); options include dopamine, adrenaline, and/or noradrenaline infusions.

6. Sodium bicarbonate: Use 50-100 mEq sodium bicarbonate (0.5-1.0 mEq/kg in children) in cases where a severe metabolic acidosis develops.

7. Cardiac pacing: It can be difficult to achieve electrical capture, and it may not improve overall perfusion.
Bypass AV blockade with ventricular pacing, which is usually done at a rate of less than 60 beats per minute.

8. Intralipid transport
Calcium channel blockers are lipid-soluble agents, so they should be used in refractory cases.

Adrenaline (epinephrine) is a sympathomimetic amine that binds to alpha- and beta-adrenergic receptors and acts as an agonist. It is active at both alpha and beta receptors in roughly equal amounts.

When taken orally, it becomes inactive. Subcutaneous absorption is slower than intramuscular absorption. In cardiac arrest, it is well absorbed from the tracheal mucosa and can be given through an endotracheal tube.

At the adrenergic synapse, catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) metabolise it primarily. The inactive products are then passed through the kidneys and excreted in the urine.

In adult cardiac arrest, the IV dose is 1 mg, which is equal to 10 ml of 1:10000 or 1 ml of 1:1000. In anaphylaxis, the IM dose is 0.5 ml of 1:1000. (500 mcg).

In open-angle glaucoma, adrenaline causes mydriasis and lowers pressure.

Adrenaline is used in cardiopulmonary resuscitation, the treatment of severe croup, and the emergency management of acute allergic and anaphylactic reactions (as a nebuliser solution).

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.

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

Side effects to nitrate therapy are common especially
The most common side effects are:
1. Headaches
2. Feeling dizzy, weak, or tired
3. Nausea
4. Flushing

The serious but less likely to occur side effects are:
1. Methemoglobinemia (rare)
2. Syncope
3. Prolonged bleeding time
4. Exfoliative dermatitis
5. Unstable angina
6. Rebound hypertension
7. Thrombocytopenia

Dry eyes, bradycardia, and metabolic acidosis have not been reported.

The use of a beta-blocker at the same time increases the risk of myocardial depression, but it is not a contraindication.
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

An antidote for digoxin overdose is digoxin-specific antibody (Digifab). It’s a lyophilized preparation of digoxin-immune ovine Fab immunoglobulin fragments that’s sterile, purified, and lyophilized. These fragments were extracted from the blood of healthy sheep that had been immunised with a digoxin derivative called digoxin-dicarboxymethoxylamine (DDMA), a digoxin analogue that contains the functionally important cyclopentaperhydrophenanthrene:lactone ring moiety coupled to keyhole limpet hemocyanin (KLH).

Digifab has a higher affinity for digoxin than digoxin does for its sodium pump receptor, which is thought to be the site of its therapeutic and toxic effects. When given to a patient who is intoxicated, Digifab binds to digoxin molecules, lowering free digoxin levels and shifting the equilibrium away from binding to receptors, reducing cardio-toxic effects. The kidney and reticuloendothelial system then clear the Fab-digoxin complexes.

The following summarises the indications for Digifab in acute and chronic digoxin toxicity:
Acute digoxin toxicity
Chronic digoxin toxicity
Cardiac arrest
Life-threatening arrhythmia
Potassium level > 5 mmol/l
>10 mg digoxin ingested (adult)
>4 mg digoxin ingested (child)
Digoxin level > 12 ng/ml
Cardiac arrest
Life-threatening arrhythmia
Significant gastrointestinal symptoms
Symptoms of digoxin toxicity

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.

Angiotensin-converting enzyme (ACE) inhibitors prevent angiotensin I from being converted to angiotensin II. Angiotensin II has a variety of effects:
Sympathetic activity has increased.
Vasoconstriction in the arteries
Secretion of Vasopressin
Secretion of aldosterone

The increase in systemic blood pressure is caused by arteriolar vasoconstriction. Vasopressin stimulates water reabsorption in the kidneys as well as the thirst sensation. In the distal convoluted tubules and collecting ducts, aldosterone causes the reabsorption of sodium and water from the urine in exchange for potassium secretion. As a result, ACE inhibitors lower systemic blood pressure while also causing hyperkalaemia.

Angiotensin-converting enzyme inhibitors (ACE inhibitors) are used in a variety of clinical settings, including heart failure. According to a meta-analysis, ACE inhibitors reduce death, MI, and overall admission in patients with heart failure by 28%.
ACE inhibitors are also used in the following clinical settings:
Hypertension
Chronic kidney disease
Diabetic nephropathy 
Following a myocardial infarction

In the presence of renal artery stenosis, ACE inhibitors are contraindicated because they can cause or exacerbate renal failure.
The most common side effect of ACE inhibitors is a dry cough caused by increased bradykinin production. There is, however, no known link to fibrosis of the lungs.