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.

A patient suffering from acute ischemic stroke can commonly present with hypertensive emergencies. Thrombolytic therapy is contraindicated in a patient with:
1. Systolic blood pressure greater than 185 mmHg
2. Diastolic blood pressure greater than 110 mmHg

But delaying thrombolytic therapy is associated with increased morbidity in patients with acute ischemic stroke.

Managing high blood pressure in acute ischemic stroke requires a slower and more controlled reduction in BP. In the presence of an ischaemic stroke, rapid reduction of MAP can compromise blood flow, causing further ischemia and worsening of the neurological deficit.

Intravenous labetalol is the agent of choice. The dose is 10 mg IV over 1-2 minutes. This dose can be repeated, or an infusion can be set up that runs at 2-8 mg/minute. Thrombolysis can be performed once the blood pressure is brought down to less than 180/105 mmHg.

A nitrate infusion (for example, Isoket) can be used as an alternative in patients with contraindications to the use of beta-blockers (e.g., asthma, heart block, cardiac failure).

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.

It is infused intravenously after being diluted to a volume of at least 50 ml in a suitable crystalloid solution. The dose is titrated to response and ranges from 0.5 to 40 g/kg/min. Extravasation-induced skin necrosis is uncommon, and dobutamine can be administered through a peripheral line.

At doses below 10 g/kg/min, side effects are rare, but at higher doses, they can include:
Nausea and vomiting
Tachycardia
Dysrhythmias
Angina
Hypertension
Headache

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

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.

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.

Hypoperfusion, renal failure, and the oligohydramnios sequence are all linked to ACE inhibitor use in the second and third trimesters.

The oligohydramnios sequence refers to a foetus’ or neonate’s atypical physical appearance as a result of oligohydramnios in the uterus. It’s also linked to aortic arch obstructive malformations and patent ductus arteriosus.

The inhibitory effects on the renin-angiotensin-aldosterone system appear to be the cause of these defects. To avoid these risks, ACE inhibitors should be stopped before the second trimester.

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).

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

End-organ damage (e.g. encephalopathy, intracranial haemorrhage, acute myocardial infarction or ischaemia, dissection, pulmonary oedema, nephropathy, eclampsia, papilledema, and/or angiopathic haemolytic anaemia) characterises a hypertensive emergency (also known as ‘accelerated hypertension’ or malignant hypertension’ It’s a life-threatening condition that necessitates rapid blood pressure reduction to avoid end-organ damage and a negative outcome.

Hypertensive encephalopathy is a syndrome that includes headaches, seizures, visual changes, and other neurologic symptoms in people who have high blood pressure. It is reversible if treated quickly, but it can progress to coma and death if not treated properly.

Any patient with suspected hypertensive encephalopathy should have an urgent CT scan to rule out an intracranial haemorrhage, as rapid blood pressure reduction could be dangerous in these circumstances.

The drug of choice is labetalol, which reduces blood pressure steadily and consistently without compromising cerebral blood flow.
An initial reduction of approximately 25% in mean arterial pressure (MAP) over an hour should be aimed for, followed by a further controlled MAP reduction over the next 24 hours. In patients who are unable to take beta-blockers, nicardipine can be used as a substitute.

Many medications, including warfarin, require cytochrome P450 enzymes for their metabolism. When co-prescribing cytochrome p450 enzyme inducers and inhibitors with warfarin, it’s critical to be cautious.

Inhibitors of the cytochrome p450 enzyme potentiate the effects of warfarin, resulting in a higher INR. To remember the most commonly encountered cytochrome p450 enzyme inhibitors, use the mnemonic O DEVICES:

O– Omeprazole
D– Disulfiram
E– Erythromycin (And other macrolide antibiotics)
V– Valproate (sodium valproate)
I– Isoniazid
C– Ciprofloxacin
E– Ethanol (acute ingestion)
S- Sulphonamides

Amiodarone is an anti-arrhythmic medication that can be used to treat both ventricular and atrial arrhythmias.

The use of amiodarone is contraindicated in the following situations:
Conduction disturbances that are severe (unless pacemaker fitted)
Sinus node disease is a condition that affects the lymph nodes in (unless pacemaker fitted)
Sensitivity to iodine
Blockage of the Sino-atrial heart valve (except in cardiac arrest)
Bradycardia in the sinuses (except in cardiac arrest)
Thyroid disorders

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.

Nitrates are used in the treatment of angina pectoris and the prevention of myocardial ischaemia. Commonly used examples of nitrates are glyceryl trinitrate and isosorbide dinitrate. Unwanted effects, however, are common and can limit therapy, particularly when angina is severe or when patients are unusually sensitive to the effects of nitrates.

The following are common or very common side effects of nitrates:

• Arrhythmias
• Asthenia
• Cerebral ischaemia
• Dizziness
• Drowsiness
• Flushing
• Headache
• Hypotension
• Nausea and vomiting
• Diarrhoea, syncope and cyanosis can occur, but these are rare side effects.

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

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.

Digoxin is excreted through the kidneys, and impaired renal function can lead to elevated digoxin levels and toxicity.
The patient’s digoxin dose should be reduced in this case, and their digoxin level and electrolytes should be closely monitored.

Propranolol, like other non-selective beta-blockers, is contraindicated in patients with asthma. These drugs can cause acute bronchospasm, therefore worsening symptoms, especially in high doses. However, there has been some recent evidence that long-term use of selective beta-blockers in mild or moderate asthma patients can be safe.

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.

Dopamine is a catecholamine that occurs naturally and is used to treat low cardiac output, septic shock, and renal failure. It is both adrenaline and noradrenaline’s immediate precursor.

Dopamine acts on D1 and D2 dopamine receptors in the renal, mesenteric, and coronary beds at low doses (1-5 g/kg/min). Dopamine causes a significant decrease in renal vascular resistance and an increase in renal blood flow at these doses. Within this dose range, it is also involved in central modulation of behaviour and movement.

Dopamine stimulates beta- and alpha-adrenergic receptors directly and indirectly at higher doses. Beta-stimulation predominates at a rate of 5-10 g/kg/min, resulting in a positive inotropic effect that increases cardiac output and coronary blood flow. Alpha-stimulation predominates at infusion rates greater than 15 g/kg/min, resulting in peripheral vasoconstriction and an increase in venous return and systolic blood pressure.

Below is a summary of the mechanisms and effects of various inotropic agents:
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