Med School Hub List Emergency Drugs

Emergency Drugs

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Here I have listed a set of drugs that are being used in emergency situations. Some of these drugs may have been replaced by more recent and effective drugs in developed countries, but most are still been used in hospital settings.

What is an Emergency Drug?

Emergency drug means a drug required to meet the immediate therapeutic needs of patients that is not available from any other authorized source in sufficient time to prevent risk of harm to patients because of delay (lawinsider.com)

As medical health professionals, we are expected to memorize thousands of drugs, their actions and dosage. Unless you have a knack for memorizing hundreds of confusing and tongue twisting names, you may find it exhausting to prepare for a pharmacology exam. Fortunately, we only have to go through this burden during our medical student years, after which we have the liberty to google anything we simply can’t be bothered to remember.

Drugs for cardiac arrhythmia

When we keep a stethoscope near our heart, we can hear the sounds ‘lub’ and ‘dub’; these are what we call as heart sounds. In a healthy person, the heart should beat at a rate of 60-100 beats per minute; in trained athletes, this may be lower.

An abnormality in the cardiac rhythm is known as cardiac arrhythmias. These patients typically present with chest pains, dizziness or palpitations and sometimes no symptoms at all. When the heart rate has decreased, we call it as bradycardia; when it has increased we call it as tachycardia.

Antiarrhythmic drugs have not been shown to prolong life. The type of antiarrhythmic therapy depends mainly on the patients’ safety among other factors.

Amidarone

This is the most powerful antiarrhythmic drug available for the treatment and prevention of both atrial and ventricular arrhythmias. It is classified under class III of Vaughan-Williams classification of antiarrhythmic drugs. It prolongs the effective refractory period of myocardial cells, the AV node and anomalous pathway (due to potassium channel blockade).

Due to its powerful effect, it can result in serious toxicity even in short term use. Amidarone contains iodine so both hyperthyroidism and hypothyroidism are commonly seen among patients on this drug.

Dosage and administration – 5 mg/kg in 100 cc of 5% dextrose IV over 60 minutes (max dose 1.2 g/day) with ECG monitoring.

Verapamil

This has marked negative myocardial inotropic (contractility) and chronotropic (rate) actions. It is classified under class IV of Vaughan-Williams classification of antiarrhythmic drugs. It prolongs conduction and refractoriness in the AV node and depress the rate of discharge of the SA node (due to calcium channel blockade).

If adenosine is not available, this is a safe alternative for terminating narrow complex paroxysmal supraventricular tachycardia. Verapamil should not be given to patients with bradycardia, second or third degree heart block, or patients with Wolf-Parkinson-White syndrome to relieve atrial flutter or fibrillation. Dosage and administration – 5-10 mg of slow IV over 2 minutes.

Adenosine

Adenosine slows AV conduction and dilates coronary and peripheral arteries. It has a very brief plasma half-life (<2s) so it must be given rapidly intravenously. It is effective for terminating paroxysmal supraventricular tachycardia, including episodes in patients with Wolf-Parkinson-White syndrome. It is a safer option to treat supraventricular tachycardia than verapamil, since it is short acting and not negatively inotropic.

Adenosine should not be given to asthmatics or patients with second or third degree AV block or sick sinus syndrome (unless a pacemaker is in place).

Dosage and administration – 3 mg over 2 seconds into a central or large peripheral vein with cardiac monitoring. Can repeat with 6 mg after 1-2 minutes and 12 mg after another 1-2 minutes.

Digoxin

Digoxin is a cardiac glycoside which affect the heart both directly and indirectly. Its direct effect is to inhibit the Na+/K+ ATPase pump and raise the intracellular Ca2+ thus increasing cardiac muscle contractility. Its indirect effect is to enhance vagal activity which results in lower heart rate and conduction velocity.

This is not strictly an antiarrhythmic drug. It helps to modulate the response to arrhythmias. It is mainly used for atrial fibrillation, atrial flutter, and heart failure.

Dosage and administration – in AF: 0.75-1 mg over 2 hours in 100 ml of 0.9% saline.

Catecholamines

Adrenaline, noradrenaline and dopamine fall under this group. They are synthesized in the body. The pathway is; Tyrosine à dopa à dopamineà noradrenaline à adrenaline. They act on α and β receptors.

The above when given as a drug can mimic the action of the sympathetic nerves, hence the name sympathomimetic was given. The overall effects of sympathomimetic depends on the site of action (receptor agonist or indirect action), on receptor specificity and on dose; for example, adrenaline normally dilates muscle blood vessels (β2 effect) but in very large doses can cause them to constrict. The end results are often complex and unpredictable.

Sympathomimetic drugs can have adverse effects such as tissue necrosis due to intense vasoconstriction (α), or effects on heart (β1) such as tachycardia, palpitations and cardiac arrhythmias. Therefore, these drugs should be used with extreme caution on patients with heart diseases.

Adrenaline/epinephrine

Adrenaline can be used in many instances. It is used as a vasoconstrictor with local anesthetics to prolong their effects. It can also be used as a topical mydriatic during eye examinations. It’s used as a topical agent for epistaxis (nosebleed) as it stops the hemorrhage by local vasoconstriction. It’s also very important in anaphylactic shock.

Dosage and administration –

In CPR: 10 ml 1:10000 IV (dilute 1 vial in 10 ml of 0.9% saline flush with 20 ml of 0.9% saline. Can be repeated every 3-5 minutes) 1 vial = 1 mg

In anaphylactic shock: 500 µg IM (intramuscular), can be repeated every 5 minutes. (1/2 vial = 1:1000, without diluting)

Noradrenaline/norepinephrine

Its main effect is to raise the blood pressure by constricting the arterioles and so increasing the peripheral resistance. Though it has some effect on the heart (tachycardia), this is masked by the more profound reflex bradycardia caused by hypertension.

Dosage and administration – 0.1-1 µg/kg/min IV infusion titrated on BP

Dopamine

Dopamine activates different receptors depending on the dose used. Low doses activates dopamine receptors in the CNS and the renal and other vascular beds. When the dose is increased, it stimulates the β1 receptors in the heart. At high doses it activates α adrenoceptors and cause vasoconstriction. Levodopa is the precursor to dopamine that is used in the treatment of Parkinson’s disease.

Dosage and administration – 2-5 µg/kg/minute IV in 100 ml of 0.9% saline in syringe pump. (1 vial = 200 mg) OR 1 vial in 500 cc of 0.9% saline slowly titrated on BP

Dobutamine

It is an agonist for β adrenoceptors with greater inotropic than chronotropic effect on the heart. It has some α agonist effect. It is useful in shock (with dopamine) and in low output heart failure.

Dosage and administration – 2.5-10 µg/kg/minute in 100 ml of 0.9% saline in syringe pump or 1 vial (250mg) in 500 cc 0.9% saline slowly titrated on BP

Salbutamol

Salbutamol is a non-catecholamine that is relatively selective for β2 receptors. You might have come across this name in the puff/inhalers given for asthma patients. It causes bronchodilation by acting on β2 receptors on bronchial smooth muscles and help to alleviate the symptoms of asthma. It is also given as an injection in premature labor to reduce uterine contractions and for cardiac inotropic effect in heart failure.

Dosage and administration –in acute asthma: start with 5 µg/min, adjusted in every 15-30 min according to response and HR. Max 20 µg/in

Some drugs blocks the actions of these receptors by competitively binding with them.

Propranolol

Propranolol is a non-selective β blocker which effectively decreases the sympathetic activity in the body. It reduces the heart rate, blood pressure and cardiac work. Β blockers are given to patients with chest pain (angina pectoris), hypertension, and cardiac tachyarrhythmia’s. As an emergency drug, it is used after a heart attack to improve the chance of survival. It is also used in the treatment of endocrine disorders such as hyperthyroidism and phaeochromocytoma.

Dosage and administration – 1 mg over 1 minute (max 10 mg)

Atropine

Atropine is an antimuscarinic drug which act principally on postganglionic cholinergic nerve endings. It is an alkaloid from the deadly nightshade, Atropa belladonna, which was used as a homicidal poison many years ago.

Antimuscarinic drugs competitively prevent acetyl choline from binding to muscarinic receptors. Atropine can act on both peripheral and CNS receptors and essentially reduce the parasympathetic and some sympathetic actions in the body.

It is used against tremors and rigidity of Parkinsonism. It prevents or reduces motion sickness. It is used in ophthalmology to dilate the pupil and to paralyze ocular accommodation (you can’t read or drive for 3-4 hours). It is also useful in bradycardia following myocardial infarction.

Disadvantages include glaucoma and urinary retention when the prostate is enlarged.

Dosage and administration – In CPR: 3 mg bolus or 0.6 mg IV repeat 5 times

Streptokinase

Streptokinase is a drug that promotes fibrinolysis. It is derived from the microorganism Streptococcus haemolyticus. It is used to break down clots in acute myocardial infarction, deep vein thrombosis and pulmonary embolism, and arterial thromboembolism.

Currently, despite the wide use of tissue plasminogen activator in developed nations, streptokinase is still essential for managing acute MI in developing nations.

Dosage and administration – 1.5 MU in 100 ml of 0.9% saline over 1 hour.

As I mentioned before, memorizing all these emergency drugs is no easy feat but with time and practice, like many other medical professionals before us, it just becomes second-nature; much like learning to drive a vehicle. You just have to put the effort in being a good driver.

References :

Clinical pharmacology (12th edition) – Morris J. Brown

Kumar & Clark’s Clinical Medicine (10th edition)

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