EMERGENCY DRUGS

INTRODUCTION

Emergency drugs are chemical compounds used in patients during life threatening conditions so that
the symptoms can be controlled and the life of a patient can be saved.

For a drug to be useful in emergency, it must have a short onset of action and be administered in such a
way as to facilitate rapid onset of action.

PURPOSE OF EMERGENCY DRUGS

 To provide initial treatment for life threatening illness and injuries.
 To control the symptoms.
 To save the life of the patient.
 To reach the site of action as soon as possible.
 To normalize the vital bodily functions.
 To diverge the patient from the possible risks.

LIST OF DRUGS
 Atropine
 Amiodarone
 Epinephrine
 Norepinephrine
 Lidocaine
 Adenosine
 Dopamine
 Heparin
 Magnesium sulphate
 Calcium gluconate
 Rocuronium bromide
 Sodium bicarbonate
 Potassium chloride
 NERVOUS SYSTEM

SYMPATHETIC NERVOUS SYSTEM PARASYMPATHETIC NERVOUS SYSTEM

(Also known as adrenergic) (Also known as cholinergic )
Dilates pupils Constricts pupils
Relaxes bronchi Stimulate saliva production
Increases HR, BP Constricts bronchi
Inhibits peristalsis &secretion Dilates blood vessel,decreases HR, BP
Stimulates glucose production & release Increases appetite, Stimulates digestion
Diverts blood flow to working muscles Promotes energy storage
Inhibits bladder contraction Bladder contracts

Neurotransmitters: Norepinephrine Neurotransmitter: Acetylcholine

&Epinephrine
 ATROPINE SULFATE

Class: Anticholinergic Agent(Antimuscarinic)

Route: Intravenous
Available form: 0.6mg/ml 1ml ampoule
Dose: 0.5 mg upto maxim 3mg (bradycardia)
Titrate as per respiratory distress (Poisoning)
Half-life: 2-3 hr.
Onset: Rapid.
Note: Administer fast IV push.
Drug of choice for Symptomatic bradycardia and
Organophosphorus poisoning.
Antidote: Physostigmine

INDICATIONS
 Sinus bradycardia: Atropine blocks vagus nerve action and increases heart rate.
 Bronchospasm: Atropine causes muscle relaxation. Also, suppress secretion production.
 Preoperative and preanaesthetic medication: To inhibit secretory functions of glands thereby airway
patency can be maintained.
 Antidote for organophosphate or carbamate poisoning: It causes muscle relaxation by neuro
transmitter blockage.
 Ophthalmic: It causes smooth muscle relaxation thereby produce mydriasis and cycloplegia for
examination of the retina and optic disc and accurate measurement of refractive errors. It produce pupillary
dilation in inflammatory conditions (eg: uveitis).

CONTRAINDICATIONS
 Narrow Angle Glaucoma: Atropine causes ciliary muscle relaxation, which result in incomplete drainage
of aqueous humor.
 Benign Prostatic Hypertrophy(BPH): Atropine causes relaxation of bladder sphincter. It will block
urination so, condition will worsen.
 Thyrotoxicosis: Atropine increases HR and reduces secretion of glands.
 Cardiac Failure, Tachycardia: It blocks vagus nerve action and increases heart rate.
COMMON SIDE EFFECTS
 Cardiovascular: Arrhythmia, flushing, hypotension, palpitation, tachycardia. (due to vagal nerve blockage)
(Flushing is secondary to overheating due to block of sweat gland)
 Central nervous system: Ataxia, coma, delirium, disorientation, dizziness, drowsiness, excitement, fever,
hallucinations, headache, insomnia, nervousness. (hyperthetmia due to hypothalamic regulation of body
temperature is overwhelmed and an uncontrolled increase in body temperature exceeds the body's ability to
lose heat.)
 Dermatologic: Anhidrosis, urticaria, rash, scarlatiniform rash.
 Gastrointestinal: Bloating, constipation, delayed gastric emptying, loss of taste, nausea, paralytic ileus,
vomiting, xerostomia, dry throat, nasal dryness. (muscle movement affected so no persistalsis, gastric
emptying, this all will lead to gastrointestinal problems)
 Genitourinary: Urinary hesitancy, urinary retention. ( due to muscle relaxation , sphincter relaxation)
 Neuromuscular & skeletal: Weakness.
 Ocular: Angle closure glaucoma, blurred vision, cycloplegia, dry eyes, mydriasis, ocular tension increased.
(due to ciliary muscle relaxation blockage aqueous humor increases pressure)
 Respiratory: Dyspnoea, laryngospasm, pulmonary oedema.
 Miscellaneous: Anaphylaxis.

NURSING CONSIDERATIONS

 Observe IV site for signs of extravasation. The pH of atropine is less(acidic). Hence, it may cause cell
damage.
 Rapid IV push.
 Assess for signs of adverse effects, especially pupillary reaction: Due to smooth muscle relaxation
pupillary dilation occurs.
 Continuous monitoring of vital signs and cardiorespiratory functioning before and after administration:
Atropine causes tachycardia, palpitations, temperature variation.
 Monitor fluid balance. Strict I/O charting: Urinary retention may occur due to muscle relaxation and
sphincter relaxation.
 Observe for gastric distension. Assess gastric motility: Atropine causes smooth muscle relaxation.
 Check for any dryness of mucus membrane: Atropine reduces the secretion.
 AMIODARONE HYDROCHLORIDE

Class: Class III antiarrhythmic.

Route: Intravenous
Available form: 50 mg/mL, 3 ml ampoule.
AFib Loading dose: 150 mg/100 ml 5%DW or NS over 10 minutes
(15 mg/min),
Maintenance infusion: following 360 mg over the next 6 hours (1 mg/min).
540 mg over the remaining 18 hours (0.5 mg/min).
VT with pulse: Loading dose: 150 mg direct IV push over 10 minutes during CPR.(IV push)
Pulseless VT: Loading dose: 300 mg direct IV push during CPR.(IV push)
Normal dose: 5mg/Kg.
Half-life: 14-110 days.
Onset: 1-30 minutes.
Note: Administer slowly.
The drug of choice in Ventricular Tachycardia & Atrial Fibrillation .
Amiodarone is incompatible with NS.

INDICATIONS
 Atrial arrhythmias: Atrial Fibrillation with a rapid ventricular response.
 Supraventricular tachyarrhythmias: Atrial
flutter, refractory AV nodal, and AV re-entrant tachycardia.
 Ventricular arrhythmias: Monomorphic VT, Rationale: Amiodarone is an
Non Torsades polymorphic VT and pulseless VF. antiarrhythmic drug. It works
 Pulseless VT that fail to convert even after CPR, primarily by blocking potassium
defibrillation and epinephrine administered. rectifier currents that are responsible
 Hemodynamically unstable patients. for the repolarization of the heart.
 Patients with congestive heart failure.

CONTRAINDICATIONS
 Hypersensitivity
 2nd or 3rd degree AV block, Cardiogenic Shock, Bradycardia, Severe sinus node
dysfunction, Patients with baseline QT prolongation, Hypotension: Increased action potential
duration and a prolonged effective refractory period in cardiac myocytes. So HR reduced, thereby,
cardiac output reduced and arrest occurs.
 Avoid during breastfeeding: It passes through breast milk. Hence newborn HR will be altered.
 Lung disease or other breathing problems: Cardiac output is reduced. This will lead to
decreased blood supply to lungs hence result in breathing problems.
 Thyroid problems: Amiodarone is iodine rich which causes alteration in thyroid function.

SIDE EFFECTS
 Hypotension, AV BLOCK, Congestive Heart Failure, Bradycardia, Cardiogenic Shock:
Increased action potential duration and a prolonged effective refractory period in cardiac myocytes.
So HR reduced , output reduced and arrest occurs. This will result in hypotension.
 Dizziness, lightheadedness
 Neurologic toxicity
 Painful breathing
 Headache
 Sleep disturbances
 Hypothyroidism, Hyperthyroidism, Sensitivity of the skin to sunlight, skin discolouration,
constipation: Amiodarone is iodine rich which causes alteration in thyroid function and
constipation.
 Loss of appetite
 Hepatitis and cirrhosis
 Visual disturbances, Optic neuritis

NURSING CONSIDERATIONS

 Administer slowly except in case of VT with and without pulse.

 Peripheral IV administration of amiodarone can result in phlebitis: Phlebitis is caused by
amiodarone’s acidic pH range. Also, amiodarone can precipitate at the time of administration
resulting in needle-shaped crystals adhering to the vein intima and irritating the delicate
endothelium. This process is known as crystallization.
 Drug interactions and flush the line properly: Amiodarone can slow down the removal of
other medications from your body, which may affect how they work. Examples of affected
drugs include clopidogrel, phenytoin, certain "statin" drugs (atorvastatin, lovastatin), trazodone,
warfarin, among others.Also, it will get precipitate with drug interactions.
 Cardiac monitoring especially, rhythm and hypotension: It is an anti arrhythmic drug.
Hence cardiac measures need to be monitored.
 Assess for drug reactions especially, bradycardia, nausea, vomiting and headache.
 ADRENALINE/ EPINEPHRINE

Class: Sympathomimetic catecholamine, Alpha-adrenergic agonist, Beta adrenergic agonist.

Route: Intravenous
Available form: 1mg/ml.1ml ampoule
Dose: 1mg in 10 ml NS (0.01mg/kg body weight.)
Onset: 1-3minutes. Rapid and short duration of action.
Half life: 2-3 minute
Note: Administer fast.
Drug of choice in anaphylactic shock.
Antidote: Beta blockers( labetalol)

INDICATIONS
 Treatment of allergic reactions: It increases blood flow through to liver. In liver
immunoglobulins are produced. This help in allergy management.
 In restoring cardiac rhythm in cardiac arrest: Epinephrine increases arterial blood pressure and
coronary perfusion during CPR via alpha-1-adrenoceptor agonist effects. In the heart, it increases
the HR and force of contraction, thus increases cardiac output and blood pressure.
 Hemostatic agent: Epinephrine causes constriction in many networks of minute blood vessels.
 Acute asthmatic attack: Epinephrine is a bronchodilator that works by opening breathing
passages to make breathing easier.

CONTRAINDICATIONS
 Narrow angle glaucoma
 Hyperthyroidism
 Organic brain damage: Hypertension leads to haemorrahage.
 Shock (other than anaphylactic shock)
 Ischemic disease, Coronary insufficiency: Adrenaline have chronotropic, inotropic, and
arrhythmogenic properties. Hence HR and oxygen demand increases. This worsens the condition.
 Labor: It inhibits spontaneous or oxytocin induced contraction of uterus. Thus labor is delayed.
 Breast feeding mothers: Adrenaline is excreted through breast milk. Hence tachycardia occurs
for newborn.
SIDE EFFECTS
 Central nervous system: Anxiety, dizziness, nervousness, agitation, headache, Parkinson’s
disease exacerbation.
 Cardiovascular: Arrhythmias, chest pain, hypertension, palpitations, tachycardia, cerebrovascular
accidents, ventricular ectopy, vasospasm, tissue ischemia.
 Dermatologic: Gangrene at the injection site, skin necrosis with extravasation: (vasoconstriction
causes gangrene.)
 Endocrine: Hyperglycemia, hypokalemia, lactic acidosis: (When blood glucose levels drop too
low, the adrenal glands secrete epinephrine, causing the liver to convert stored glycogen to
glucose and release it, raising blood glucose levels.)
 Gastrointestinal: Nausea, vomiting, increase in AST and ALT.
 Neuromuscular: Tremors, weakness.
 Renal: Decreased renal perfusion. (Vasoconstriction leads to reduced renal perfusion- reduce
urine.)
 Respiratory: Dyspnea, pulmonary edema (Tachycardia and increased systemic resistance causes
excess load on left ventricle, causing pulmonary congestion.

NURSING CONSIDERATIONS

 Strict I/O maintenance: Epinephrine causes renal blood vessel constriction and can decrease
urine impairment.
 Administer as IV push.
 Double-check: Epinephrine is a very potent drug; small errors in dosage can cause serious adverse
effects.
 Use minimal doses for minimal periods of time; “epinephrine-fastness” (a form of drug
tolerance) can occur with prolonged use.
 Assess for drug reactions such as pounding heart beat,dizziness, tremors and weakness.
 Protect drug solutions from light, extreme heat, and freezing; do not use precipitated solutions.
 Shake the suspension for injection well before withdrawing the dose.
 Keep a rapidly acting alpha-adrenergic blocker (phentolamine) or a vasodilator (a nitrate) readily
available in case of excessive hypertensive reaction.
 Have an alpha-adrenergic blocker or facilities for intermittent positive pressure breathing readily
available in case pulmonary edema occurs.
 Keep a beta-adrenergic blocker (propranolol, atenolol, should be used in patients with respiratory
distress) readily available in case cardiac arrhythmias occur.
 NORADRENALINE/NOREPINEPHRINE

Class: Vasopressor, Alpha/Beta Adrenergic Agonists.

Route: Intravenous.
Available form: 1mg/ml; 2ml ampoule.
Dose: 4mg in 46 ml NS. (0.05-0.1mcg/kg/min)
Onset: Rapid: 1- 2 minutes.
Half life: 1- 2 minutes.
Note: Administer slowly.
Drug of choice for septic shock.

INDICATIONS
 Cardiac surgery-post operative low cardiac output: Due to inotropic effect it increases
myocardial contractility.
 Hypotension: It causes vasoconstriction which helps to improve BP.
 Circulatory failure resistant to other drug management.

CONTRAINDICATIONS
 Hypertension
 Hypotension from volume deficit: Again noradrenaline will cause vasoconstriction. It leads to
decreased tissue perfusion,urine output, lactate acidosis.
 Blood clot and blockage of blood vessels: Due to vasoconstriction clot will get stuck in major
organs or blood vessel. Which will which will hamper blood supply and thereby tissue necrosis.
 Increase of carbon dioxide in the blood or decreased oxygen in the tissues or blood: As
vasoconstriction occurs, blood supply to tissues will be hampered, which will result in lack of
oxygen to tissue.
SIDE EFFECTS
 Cardiac arrhythmia.
 Renal vascular ischaemia: It causes vasoconstriction in the peripheral vasculature.
 Severe hypertension with possible intracranial hemorrhage: It causes vasoconstriction and
hypertension. Hence chance for intracranial hemorrhage due to hypertension.
 Increases myocardial oxygen consumption: As inotropic activity increases it requires more
oxygen.
 Therapeutic doses may cause hypokalemia.
 Plasma volume depletion.
 NURSING CONSIDERATIONS

 Monitor blood pressure and heart rate: Myocardial contractility will increase more oxygen
consumption and it will cause cardiac arrhythmias.Hence vital parameters need to be monitored.
 Monitor peripheral perfusion: Peripheral vasoconstriction will hamper blood supply to
peripheries.
 Monitor urine output: It causes renal vasoconstriction. Thereby urine output will decrease.
 Do not administer bolus doses, administer slowly: It causes arrhythmias due to sudden inotropic
effect of the drug.
 Monitor for adverse drug effects such as arrhythmias, dyspnoea and confusion.
ADENOSINE

Class: Antidysrhythmics

Route: Intravenous

Available form: 3 mg/ml, 2 ml ampoule.

Dose: Bolus dose: 6 mg IV bolus over 1 to 2 seconds. Maximum dose: 12 mg.

Onset: Rapid, 20-30 sec

Half-life: Less than 10 seconds.

Note: The drug of choice for paroxysmal tachycardia, SVT.

Administration is to be done over 1-3 seconds (maybe given IO)
Following rapid flush with 20 ml NS. IV line is started as
proximal to the heart as possible, such as the antecubital fossa.
Adenosine have extremely short half-life.

INDICATIONS
 Supraventricular tachycardia: Adenosine injection slows conduction time through the A-V
node and can interrupt the reentry pathways through the A-V node. This prevents atrial impulses
from reaching the ventricles through the AV node and blocks re-entrant tachycardia that rely on
conduction through the AV node.
 It is used during a stress test of the heart: Adenosine injection is a vasodilator used in
combination with thallium-201 for nuclear heart stress tests when the patient is unable to exercise
adequately.
CONTRAINDICATIONS
 Second- or third-degree A-V block, Sinus node disease, Symptomatic bradycardia(except in
patients with a functioning artificial pacemaker): Adenosine causes blockage of conduction
through AV node. So in this cardiac case, it delay the already delayed conduction system. Hence
condition worsens and arrest occurs.
 Hypersensitivity to adenosine.

SIDE EFFECTS

 Cardiovascular: Facial flushing, sweating, palpitations, chest pain, hypotension. (The

administration of adenosine reduces blood flow to coronary arteries past the occlusion. Other
coronary arteries dilate when adenosine administration. While the segment past the occlusion is
already maximally dilated, which is a process called coronary steal. This leads to less blood
reaching the ischemic tissue, which in turn produces the characteristic chest pain.)
 Respiratory: dyspnea, chest congestion, hyperventilation (It cause bronchospasm and thereby
dyspnea and to manage this hyperventilation occurs.)
 Central Nervous System: Lightheadedness , dizziness, tingling in arms, numbness, apprehension,
blurred vision, burning sensation, heaviness in arms, neck and back pain.

NURSING CONSIDERATIONS

 Use IV line with no other medications.

 Administer rapidly.
 Monitor HR, RR, BP and adverse drug reactions.
 Monitor blood pressure and apical pulse prior to administration: It slows conduction time
through the A-V node. So in order to prevent complications, it needs to be monitored.
 Do not refrigerate: Crystallization may occur. If crystallization has occurred, dissolve crystals
by warming to room temperature.
 IV line is secured as proximal to the heart as possible, such as the antecubital fossa, with an
attached 3 way extension to the IV cannula. Adenoine and 20 ml flush need to be connected and
ready for administration. Soon after administration of adenosine, flush needs to be injected
without any delay.
 https://www.youtube.com/watch?v=8fpJXPSC7w8
 DOPAMINE

Class: Sympathomimetic amine vasopressor, inotropic agent.

Route: Intravenous.
Available form: 200mg/5ml/ ampoule.
Dose: 5ml in 45ml NS; (1- 5 mcg/kg/min by continuous IV infusion.)
Onset: Within 5 minutes.
Half-life: 2 minutes.
Note: Administer slowly.
The drugs of choice to improve cardiac contractility.

INDICATIONS

 Hypotension: It acts by inotropic effect on the heart muscle (causes more intense contractions)
that, in turn, can raise blood pressure. At high doses, Dopamine may help correct low blood
pressure due to low systemic vascular resistance.
 Low cardiac output
 Poor perfusion of vital organs: As adequate organ perfusion depends on maintenance of cardiac
output and systemic vascular resistance, diminished cardiac output and abnormal SVR result in
decreased organ perfusion. Dopamine increases CO.

CONTRAINDICATIONS

 Hypersensitivity to sympathomimetic amines and sulfites.

 Uncorrected tachyarrhythmias: Beta- receptor stimulation and the indirect release of
endogenous norepinephrine can result in potentially life-threatening consequences.

SIDE EFFECTS
 Cardiovascular: Ventricular arrhythmia, atrial fibrillation (at very high doses), ectopic beats,
tachycardia, anginal pain, palpitation, cardiac conduction abnormalities, widened QRS complex,
bradycardia, BP fluctuation, vasoconstriction. (Intravenous inotropic agents promote increased
myocardial contractility via elevation of myocyte calcium concentrations, a mechanism that is also
known to promote the development of cardiac arrhythmias.)
 Respiratory: Dyspnea.
 Gastrointestinal: Nausea, vomiting (dopamine is a neurotransmitters implicated in the control of
nausea and vomiting.)
 Metabolic/nutritional: Azotemia.
 Central nervous system: Headache, anxiety.
 Ocular: Increased intraocular pressure; dilated pupils (Dopamine cause changes in ciliary blood
flow and aqueous production, with ciliary vasodilation and secretory stimulation at the lowest
infusion rate and vasoconstriction and secretory inhibition at higher infusion rates.)
 Gangrene: Dopamine infusion can cause tissue ischemia or necrosis secondary to vasospasm and
extravasation.

NURSING CONSIDERATIONS
 Monitor blood pressure and HR closely: It increases myocardial activity. Hence, there are
more chances for arrhythmia.
 Infuse via central line, large vein: It may cause tissue gangrene if small blood vessels used due
to vasospasm in small blood vessels.
 Not compatible with Sodium Bicarbonate or other alkaline solutions: The drug is inactivated
in alkaline solution.
 Use infusion pump to control flow rate.
 Titrate dosage to desired hemodynamic values or optimal urine flow: In the periphery,
dopamine acts on dopamine receptors in the kidney causing increased renal blood flow, sodium
excretion, and urine volume. Increased renal blood flow occurs through dopamine-induced
smooth muscle relaxation and resulting vasodilation.
 Monitor closely for urine output, RR and ventricular arrhythmias.
 Monitor when administered to feeding mother.
 HEPARIN SODIUM
Class: Anticoagulant, Blood thinners.
Route: Intravenous
Available form: 1000IU/ml, 5000IU/ml: 5ml vial.
Dose: Loadig dose: 5000IU IV push following 25000IU in 45 ml NS.
(150 units/kg-300units/Kg)
Half life: 1.5 hours
Onset: IV (immediate)

Note: Administer fastly.

Heparin sodium injections should be stored at 20 C to 25 C.
Antidote: Protamine sulfate

INDICATIONS
 Prophylaxis and treatment of venous thrombosis and pulmonary embolism.
 Treatment of acute and chronic consumptive coagulopathies (disseminated intravascular
coagulation.)
 Prevention of clotting in cardiovascular surgery.
 Anticoagulant use in blood transfusions, extracorporeal circulation and dialysis procedures.

CONTRAINDICATIONS

 Patient with severe thrombocytopenia: platelet count is less in thrombocytopenia, which is

responsible for coagulation . if heparin used it will trigger bleeding
 Hypersensitivity to heparin or pork products
 Severe hypertension, intracranial haemorrhage: Condition will worsen if heparin administered.
 Ulcerative gastrointestinal lesion: Heparin administration enhances bleeding in the stomach.

SIDE EFFECTS
 Hemorrhage. Rationale:
 Thrombocytopenia. Heparin will form antibodies against
 Hypersensitivity reactions. platelet factor 4. Therefore, more platelet
activation occurs, this formed platelet
 Increased aminotransferase levels.
aggregate and clump together. So less free
platelet to work. This leads to bleeding.
 NURSING CONSIDERATIONS

 Monitoring blood report:

 Coagulation profile.(APtt)
 Platelet count and haematocrit: For early detection of anticoagulant related complications.
 Prevention of injury and fall.
 Assess for bleeding, hypertension and recent surgical procedures.
 LIDOCAINE

Class: Anaesthetic drug, Type I Antiarrythmic drug

Route: Intravenous (slow)
Available form: 20mg/ml
Dose: 50 to 100 mg IV bolus over 2 to 3 minutes.
Maximum dose upto 300 mg in an hour.
Onset: 2-5 minutes
Half life: 1.5 to 2.0 hours
Note: The drug of choice in the acute management of ventricular arrhythmias.
Antidote: Intravenous lipid emulsion.

INDICATIONS
 Production of local and regional anesthesia: Blocks sodium channel and thereby no message
transmission
 Digoxin toxicity
 Ventricular dysrrhythmias: It prolong repolarization time in heart.

CONTRAINDICATIONS
 Hypersensitivity
 Hypokalemia: Sodium channel is blocked which will result in hypokalemia.
 Myasthenia Gravis: Neurological transmission is already altered in neurological condition, which
will be worsened.
 Heart block, Atrial fibrillation: Its use will conduct atrial impulse which result in excessive
ventricular rates.
 Congestive heart failure
 Shock, Hypovolemia
 Liver disease: It is extensively metabolized by the liver with a high extraction ratio; therefore, its
clearance is dependent on hepatic blood flow.
 Hypoxia
 Chronic kidney disease: Lidocaine is primarily eliminated by the kidney. Therefore, in CKD
elimination of the drug will be affected.
SIDE EFFECTS
 Cardiovascular: Bradycardia, hypo and hyper tension, cardiovascular collapse, cardiac arrest,
circulatory collapse, arrhythmia, shock, tachycardia, ventricular fibrillation, heart block,
myocardial depression, peripheral vasodilation. (It works by blocking sodium channels and thus
decreasing the rate of contractions of the heart. Causing arrhythmias.)
 Nervous system: Light headedness, headache, dizziness, drowsiness, cold/numbness, tremor,
convulsions, unconsciousness, spinal cord deficit, paraesthesia, slurred speech, arachnoiditis,
peripheral nerve injury, coma, cauda equina syndrome, Horner's syndrome, nystagmus.
 Gastrointestinal: Vomiting, nausea, bowel control loss, swallowing difficult, numbness of tongue.
(Muscle relaxation due to sodium channel block, hence no peristalsis and muscle movement.)
 Psychiatric: Nervousness, apprehension, euphoria, confusion, agitation, disorientation, psychosis,
restlessness, excitement.
 Hematologic: Methemoglobinemia.
 Dermatologic: Urticaria, cutaneous lesion, dermatitis, rash, edema.
 Genitourinary: Loss of control of genitourinary system, sexual function loss, urinary retention.
(The anaesthetic agents decrease the intrabladder pressure and inhibit the micturition reflex.)
 Immunologic: Anaphylaxis.

NURSING CONSIDERATIONS
 Continuous ECG monitoring: Blocking sodium channels in the conduction system, as well as
the muscle cells of the heart, raises the depolarization threshold, making the heart less likely to
initiate or conduct early action potentials that may cause an arrhythmia.
 Administer slowly.
 I/O chart maintenance: Sodium channel blocked by lidocaine administration. Sodium regulates
water in body. Also, muscle relaxation cause inadequate emptying.
 Seizure probability: High dose lidocaine causes sodium channel block. Electrical impulses are not
transmitted to brain. This causes seizure.
 Absorbed across mucous membranes and damaged skin but poorly through intact skin.
 MAGNESIUM SULPHATE

Class: Antidysrrhythmics, Anticonvulsant, Electrolytes

Route: Intravenous
Available form: 50/ w 2ml , 5ml ampoule
Convulsion Dose: Loading dose: 4 g by IV infusion in 12 ml of 0.9% NS
over 15 to 20 minutes then, 10 g by IM route then,
Maintenance dose: 5 g by IM route every 4 hours.(25-50 mg/kg)
Hypomagnesemia
& Cardiac arrest: 2 g in 100ml NS over 20-30 minutes.
Onset: Immediate
Half life: 4 hours
Note: Administer slowly.
The drug of choice for the prevention and treatment of seizures in eclampsia.
Antidote: Calcium gluconate.

INDICATIONS
 Convulsions: The mechanism of action of magnesium sulfate is thought to trigger cerebral
vasodilation, thus reducing ischemia generated by cerebral vasospasm during an eclamptic event.
The substance also acts competitively in blocking the entry of calcium into synaptic endings,
thereby altering neuromuscular transmission.
 Hypomagnesemia: (prophylaxis and treatment) (in patients receiving total parenteral nutrition.)
 Tetany : Magnesium sulphate causes muscle relaxation and thereby muscle spasm will be
released.
 Torsades de Pointes, Refractory V-Fib and Pulseless V-Tach: Rapid administration of
magnesium decreases the influx of calcium into cardiac cells, lowering the amplitude and
suppressing early after depolarizations. It improves potassium transport through myocardial
potassium channels and shortening of the action potential duration.
CONTRAINDICATIONS
 Hypersensitivity
 Myocardial damage, diabetic coma, heart block.
 Hypermagnesemia & Hypercalcemia
 Administration during 2 hours preceding delivery for mothers with toxemia of pregnancy: In a
baby, magnesium toxicity can cause low muscle tone. This is caused by poor muscle control and
low bone density. These conditions can put a baby at greater risk for injuries, such as bone
 fractures, and even death. Also, the newborn may show signs of magnesium toxicity, including
neuromuscular or respiratory depression.
 Myasthenia gravis: Magnesium has a significant inhibitory effect on acetyl choline release and
thereby it impairs already slowed nerve-muscle connections.

SIDE EFFECTS
 Flushing, Sweating.
 Hypotension: Peripherally, causing vasodilation.
 Hypothermia,Circulatory collapse &respiratory depression: Magnesium causes CNS depression.
 Stupor.
 Stomach upset and diarrhea.

NURSING CONSIDERATIONS
 Use with caution in:
 Digitalized patients: Digoxin reduces tubular magnesium reabsorption, and in patients with
congestive heart failure this interaction may be cumulative with other causes of magnesium
deficiency (diuretics, diet, poor intestinal absorption).
 Neuromuscular disease: Magnesium has a significant inhibitory effect on acetyl choline
release thereby it impairs already slowed nerve-muscle connections.
 Potassium levels must be normalized: Hypomagnesemia is usually associated with hypokalemia
and ECG variations are similar. Hypomagnesemia impairs Na-K-ATPase, which would decrease
cellular uptake of K+. A decrease in cellular uptake of K+, if it occurs along with increased
urinary or gastrointestinal excretion, would lead to K+ wasting and hypokalemia.
 Administer slowly.
 Monitor renal function, blood pressure, respiratory rate, and deep tendon reflex : It causes
CNS depression.
 Observe neonates for skeletal abnormalities: Fetal skeletal demineralization, hypocalcemia, and
hypermagnesemia abnormalities to be monitored in new born.
 CALCIUM GLUCONATE

Class: Membrane stabilizer, Antidote.

Route: Intravenous
Available form: 10 ml of 10% solution contains 93 mg (4.65 meq) of calcium.
Dose: Can be administered directly and in 100 ml NS.
Onset: 1-3 minutes.
Half life: Not applicable.
Note: Administer slowly.

ACTION
 Stabilizes the membrane of cardiac muscles.
 Counteracts the toxicity of hyperkalemia.
 Antidote for magnesium intoxication.

INDICATIONS
 Severe hypocalcaemia (hypocalcemic tetany, neonatal hypocalcaemia, etc.)
 Hyperkalemia: As a membrane stabilizer. Reverses EKG changes pending correction of the
extracellular potassium concentration. It reduces the excitability of cardiomyocytes, thereby
lowering the likelihood of cardiac arrhythmias.It raises the cell depolarization threshold and
reduces myocardial irritability.
 As a potential antidote in suspected calcium channel blocker overdoses, hydrofluoric acid
poisoning and iatrogenic magnesium intoxication: CCBs block intracellular entry of calcium by
binding L-type calcium channels located primarily in cardiac and vascular smooth muscle. The
results include decreased rate of firing of the sinus node pacemaker, decreased rate of conduction
through the AV node, decreased cardiac contractility, and decreased vascular tone.

CONTRAINDICATIONS
 Hypersensitivity
 Ventricular fibrillation during CPR
 Hypercalcemia
 Digoxin poisonings: Calcium can augment the positive inotropic and negative chronotropic
effects of digitalis preparations.
 Sarcoidosis
SIDE EFFECTS
 Cardiovascular: Arrhythmias, Hypotension, Bradycardia, Vasodilation, Cardiac arrest: calcium
causes muscle contraction. Hypotension is due to vasodilation.
 Local: Tissue necrosis, Local soft tissue inflammation, Calcification due to extravasation

NURSING CONSIDERATIONS

 Administer slowly and stop if the patient complains of pain: Rapid intravenous injections of
calcium gluconate may cause hypercalcemia, which can result in vasodilation, cardiac arrhythmias,
decreased blood pressure, and bradycardia.
 Calcium gluconate should be injected through a small needle into a large vein: In order to
avoid too rapid increase in serum calcium and extravasation of calcium solution into the
surrounding tissue with resultant necrosis.
 Do not mix with bicarbonate: Calcium-gluconate has been shown to be incompatible and forms
precipitate when mixed with sodium bicarbonate.
 Avoid use with patients who are on Digoxin: Calcium can augment the positive inotropic and
negative chronotropic effects of digitalis preparations.
 Check potassium level: Hyperkalemia may occur in association with calcium alteration in patient
with renal failure.
 ROCURONIUM BROMIDE

Class: Neuromuscular blocker.

Route: Intravenous
Available form: 10 mg/ml - 10 ml/5 ml - vial
Dose: 50mg.(0.15 mg/Kg)
Onset: Rapid
Half-life: 1-2 minutes
Note: Administer fast as direct IV.

INDICATIONS
 Paralyzation after intubation: It helps in smooth muscle relaxation.

CONTRAINDICATIONS
 Hypersensitivity
 Lack of ventilatory support: It causes smooth muscle relaxation so respiratory depression will
happen. Hence respiratory support required.
 Neuromuscular disease: Rocuronium blocks acetyl choline transmission, which is essential in
neurotransmission. Hence neurological condition will worsen.
 Other neuromuscular blocking agents.

SIDE EFFECTS
 Airway compromise, Respiratory arrest: Neuromuscular blocking agents cause respiratory
insufficiency by paralyzing respiratory muscles.
 Light-headedness
 Feel incontinence: It is a muscle relaxant.
 Hypertension, tachycardia (severe headache, blurred vision, pounding in neck or ears, anxiety,
confusion): These cardiovascular effects are caused by the combination of vagal blockade and
catecholamine release from adrenergic nerve endings.
 NURSING CONSIDERATIONS

 Administer fast.
 Observe the patient for residual muscle weakness and respiratory distress during the recovery
period: Neuromuscular blocking agents cause respiratory insufficiency by paralyzing respiratory
muscles.
 Check for consciousness of patient. Sedation should be administered: Sedation should be
administered to reduce the physiological stress of respiratory failure and improve the tolerance of
invasive life support.
 Monitor ECG, heart rate, BP and respiratory rate throughout administration:These
cardiovascular effects are caused by the combination of vagal blockade and catecholamine release
from adrenergic nerve endings.
 Use rocuronium with caution in patients with pulmonary hypertension or valvular heart
disease: It has been associated with transient increases pulmonary vascular resistance.
 SODIUM BICARBONATE

Class: Alkalizing agent.

Route: Intravenous
Dose: 75 ml NaHCO3 in 5 % D
Available form:7.5% solution(44.6 mEq) 25 ml ampoule.
Onset: Within 30 minutes.
Note: Administer slowly as direct IV.

INDICATIONS
 Metabolic acidosis.
 Hyperkalemia: By alkalinizing the serum, bicarbonate may indirectly cause movement of potassium into
cells via an H+/K+ exchange mechanism. So K goes into intracellular space. Additionally, it facilitate
potassium excretion.
 Tricyclic antidepressant overdose.
 To correct bicarbonate deficit due to renal or GI losses.

CONTRAINDICATIONS
 Hypokalemia

SIDE EFFECTS
 Metabolic alkalosis: It is an alkalizing agent.
 Hypernatremia &hypokalemia: Alkalosis caused a slight increase in potassium secretion. Also, sodium
bicarbonate contains sodium. Sodium bicarbonate intake can also raise your blood sodium levels, which
may increases blood pressure. In addition, large amounts of sodium can make your body to retain water.
 Frequent urge to urinate: Sodium bicarbonate produced a significant metabolic alkalosis and an increase
in urine pH. Both sodium bicarbonate and sodium chloride produced a profound diuresis
 Headache
 Loss of appetite: As an antacid, sodium bicarbonate, especially after excess food or liquid, can cause
excess gas release, which causes stomach pain.
 Mood or mental changes
 Muscle pain or twitching
 Nausea or vomiting
 Nervousness or restlessness, irritability, confusion: Due to greater permeability of the blood-brain
barrier to hydrogen than to bicarbonate, the pH of cerebrospinal fluid may significantly decrease during
sodium bicarbonate administration, which can cause mental stupor or coma.
 Slow breathing
 Swelling of feet or lower legs
 Unpleasant taste
 Unusual tiredness or weakness: Intravenous sodium bicarbonate has been associated with increased
serum osmolality, decreased ionized serum calcium (which is associated with decreased myocardial
contractility) and peripheral vasodilation. Hence, blood supply is reduced.

NURSING CONSIDERATIONS

 Flush line well when administering any other drug into the same IV site, particularly with calcium or
phosphate preparations: It will precipitate.
 Monitor blood gases, serum calcium and electrolyte especially, bicarbonate, sodium, potassium: It will
alter blood PH, bicarbonate level and electrolytes.
 Do not use if unclear or precipitated.
 Assess fluid balance and for side effects. I/O chart to be maintained: Overdose of intravenous sodium
bicarbonate results in solute and/or fluid overload, potentially leading to edema, including pulmonary
edema.
 Observe IV site: It is alkaline in nature. So causes cell necrosis.

POTASSIUM CHLORIDE

Class: Electrolytes
Route: Intravenous
Dose: 5ml (10 meq) / 45ml NS.
Available form: 2 meq/ml, 10 ml ampoule.
Onset: Within 15 minutes.
Half life: 16 sec.
Note: Potassium chloride must always be administered by
slow IV infusion, following dilution.
ACTION
 It helps to regulate fluid balance, muscle contractions and nerve signals.

INDICATIONS
 Hypokalemia

CONTRAINDICATIONS
 Hyperkalemia
 Hypersensitivity
SIDE EFFECTS

 Immune system disorders: Hypersensitivity. (rash and angioedema)

 Metabolism and nutrition disorders: Hyperkalemia, hyponatremia.
 Cardiac disorders: Cardiac arrest, asystole, ventricular fibrillation, bradycardia (rapid intravenous
administration and /or of hyperkalemia.)
 General disorders and administration site conditions: Chest pain, infusion site thrombosis, infusion site
phlebitis, infusion site erythema, infusion site swelling, infusion site pain, infusion site irritation, and/or a
burning sensation.
 Nervous System Disorders: Hyponatremic encephalopathy.

NURSING CONSIDERATIONS

 Potassium salts should never be administered by IV push: I.V. push or bolus, can trigger cardiac
dysrhythmias and cardiac arrest.
 IV potassium must NEVER be given by direct IV injection. It must always be diluted in infusion fluid
since it can trigger cardiac dysrhythmias and cardiac arrest
 It must never be administered intramuscularly. It will cause tissue necrosis.
 Monitor serum potassium concentrations. If serum potassium level is not rising with effective
potassium supplementation, consider checking a magnesium level. Hypomagnesemia also have similar
ECG changes.
 Continuous cardiac monitoring is mandatory for IV replacement especially, for central infusions. It
causes peaking of T waves, loss of P waves and QRS widening.
 Watch IV site for signs of irritation or phlebitis. It will cause cell damage-extravasation
 NURSING RESPONSIBILITY DURING
EMERGENCY DRUG ADMINISTRATION

 High risk policy and LASA policy need to be followed.

 All high risk medications are to be given to patient only after written orders (except emergency
conditions).
 All high risk medication orders are to be verified by 2 seniors.
 A loaded syringe must be labeled with name, strength, frequency of
administration, date & time of loading and dilution ratio.
 To avoid medication errors due to multiple drug colour coding is done
Fluorescent Green - High Risk.
 Document in the nursing note regarding the medication administration with if anything occurs.
Check the IV site for
extravasation.

Double check for any prescribed

dilution.

Administer as per the prescription

to obtain optimum effect.

Drug solutions should be clear

without precipitation.

Monitor the vitals before during

and after drug administration.

Observe for any side effects.

Shake the suspension for

injection gently, well before
withdrawing the dose.

High risk policy and LASA

policy need to be followed.

Documentation: time, indication,

dose, route, patient response and
complications.
Drug name Dose Route Indications
Contraindications
Side effects Nursing considerations

Atropine 0.6mg IV  Sinus bradycardia  Narrow Angle  Dry mouth  Observe IV site for signs of
sulphate /ml  Bronchospasm Glaucoma  Blurred vision extravasation.
 Organophosphate  Prostatic  Sensitivity to light  Rapid IV push.
poisoning Hypertrophy  Lack of sweating  Assess for signs of adverse effects,
 Preoperative  Thyrotoxicosis  Dizziness especially, pupillary reaction and
 Ophthalmic  Cardiac Failure  Nausea dryness of mucus membrane.
 Tachycardia  Loss of balance  Continuous monitoring of vital
 Hypersensitivity reactions signs and cardio respiratory
 Tachycardia functioning.
 Monitor fluid balance.
 Observe for gastric distension.
Amiodarone 50mg IV  Ventricular arrhythmias  Hypersensitivity  Dizziness, lightheadedness, or  Administer slowly except in case of
/ml  Atrial arrhythmias  2nd or 3rd degree fainting VT with and without pulse.
 Hemodynamically AV block  Neurologic toxicity  Peripheral IV administration of
unstable patients  Cardiogenic Shock,  Painful breathing amiodarone can result in phlebitis.
 Patients with CHF Bradycardia,  Sensitivity of the skin to  Cardiac monitoring especially,
Hypotension sunlight, skin discoloration rhythm and hypotension.
 Severe sinus node  Sleep disturbances  Assess for drug reactions especially,
dysfunction  Constipation bradycardia, nausea, vomiting and
 Breastfeeding  Loss of appetite headache.
 Lung disease  Thyroid abnormality  Drug interactions; flush the line
 Thyroid problems properly.
Adrenline/ 1mg/ IV  Treatment of allergic  Hyperthyroidism  CNS: Anxiety, dizziness,  Strict I/O maintenance.
Epinephrine ml reactions  Shock nervousness, agitation, headache  Administer as IV push.
 In restoring cardiac  Ischemic disease  Cardiovascular: Arrhythmias,  Double-check:
rhythm in cardiac arrest  Coronary chest pain, hypertension,  Use minimal doses for minimal
 Hemostatic agent insufficiency palpitations, tachycardia periods of time.
 Acute asthmatic attack  Labor and Breast  Dermatologic: Gangrene  Gently shake the suspension for
feeding mothers  Endocrine: Hyperglycemia, injection well before withdrawing
  Organic brain hypokalemia, lactic acidosis the dose
damage  GI: Nausea, vomiting
 Narrow angle  Neuromuscular: Tremors,
glaucoma weakness
 Renal: decreased urine output
 Respiratory: Dyspnea,
pulmonary edema
Noradrenline 1mg IV  Low cardiac output  Hypertension  Cardiac arrhythmia  Monitor BP and HR
/ /ml  Hypotension  Hypotension from  Renal vascular ischemia  Monitor peripheral perfusion
 Circulatory failure volume deficit  Severe hypertension with  Monitor urine output
Norepinephr
 Blood clot, blockage possible intracranial hemorrhage  Do not administer bolus doses,
ine or closing off of  Plasma volume depletion. administer slowly
blood vessels  Monitor for adverse drug effects
Adenosine 3mg IV  Arrhythmias  Second- or third-  Cardiovascular: Facial flushing,  Use IV line with no other
/ml  It is used during a stress degree A-V block sweating, palpitations, chest medications
test of the heart  Sinus node disease pain, hypotension.  Administer rapidly
or symptomatic  Respiratory: dyspnea, chest  Monitor HR, RR,BP and adverse
bradycardia congestion, hyperventilation drug reactions.
 Hypersensitivity  CNS: Lightheadedness ,  Do not refrigerate
dizziness, tingling in arms,  IV line is secured as proximal to the
numbness , apprehension, heart as possible
blurred vision, burning
sensation, heaviness in arms,
neck and back pain
Dopamine 40mg IV  Hypotension  Hypersensitivity to  Cardiovascular: Ventricular  Monitor BP and HR closely
/ml  Low cardiac output sympathomimetic arrhythmia, atrial fibrillation,  Infuse via large vein
 Poor perfusion of vital amines and sulfites. ectopic beats, tachycardia,  Not compatible with Sodium
organs  Uncorrected anginal pain, palpitation, cardiac bicarbonate or other alkaline
tachyarrhythmia conduction abnormalities, solutions
bradycardia, vasoconstriction  Use infusion pump to control flow
 Respiratory: Dyspnea rate
 Gastrointestinal: Nausea,  Titrate dosage to desired
vomiting hemodynamic values or optimal
  CNS: Headache, anxiety urine flow.
 Gangrene: tissue necrosis
Heparin 1000 IV  DVT and pulmonary  Thrombocytopenia  Hemorrhage  Monitoring blood report:
Sodium IU embolism  Hypersensitivity  Thrombocytopenia Coagulation profile.
 Coagulopathies  Severe  Hypersensitivity reactions Platelet count and haematocrit
/ml
 Cardio vascular hypertension,  Prevention of injury and fall.
5000 surgery intracranial  Assess for bleeding, hypertension
IU/  blood transfusions, hemorrhage and recent surgical procedures.
extracorporeal  Ulcerative
ml
circulation and dialysis gastrointestinal
procedures lesion

Lidocaine 20mg  Production of local and  Hypersensitivity  Cardiovascular: hypo and hyper  Continuous ECG monitoring
/ml IV regional anesthesia  Hypokalemia tension, cardiovascular collapse,  Administer slowly.
 Digoxin toxicity  Myasthenia Gravis arrhythmia, shock, heart block,  I/O chart maintenance
 Ventricular  Heart block, peripheral vasodilatation  Seizure probability
dysrrhythmias AF,CHF Shock,  Nervous system: Light
Hypovolemia headedness, headache, dizziness,
 Liver disease drowsiness, tremor,
 Hypoxia convulsions, paresthesia,
 Chronic kidney slurred speech, peripheral nerve
disease injury, coma
 GI: Vomiting, nausea, bowel
control loss, dysphagia
 Psychiatric: Nervousness,
euphoria, confusion, agitation,
restlessness, excitement
 Hematologic:
Methemoglobinemia
 Dermatologic: Urticaria,
 Genitourinary: Loss of control,
sexual function loss, urinary
retention
  Immunologic: anaphylaxis
Magnesium IV  Convulsions  Hypersensitivity  Flushing  Use with caution in:
50w/v
sulphate  Hypomagnesemia  Myocardial damage,  Sweating Digitalized patients:
 Uterine tetany diabetic coma, heart  Hypotension Neuromuscular disease
 Torsades de Pointes , block  Circulatory collapse  Potassium levels must be
Refractory V-Fib and  Hypermagnesemia &respiratory depression normalized.
Pulseless V-Tach & Hypercalcemia  Hypothermia  Administer slowly.
 2 hours preceding  Stupor  Monitor renal function, blood
delivery for mothers  Stomach upset and diarrhea pressure, RR and deep tendon reflex
with toxemia of  Observe neonates for skeletal
pregnancy abnormalities.
 Myasthenia gravis
Calcium IV  Severe hypocalcaemia  Hypersensitivity  Cardiovascular: Arrhythmias  Administer slowly
1 gm/
gluconate  Hyperkalemia  Ventricular Hypotension, Vasodilation,  Inject through a small needle into a
10 ml
 Antidote in suspected fibrillation during Cardiac arrest large vein
calcium channel CPR  Local: Tissue necrosis,  Do not mix with bicarbonate
blocker overdoses,  Hypercalcemia Calcification due to  Avoid use with patients who are on
hydrofluoric acid  Digoxin poisonings extravasation Digoxin
poisoning and  Sarcoidosis  Check potassium level
iatrogenic magnesium
intoxication.
Rocuronium IV  Paralyzation after  Hypersensitivity  Airway compromise,  Administer fast.
10mg
bromide intubation  Lack of ventilatory Respiratory arrest  Observe the patient for residual
/ml
support  Light-headedness muscle weakness and respiratory
 Neuromuscular  Feel incontinence distress
disease  Hypertension  Monitor ECG, heart rate, BP and
 Other respiratory rate
neuromuscular  Monitor infusion site frequently
blocking agents  Check for consciousness of patient.
Sedation should be administered.
Sodium IV  Metabolic acidosis  Hypokalemia  Metabolic alkalosis  Flush the line well.
10mg
bicarbonate  Hyperkalemia  Hypernatremia &hypokalemia  Monitor blood gases, serum calcium
/ml
 Tricyclic antidepressant  Frequent urge to urinate and electrolyte.
 overdose  Loss of appetite Mood or mental  Do not use if unclear or
 To correct bicarbonate changes precipitated.
deficit  Nausea or vomiting  I/O chart to be maintained.
 Nervousness or  Observe IV site.
restlessness,headache
 Slow breathing
 Unpleasant taste
 Unusual tiredness or weakness
Potassium IV  Hypokalemia  Hyperkalemia  Immune system disorders:  Never be administered by IV push
2meq/
chloride  Hypersensitivity Hypersensitivity  NEVER be given by direct IV
ml
 Metabolism and nutrition injection
disorders: Hyperkalemia,  Never be administered
hyponatremia intramuscularly/subcutaneously.
 Cardiac disorders: Cardiac  Monitor serum potassium
arrest, asystole, ventricular concentrations
fibrillation, bradycardia  Continuous cardiac monitoring
 General disorders and  Watch IV site for extravasation.
administration site conditions:
Chest pain, infusion site
phlebitis
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