Page 1

ORAL MAXILLOFACIAL AND RECONSTRUCTIVE SURGERY BAPUJI DENTAL COLLEGE AND HOSPITAL

SEMINAR ON

EMERGENCY DRUGS

Moderator: Dr. Dayananda Presenter:

Dr. Neeraja Singhla

1


CONTENTS 1. INTRODUCTION 2. EMERGENCY DRUG KIT 3. EMERGENCY DRUG MODULES OR LEVELS 4. EMERGENCY DRUGS IN - Cardiovascular system - Respiratory system - Central Nervous system - Endocrine system - Allergic reactions. 5. OTHER

EMERGENCY

DRUGS

EMERGENCIES 6. CONCLUSION 7. REFERENCES.

2

USED

IN

DIFFERENT


INTRODUCTION An emergency is a serious situation that arises suddenly and threatens the life or welfare of a person or a group of people, as a natural disaster or a medical crises. Emergency department is a section of an institution that is staffed and equipped to provide rapid and varied emergency care, especially for those stricken with sudden and acute illness or those who are the victims of severe trauma. In spite of the most meticulous protocols designed to prevent the development of life- threatening situations, emergencies still occur. Prevention, as successful it may be, is not always enough. The entire office staff must be prepared fully to assist in the recognition and management of any potential emergency situation. The management of an emergency begins with the application of the steps of basic life support: P (positioning), A (airway), B (breathing), C (circulation) and D (definitive treatment), including the administration of drugs and hence emergency drugs and equipment must be available in every dental office.

3


EMERGENCY KITS A number of emergency kits are available commercially for the in the dental and medical offices. The best emergency drug kit is one the doctor designs personally to meet his special requirements and capabilities. The emergency kit should not be complicated. It should be as simple as possible organized collection of drugs and equipment that is highly effective in the management of life- threatening situations. Pallach’s statement that “complexity in a time of adversity breeds chaos� is all true. The doctor should remember three things in preparing and using emergency drug kits: i)

Primary management of all emergencies involves BLS

ii)

Drug administration is not necessary for the immediate management of medical emergencies except in certain conditions such as anaphylaxis

iii)

When in doubt, never medicate.

All the drugs come with drug package inserts. Doctors should save this information sheet from each drug included in their kit, read it, and take a note of important information about the drug, including its indications, usual doses (pediatric, adult and geriatric), adverse reactions, and expiry dates.

4


EMERGENCY DRUGS The emergency drugs and equipment are now described according to four levels or modules. • Module one: basic emergency kit (critical drugs and equipment) • Module two: non critical drugs and equipment • Module three: ACLS • Module four: antidotal drugs Two categories of drugs are described for each module as well as emergency equipment: 1) Injectable drugs 2) Non-injectable drugs Most Injectable drugs are prepared in a 1-ml glass ampule or vial. The number of mgs of drug present in 1 ml of solution varies from drug to drug. E.g. diazepam is 5mg/ ml, whereas diphenhydramine is 50 mg/ ml and ephedrine is 10 mg/ ml. the one ml form of the drug is known as its therapeutic dose or unit dose. However, epinephrine is a major exception to this basic rule of doses. Although the 1- ml form of 1: 1000 epinephrine is considered the adult therapeutic dose, a smaller dose- 0.3 ml- is recommended, with subsequent doses based on patient’s response. Noninjectable drugs usually are prepared so that one tablet or spray is the adult therapeutic dose. Many of them are also prepared in pediatric forms to simplify administration. Other items of emergency equipment should be available in both pediatric and adult forms. E.g. face masks, airways etc.

5


ADMINISTRATION OF INJECTABLE DRUGS: For a drug to exert a therapeutic effect a minimum therapeutic blood level must be achieved in the target organ. Therefore the ideal route for emergency drug administration is IV; onset of action is approximately 20 sec, and the drug effect the most reliable of all routes of administration. Emergency drugs may be administered via the IM route into various sites; most often the anterolateral aspect of the thigh (vastus lateralis), the mid-deltoid region of the upper arm, and the upper outer quadrant of the gluteal region. I.m. administered drugs have an onset of action of about 10 min with normal tissue perfusion. This is somewhat slower with decreased BP (hypotension). Of these three traditional i.m injectional sites, the middeltoid provides the most rapid uptake of most drugs (because of its greater tissue perfusion) and is therefore the site of choice. The vastus lateralis is a close second because of its accessibility and anatomic safety. One additional site provides an even more effective and rapid uptake than the mid-deltoid region- the tongue. Emergency drugs can be injected either into the body of the tongue (intralingual injection) or sublingually for a more rapid uptake and onset of clinical action. The drug may be administered in the body of the tongue or floor of the mouth, either intraorally or extra-orally. Onset of action is approximately 5-10 min in the presence of effective circulation, but slower in patients with hypotension. The steps of BLS must continue as needed while the emergency team awaits the onset of the drugs action.

6


MODULE ONE: critical emergency drugs and equipment: Injectable drugs: i)

Epinephrine

ii)

Histamine blockers • Chlorpheneramine • Dipenhydramine

Noninjectable drugs: i)

Oxygen

ii)

Vasodialators • Nitroglycerine • Amyl nitrate

iii)

Bronchodialator • Albuterol • Metaproterol

iv)

Antihypoglycemics

v)

Asprin

Emergency equipment: i)

Oxygen delivery system

ii)

Suction and suction tips

iii)

Tourniquets

iv)

Syringes

v)

Magill intubation forceps

7


MODULE TWO: secondary (non critical) emergency drugs and equipment: Injectable drugs: i)

Anticonvulsants • Midazolam • diazepam

ii)

Analgesics • Morphine sulphate • Meperidine

iii)

Vasopressors • Methoxamine • Phenylephrine

iv)

Antihypoglycemics • Dextrose 5% • Glucagon

v)

Corticosteroids • Hydrocortisone sodium succinate

vi)

Antihypertensives • Esmolol • propranolol

vii)

Anticholinergics • atropine

Noninjectable drugs: i)

Respiratory stimulant • Aromatic ammonia

ii)

Antihypertensives • Nifedipine 8


• Nitroglycerine Emergency equipment: i)

Scalpel or cricothyrotomy needle

ii)

Artificial airways

iii)

Laryngoscope and endotracheal tubes

MODULE THREE: ACLS: ACLS essential drugs: i)

Epinephrine

ii)

Oxygen

iii)

Lidocaine

iv)

Atropine

v)

Dopamine

vi)

Morphine sulphate

vii)

Verapamil

MODULE FOUR: anti dotal drugs: i)

Opioid antagonist • Naloxane • Nalbuphine

ii)

Benzodiazepine antagonist • Flumazenil

iii)

Antiemergence delirium drug • Physostigmine

iv)

Vasodilator / local anesthetic • Procaine

9


PRIMARY INJECTABLE DRUGS: DRUG FOR ACUTE ALLERGIC REACTION Drug of choice : EPINEPHRINE Drug class : Natural catecholamine. - Epinephrine (Adrenalin) is the drug of choice for the management of the acute allergic reaction (signs and symptoms appearing within 1 hour of drug administration) - Epinephrine will be of primary value in the management of the respiratory and cardiovascular manifestations of allergic reactions. - Desirable properties of this agent include. • Rapid onset of action. • Potent action as a bronchial smooth muscle dilator (beta properties) • Antihistaminic properties. • Vasopressor properties. And its action on heat which include. • Increase heart rate (21%) • Increase systolic blood pressure (5%) • Decrease diastolic B.P. (14%) • Increased cardiac output (51%) • Increased coronary blood flow. Undesirable actions : Its tendency to predispose the heart to arrythmias and its relatively short duration of action.

10


Therapeutic considerations : - Acute allergic reaction. - Acute asthmatic attacks. - Cardiac arrest. Side effects, contraindications precautions : - Tachyarrhythmias, both supraventicular and ventricular may develop. - Epinephrine should be used with contain in pregnancy because it decreases placental blood flow and may induce premature labor. - An vital signs should be frequently monitored Availability : - Epinephrine for parenteral administration will be supplied in 1:1000 concentration: thus each milliliter will contain 1mg of the agent. - Because of short duration of action of epinephrine, multiple administrations maybe necessary during the acute phase of it. - Unit dose (1ml) ampule are preferred over multiple dose vials because the unit dose form will prevent the rescuer from inadvertently administering an overdose. - A little epinephrine may be life-saving but a lot may be lethal. - It is used to start administration of epinephrine with 0.3 to 0.5 ml of solution, I.m or Sc. Suggested for emergency kit : On preloaded syringe [1ml of 1:1000 (1mg epinephrine)] and three to four ampules of 1:1000 epinephrine. Action: β-adrenergic agonist with some ι- effects.

11


PHARMACOLOGY Epinephrine is an endogenous catecholamine Epinephrine is a direct-acting sympathomimetic agent that exerts its effects on both ι and β-adrenoceptors. Clinical pharmacology: - Parenteral administration of epinephrine produces hemodynamic metabolic and electrocardiographic effects. - Rapid intravenous injection produces rapid rises in systolic and diastolic blood pressure. - Slow IV or subcutaneous injection, however produces a moderate increase in systolic BP and drop in diastolic BP caused by a predominantly B2 stimulant vasodilator effect or blood vessels in skeletal muscle. - In infusion produces hypokalemia. Pharmacokinetics - Pharmacologically active concentrations of epinephrine are not achieved following oral administration as it is rapidly oxidized and conjugated in the gastrointestinal mucosa and liver. - Absorption from subcutaneous tissue is slow because of local vasoconstriction : effects are produced within 5 min. - Absorption is more rapid after I.m than after subcutaneous injection. - Epinephrine is rapidly metabolized in the liver, neuronal tissues and else where. - Upto 91% of IV dose is excreted in urine.

12


Metabolism : Rapidly metabolized by oxidation de-amination and O-methylation, catalyzed by enzymes monoamine oxidase and catechol-O-methyl transferase respectively. Therapeutic use : 1) TT of acute allergic reactions. 2) Emergency ft of life-threatening angioedema and anaphylactic shock. 3) Adjunctive use in management of cardiac arrest 4) Open-angle glaucoma. Mode of use : - Route of administration and dose vary with the indication and the severity of condition. - Repeated doses may be given in life threatening situations but dosing more frequently than every 5 min is associated with higher incidence of side effects and caution is susceptible patients. Indications : 1) Acute allergic reactions : Acute allergic reactions with airways obstruction should be treated with 200 to 5mg epinephrine by SC or IM injection. - This may repeated at internals of 15 to 30 min. depending on response. - SC should be preferred 2) Life threatening angioedema and anaphylactic shock : - 1st line of treatment in these medical emergencies, mode of action of epinephrine is not entirely clear but it is likely that its Îą-agonist

13


action reverses vasodilation and edema and B2 receptor stimulation relates bronchial smooth muscle in bronchoconstriction. - A dose of 500 Âľg to 10mg (0.5-1ml of epinephrine 1 in 1000 injection) should be IM as soon as possible and repeated every 10 min until improvement occur. 3) Cardiac Arrest : - Epinephrine is one of a number of tt 1 used in management of cardiac arrest. Myocardial and cerebral blood flow is substantially increased by epinephrine during CPR owing to prevention of arterial collapse and augmentation of coronary and cerebral perfusion pressures. - 1mg (10ml of a 1 in 1000) injection of epinephrine should be given by peripheral or central IV route. - Endotracheal administration is venous access is difficult - Intracardiac administration should be regarded as last resort as it carries the risk of coronary artery laceration, cardiac tamponade, and pnuemothorax, in addition. Intra cardiac injections cause interruption of external chest compression and ventilation. 4) Open-angle glaucoma : Epinephrine 0.5% and 1% eye drops are used to reduce intraocular pressure in open-angle glaucomas may act by decreasing the rate of aqueous humor production, enhancing aqueous outflow or by both mechanisms. Contraindications : 1) Hyperthyroidism : patients with hyperthyroidism are hypersensitive to the effects of epinephrine. Toxic effects may be produced with low doses of epinephrine and therefore great caution must be exercised.

14


2) Hypertension : The pressor effects or epinephrine are exaggerated in hypertensive patients and great care must be taken to avoid severe hypertension. 3) Ischemic heart disease : Angina and further myocardial ischemia may be precipitated by epinephrine in patients with underlying ischemic heart disease. Ventricular fibrillation is particularly likely to be induced in such patients. 4) Diabetes : Epinephrine should be used with case in diabetic patient as hyperglycemia, caused by α-receptor mediated suppression of insulin release will occur. 5) Angle-closure glaucoma : Papillary dilation caused by epinephrine may

worsen

angle

closure

glaucoma

and

epinephrine

is

contraindicated in this condition. Adverse reactions : • Acute over dosage : Over dosage may cause cardiac arrythmias, cerebral hemorrhage and pulmonary edema. • Severe or irreversible adverse effects Local ischemic necrosis may be produced if epinephrine is used in excess in combination with L.A. • Symptomatic adverse effects : Adverse effects such as anxiety, dyspnea, restlessness, palpitations, tachycardia, tremors, weakness, dizziness, headache and coldness of extremities may occur with even small doses of epinephrine. • Children The use of epinephrine in children requires that the body weight of the patient be known, or atleast carefully estimated. 15


The dose recommended in cardio pulmonary resuscitation is 10 mg.kg -1 (0.1ml. Kg-1 of 1 in 1000 ml) Cardiovascular effects : The cardiovascular effects of epinephrine results from epinephrine induced stimulation of α and β- adrenergic receptors. Small doses of epinephrine (1 to 2 mg/min IV) administered to adults stimulate principally beta2 receptors in peripheral vasculature. Stimulation of beta1 receptors occurs at somewhat larger doses (4mg/min IV) where as large doses of epinephrine (10 to 20 mg/min IV) stimulate both α and β-adrenergic receptors with the effects of α stimulation predominantly in most vascular beds, - Epinephrine stimulates β1 receptors to cause an increase in systolic BP, heart rate, and cardiac output. There is modest decrease in diastolic BP, reflecting vasodilation in skeletal muscle vasculature due to stimulation of B2 receptors. - The net effect of these systemic blood pressure changes is an increase in pulse pressure and minimal changes in mean arterial pressure. - Epinephrine predominantly stimulates alpha, receptors in the skin, mucosa,

and hepatocellular

vasculature producing increasing

vasoconstriction. - In skeletal muscle vasculature epinephrine principally stimulation β2 receptors producing vasodilation. - The net effect of these peripheral vasculature changes is preferential distribution of cardiac output to skeletal muscles and decreased systemic vascular resistance.

16


Airway smooth muscle : Smooth muscle of the bronchi are related by virtue of epinephrine induced activation of β2-adunnjic blockade, reflecting epinephrine-induced stimulation of α-receptors. β2- Stimulation, by increasing intracellular concentration of camp decreases release of vasoactive mediators associated with symptoms of bronchial asthma. Coagulation : Blood coagulation is accelerated by epinephrine, presumably due to increased activity of factor V. A hypercoagulable state present during the intraoperative and post operative period may reflect stress associated release of epinephrine. Epinephrine increases the total leukocyte count but at the same time causes eosinopenia. ANTIHISTAMINE : Drug of choice : CHLORPHENIRAMINE (CHLOR-TRI-METON) Alternative drug : DIPHENHYDRAMINE HCL (Benadryl) - Antihistamines will be of value in the treatment of the delayed allergic response (onset of symptoms more than 1 hour after administration of allergen) and in the definitive management of the acute allergic reaction (administered after epinephrine has terminated the acute life-threatening phase of the reaction. - Antihistamines are competitive antagonists of histamine. They do not prevent the release of histamine from cells in response to injury, drugs or antigens but do prevent access of histamine to its receptor site in the cell and there by block the response of the effector cell to histamine. - Antihistamines are more potent in preventing the actions of histamine than in reversing these actions once they develop. 17


- An interesting action of many antihistamines is that they are also potent local anesthetics, E.g. diphenhydramine and tripelennamine. - The choice of an antihistamine for the emergency kit was made after considering that most dental patients are ambulatory and may leave the dental office unescorted. Therapeutic indications : - Delayed allergy, - Definitive management of acute allergy - For local anesthesia. - When history of alleged allergy is present. Side effects, contraindications and precautions : - Side effects include CNS depression, b) Decreases BP c) Thickening of bronchial secretions resulting from drugi drying action - Contraindicated in treatment of acute asthamatic episodes. Availability : Chlorpheniramine, 10 mg / ml (1ml ampule) Diphenhydramine, 10 mg / ml (10 and 30 ml multidose vial) Suggested for emergency kit : Chlorpheniramine, 10mg / ml (3 to 4 ampules) Diphenhydramine, 50 mg/ ml (3 to 4 ampules)

18


CHLORPHENIRAMINE (MALEATE) Belongs to the alkylamine group of classic H1 Histamines. Pharmacology : It clinically most relevant effect is on the smooth muscle of the vascular the where it blocks histamine-induced increased capillary permeability, and incompletely prevents the histamine-induced fall in the blood pressure. Clinical pharmacology : Like other H1 antihistamines, chlorpheniramine antagonizes various physiological and pathophysiological effects of histamine including increased capillary permeability and dilatation the formation of edema, the ‘flare’ and ‘itch’ response, and the constriction of gastrointestinal and respiratory smooth muscle. Acute overdose : When taken in excessive doses the intoxicated patient is unconscious and shows hypertension, coma, and occasionally, convulsions which are difficult to it. DIPHENHYDRAMINE - is a H1 histamine receptor antagonist. Clinical pharmacology : - Histamine is found in high concentrations in most cells in skin, lung and intestinal mucosa. - Its actions at H1 sites include contraction of bronchial intestinal and vascular smooth muscle, but relaxation of smooth muscle in blood vessels. 19


- Histamine is responsible for triple response of flore, swelling and vasodilation which follows tissue injury. Use : Premeditation, emesis, motion sickness. ANTICONVULSANT : Drug of choice : Diazepam- benzodiazepine Alternative drug: Barbiturates (thiopentone) Seizures disorders may occur in dental office in several circumstances :Over dose reactions of L.S. Epileptic seizures. Febrile convulsions. Diazepam is the preferred drug because seizure disorders are characterized by stimulation of CNS and cardio respiratory systems followed by a period of depression of these same systems. - Diazepam will usually terminate seizure activity without pronounced depression of the respiratory and cardiovascular systems. - When barbiturates are administered to terminate seizure activity, the degree of depression is accentuated and its duration prolonged because of pharmacologic actions of barbiturate leading to respiratory arrest and a profound cardiovascular depression or collapse. Therapeutic indications : - Termination of prolonged seizures - Local anesthetic seizures - Hyperventilation syndrome - Thyroid stone.

20


Side effects : Major side effect of diazepam is respiratory depression or arrest, however careful titration during administration this is unlikely to occur. Availability : Diazepam (valium)

5mg/ml (2ml preloaded syringe) 5mg / ml (2m, 10ml vial)

Suggested for emergency kit : One 10 ml vial of diazepam, 5mg / ml - IV injections of diazepam should always be administered slowly (about 5-1 ml/min) because unduly rapid injection may induce apnea. - Intra-arterial and extravasation must be avoided. - The absorption of diazepam administered rectally in the form of a rectal solution is rapid, peak plasma diazepam levels occurring within 10 min. - IM injection may cause local pain and erythema : IM administration of diazepam (but not IV administration) can lead to rise in creatinine phosphokinase activity as a result of muscle damage. - Where a very rapid onset of effect is needed but parenteral administration is inadvisable, a rectal solution can be used. E.g. : for emergency control of febrile convulsions. Indications For IV Administration : Diazepam is indicated IV when a rapid response is desired and may be useful in acute anxiety or tension states related to stressful conditions, to control prolonged seizure activity (status epilepticus) including severe recurrent seizures: for the relief of muscle spasm in cerebral palsy, athetosis, the rare stiff mass syndrome and adjunctively in tetanus. 21


The absorption of diazepam given. IM is slow and unreliable. Oral administration is preferable when IV route is unnecessary. Indications : Status epilepticus : The dose is 0.15 – 0.25 mg/ kg body weight .IV repeated if necessary after 10-15 min, or continuous drip infusion but not more than 3mg. kg body weight in 24 hours. TETANUS : 0.1-0.3 mg. kg body weight IV at intervals of 1-4hours. EXCITATION STATES : 0.1-0.2 mg.kg-1 body weight IV and repeated 8 hours interval.

NARCOTIC ANTAGONIST : Drug of choice : Naloxone (Narcan) Alternative drug : nalbuphine (Nubain) - If a narcotic analgesic or pentazoline is used for psychosedation techniques, a narcotic antagonist must be readily available. - Narcotic antagonist are indicated for reversal of narcotic depression, including respiratory depression. Side effects : Contraindications : precautions The duration of naloxone is short – quite possibly shorter than that of the narcotic it is reversing. This situation may lead to recurrence of respiratory depression following a period of apparent recovery. For this reason all patients receiving naloxone must be observed for at least 1 hour after its administration. 22


Availability : Naloxone (Narlam), 0.4 mg/ml (1m ampule) Emergency kit :

Naloxone (Narlam), 0.4 mg/ml (1m ampule)

Mode Of Use - Naloxone can be administered by IV, IM or SC in opioid over dose, 5-10 mg. kg is the used initial IV dose and may be repeated at 2-3 min intervals until the desired response is seen. - At least 2mg should be used to constitute an adequate trial in overdose of unknown cause. - The duration of action of long acting opioids may outlast that of an IV dose of naloxone so patient should be carefully monitored for signs of returning opioid depression. - Iv infusions have been employed to avoid this problem commencing at 2-5 mg. kg hourly and adjusted act to response. - Absorption is good from IM and SC sites but rate of onset is slower than via the IV route. Action: Competitive antagonist at opioid receptors. Antagonizes endogenous or exogenous opioids, reverses all effects such as analgesia, respiratory depression, papillary constriction, coma and convulsion. NALOXONE (HYDROCHLORIDE) Naloxone is the 1st opioid antagonist to be developed that is devoid of agonist activity. Indications : 1) Reversal of effects of opioid drugs. 2) Diagnosis and treatment of opioid addiction. 23


3) Prevention of intravenous abuse of opoiod tablets. 1) Reversal Of Effects Of Opioid Drugs The treatment of the life threatening consequences of known or suspected opioid overdose is the prime indication for naloxone. In case of over dose following therapeutic use of opioids E.g. postoperatively, a small initial dose is used in an attempt to reverse a respiratory depression without loss of the opioid analgesia. In such cases 0.1mg doses may be administered at 2-3 min intervals until the required effect is achieved. 2) Diagnosis and treatment of opoid addiction: The precipitation of a withdrawal reaction by naloxone has been used as a diagnostic test in cases of suspected opioid dependence, though care must be taken to avoid a severe withdrawal reaction. Adverse reactions : Extreme hypertension may follow naloxone administration both in opioid addicts and after large therapeutic doses of opioid for pain relief.

SECONDARY INJECTABLE DRUGS : Secondary injectable drugs are agents that are deemed important but not absolutely essential to the successful management of emergency situation. ANALGESIC DRUGS : Drugs of choice : Morphine sulfate – opioid agonist. Alternative drug : Meperidine (Demerol) 24


Actions : Narcotic analgesic. - Analgesic medications will be useful during emergency situations in which acute pain or anxiety is present. In most instances, the presence of pain or anxiety will cause an increase in the workload of the heart that may prove detrimental to the well being of patient. To such circumstances are acute myocardial injection and congestive heart failure. The choice of drugs include the narcotic agonists morphine sulfate and meperidine (Demerol) Therapeutic indications : - Intense, prolonged pain and / or anxiety. - Acute myocardial infarction - Congestive heart failure. Side effects : precautions : contra indications : - Potent CNS and respiratory depressants. - Vigilant-monitoring of vital signs is mandatory - Use of narcotics is contraindicated in victims of head injury and multiple trauma. - Use with car in patients with compromised respiration. Availability :

Morphine sulfate, 10mg/ml (in 1ml ampule) Meperidine (Demerol), 50mg/ml (in 2ml ampule)

Suggested for emergency kit : Morphine sulfate, 10 mg/ml (2 or 3 1 ml ampules) or Meperidine 50 mg / ml (2 or 3 1ml ampules).

25


VASOPRESSORS : Drugs of choice – methoxamine ( vasoxyl) Alternative drug – phenylephrine (Neo-symphrine) - Vasopressors such as methoxamine (vasoxyl) and phenylephrine (neo-synephrine) are drugs that produce moderate blood pressure elevations through the mechanism of peripheral vasoconstrictions. - Methoxamine is a clinically useful Vasopressor with, sustained action and with little effect on the myocardium or CNS. - Its vasopressor action is associated with marked increase in the peripheral resistance and no increase in cardiac output. A compensatory bradycardia accompanies the rise in BP. - Onset of the vasopressor action is almost immediate following IV administration and may persist for upto 60 min. Therapeutic indications : - Management of hypotension, in which the state of the heart is unknown and the intent is to raise the blood pressure without cardiac stimulation. - Possible uses are in syncopal reactions, drug over dose reaction, post seizure states, acute adrenal insufficiency, allergy. Side effects, contraindications, precautions : - Parenteral administration of most vasopressor is contraindicated in patient with high BP or ventricular tachycardia. - Extreme caution in patient with hyperthyroidism, Bradycardia, partial heart block, Myocardial disease or severe arthrosclerosis.

26


Availability : - Methoxamine (vasoxyl), 10mg/ml, and 20mg/ml 91ml ampules and 10ml vials) - Phenylephrine 10mg/ml (1ml ampule) Suggested for emergency kit : - Methoxamine 10mg/ml (2 or 3 1ml ampules) - Phenylephrine 10mg / ml (2 or 3 ml ampules) METHOXAMINE : Methoxamine is a pure a1- adrenoceptor agonist used to treat hypotension resulting form vasodilation. Pharmacology : It is a constrictor of vascular smooth muscle through its action upon post synaptic α-receptors. Clinical pharmacology : Methoxamine produces its effects by a direct α-adrenoreceptor stimulant action on both resistance and capacitance vessels. There is resultant dose-related increase in systemic vascular resistance and arterial blood pressure. Bradycardia occurs as a result of increased vagal activity as a reflex response to the vasopressor effects of methoxamine – Bradycardia can be abolished by atropine.

27


Contraindications : 1) Hyperthyroidism: High doses of methoxamine cause marked increases in BP associated with severe bradycardia. 2) Severe hypertension : High doses of methoxamine cause marked increases in BP associated with severe bradycardia. 3) Myocardial disease : The increase in systemic vascular resistance

cause by methoxamine results in increased cardiac work and O2 demand. CORTICOSTEROIDS : Drug of choice : hydrocortisone sodium succinate Alternative drug : Methyl prednisolone sodium succinate. - The primary value of the corticosteroids is in the prevention of recurrent episodes of anaphylaxis. - Corticosteroids are also important in the management of acute adrenal insufficiency. - Studies showed that maximal effectiveness may not occur for upto 60 min after IV administration. - It appears likely that the anti-allergic effects of the corticosteroids are simply a manifestation of the nonspecific anti-inflammatory action of the adrenal glucocorticoids. Therapeutic indications : - Definitive management of acute allergy - Acute adrenal insufficiency.

28


Side effects, contraindications and precautions : When administered for an emergency treatment there are many factors to be considered, such as presence of pre-existing injection, pepticulcer, and hyperglycemia. Availability : Hydrocortisone sodium succinate, 50mg/ml (2ml vial) Methyl prednisolone sodium succinate 50mg/ml (1ml vial) Action : suppression of anti-inflammatory response rather than to inhibition of production of immunoglobulin. HYDROCURTISONE : Hydrocortisone

is

a

naturally

occurring

corticosteroid

used

principally for its anti-inflammatory and immunosuppressive actions, or as hormone replacement therapy. Pharmacology Hydrocortisone is the principal gluco-corticosteroid synthesized by the adrenal cortex in man. It influences carbohydrate, protein and lipid metabolism. The anti-inflammatory and immunosuppressive effects of hydrocortisone are its main therapeutic actions. Hydrocortisone inhibits the inflammatory response whatever the inciting agent, and is thought to be mediated by reduction in the formation of various vasoactive chemicals released during inflammation such as kinins histamines, lysosomal enzymes, and the complement system.

29


INDICATIONS : 1) Replacement therapy for adrenocortical failure or hypopituitarism. 2) Status asthamaticus. 3) Anaphylactic reaction. 4) Soft tissue or joint inflammation. 5) Congenital adrenal hyperplasia. 6) Apthous ulcer. 1) Replacement therapy for adrenocortical failure or hypopituitarism. Acute adrenal failure is a medical emergency, and may follow abrupt cessation of corticosteroid therapy. in chronic primary adrenal failure, hydrocortisone is usually administered usually at a dose of 20-30 mg daily. A common dose schedule is long hydrocortisone in morning and 10mg late afternoon. Apart from adequate IV saline and glucose fluid replacement IV hydrocortisone as sodium succinate or phosphate derivative should be given at a dose of 100 mg 8 hourly adrenal failure secondary to hypopituitarism is treated as a chronic adrenal failure. Therapy is generally guided by the sense of well being, alertness, postural changes in BP, weight and strength. 2) Status asthamaticus : IV hydrocortisone succinate in doses of 100-200 mg every 6 hour is usually administered. 3) Allergic and anaphylactic reactions : Allergic and anaphylactic reactions manifest in a variety of ways including has sever, urticaria, angioneurotic edema, and shock. Life threatening reactions should be treated with large doses (100-500 mg every 6 hours) of IV hydrocortisone succinate. The effects of hydrocortisone takes 30


some hours to develop, and other therapy such as IM or SC epinephrine (0.3-1mg) should be considered. ANTIHYPOGLYCEMICS : Drug of choice – 5% dextrose sol. Alternative drug – glucagon. - In management of hypoglycemic patient the mode of therapy will depend in large part on the patient’s level of consciousness. - Oral carbohydrate is much the preferred mode of therapy; however is a patient is unconscious or severely obtunded, the oral route must not be employed; - At this situation 50 ml of a 50% dextrose solution may be administered IV. When IV route not available, glucagons may be administered. - Glucagon is normally produced in pancreas and acts to rapidly elevate the blood glucose level by mobilizing hepatic glycogen and converting it to glucose; thus glucagon will be effective only if hepatic glycogen is available. - Not be effective in starvation or chronic hypoglycemic states. - Oral carbohydrates are administered as soon as the patient begins to respond. Therapeutic indications : - Hypoglycemia - Diagnostic tool in unconsciousness or seizures of unknown origin. Side effects : Contraindications and precautions : - 50% dextrose may produce tissue necrosis should infiltration occur.

31


- Glucagon either IM or IV is contraindicated in starvation states and in chronic hypoglycemia. Availability : Glucagon,

1mg (1 unit) dry powder with 1ml diluent 10mg dry powder with 10 ml diluent, 50% dextrose (50mg bottle)

Suggested for emergency kit : Glucagon, 1mg/ml (two or three 1ml viols) or 50% dextrose (1 bottle) DEXTROSE : Dextrose also called glucose, is a physiological carbohydrate used as an energy source in parenteral nutrition. Clinical pharmacology : Physiological amounts of dextrose given IV have no measurable acute pharmacodynamic effect although the volume of fluid given with in may cause circulatory overload in a patient with limited cardiac reserve. Adverse effects : - Dextrose administration must be cautions in severe under nutrition. Sodium retention, edema, and heart failure may be induced. - Hypophosphatesia occurs is dextrose is administered as feed without added phosphate. This may result in parasthesia, seizure, coma and death. - The hypophosphatemia is presumably the result of phosphorylation of dextrose as it enters the cell. 32


- Anaphylactoid reactions were reported in 2 patients with asthma and diabetes mellitus after IV infusion of 50% dextrose solution, probably as a result of dextrose induced histamine release.

INJECTABLE DRUG FOR ADVANCED CARDIC LIFE SUPPORT (ACLS) SODIUM BICARBONATE (NaHCO3) : - During cardiopulmonary arrest, both metabolic and respiratory acidosis occur. - Effective ventilation of the lungs is major factor in management of the acidosis accompanying cardiac arrest, especially in the removal of CO2 that has been retained (hypercarbia) by ventilatory failure or insufficiency. - NaHCO3 is effective in management of metabolic acidosis. The HCO3- ion combines with the hydrogen (H+) ion in the blood, there by elevating the pH of the blood adequate ventilation is necessary wherever NaHCO3 is administered because CO2 is produced during the reaction. HCO3- + H+ ⇔ H2CO3 ⇔ CO2 + H2O Therapeutic indications : Reversal

of

metabolic

acidosis

metabolism in cardiopulmonary arrest. Side effects : - Metabolic alkalosis - Hypernatremia, ad hyperosmolatity Availability : 1 mEq / ml (50 ml ampule)

33

occurring

during

anaerobic


ATROPINE SULPATE : Atropine is a parasympatholytic drug that decreases vagal tone through its vagolytic action, there by increasing the rate of discharge of the sinoatrial node. Indications : Management of severe sinus bradycardia when accompanied by symptomatic hypotension or hypotension that might impair coronary artery blood flow. Side effects : contraindications Atropine administration is therefore not recommended when bradycardia is not associated with hemodynamic compromise (hypotension) Availability : Atropine 5 mg [ 5ml (0.1 mg / ml) reloaded syringe] Suggested kit : one preloaded syringe CALCIUM CHLORIDE (CaCl2) : Indications : Cardiac arrest Electro mechanical dissociation and Ventricular asystole Calcium chlorides is effective in profound cardiovascular collapse in which an orderly electrical rhythm is associated with an ineffective ejection of blood from the heart (electromechanical dissociation). Side effects - Rapid administration of CaCl2 can produce a severe sinus bradycardia or sinus arrest is the heart is beating. 34


- Calcium cannot be administered along with sodium bicarbonate because calcium will precipitate out SODIUM BICARBONATE : NaHCO3 is a systemic alkalinizing agent. It increases plasma bicarbonate, buffers excess hydrogen ion concentration and raises blood pH, there by reversing the clinical manifestations of acidosis. Also be used to replenish electrolyte imbalance as a it adjacent for fevers diarrhea where the loss of bicarbonate can be significant. Pharmacology Sodium bicarbonate is a felt which on reaction with acid will raise the pH by lowering the concentration of hydrogen ion. NaHCO3 + HCl = CO2 + NaCl + H2O Thus NaHCO3 is used as an antacid in stomach or as an agent to increase the pH of urine or whole body. Indications : 1) Management of acidosis in cardiac arrest. 2) Management of metabolic acidosis in a) fever send disease b) uncontrolled diabetes c) circulatory in sufficiency from shock or dehydration 3) Alkalinization of urine. Contraindications 1) In hypoventilatory states 2) Metabolic and / or respiratory alkalosis. 3) Hypocalcemia 35


4) Chloride depletion Indications : 1) Cardiac arrest Cardiac arrest is often associated with a systemic acidosis with both respiratory and metabolic components. It was believed that this acidosis exacerbated

electrolyte

disturbances,

antagonized

the

effects

of

catecholamines, and reduced the threshold for ventricular fibrillation. This provides the rationale for the aggressive use of NaHCO 3 during CPR. The suggested initial dose is 1 m Eq. Kg body wt and further administration is to be guided by the measurement of arterial / venous blood pH and CO2 levels. NaHCO3 should never be given to its who are not ventilating adequately. 2) Metabolic Acidosis In

other

acute

forms

of

metabolic

acidosis,

Na

HCO3 may be added to other IV infusions. Parenteral solutions containing calcium ions should be avoided as precipitation may result. Recommended dose is one half of the calculated requirement followed by reassessment of the acids base. Contraindications 1) Hypoventilation : The respiratory acidosis from hypoventilation should be connected by improving the ventilation of the patient. Bicarbonate should never be given if the patient is not breathing normally.

36


2) Chloride depletion : Bicarbonate should not be used in patients losing chloride owing to vomiting or a continuous gastrointestinal fution . there is increased risk of severe metabolic alkalosis. 3) Hypocalcemia : There is increased risk that alkalosis may induce tetany 4) Hyperosmolar states : 8.4% bicarbonate high osmolar value ; so use of NaHCO3 should be carefully considered in a) Anuria or oliguria – because of increased risk of sodium retention. b) Edematous sodium-retaining conditions such as hepatic cirrhasis, CHF, impaired renal function, toxemia of pregnancy. CALCIUM CHLORIDE : Calcium has long bean known to increase the force of myocardial contraction. In addition, calcium ions also each enhance ventricular excitability. ATROPINE Atropine, an alkaloid extracted from atropa belladonna. Clinical pharmacology Major actions : Atropine has widespread central and peripheral effects. In the usual clinical dose of .5 to 1.0 mg its peripheral effects may include tachycardia without increased contractility, decreased production of sweat, bronchial, nasal, lacrimal and gastric secretions, and inhibition of micturition.

37


Cardiac Action Atropine increases sinus rate, and sinoatrial and Av conduction. Although it is generally believed that the usual therapeutic dose (0.4 – 1 mg, commonly 0.6 mg) causes tachycardia. Atropine inhibits salivary secretion, producing a dry mouth and difficulty in talking. Indications: I) BRADYARAYTHMIAS AND MYOCARDIAL INFARCTION Atropine is the it of choice in the severe bradycardia and hypotension or syncope associated with a hyperactive carotid sinus reflex and vagal over activity (vaso vagal syndrome). Atropine is also useful in severe bradycardia or temporary sinus arrest occurs during cardiac investigation initial dose of 0.6 or 1.2 mg is sufficient. Atropine may be of value in the it of Av conduction block caused by excessive vagal tone after acute myocardial infarction; it may reduce the degree of block. Atropine should be given only when bradycardia is associated with signs or symptoms of hypotension and hypoperfusion, conduction disturbance or entopic arrhythmias. 2) ANESTHETIC PREMEDICATION : Inhibition of secretion. Atropine is a long standing anesthetic premedication, used to reduce salivary and tracheobronchial secretions caused by many inhaled anesthetics, especially diethyl ether. It is less potent antisialogogue to than scopolamine but has less prolonged action and less postoperative sedation and confusion. The concomitant bronchodilator action of atropine may be a useful bonus in anesthetic use. Conventional dose 300 – 600 mg in adults 38


3) ANESTHETIC PREMEDICATION : INHIBITION OF CARDIAC REFLEXES Atropine is the traditional premedication for the prevention of the reflex bradycardia that may be associated with laryngoscopy, tracheal intubation and for the prevention of occulo-cardiac reflex during ophthalmic surgery. 4) Ophthalmic use : Local administration of atropine in form of eye drops is used in ophthalmology to produce mydriasis and cycloplegia. CONTRAINDICATION 1) Glaucoma Both local and systemic use of atropine can precipitate acute glaucoma, especially in patients predisposed to narrow – angle glaucoma. 2) Chronic lung disease Because of the reduction of bronchial secretions there may be a marked increase in viscosity

PRIMARY NON INJECTABLE DRUGS OXYGEN : 

Alternative drug : none

Most important drug in the entire emergency kit

O2 is supplied in variety of cylinder sizes but the minimal acceptable size is E cylinder. E – cylinder provide O2 – 30 min in emergency. haye cylinders (H) smaller (A through D)

O2 supplied in canisters through a chemical reaction is not adequate for the emergency kit. 39


Availability 

Compressed gas cylinders in variety of sizes.

VASODILATOR Drug of choice : Nitro glycerin Alternative drug : Amyl nitrite 

Vasodilators are used in the immediate management of chest pain – (angina pectoris and acute myocardial infraction) Two varieties – Nitroglycerin (TNG) as a tablet ad spray and an inhalant, amyl nitrite.

Nitroglycerin acts in 1 to 2 min. when placed sublingually

Amyl nitrite is available as an inhalant it is supplied in yellow vapourule, 0 – 3 ml, which when crushed and placed under the victims nose will act in about 10 sec to produce profound vasodilation.

Duration of action of amyl nitrite is shorter than that of TNG.

Side Effects : Contraindications And Precautions 

Transient pulsating headache, Facial flushing Hypotension

Contraindicated in hypotensive patients

Side effects of amyl nitrite are more intense which include flushing of the

face

pounding

pulse

dizziness,

intense

headache

hypotension. Availability: Nitroglycerin tablets , 0.1, 0.3, 0.6 mg tablet nitroglycerin spray. Nitrite vapuroles (yellow), 0.3 ml. 40

and


Emergency kit : One spray bottle of nitroglycerin (0.4 mg) NITROGLYCERIN Indications 1) Relief of angina pectoris 2) Prophylaxis of angina pectoris 3) Management of angina pectoris 4) Management of acute cardiac pulmonary edema 5) Management of chromic heat failure 6) Management of acute myocardial infraction. 7) Management of postoperative hypertension. Contraindications 1) Obstructive hypertrophic cardiomyopathy 2) Raised intracranial pressure. 3) Cardiac tamponade. Relating contraindication 1) Glaucoma 2) Mitral value proplapse Mode of Use All the clinical use depends upon production of venous and arterial dilatation and to some extent of dilatation of coronary arteries. 1) Relief of angina pectoris Sublingual nitroglycerin is widely used for the relief of effort induced and resting angina. It acts by reducing cardiac work. Effects are more 41


pronounced in the standing than in the supine position and may lead to syncope if vasodilation is pronounced. It is preferable to take nitroglycerin in sitting position. Nitroglycerin sublingually in a dose of 0.3 – 0.4 mg and repeated every 3 min until either the pain resolves or max of 4 to 5 tablets have been taken. 2) Prophylaxis of angina pectoris For prophylaxis of angina pectoris, sublingual nitroglycerin is very effective but its duration of effect last only for a few min to max of half an hour. Nitroglycerin ointment every 4 to 6 hr may be prescribed and effects last for several hours. Another alternative is buccal nitroglycerin in dose of 3 – 5 mg every 6 hr. Nitroglycerin patches, although claimed to have 24 hrs efficacies, have been shown to be ineffective for 24 h prophylaxis of angina pectoris. 3) Unstable angina Intravenous nitroglycerin is a very effective dry for relief of chest pain by myocardial ischemia dose of upto 200 mg min or higher have to be used. 4) Management of CHF : Nitroglycerin by reducing venous return, lowers elevated end – diastolic pressure in the right and left ventricles and improves myocardial function. The cardiac output either does not change or increases.

42


5) Management of hypertension IV nitroglycerin lower raised arterial presence and effective in selected group of patient. Contraindications : 1) Obstructive hypertrophic cardiomyopathy By causing vasodilatation nitroglycerin reduces venous return to heart and increases left ventricular out flow obstruction. 2) Raised intracranial pressure Should be avoided, or venodilatation may further increased already raised intracranial pressure 3) Cardiac tamponade Filling of the ventricles is impaired and nitroglycerin may further reduce this and cause syncope. 4) Glaucoma This is a relative contraindication of nitroglycerin as intraoculas pressure may increase. Acute over dosage Include hypotension, tachycardia, warm flushed skin, headache, palpitations and syncope. SECONDARY NONINJECTABLE DRUGS Drug of choice : Aromatic ammonia - Aromatic ammonia is the agent of choice as a respiratory stimulant for the emergency kit. 43


- Available in a silver – gray vapourule, which is crushed and placed under the victims nose until respiratory stimulation is effected. Aromatic ammonia (a noxious odor) acts by irritating the mucous membrane of the upper respiratory tract, thereby stimulating the respiratory and vasomotor centers of the medulla ; this in turn increases respiration and B.P. Therapeutic Indications Respiratory

depression

not

induced

by

narcotic

andgesies

vasodepressor syncope. Side effects : contra indications ad precautions Caution with person with chronic obstructive pulmonary disease (OPD) or asthma because it may precipitate bronchospasm resulting from its irritating effects on the mucous membranes of the upper – respiratory tract. Availability : Silver gray vaporole (0.3 ml aromatic ammonia) Suggested for emergency kit : 12 vaporoles next to O2, aromatic ammonia is the most commonly used drug in emergency kit. ANTIHYPOGLYCEMIC (ORAL) Agent of choice – carbohydrate Antihypoglycemic agents will be useful in the management of hypoglycemic reactions occurring in patient with diabetes mellitus or in the non – diabetic patient with hypoglycemia. 44


Therapeutic Indications Hypoglycemic state secondary to diabetes mellitus or forting hypoglycemia (in conscious patient) Slide Effects : Contraindications : Precautions 

Oral carbohydrates should not be administered to patient who do not have an active gag reflex or who are unable to dink without assistance.

Parental antihypoglycemics should be administered in these situations.

No side effects

Small tubes of decorative icing are useful in the management of unconscious hypoglycemic individuals. These tubes contain a thickened posts of concentrated sugar that can be applied in the form of a ribbon to buccal mucosa

Availability : Glucola, gluco-stat, fruit juices, sugar, tubes of BRONCHODILATING AGENT Drug of choice : METAPROTERENOL – 1ST NON – CATECHOLAMINE B- AGONIST Alternative drug : Epinephrine, isoproteronol 

Asthmatic patients and patients with allergic reactions manifested primarily by respiratory difficulty will require the use of bronchodilator drugs.

Although epinephrine remains the drug of choice in bronchospasm, its wide ranging effects on system lead to introduction of more specific

agents.

Metraproterenol

a

specific

beta

2

sympathomimetic has specific bronchial, smooth muscle relaxing 45


properties with little or no stimulatory effect on the cardiovascular and gastrointestinal systems (beta 1) 

In emergency situation in which the patients cardiovascular status is unknown, beta – 2 stimulations appear more attractive for management of acute asthmatic episode than agents such as epinephrine and isoproterernol, which have both beta – 1 ad beta – 2 stimulating properties.

It will be in an inhalator that dispenses a calibrated dosage of the medication. When the patient inhales as the agent is dispensed, allowing the drug to reach the bronchial mucosa, where it acts directly on bronchial smooth muscle.

One or two inhalations every hour is the maximal recommended dosage.

Therapeutic Indications 

Respiratory distress as seen in asthma.

Allergic reactions with primary respiratory phenomena.

Side effects : contraindications and precautions 

Metraproterenol,

epinephrine,

isoproteronol

has

potential

cardiovascular side effects. Producing tachycardia, and ventricular arrhythmias. 

Contraindicated in patients with preexisting tachyarrhythmias

Availability : Metraproterenol inhaler (alupent) : Epinephrine mistometer (medihales – epi) Isoproterenol mistometer (mediholar – 750)

46


EMERGENCY DRUGS I. Cardiovascular emergencies – drugs used 1) Acute myocardial infarction • Aspirin therapy • Nitroglycerine • Analgesics –morphine sulphate • Streptokinase 2) Unstable angina • Aspirin • Nitrates • β-blockers 3) Congestive heart failure • Vasodilators • Sodium nitroprusside • Digitalis 4) Hypertensive crisis • Nifedipine • Sodium nitroprusside • Nitroglycerine • Labetolol • Nicardipine • Esmolol 5) Shock • Fluid resuscitation • Vasopressors and inotropes • Dopamine 47


• Dobutamine 6) Malignant hyperthermia II. Respiratory : 1) Bronchial asthma : • O2 • Bronchodilators • Epinephrine • Systemic corticosteroids 2) Acute respiratory failure : • Bronchodilators • Corticosteroids III. Neurological emergencies : 1) Status epilepticus – Anticonvulsant • Diazepam • Phenytoin • Phenobarbital 2) Stroke : transient ischemic attack • Antiplatelet therapy • Anticoagulant therapy • Heparin and Warfarin IV. Endocrine emergencies 1) Thyroid crisis : • Antithyroid drugs – carbimazole • Antisympathetic drugs 48


• Corticosteroids

2) Acute adrenal insufficiency • Vol replacement – 5% dextrose • Corticosteroids 3) Myxedema crisis : • Thyroid hormone – levothyroxine • Corticosteroids V. Allergic reactions and syncope • Epinephrine VI. Metabolic emergencies • Hypoglycemia • Diabetic ketoacidosis

49


CARDIOVASCULAR EMERGENCIES : DRUGS USED I. ACUTE MYOCARDIAL INFARCTION : 1. ASPIRIN THERAPY : Aspirin produces a rapid antithrombotic effect by inhibiting cyclooxygenase and blocking formation of thromboxane A2 in platelets almost instantly. The best way is to ask the patient to chew half to one tablet (160-325 mg) of aspirin since buccal absorption of the drug is faster than absorption through the gastric mucosa. Ideally should be administered within 6 hrs of onset of symptom. - Aspirin is acetylsalicylic acid. It is rapidly converted in the body to salicylic acid which is responsible for most of the action. Precautions and contraindications : • Aspirin is contraindicated in patients who are sensitive to it and in peptic ulcer, bleeding tendencies. • An association between salicylate therapy and “Reyes syndrome”, a rare form of hepatic encephalopathy seen in children having viral (influenza, varicella) infection has been seen. So contraindicated in children. • In chronic lines disease cases of hepatic necrosis. Uses : 1) As analgesic, antipyretic 2) Acute rheumatic fever 3) Rheumatoid arthritis

50


2) NITROGLYCERINE : VASODILATOR Nitrates cause vascular smooth muscle relaxation by conversion to nitric oxide. This dilatation is more marked on the venous than the arterial side of the circulation, so that myocardial preload is reduced proportionately more than after load. - Nitrates also dilate the coronary arteries, relieving spasm and redistributing flow from epicardial to endocardial regions by opening up collateral channels. - Nitroglycerin sublingually in a dose of 0.3-0.4 mg and repeated every 3 min. - Nitroglycerin acts in 1 to 2 min when placed sublingually. Side effects : contraindications : precautions • Transient pulsating headache Facial flushing Contraindicated in hypotensive patients Nitroglycerin also available in spray bottles. 3) ANALGESICS : It is hear that the pain of AMJ is due to continuing ischemia of living jeopardized myocardium rather than to the effects of completed myocardial necrosis. Morphine sulfate and pethidine hydrochloride are the two traditional drugs used to control ischemic pain. Used dose is 10-15 mg – morphine If pain very intense IV in a dose of 2-5mg to be repeated 10-15 min half the dosage, 51


- Total dose in 24 hrs should not exceed 60 mg morphine Contraindications : It is also useful to remember that morphine may produce hypotension (due to venous pooling) and bradycardia (due to enhanced tone) and therefore should be avoided if any of these complications is present or anticipated, especially in inferior MI. Morphine sulfate : Opioid agonist Suggested for emergency kit : Morphine sulfate, 10mg /ml (2 or 3 mg/ml ampules) Treatment in the hospital 1. O2 Therapy : 3-4 lit / min 2. Thrombolytic therapy : – 3 thrombolytic agents a) Streptokinase b) Recombinant tissue plasminogen activator c) Anisolyated plasminogen activator complex Streptokinase : Is a non selective agent that induces a generalized fibrinolytic state characterized by extensive fibrinogen degradation. Half life- 30min. It is administered as an IV infusion of 1.5 million units over 60 min. - Before starting streptokinase therapy 100mg hydrocortisone and 25mg rhyriramine are administered IV to minimize risk of allergic reactions which include fever, rash, hypotension.

52


3. β - blockers : Atenolol or metaprolol (selective) Therapy can be initiated with an IV bolus of metaprolol 5mg this dose can be repeated a 5 min to a total dose of 15mg : with monitoring of vitals signs. 4. Nitroglycerin : IV nitroglycerin 10 µg / min β - blockers : IV β - adrenoreceptor blockers given early in the course of acute myocardial infarction reduce heart rate, BP and cardiac index, and thus help to limit the infarct size, relieve chest pain and decrease risk of ventricular arrhythmias. Contraindications to β-blockers : Hypotension - In case of uncertainly regarding the safety of β-blockade, an ultra short acting β-blocking agent (ESMOLOL) with half life of only 9min may be used to determine whether the patient can tolerate beta blockade. UNSTABLE ANGINA : 1) Aspirin therapy : In view of the widely accepted role of platelet aggregates in the genesis of ischemic episodes in unstable angina, aspirin is routinely prescribed. The inhibitory effects of aspirin on platelet aggregation occurs immediately and continue for 4-6 days after a single dose. - Aspirin has been shown not only to relieve ischemic episodes in unstable angina, but also to reduce the incidence of fatal and non fatal MI - A dose of 60-100mg – OD - When aspirin contraindicated, TICLOPIDINE – 20mg BD antiplatelet agents.

53


2) Nitrates : These are main stay in it of UA. By promoting coronary blood flow nitrates not only relieve anginal pain and prevent its recurrence, but also improves LV function. - Can be given sublingually, orally, tonically or IV sublingual nitroglycerin is available as 0.3, 0.4, and 0.6 mg tablets or metered dose spray (0.4mg) usually 0.4 mg tablets are prescribed. - Peak pharmacologic action occurs within 2min - Can be repeated at 5mm if symptoms persists. 3) β-adrenergic blocking agents : unless contraindications exists, 13 blockers should be combined with nitrates in all cases of unstable angina, adjusting the dose so as to maintain the heart rate between 50 – 60 beats / min. the combination (nitrates and B blockers) not only reduces the frequency of recurring ischemic episodes but also the occurrence of MI. even if the patient is taking nitrates and calcium antagonists, β blockers should be added. - However, such patients should be carefully monitored since a combination of β-blockers and calcium antagonists (especially veraparnil or diltiazm) may precipitate heart failure and / or severe bradycardia. Side effects : - Bronchospasm, Postural hypotension, depression. CONGESTIVE HEART FAILURE : Main drugs are 1) Digitalis which augments myocardial contractility 2) Diuretics which reduce the preload of heart 54


3) Vasodilators which reduce elevated after load and decrease left ventricular work. These 3 groups of drugs are complementary to each other and are used together in various combinations upon type and severity of HF. Vasodilators : are main stay of TT in HF. As venous and arterial vasoconstriction is important accompaniments of CHF, vasodilators are now used extensively in HF. The drugs currently employed most often are angiotensin – converting enzyme (ACE) inhibitors which are “balanced vasodilators” having action on venous and arterial beds. ACE inhibitors, as a class, effectively antagonize the rennin – angiotensin system and, by their direct action on peripheral vascular bed, decrease the impedance (resistance) against which the heart pumps in heart failure. ACE inhibitors have revolutionized the it of CHF, and are now front time drugs in management of HF both mild and severe. Besides being potent vasodilator, such drugs have additional properties beneficial in such patients. 1) Suppress angiotensin and aldosterone levels, and there by decrease salt and fluid retention. 2) Reduce neurohormonal stimulation (catecholamine concentration) and thus reduce the risk of sudden death. 3) Probably posses antianginal effect due to reduction in arterial pressure

without

causing

reflex

tachycardia

(thus

lowering

and

improve

myocardial oxygen demands). ACE

inhibitors

not

only

relieve

symptoms

hemodynamic profile, but have also (the only drug) been found to improve survival especially in cases with moderate and severe chronic HF. 55


TT may be started with any ACE inhibitor but in cases with borderline BP, especially when on diuretic therapy, captopril or enalapril may be safer because of their shorter duration of action. Initial dose should be small (captopril 6.25mg; enalapril 2.5mg), patient closely observed, and if there is no unusual drop in BP the next dose may be doubled. ACE inhibitors are generally safe, the only hazard being excessive hypotension. All ACE inhibitors are contraindicated in patients with intrinsic rend disease, systemic hypotension. Digitalis : Digoxin : This should be used as first line therapy in patient with failure and atrial fibrillation when it will usually provide adequate control of the ventricular rate together with a small positive inotropic effect. In emergency situation, 0.5 mg out of the total calculated dose should be given IV slowly over 5-10 min and remaining by oral route over next 24 hours (rapid digitalization). Digoxin toxicity : - Gastrointestinal – Anorexia, nausea, vomiting - SVS – bradycardia, ectopic beats. - Miscellaneous – fatigue, headache, confusion, hallucination. Diuretics : Diuretics in one form or the other are always used in HF whenever there is evidence of fluid retention. When diuretics are initiated for an acute exacerbation of heart failure, the goal of therapy should be a maximum net loss of 0.5-1.0 L of fluid / day (0.5-1.0 kg body weight) to prevent intravascular volume depletion. 56


- When treating advanced / refractory cases of HF, high potency loop diuretics. (furosemide and ethacrynic acid) are employed. Given IV their diuretic action starts within 15min, peaks in about 30-45 min and lasts for2-4 hours. - Large single daily doses are to be avoided since by causing acute volume depletion, such a regime is likely to activate resin – angiotensin aldosterone system which may prove counterproductive and may actually increase myocardial O2 demand. - Thiazide diuretics (hydrochlorothiazide, chlorthiolidone) can be used as initial agents in patients with normal renal function in whom only a mild diuresis is desired. Action : In heart failure diuretics produce an increase in urinary sodium excretion, leading to a reduction in blood and plasma vol, and may also cause a small but significant degree of arterial and venous dilatation. Diuretic therapy will, therefore, reduce preload and improve pulmonary and systemic venous congestion therefore it may also cause a small reduction in after load and ventricular vol leading to a fall in wall tension and increased cardiac efficiency. HYPERTENSIVE CRISIS : Hypertensive crisis is an all encompassing term which includes various acute life-threatening situations associated with hypertension. Conventionally classified as Hypertensive emergencies and hypertensive urgencies. Hypertensive emrgencies : are defined as a substantial increase in BP usually with a diastolic BP of greater than 120-130 mm/sy. - Accelerated – malignant hypertension. - Perioperative hypertension. 57


- Severe hypertension associated with a) CHF b) Stable angina. c) Transient ischemic attacks. Hypertensive emergencies include accelerated hypertension: defined as systolic BP typically exceeding 210 and diastolic BP greater than 130 presenting with headache, blurred vision, and malignant hypertension. - Hypertensive emergencies require immediate BP reduction (not necessary to normal ranges) to prevent or minimize end-organ damage i.e. - Hypertensive encephalopathy - Intracranial hemorrhage - Unstable angina pectoris. - Acute MI - Acute LVF with pulmonary edema. Immediate lowering of BP is required in these cases, and therefore parenteral therapy is preferred. The aim should be to reduce mean pressure (diastolic BP + 1/3 pulse pressure) to 120mm 14 or to lower mean pressure by 20-25%k, over 30-90 min. Initial therapy : If there is likely to be some delay in instituting parenteral antihypertensive therapy, nifedipine 5mg should be given sublingually. This may reduce the BP by 10-20% of the pretreatment level. Nifedipine is a calcium channel antagonist. Action : is to cause arteriolar vasodilation by selective blockade of the slow inward calcium channels in vascular smooth muscle cells. 58


The effect starts within 1-5 min and is maximum at15-20min. Such rapid reduction of BP is, however not without risk and therefore sublingual dose should not exceed 5mg at a time. Parentral drugs : 1) SODIUM NITROPRUSSIDE : It is most potent of the parenteral hypotensive agents, with a rapid onset of action and immediate reversibility. It also has minimal side effects. These qualities make it an ideal drug for most of the hypertensive emergencies. Action : It lowers the BP by primary vasodilation of both arterioles and veins. Nitroprusside may therefore, increase pressure but still the best drug in patients of hypertensive encephalopathy. The drug is administered IV through an infusion pump at a rate of 0.25 to 0.5mg/kg/min, with constant monitoring of BP. The dosage is adjusted according to BP response but should not exceed generally 3mg / Kg/min and infusion not continued beyond 12 hours. At this risk of (cyanide toxicity. 2) NITROGLYCERINE : it is a vasodilator, which given as a continuous IV infusion may be appropriate in situations in which sodium nitroprusside is relatively contraindicated, such as in patients with severe coronary insufficiency or advanced send on hepatic disease. It is preferred agent for patient with moderate hypertension because of its more favorable effects on pulmonary gas exchange and collateral coronary blood flow. Nitroglycerin reduces preload more than after load, and should be used in caution in acute MI. 59


3) Labetolol : This is combined α-β blocker, bit α - blocking properties predominate clinically in the it of hypertensive emergencies. Marked reduction in systemic vascular resistance results in lowering of BP with little change in cardiac output or heart rate. Because of the associated betablocade effect, the drug should be avoided in severe sinus bradycardia heart failure, and asthma. Labetalol : It bolus 20 – 80 mg every 10 min. Onset – 5 – 10 min. Duration of action – 3 – 6 hrs. Its infusion :- 2 mg / min 4) Nicardipine : are effective IV calcium antagonist. Used for it in post – operative hypertension and when given IV are as effective as nitroprusside in rapidity of antihypertensive action. There is little change in heart rate, and only a small increase in cardiac output, Nicardipine has apparently greater selectivity for cerebral vessels and is perhaps the drug of choice in management of cerebrovascular hypertensive emergencies. Nicardipine : IV, 5 – 10 mg / Action :- Continuous during infusion 5) Esmolol : Is a parenteral, short acting, cardio selective β adrenergic antagonist that can be used in it of hypertensive emergencies in patient whom β blocker intolerance is a concern. β - adrenergic antagonist may be infective when used as monotherapy in case of severe hypertension and frequently combined with other agents

60


SHOCK Fluid resuscitation : usually is the 1st it used. All patients in shock should receive an initial IV fluid challenge. The amount of fluid necessary is unpredictable but should be based on changes in clinical parameters, including arterial BP, urine output, cardiac filling pressures and Co., crystalloid fluid solutions (0.9 % NaCl or Ringer’s lactate) usually are administered. Blood Volume should be administered to patient with significant anemia or active hemorrhage. Vasopressors and Inotropes DOPAMINE : (3 , 4 – dihydroxphenylethylamine) is immediate metabolic precursor of norepinephrine and epinephrine. Like norepinephrine, it also acts as both α and β adrenergic receptors, but imp difference is that the effects are dose dependent. When used in low doses ( 2- 5 mg / kg / min) it has a predominantly beta – 1 adrenergic stimulant action on myocardial contractility and therefore results in significant increase in stroke volume and cardiac output. In this dosage it also produces vasodilation (promotes renal perfusion) and lacks (the undesirable) chronotropic or peripheral vasoconstrictor effect of norepinephrine with increasing doses, there is dose dependant increase in chronotropic and α - adrenergic vasoconstrictor effects with consequent decrease in tissue perfusion. At larger doses ( > 15 – 20 mg / kg/ min) its hemodynamic effects come to resemble those of epinephrine with predominant chronotropic and α adrenergic stimulant action. Accordingly, systemic vascular resistance (after load) increases and this coupled with tachycardia may aggravate myocardial ischemia. 61


In cases with cardioagenic shock, dopamine infusion should be started at a low dose ( 2- 5 µg / kg /min) to improve cardiac output and renal perfusion and the dose carefully increased to maintain a systolic 13 p of 90 – 100 8) Dobutamine : This is a synthetic catecholamine with predominantly beta – adrenergic agonist properties which amount for its inotropic and chronotropic effects. Unlike dopamine, it lacks any appreciable beta – adrenergic agonist action, and therefore, has little effect on systemic vascular resistance even at larger doses. In the case of cardiogenic shock it has therefore near ideal vasopressor properties. However when compared to dopamine, it lacks renal vasodilator action. It should not therefore, be used alone in the severely hypotensive patient rather it should be given simultaneously with dopamine infusion. Used in this manner, dobutamine may reduce dopamine requirement, and thus pharmacologically the best possible improvement in hemodynamic profile viz., increase in stroke volume and cardiac output, and reduction in left ventricular filling pressure with only minimal increase in heart rate, peripheral vascular resistance and myocardial O2 requirement. 9) Norepinephrine : It is a powerful catecholamine producing both α and β – adrenergic stimulation, and used to be the mainstay of patient of (cardiogenic) shock before the availability of dopamine. Though its α – adrenergic stimulation (which predominates) it acts as a potent vasoconstrictor (increases afterload) while through the β – adrenergic stimulation it has relatively modest (myocardial) inotropic and chronotropic effects.

62


All these pharmacological actions result in increased myocardial O 2 demand

and

hence

are

likely

to

worsen

myocardial

ischemia.

Norepinephrine is therefore now notused in cardiogenic shock. MALIGNANT HYPERTHERMIA Obtundation

and

muscular

rigidity

characterize

malignant

hyperthermia syndrome. - Serums creative kinase is markedly elevated. - Multiple

genetic

mutations

are

associated

with

malignant

hyperthermia syndrome, with a likely common abnormal elevation in intracellular calcium, following triggering factors (e.g. halothane anesthesia) Management - Discontinuation of offending anesthetic agent, aggressive supportive care that focuses on oxygenation, ventilation, circulation, correction of acid – base and electrolyte derangements and dantrolene sodium, 1 – 10 mg / kg / day, to reduce muscular rigidity.

RESPIRATORY EMERGENCIES – DRUGS USED BRONCHIAL ASTHMA 1) Supplemental O2 2) Bronchodilators : are first line of it is an asthma attack and act by relaxing the smooth muscle in all always. - When given by nebulizer beta 2 agonist constitute the first line of therapy of acute sever asthma. 1 or 2 ampoule of salbutamol 2.5 – 3 mg or terbutaline 5 – 10 mg should be given initially and should be neubulized even 30 min. - Intermittent aerosol it with salbutamol 2 – 5 mg should be continued every 4 hrs. 63


- When beta-2 agonists cannot be mobilized (e.g. patients on mechanical ventilation), Terbutaline should be used SC in a dose of 0.25-0.5 mg every 6-8 hours. Additional Bronchodilators : Include anticholinergics (ipratopium bromide) and theophyllines. Though less potent that beta agonist, these are invariably used in management of ASA. Ipratopium bromide

is particularly useful in patients with

bronchospasm induced by beta blockers or when acute asthma is exceptionally severe. b) EPINEPHRINE (Adrenaline) : This is a non selective β-adrenergic agonist and is associated with a high incidence of cardiovascular side effects due beta-1-adrenergic receptor stimulation. However since the drug is a powerful bronchodilator, a trial is worthwhile, and 1ml of1:1000 adrenaline hydrochloride may be injected SC slowly in 2 or3divided doses 15 minutes apart provided the patient is not over 40, and does not have already tachycardia. - Avoided in patients with cardiac disease, hypotension, hyperthyroidism or diabetes. 3. Systemic corticosteroids : Corticosteroids control airway wall inflammation by inhibiting release of mediators from macrophages and eosinophils (but not from most cells). Corticosteroids thus block the late phase reaction and subsequent hyper-responsiveness. Additionally, steroids decrease mucus production and are mucosal edema resulting from microvascular leakage in the air ways.

64


ACUTE RESPIRATORY FAILURE - 1st relief of bronchoconstriction - maintaining acceptable level of PaO2 and PaCO2 - Control of infection. 1) Bronchodilators : Best given by nebulizer every 2-45 hours. - oral administration may aggravate tachycardia, and produce tremor and tachyphylaxis. - Parenteral beta- agonists are rarely indicated - Anticholinergic drugs are also beneficial. 2) Corticosteroids 3) O2 Therapy 4) Antibiotics NEUROLOGICAL EMERGENCIES : STATUS EPILEPTICUS ANTICONVULSANTS 1. DIAZEPAM (Calmpose) : very rapid action when given IV, and drug of choice in instant control of seizures. Adult dose 0.2mg/kg IV at rate of 5 mg /min. Because of short action, it should be followed by phenytoin to prevent recurrence of seizures. Diazepam must be given IV because when administered by IM route, it does not have anticonvulsant action. If parental preparation of lorazepam is available, it is preferable (over diazepam), in the initial management of convulsive status since, being fewer lipids soluble, it has a longer effective anticonvulsant half life. IV dose of lorazepam is 0.1 mg/kg administered at a rate of 2mg /min.

65


2. PHENYTOIN (Dilantin) : After IV diazepam has terminated the seizure, phenytoin should be given IV to prevent its recurrence, or to control status epilepticus in case it persists following diazepam. The used adult dose in adults is 15-20 mg/kg (not glucose containing solution in which phenytoin precipitates) and administered gradually at rate not exceeding 50mg / min. Advantages of Phenytoin are - High effectiveness in controlling convulsions, - Relatively long half-life and its lack of CNS depression. Side effects : - Hypotension - Cardiac arrhythmia : therefore BP and ECG- monitored. - IV phenytoin is contraindicated in patients with heart block or severe myocardial disease. - Phenytoin should not be given 1m since it is poorly absorbed. 3. PHENOBARBITAL : long acting. If the patient continues to have seizures 15-20 min after the loading dose of phenytoin, (5-10 mg/kg of phenytoin), Phenobarbital should be given IV 10mg/kg at a rate of 50100 mg / min. If the seizure still continue, a similar dose can be repeated (upto total dose of 20mg/kg).

Note : When diazepam and phenobarbitone are used simultaneously or sequentially, the patient must be intubated (for emergency ventilation) as this combination may result in respiratory depression and even respiratory arrest.

66


CEREBROVASCULAR CATASTROPHES / ACCIDENTS (CVA) Acute vascular disruption to a specific region of the brain (“STROKE”) constitutes one of the emergencies encountered Stroke encompasses several entities with vastly different clinical presentation all of which arise from either lack of blood supply (ischemia) or leakage of blood outside the normal vessels (Haemorrhage) stroke can be classified as pathophysiological basis into 2 broad categories – Ischemic stroke, Haemorrhagic stroke. Transient ischemic attacks : 1) These comprise briefly and transient episodes of focal dysfunction of the brain, without any clinical sequelae. The symptoms came suddenly, reach the peak within a few seconds or a few minutes and are generally over in less than half an hour. On some occasions, TIA may continue for several hours through seldom more than 24 hours. Such transient ischemic episodes are through to result from either an intermittent decrease in perfusion in an area of the brain (“Low flow” with inadequate collateral circulation) or from embolization of platelet fibrin material from heart or from atherosclerotic lesions in large arteries in neck (artery to artery embolus) 1) ANTIPLATELET THERAPY Aspirin is now universally accepted as the most effective drug available to prevent TIA’s as well as to reduce the incidence of subsequent stroke. It has been shown that Aspirin produces a rapid antithrombotic effect by inhibiting cyclooxygenase and blocking formation of thromboxane A 2 in

67


platelets almost instantly, when given in small doses than in large doses. A common dose is 325 mg/day. The combination of aspirin (25mg bid) and extended release dipyridamole (200mg bid) may be more effective in stroke prevention after TIA. Dipyridamole is a vasodilator that in combination with aspiration reduces thrombosis in patient with thrombotic disease. 8.

Patient

who

TILOPIDINE.

cannot This

tolerate

newer

aspirin

antiplatelet

should agent

be

prescribed

prevents

platelet

aggregation by inhibiting fibrinogen binding on to the platelet membrane. 9.

However the drug carries a small rise of producing leucopenia and rash.

2) ANTICOAGULANT THERAPY : Therefore Heparin and warfarin controversies. Heparin anticoagulant effect of Heparin is medicated by an endogenous component of plasma termed heparin factor. Patient has not yet been firmly established that anticoagulation effectively reduces the stroke after TIA. RENAL EMERGENCIES : PRINCIPLES OF MANAGEMENT 1) Identification and several of underlying cause. 2) Fluid management 3) Control of Electrolytes 4) Acid base homeostasis. 5) Maintenance of nutrition 6) Institution of dialysis. ENDOCRINE EMERGENCIES : 68


THYROID CRISIS : Aim 1) Inhibit both hormone synthesis and release. 2) Suppress the sympathetic aspect of paripheral 3) To control precipitating factor. 1) Antithyroid drugs : These are required to block thyroid hormone synthesis and release. Thyroid hormone synthesis is achieved by use of carbimazole (Neomercazole) 60-80 mg or propylthiouracil 600-100 mg daily in divided doses orally or through Ryles tube if oral medication is not possible. -Propylthiouracil also blocks peripheral conversion of T4 to T3, - disease – is these drugs may take about a week to lower serum T3 level. -To inhibit hormone release. Iodine should be given in large doses IV. In emergent situations, iodine can be given IV as sodium iodide, 0.5-1.0 g in one litre of normal saline every 8-12 hours for 24 hours. -An alternative approach is to administer iodinated X-ray contrast agent, sodium ipodate, instead of iodide. It has additional advantage of inhibiting peripheral conversion of T4 to T3. 2) ANTISYMPATHETIC DRUGS : β-blockers often give dramatic results decreasing heart rate within 2-3 hours when given orally, and within minutes when given IV. To relieve symptom of hyperthyroidism such as palpitations humor and anxiety. Propranolol 1-3 mg given slow IV and repeated 1mg after 3-4 hours. During this patient should be loosely observed for pulmonary edema, bronchospasm.

69


3) CORTICOSTERIODS : Since biological half-life of cortisol is sheltered and adrenocortical reserve is reduced in thyrotoxic crisis, large doses of corticosteroids should be given E.g. Hydrocortisone 200 mg IV initially, forward by 100 mg every 6 hours. ACUTE ADRENAL INSUFFICIENCY : - Key element in it is speed of action, replenishment of intravascular volume and administration of corticosteroids. 1) Volume replacement : Severe volume depletion, hyponatremia and hypoglycemia invariably exist together in acute adrenal insufficiency. The fluid deficit often exceeds 6% of body weight. 5% dextrose in normal saline is fluid of choice and should be infused at an initial rate of 500-1000 ml/hr. therapy guided by hourly record of pulse, BP. 2) Corticosteroids : Hydrocortisone provides the best steroid replacement as it contains both glucocorticoid and mineralocorticoid activity. An initial dose of 200mg IV over 3-5 min should be followed by 100mg (1.5mg/kg) every 6 hours. IV should be continued for 24 hours after recovery from adrenal crisis. Thereafter prednisolone in daily dose of 20-40 mg. 3) Other measures : If hypotension – vasopressors such as Dopamine. MYXEDEMA CRISIS : 1) Thyroid hormone : For quick improvement in thyroid status, it should be started with levothyroxine IV in a loading dose of 200-400 microgram followed by 50-100 microgram IV daily until oral therapy can be relied upon.

70


2) Corticosteroids : Adrenal corticosteroids have been found deficient in myxedema coma and therefore, should be replenished especially if hypotension is a problem. For this purpose 200 mg hydrocortisone should be given IV initially followed by 100 mg 3-4 times daily. 3) Rewarming: Hypothermia. AILERGIC REACTIONS Regardless of the cause, prompt treatment of anaphylactic and anaphylactoid reaction is mandatory, since death may occur within minutes or hours after the onset of 1st symptom. The specific drug fro all such reactions is EPINEPHRINE. It prevents continued mast cell activation, reduces mast cell mediator release and reverse the action of mediators on target tissues. If hypersensitivity is acute and generalized but not life threatening (eg. pruritis, or urticaria, laryngeal edema, acute bronchospasm). 0.3-0.5ml of 1:1000 epinephrine should be given SC and repeated 2 or 3 times at 5-7 minute intervals as required. In cases who develop shock, SC epinephrine is not enough. Such cases should be given 0.3ml epinephrine IV diluted 1:50,000 along with volume expanders and vasopressors (dopamine) is intractable hypotension develops. Other measures is antihistamine IM and (when severe bronchospasm exist) IV aminophylline. SYNCOPE : 10.Trendelenburg position and 100% O2. 11.Spirit of ammonia may be placed under right nose. This noxious odor stimulates the respiratory and vasomotor centers of the medulla. 71


HYPOGLYCEMIA : 1) Autonomic (or neurogenic) symptoms : Include sweating, palpitation, and hunger. Increased secretion of counter-regulatory hormones (e.g. Epinephrine) account for these symptoms. 2) Neuroglycopenic symptoms : develop as blood glucose decreases further include impaired concentration, irritability, blurred vision, lethargy, and development of Seizure or lama. TT: 1) Readily absorbable carbohydrates : (e.g. Glucose, and sugar containing beverages ) can be administered orally to conscious patients for rapid effect. Hypoglycemia associated with a carbose or miglitol therapy should be preferentially be treated with glucose, because these Îą-glucosidase inhibitors block the digestion of disaccharides and complex carbohydrates. 2) IV Dextrose : Is indicated for severe hypoglycemia, in patients with altered consciousness, and during restriction of oral intake. An initial bolus 20-50 ml 50% dextrose, should be given immediately followed by infusion of D5 to maintain blood glucose above 100 mg/dl. 3) Glucagon : 1mg / ml (or SC) is an effective initial therapy for severe hypoglycemia in patients who are unable to maintain oral intake or in whom on an IV access cannot be secured immediately. DIABETIC KETOACIDOSIS AND COMA : Specific measures : 1) Fluid therapy: Severe dehydration (due to osmotic diuersis) is an important accompaniment of DKA and needs to be managed aggressively. 72


The usual fluid deficit is 4-6 liters (80-100 ml/kg body weight) IV fluid therapy should be started. Initially 1 liter of fluid –1st hour followed by 250-500 ml / hr. for next 24 hours. Until BP is stabilized. Thereafter, 1 liter of fluid – every 4 to 6 hours for 24 hour. Type of fluid : 12.Normal saline solution is the fluid of choice in the initial stages as it quickly restores intravascular volume and avoids a rapid fall in extracellular osmolarity. PRACTICAL APPROACH : As soon as DKA is diagnosed 20-40 units of soluble insulin should be given, half IU and half IM, depending upon one severity and duration of ketosis and the degree of impairment of consciousness. Note : SC insulin should never be used in DKA. It is slowly absorbed and has a long half life (about 4 hrs), so there is a delay in onset of action. IM insulin should be given in deltoid muscle (not in glutted lesion)

73


REFERENCES : 1. medical emergencies in the dental office, Malamed 2. The pharmacological basis of therapeutics Goodman and Gillman’s 3. Essentials of Medical Pharmacology K.D. Tripathi 4. Washington Manual of Medical Therapeutics 5. Pharmacology and Pharmacokinetics Satoskar and Bandarkar 6. Principles and Practice of Medicine Davidson’s 7. Medical Emergencies in General Practice SP Gupta and Dinesh K Gupta 8. Current Medical Diagnosis and Treatment CMDT 2003. 9. OMSCNA- PHARMOCOLOGY- Vol 13, no. 1, Feb 2001.

74

Emergency drugs / dental implant courses by Indian dental academy  

The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide r...

Read more
Read more
Similar to
Popular now
Just for you