Week 6 chapter Pharmacology of Emergency Medications Flashcards
advanced cardiac life support (ACLS)
The American Heart Association (AHA) states that the highest survival rate after cardiac arrest occurs in patients who receive cardiopulmonary resuscitation (CPR) within 4 minutes and who are additionally provided medications through advanced cardiac life support (ACLS) within 8 minutes. Time is life! The patient with no blood circulation for more than 4 minutes will likely have brain damage. If spontaneous circulation is not restored within 8 minutes, the patient will probably die. For these reasons, the technologist cannot rely solely on other medical professionals to provide care to patients experiencing a life-threatening emergent condition.
alpha receptors
Pharmacodynamics.
Epinephrine elicits sympathomimetic (mimics the sympathetic nervous system) effects on various organ systems by attaching to and stimulating the alpha-1 (α1), alpha-2 (α2), beta-1 (β1), and beta-2 (β2) receptors. Table 11-1 outlines the various effects that can occur when these receptors are stimulated by epinephrine. The effects of epinephrine on the various receptors are dose dependent. Low doses generally result in a predominance of beta receptors, whereas higher doses result in a predominance of alpha receptors. In cardiac arrest, epinephrine is primarily given in doses sufficient to stimulate α1 receptors so that arterioles (small blood vessels) can constrict. This produces a marked increase in blood pressure. When combined with chest compressions, epinephrine is used to cause a return of spontaneous circulation (ROSC).
basic life support (BLS)
CARDIORESPIRATORY ARREST
The American Heart Association (AHA) states that the highest survival rate after cardiac arrest occurs in patients who receive cardiopulmonary resuscitation (CPR) within 4 minutes and who are additionally provided medications through advanced cardiac life support (ACLS) within 8 minutes. Time is life! The patient with no blood circulation for more than 4 minutes will likely have brain damage. If spontaneous circulation is not restored within 8 minutes, the patient will probably die. For these reasons, the technologist cannot rely solely on other medical professionals to provide care to patients experiencing a life-threatening emergent condition. A medical imaging technologist can call for help and then begin basic life support (BLS), as outlined by the AHA or American Red Cross, until assistance arrives. Every technologist should be certified in BLS. However, prudence would dictate the technologist be prepared for the possibility that the emergency team may be delayed or may need extra assistance. Therefore, familiarity with advanced life support procedures and medications is recommended.
amiodarone
Amiodarone
Amiodarone is an antidysrhythmic agent used in patients experiencing cardiac arrest. Amiodarone use has become more frequent over the years because it contains actions that mimic all classes of antidysrhythmic medications. Therefore, amiodarone is a relatively good choice in emergency situations when the exact focus of rhythm disturbance is unknown and when a patient has a heart condition.
Pharmacodynamics.
Amiodarone suppresses dysrhythmias by various mechanisms, including sodium channel blockade (see lidocaine discussion), beta-receptor blockade, calcium channel blockade, and membrane stabilization. These actions result in delayed repolarization of cardiac cells by prolonging the action potential and the refractory period in myocardial cells.
Pharmacokinetics.
Amiodarone is distributed extensively in many tissues, with an elimination half-life as long as 58 days. Because of rapid distribution into multiple tissues, amiodarone must be given by an initial bolus, followed by a continuous IV drip, in patients with cardiac arrest. When the patient stabilizes, the drug can be converted to oral therapy. Amiodarone is metabolized by the liver to the metabolite N-desethylamiodarone. Both amiodarone and N-desethylamiodarone are excreted in the urine.
Indications.
Amiodarone is recommended for pulseless ventricular tachycardia, shock-resistant ventricular fibrillation, polymorphic ventricular tachycardia, and wide-complex tachycardia, as well as for rate control in atrial fibrillation or flutter.
Dosage and administration.
For pulseless ventricular tachycardia or shock-resistant ventricular fibrillation, amiodarone should be administered by IV push as a 300 mg/30 ml D5W solution. A second dose of 150 mg/30 ml D5W may be given in 3 to 5 minutes if no effect has occurred. It is important to note that amiodarone will cause hypotension; thus, if the patient has hypotension, it is strongly recommended to administer this bolus over a 10-minute period. If amiodarone is effective, a continuous IV drip containing 450 mg/250 ml D5W should be set to infuse at 1 mg/min for 6 hours, then 0.5 mg/min for at least 18 hours over a minimum of 24 hours. In the event that a higher dose is required, the maximum daily dose should not exceed 2200 mg.
Adverse effects.
The most frequent adverse effect seen with IV amiodarone is hypotension. Other cardiac effects may include dysrhythmia production. Long-term use can lead to pulmonary fibrosis (reported within 6 hours of initiation) and hypothyroidism.
Stability.
Commercially prepared amiodarone injections are stable until the expiration date listed on the product. Amiodarone injection is stable at temperatures ranging from 20° to 30° C when protected from light. Once diluted in D5W, the drug does not need protection from light and should be discarded after 24 hours. This medication loses approximately 10% of its potency when placed in a polyvinyl chloride bag; thus, a glass bottle or polyolefin bag is recommended for preparing IV drips of more than 2 hours. Amiodarone is incompatible with many medications, including aminophylline, cefamandole, cefazolin, mezlocillin, heparin, and sodium bicarbonate. Either a separate IV line should be used or the line should be flushed with NS before amiodarone injection.
antidiuretic hormone (ADH)
Epinephrine also stimulates β1 receptors in the posterior pituitary gland (located at the base of the brain) to cause release of antidiuretic hormone (ADH, vasopressin), which is also a potent vasoconstrictor and water preserver. Again, the combination of vasoconstriction and water preservation leads to an increase in blood pressure.
atropine
Atropine
Atropine is an antimuscarinic agent frequently used in patients experiencing cardiac arrest.
Pharmacodynamics.
Atropine competitively inhibits the action of acetylcholine or other cholinergic stimuli at the muscarinic receptors in the parasympathetic nervous system. Box 11-1 lists the various effects that occur when muscarinic receptors are stimulated in the parasympathetic nervous system; the competitive inhibition of these receptors by atropine generally yields the opposite effect.
Atropine is an antimuscarinic agent frequently used in patients experiencing cardiac arrest.
Pharmacodynamics.
Atropine competitively inhibits the action of acetylcholine or other cholinergic stimuli at the muscarinic receptors in the parasympathetic nervous system. Box 11-1 lists the various effects that occur when muscarinic receptors are stimulated in the parasympathetic nervous system; the competitive inhibition of these receptors by atropine generally yields the opposite effect.
Pharmacokinetics.
Atropine has an onset of action of 2 to 4 minutes after IV administration. Atropine is absorbed through the oral, intramuscular, and pulmonary routes; however, the IV and ET (pulmonary) routes are the only accepted routes for cardiac arrest victims. Atropine distributes well throughout the body and will lead to side effects in the parasympathetic nervous system. Atropine is metabolized by the liver to tropic acid, tropine, tropic acid esters, and glucuronide conjugates. The half-life of elimination for atropine is 2 to 3 hours. Atropine and its metabolites are eliminated principally in the urine, but some may be excreted by pulmonary exhalation.
Indications.
Atropine is indicated for cardiac arrest patients with hemodynamically significant bradycardia, first-degree atrioventricular block, and ventricular asystole (flat line). Atropine may also be used when attempts at intubation lead to vagal nerve (a parasympathetic nerve) stimulation resulting in symptomatic bradycardia.
Dosage and administration.
Atropine should be given via rapid IV push at doses ranging from 0.5 to 1.0 mg every 3 to 5 minutes until the desired heart rate is achieved. Ventricular asystole generally requires at least 1.0 mg. A cumulative dose of 3.0 mg generally should not be exceeded, since this will lead to complete vagus nerve blockade. Pediatric patients require 0.02 mg/kg, with a minimum dose of 0.1 mg and a maximum single dose of 0.5 mg in children and 1.0 mg in adolescents; the cumulative maximum dose for children is 1.0 mg and for adolescents is 2.0 mg.
If atropine is given via slow IV push, a paradoxical action may occur leading to a further decrease in heart rate that could be lethal. If the IV route is unavailable, either the ET or the IO route can be used. The technique for ET administration is the same as for epinephrine, discussed earlier.
Adverse effects.
Serious adverse effects of atropine include a worsening of myocardial ischemia or extension of infarct zone, ventricular fibrillation, and ventricular tachycardia. A paradoxical slowing of heart rate may occur with low doses of atropine and in patients who receive the drug by slow IV push. Less severe adverse effects include dry mouth, blurred vision, constipation, urinary retention, pupillary dilation (mydriasis), headache, nervousness, progression of angle-closure glaucoma, drowsiness, weakness, dizziness, flushing, insomnia, nausea, vomiting, gastrointestinal bloating, bad taste in mouth, mental confusion, and central nervous system excitement.
Stability.
Commercially prepared atropine injections are stable until the expiration date listed on the product. Atropine products are unstable when exposed to light for long periods and should be protected from light when in storage. Atropine is incompatible with sodium bicarbonate, norepinephrine, metaraminol bitartrate, methohexital, and pentobarbital.
beta receptors
Pharmacodynamics.
Epinephrine elicits sympathomimetic (mimics the sympathetic nervous system) effects on various organ systems by attaching to and stimulating the alpha-1 (α1), alpha-2 (α2), beta-1 (β1), and beta-2 (β2) receptors. Table 11-1 outlines the various effects that can occur when these receptors are stimulated by epinephrine. The effects of epinephrine on the various receptors are dose dependent. Low doses generally result in a predominance of beta receptors, whereas higher doses result in a predominance of alpha receptors. In cardiac arrest, epinephrine is primarily given in doses sufficient to stimulate α1 receptors so that arterioles (small blood vessels) can constrict. This produces a marked increase in blood pressure. When combined with chest compressions, epinephrine is used to cause a return of spontaneous circulation (ROSC).
cardiac arrest
**Cardiac arrest **is a condition in which the heart ceases to pump blood adequately to the rest of the body. A respiratory arrest is a condition in which the patient becomes unable to breathe; thus the body is inadequately oxygenated. If not treated promptly, a respiratory arrest will progress to a full cardiac arrest, known as cardiorespiratory arrest. A full cardiac arrest becomes lethal if immediate intervention does not occur. Management of cardiac arrest requires a systematic approach.
cardiopulmonary resuscitation (CPR)
CARDIORESPIRATORY ARREST
Cardiac arrest is a condition in which the heart ceases to pump blood adequately to the rest of the body. A respiratory arrest is a condition in which the patient becomes unable to breathe; thus the body is inadequately oxygenated. If not treated promptly, a respiratory arrest will progress to a full cardiac arrest, known as cardiorespiratory arrest. A full cardiac arrest becomes lethal if immediate intervention does not occur. Management of cardiac arrest requires a systematic approach.
The American Heart Association (AHA) states that the highest survival rate after cardiac arrest occurs in patients who receive cardiopulmonary resuscitation (CPR) within 4 minutes and who are additionally provided medications through advanced cardiac life support (ACLS) within 8 minutes. Time is life! The patient with no blood circulation for more than 4 minutes will likely have brain damage. If spontaneous circulation is not restored within 8 minutes, the patient will probably die. For these reasons, the technologist cannot rely solely on other medical professionals to provide care to patients experiencing a life-threatening emergent condition. A medical imaging technologist can call for help and then begin basic life support (BLS), as outlined by the AHA or American Red Cross, until assistance arrives. Every technologist should be certified in BLS. However, prudence would dictate the technologist be prepared for the possibility that the emergency team may be delayed or may need extra assistance. Therefore, familiarity with advanced life support procedures and medications is recommended.
Code Blue
The technologist should also be familiar with emergency pager systems so that emergency assistance can be summoned swiftly and efficiently. Generally, a standardized phrase such as Code Blue or a fictitious physician’s name such as “Dr. Stat” is used to summon an emergency team to the area where immediate assistance is required. Each medical facility has its own procedure to call for emergency assistance. It is the professional duty of the medical imaging technologist to know this procedure clearly.
dopamine
Dopamine (Intropin)
Dopamine is the pharmaceutical equivalent of endogenous dopamine. Endogenous dopamine is a precursor to norepinephrine and epinephrine naturally produced by the body.
Pharmacodynamics.
Dopamine has dose-dependent effects on the various sympathetic (adrenergic) nervous system receptors. At low doses, dopamine primarily stimulates the dopamine receptors in the renal, coronary, intracerebral, and mesenteric arteries. This leads to arteriolar vasodilation with increased blood flow to the respective organs. At moderate doses, dopamine will also begin stimulating the β1 receptors to cause increases in contractility, force of contraction, and stroke volume in the myocardium. This effectively increases cardiac output in patients in shock or with congestive heart failure. At high doses, dopamine begins stimulating alpha receptors. When high doses are used, the net effects are a combination of dopamine receptor and β1-, α1-, and α2-receptor stimulation; no β2-receptor stimulation occurs. At very high doses, the primary pharmacodynamic effects seen are those associated with α1-receptor stimulation.
Pharmacokinetics.
Dopamine has an onset of action of 2 to 4 minutes, with a duration of action of less than 10 minutes. Renal vasodilation with increased urine output may take up to 20 minutes. Dopamine is metabolized to homovallinic acid (HVA), norepinephrine, and other chemicals by the enzymes COMT and MAO. The resulting metabolites of dopamine are excreted in the urine. A small fraction of dopamine is excreted unchanged in the urine.
Indications.
Dopamine is indicated for treating hypotension secondary to congestive heart failure, myocardial infarction, trauma, sepsis, and overt heart failure. Dopamine is also used to increase urine output in patients with renal failure. In cardiac arrest, dopamine is used as second-line therapy, after epinephrine and fluids have failed to attain ROSC. Dopamine is also used to support blood pressure further after successful ROSC in cardiac arrest victims.
Dosage and administration.
Dopamine is administered by IV infusion through a controlled delivery device such as an electronic pump. The appropriate total dose should be diluted in either NS or 5% dextrose in water (D5W). Low-dose dopamine is considered to be less than 5 μg/kg/min. Intermediate dosing is between 5 and 10 μg/kg/min. High-dose dopamine is generally considered to be any dose above 10 μg/kg/min.
Generally, dopamine is used as the premixed solution. Table 11-2 lists available dopamine preparations. If mixing the solution is required, then an easy method is by placing 800 mg into 500 ml of either D5W or NS and attaching a microdrip (60 drops/ml calibration) tubing set to the infusion bag. This gives a total concentration of 1600 μg/ml. An average 70-kg patient would then require approximately 700 μg/min (10 μg/kg/min) for α1-receptor effects to increase blood pressure. This calculates to be 42,000 μg/hr (700 μg/min for 60 minutes), which is approximately 26 ml/hr of the 1600-μg/ml solution. By using the microdrip tubing, the technologist can easily titrate the drip rate to 26 drops/min, which is equal to 26 ml/hr. (Note: If macrodrip tubing [calibrated at 15 drops/ml] is used, the drip rate per minute is equal to ml/hr divided by 4; approximately 6.5 drops/min = 26 ml/hr.)
Adverse effects.
Dopamine produces dose-dependent adverse effects. Hypotension occurs with low doses. Hypertension, cardiac dysrhythmias, headache, nausea, vomiting, angina pectoris, and tachycardia may occur with high doses. If dopamine extravasates into surrounding tissues, necrosis may occur. Gangrene of the extremities has occurred with high-dose infusions in patients with diabetes or vascular occlusive diseases. Phenytoin (Dilantin) may interact with dopamine and cause hypotension, bradycardia, and seizures.
Stability.
Dopamine is generally stable for up to 24 hours when placed into solution. Commercially prepared solutions are stable until the expiration date listed on the product. Dopamine products are unstable when exposed to light for long periods and should be protected from light when in storage. Discolored solutions should not be used because they may be ineffective. Checking the medication stock frequently can help to avoid this problem. Dopamine is incompatible with sodium bicarbonate, iron salts, and oxidizing agents.
epinephrine
Epinephrine (Adrenaline)
Epinephrine is currently one of the most valuable, potentially lifesaving therapeutic agents available to cardiac arrest victims. This drug is the pharmaceutical equivalent of adrenaline, produced by the adrenal gland.
Pharmacodynamics.
Epinephrine elicits sympathomimetic (mimics the sympathetic nervous system) effects on various organ systems by attaching to and stimulating the alpha-1 (α1), alpha-2 (α2), beta-1 (β1), and beta-2 (β2) receptors. Table 11-1 outlines the various effects that can occur when these receptors are stimulated by epinephrine. The effects of epinephrine on the various receptors are dose dependent. Low doses generally result in a predominance of beta receptors, whereas higher doses result in a predominance of alpha receptors. In cardiac arrest, epinephrine is primarily given in doses sufficient to stimulate α1 receptors so that arterioles (small blood vessels) can constrict. This produces a marked increase in blood pressure. When combined with chest compressions, epinephrine is used to cause a return of spontaneous circulation (ROSC).
Although it is thought that β1 receptors play no role in ROSC, epinephrine stimulation of these receptors in various organ systems may contribute to increasing and sustaining blood pressure. In the myocardium, β1-receptor stimulation leads to increased force of contraction, rate, and cardiac output. β1-receptor stimulation in the kidneys causes release of the hormone renin, which eventually helps produce a potent vasoconstrictive substance in the blood, angiotensin II. Angiotensin II in turn stimulates the adrenal gland to secrete the hormone aldosterone, which travels to the kidneys, where it acts to facilitate salt and water retention. The process is collectively known as the renin-angiotensin-aldosterone system and ultimately leads to increased blood pressure when activated.
Epinephrine also stimulates β1 receptors in the posterior pituitary gland (located at the base of the brain) to cause release of antidiuretic hormone (ADH, vasopressin), which is also a potent vasoconstrictor and water preserver. Again, the combination of vasoconstriction and water preservation leads to an increase in blood pressure.
Pharmacokinetics.
Epinephrine has an onset of action of 1 to 2 minutes, with a duration of action of 2 to 10 minutes. Once inside tissues, epinephrine is rapidly metabolized and inactivated by the enzymes catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO). The resulting sulfate and glucuronide metabolites of epinephrine are excreted in the urine.
Indications.
Epinephrine is indicated as first-line treatment for cardiorespiratory arrest and is used as such in ventricular fibrillation, asystole, and pulseless electrical activity (PEA). Other uses include treatment of anaphylactic or anaphylactoid reactions and acute bronchospasm. Table 11-2 lists the available epinephrine preparations used for cardiac arrest.
Dosage and administration.
Conventional ACLS guidelines recommend epinephrine 0.5 to 1.0 mg (0.01 to 0.015 mg/kg) every 5 to 10 minutes, followed immediately by 20-ml normal saline (NS) flush as needed to attain ROSC. Five to 10 ml of a 1:10,000 solution is equivalent to 0.5 to 1.0 mg. Some medication carts will carry a 30-ml vial of a 1:1000 ml solution, which is equivalent to 1 mg/ml. In the pediatric patient, 0.01 mg/kg to 0.015 mg/kg should be used.
Over the past several years, the AHA has revised its guidelines to include adult epinephrine doses greater than 1 mg after the first round of medication fails to attain ROSC. Doses greater than 1 mg are considered “high dose.” High-dose epinephrine at 0.2 mg/kg is considered appropriate if the patient fails to respond to the initial 1-mg dose.
Epinephrine may be administered intravenously through a peripheral or central vein, down the endotracheal tube (intrapulmonary administration), intraosseously (into the bone lumen) in pediatrics, or by intracardiac injection into the left ventricle. Intracardiac injection is not widely practiced at this time because myocardial necrosis can result. The intraosseous (IO) and endotracheal (ET) routes are important to keep in mind; many practitioners forget about these routes in the excitement of an actual emergency. IO injection is very effective in pediatric patients. ET administration is very effective in both pediatric and adult patients.
Endotracheal administration is generally performed when no intravenous (IV) access is available. To perform this technique, the medication should be diluted to a total volume of 10 ml, squirted down the ET tube, then followed by at least three rapid ventilations via bag-valve mask. These rapid ventilations serve to disperse the medication over the large surface area of the lung so that systemic absorption can take place. This technique has been documented to be effective at delivering epinephrine to the systemic circulation during cardiac arrest.
Adverse effects.
Major adverse effects seen with epinephrine consist of cardiac dysrhythmias, including ventricular fibrillation, through β1-receptor stimulation in the heart. Epinephrine may also lead to increased ischemia in an already-damaged heart because the oxygen demand exceeds the oxygen supply in cardiorespiratory arrest. In cardiac arrest, however, the benefits generally outweigh the risks. If the patient survives the cardiac arrest, hypertension and dysrhythmias should be expected. Other major adverse effects include a sense of nervousness, headache, and muscle twitching (fasciculations).
Stability.
Epinephrine products are unstable when exposed to light for long periods and may turn pink or brown. Discolored solutions should not be used because they may be ineffective. Checking your medication stock frequently can help to avoid this problem.
lidocaine
Lidocaine (Xylocaine)
Lidocaine is one of the most frequently used antidysrhythmic (antiarrhythmic) drugs for patients experiencing cardiac arrest.
Pharmacodynamics.
The myocardium has an extensive electrical conduction system that works in coordination with the parasympathetic and sympathetic nervous systems. Chemical electrolytes such as sodium, calcium, magnesium, and potassium play an integral role in the electrical activity of the conduction system of the heart. An improper balance of these electrolytes can lead to life-threatening cardiac dysrhythmias. Lidocaine pharmacologically blocks sodium channels, thus blocking sodium electrolytes, which affects the myocardial ventricles. This mechanism of action allows lidocaine to terminate premature ventricular contractions (PVCs) and convert a ventricular tachycardia to a slower, more stable cardiac rhythm, such as normal sinus rhythm (NSR). If multiple PVCs and ventricular tachycardia were allowed to continue in the cardiac arrest patient, a severe decrease in cardiac output could lead to the patient’s death.
Pharmacokinetics.
Lidocaine has an onset of action of 30 to 90 seconds following IV administration and 10 minutes after intramuscular (IM) administration. Lidocaine reaches significant serum levels only when absorbed via the IV, IM, and pulmonary routes. This drug distributes rapidly out of the bloodstream and into tissues throughout the body after IV administration. Lidocaine requires a steady serum concentration between 1.5 and 6.0 μg/ml to maintain therapeutic action. For this reason and because of its rapid distribution out of the bloodstream into tissues, lidocaine usually requires two bolus doses approximately 10 minutes apart initially, followed by a continuous IV drip to maintain its serum concentration in the therapeutic range. It is metabolized by the liver to monoethylglycinexylidide (MEGX) and glycinexylidide (GX). These metabolites are active in producing pharmacologic effects. Lidocaine has a half-life of elimination of 80 to 108 minutes in normal individuals, but this may be as long as 7 hours in patients with heart failure. Lidocaine and its metabolites are eliminated primarily by the kidneys.
Indications.
Lidocaine is indicated for treating ventricular dysrhythmias in heart attack or cardiac arrest. After cardiac arrest, lidocaine is primarily used to treat ventricular tachycardia. It can be used to treat ventricular fibrillation when direct-current electrical shock (i.e., defibrillation) has failed. If defibrillation is successful in converting the heart rhythm to NSR, lidocaine should be used as a follow-up measure to stabilize the heart.
Dosage and administration.
Lidocaine is administered as an initial IV bolus dose of 1.0 mg/kg body weight (the usual adult dose is 50 to 100 mg) and repeated every 5 to 10 minutes as needed to suppress ventricular dysrhythmias. The total, cumulative bolus dose should not exceed 3 mg/kg. Patients with congestive heart failure should receive only 50% of the total dose to avoid toxicity. Lidocaine is available in a prepared syringe for emergency use. (Lidocaine can also be effectively administered by ET tube and the IO route; the techniques are the same as for epinephrine.)
Immediately after the first bolus dose of lidocaine, an IV drip at the rate of 2 mg/min should be started; in pediatric patients, the infusion rate should be 20 μg/kg/min. Patients with congestive heart failure should receive only 50% of the total dose to avoid toxicity. A lidocaine infusion can be prepared by adding 1 g (1000 mg) of lidocaine to 250 ml NS or D5W for a concentration of 4 mg/ml; the IV pump rate then required to give a 2-mg/min infusion is 30 ml/hr; for pediatrics, dosage calculation should be based on 20 μg/kg/min. Table 11-2 lists other lidocaine preparations that can be used.
Adverse effects.
Adverse effects of lidocaine usually occur when it is infused too rapidly to a conscious patient, when excessive doses are used, or when a drug-drug interaction occurs. Mild lidocaine toxicity includes drowsiness, confusion, nausea, dizziness, gait disturbances (ataxia), ringing in the ears (tinnitus), numbness (paresthesias), and muscle twitching (fasciculations). Severe toxicity includes psychosis, seizures, and respiratory depression.
Stability.
Commercially prepared lidocaine injections are stable until the expiration date listed on the product. Lidocaine products are unstable when exposed to excessive heat (greater than 40° C). Preparations made by adding lidocaine to D5W or NS are stable for 24 hours at room temperature. Lidocaine may adversely affect the action of dopamine, epinephrine, norepinephrine, and isoproterenol. It is best to administer lidocaine through a separate IV line, if possible.
neuromuscular blocker
Neuromuscular Blockers
The neuromuscular blockers, also called paralyzing agents, should be used only by clinicians skilled in intubation technique. Frequently, in the setting of a cardiorespiratory arrest, a quick-onset paralyzing drug is required to relax all skeletal muscles so that the patient can be rapidly intubated. If a patient is unsuccessfully intubated after receiving a paralytic, the patient will have essentially no ability to contract the skeletal muscles required for respiration. So that the technician can at least know which drug to locate when called for by the physician, common neuromuscular blockers or paralytics include succinylcholine, vecuronium, pancuronium, atracurium, cisatracurium, rocuronium, and mivacurium. Generally, these agents are used in conjunction with a sedative, such as midazolam or lorazepam, to intubate patients rapidly if they do not breathe on their own within 8 minutes of beginning CPR and ACLS.
metabolic acidosis
During cardiorespiratory arrest, the patient generally cannot adequately ventilate. The body then begins a process of respiration known as anaerobic (without oxygen) respiration to help supply energy to tissues. Anaerobic respiration is a very ineffective way of supplying energy to tissues. The end product of anaerobic respiration is lactic acid. When lactic acid accumulates to critical levels, the body undergoes extreme metabolic acidosis. This can be lethal in cardiorespiratory arrest patients. A combination of sodium bicarbonate and artificial respiration is used to combat severe acidosis in cardiorespiratory arrest. IV sodium bicarbonate is used to restore HCO3− body stores depleted during clinical deterioration of the patient.
