PHARMACOLOGY OF EMERGENCY MEDICATIONS Flashcards
The heart ceases to pump blood adequately to the rest of the body.
cardiac arrest
The patient becomes unable to breathe; thus the body is inadequately oxygenated.
respiratory arrest
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.
CARDIORESPIRATORY ARREST
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.
• The patient with no blood circulation for more than 4 minutes will likely have brain damage.
AMERICAN HEART ASSOCIATION (AHA)
Used to summon an emergency team to the area where immediate assistance is required.
CODE BLUE
EMERGENCY MEDICATIONS FOR CARDIORESPIRATORY ARREST
• Preparation made in advance of any emergency is critical.
• Personnel should be familiar with the emergency medication box or cart.
•Medical imaging technologists should become familiar with the contents, drug names, location of drugs within the box, proper uses, and pharmacology.
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.
EPINEPHRINE (ADRENALINE)
EPINEPHRINE (ADRENALINE)
Epinephrine elicits sympathomimetic effects on various organ systems by attaching to and stimulating the alpha-1 (αι), alpha-2 (α2), beta-1 (βι), and beta-2 (B2) receptors.
PHARMACODYNAMICS
Increases blood pressure; dilates pupils; decreases ability to urinate and defecate
Alpha-1 (α₁)
Decreases blood pressure (when stimulated in the brain); causes constipation
Alpha-2 (02)
Increases heart rate, cardiac output, and dysrhythmias; causes fat to break down (lipolysis); releases renin hormone from the kidneys (may lead to increased blood pressure)
Beta-1 (β₁)
Decreases blood pressure; opens airways; causes constipation; inhibits uterine contractions; increases glucose production; releases insulin; contracts skeletal muscle
Beta-2 (B2)
Vasodilation of renal, coronary, intracerebral, and mesenteric blood vessels
Dopamine
EPINEPHRINE (ADRENALINE)
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
DOSAGE & ADMINISTRATION
EPINEPHRINE (ADRENALINE)
ADVERSE EFFECTS
• Cardiac dysrhythmias
• ventricular fibrillation
• increased ischemia
• sense of nervousnes
• Headache
• Muscle twitching
EPINEPHRINE (ADRENALINE)
• 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.
STABILITY
• Alternative to epinephrine
• Currently recommended in patients with shock-resistant ventricular fibrillation after epinephrine has failed
VASOPRESSIN (PITRESSIN)
The onset for vasoconstriction effects is immediate, whereas the water retention occurs within approximately 20 minutes.
VASOPRESSIN (PITRESSIN)
PHARMACODYNAMICS
Vasopressin has an onset of action within 3 minutes, with maximum effects occurring up to 20 minutes after injection.
VASOPRESSIN (PITRESSIN)
PHARMACOKINETICS
Vasopressin is currently recommended as an alternative to epinephrine in shock-resistant ventricular fibrillation and for cardiovascular shock.
VASOPRESSIN (PITRESSIN)
INDICATIONS
Administered to patients in cardiac arrest via direct IV push at 40 units for one dose every 20 minutes per ACLS guidelines.
VASOPRESSIN (PITRESSIN)
DOSAGE & ADMINISTRATION
VASOPRESSIN (PITRESSIN)
ADVERSE EFFECTS (LOWER DOSe)
• Circumoral pallor
• Tremor
• Sweating
• Abdominal cramps
• Nausea
• Pounding headache
• Vomiting
VASOPRESSIN (PITRESSIN)
ADVERSE EFFECTS (HIGHER DOSES)
• Hypertension
• Cardiac dysrhythmias
• Myocardial Ischemia
• Myocardial infarction
• Pharmaceutical equivalent of endogenous dopamine.
• Endogenous dopamine is a precursor to norepinephrine and epinephrine.
DOPAMINE (INTROPIN)
Has dose-dependent effects on the various sympathetic nervous system receptors.
DOPAMINE (INTROPIN)
PHARMACODYNAMICS
DOPAMINE (INTROPIN)
Stimulates the dopamine receptors in the renal, coronary, intracerebral, and mesenteric arteries
AT LOW DOSES
Begins stimulating alpha receptors
AT HIGH DOSES
• Has an onset of action of 2 to 4 mins, with a duration of action of less than 10 mins.
• The resulting metabolites of dopamine are excreted in the urine.
DOPAMINE (INTROPIN)
PHARMACOKINETICS
• Indicated for treating hypotension secondary to congestive heart failure, myocardial infarction, trauma, sepsis, and overt heart failure.
• Used to support blood pressure.
DOPAMINE (INTROPIN)
INDICATIONS
• Administered by IV infusion through an electronic pump.
• Appropriate total dose should be diluted in either NS or 5% dextrose in water (D5W).
DOPAMINE (INTROPIN)
DOSAGE & ADMINISTRATION
DOPAMINE (INTROPIN)
ADVERSE EFFECTS (DOSE DEPENDENT)
HIGH DOSES
Cardiac dysrhythmias
• Hypotension
Headache
Nausea
Vomiting
Angina pectoris
• Tachycardia
DOPAMINE (INTROPIN)
ADVERSE EFFECTS (DOSE DEPENDENT)
LOW DOSES
Hypertension
• Stable for up to 24 hours.
• Incompatible with sodium bicarbonate, iron salts, and oxidizing agents.
DOPAMINE (INTROPIN)
STABILITY
• Antimuscarinic agent frequently used in patients experiencing cardiac arrest.
ATROPINE
Inhibits the action of acetylcholine or other cholinergic stimuli.
ATROPINE
PHARMACODYNAMICS
EFFECTS OF MUSCARINIC (CHOLINERGIC) RECEPTORS WHEN STIMULATED
Pupillary constriction (miosis)
Decreased heart rate (bradycardia)
Decreased heart conduction velocity
Decreased heart contractility
Arteriolar vasodilation
Bronchial smooth muscle contraction
Bronchial gland secretions
Gastrointestinal peristalsis
Gastrointestinal secretions
Gastrointestinal sphincter relaxation
Salivation
Urinary bladder contraction
Urinary sphincter relaxation
Sweat gland secretion
Glycogen synthesis
Has an onset of action of 2 to 4 mins after IV administration.
• The half-life of elimination for atropine is 2 to 3 hours
ATROPINE
PHARMACOKINETICS
• Indicated for cardiac arrest.
• Also used when attempts at intubation lead to vagal nerve stimulation
ATROPINE
INDICATIONS
Given via rapid IV push at doses ranging from 0.5 to 1.0 mg every 3 to 5 minutes.
• If atropine given via slow IV push, a paradoxical action may occur that could be lethal.
ATROPINE
DOSAGE & ADMINISTRATION
ATROPINE
SEVERE ADVERSE EFFECTS
• Worsening of myocardial ischemia
•Extension of infarct zone
• Ventricular fibrillation
• Ventricular tachycardia
ATROPINE
LOW DOSES
• Paradoxical slowing of heart rate
ATROPINE
LESS SEVERE ADVERSE EFFECTS
• Dry mouth
• Pupillary dilation
•Headache
•Blurred vision
• Constipation
• Nervousness & etc.
• Urinary retention
• Stable until the expiration date listed on the product.
• Unstable when exposed to light for long periods
ATROPINE
STABILITY
• Frequently used antidysrhythmic drugs for patients experiencing cardiac arrest.
LIDOCAINE (XYLOCAINE)
Blocks sodium channels, thus blocking sodium electrolytes, which affects the myocardial ventricles.
LIDOCAINE (XYLOCAINE)
PHARMACODYNAMICS
Has an onset of action of 30 to 90 secs following IV administration and 10 minutes after (IM) administration.
LIDOCAINE (XYLOCAINE)
PHARMACODKINETICS
Indicated for treating ventricular dysrhythmias in heart attack or cardiac arrest.
LIDOCAINE (XYLOCAINE)
INDICATIONS
LIDOCAINE (XYLOCAINE)
DOSAGE & ADMINISTRATION
Administered via IV bolus dose of 1.0 mg/kg body weight and repeated every 5 to 10 minutes as needed to suppress ventricular dysrhythmias.
LIDOCAINE (XYLOCAINE)
ADVERSE EFFECTS
• Drowsiness
•Confusion
• Nausea
•Dizziness
• Gait disturbances
• Tinnitus
• Numbness & etc.
LIDOCAINE (XYLOCAINE)
STABILITY
• Unstable when exposed to excessive heat (greater than 40° C).
IV line is the best administration.
• Antidysrhythmic agent used in patients experiencing cardiac arrest.
• Contains actions that mimic all classes of antidysrhythmic medications.
AMIODARONE
AMIODARONE
PHARMACODYNAMICS
Suppresses dysrhythmias by various mechanisms, including sodium channel blockade, beta-receptor blockade, calcium channel blockade, and membrane stabilization.
AMIODARONE
PHARMACOKINETICS
• Half life: 58 days
• Metabolized by the liver
• Excreted in the urine
AMIODARONE
INDICATIONS
For pulseless ventricular tachycardia, shock-resistant ventricular fibrillation, polymorphic ventricular tachycardia, and wide-complex tachycardia
AMIODARONE
DOSAGE & ADMINISTRATION
• Administered by IV push as a 300 mg/30 ml D5W solution.
• If the patient has hypotension, a bolus over a 10-minute period is suggested,
AMIODARONE
ADVERSE EFFECTS
• Hypotension
• Dysrhythmia production
• Pulmonary fibrosis
• Hypothyroidism
AMIODARONE
STABILITY
•Stable at temperatures ranging from 20 to 30° C when protected from light.
• Incompatible with aminophylline, cefamandole, cefazolin, mezlocillin, heparin, and sodium
• Strong alkalinizing agent.
• Used for treating cardiac arrest.
SODIUM BICARBONATE
SODIUM BICARBONATE
PHARMACODYNAMICS
• Dissociates into its chemical components to liberate bicarbonate ion (HCO3-).
• Serves as a principal component of one of the main buffer systems, the bicarbonate-carbonic acid buffer system.
SODIUM BICARBONATE
INDICATIONS
• Used for treating severe metabolic or respiratory acidosis.
SODIUM BICARBONATE
ADVERSE EFFECTS
• Cellulitis
• Tissue necrosis
• Ulceration
• Tissue sloughing
• Congestive heart failure
SODIUM BICARBONATE
STABILITY
• Stable at temperatures ranging from 15° to 30° C.
• Incompatible calcium salts, epinephrine, dopamine, and lidocaine.
• “Paralyzing agents”
• Used in conjunction with a sedative, such as midazolam or lorazepam.
NEUROMUSCULAR BLOCKERS
