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What drugs do Beta-Lactam Antibiotics include?
Penicillins and Cephalosporins
Opioid tolerance
A state of adaptation in which exposure to a drug causes changes in drug receptors that result in reduced drug effects over time
Breakthrough pain
Occurs between doses of pain medications
What is the mechanism of action of opioid drugs?
An agonist binds to an opioid pain receptor in the brain and causes an analgesic response-the reduction of pain sensation
An agonist-antagonist, also called a partial agonist or a mixed agonist, binds to a pain receptor and causes a weaker pain response than does a full agonist
An antagonist binds to a pain receptor but does not reduce pain signals. It functions as a competitive antagonist because it competes with and reverses the effects of agonist and agonist-angtagonist drugs at the receptor sites
Suppress the medullary cough center, which results in cough suppression
What are the indications for opioids?
Used to alleviate moderate to severe pain
Many are used for postoperative pain
What are the contraindications for opioids?
Known drug allergy
Severe asthma
What are the precautions for opioids?
Respiratory insufficiency
Conditions involving ICP
Morbid obesity and/or sleep apnea
Myasthenia gravis
Paralytic ileus (bowel paralysis)
Pregnancy
What are adverse effects of opioids?
CNS: Sedation, disorientation, euphoria, light-headedness, dysphoria
CV: Hypotension, flushing, bradycardia
GI: nausea, vomiting, constipation, biliary tract spasm
GU: urinary retention
Derm: Itching, rash, wheal formation
Resp:Respiratory depression and possible aggravation of asthma
What drugs interact with opioids?
Co-administration of opioids with alcohol, antihistamines, barbiturates, benzodiazepines, phenothiazine, and other CNS depressants can result in additive respiratory depressant effects
What laboratory tests do opioids interact with?
Opioids can cause an abnormal increase in the serum levels of amylase, alanine aminotransferase, alkaline phosphatase, bilirubin, lipase, creatinine kinase, and lactate dehydraogenase
What is the normal level for alkaline phosphatase (ALP)?
30-120 units/L
What is the rationale for Alkaline phosphatase (ALP) assessment?
ALP is found in many tissues but in highest concentrations in the liver, biliary tract, and bone
Detection of this enzyme is important for determining liver and bone disorders
Enzyme levels of ALP are increased in both extrahepatic and intrahepatic obstructive biliary disease and cirrhosis and/or other liver abnormalties
What is the normal level of alanine aminotransferase (ALT)?
4-36 units/L
Elderly may have slightly higher levels than the adult
What is the rationale for alanine aminotransferase (ALT) assessment?
Formerly serum glutamic-pyruvic transaminase (SGPT)
ALT is found mainly in the liver and lesser amounts in the kidneys, heart, and skeletal muscle
If there is injury or disease to the liver parynchyma (cells), it will cause a release of this liver cellular enzyme into the bloodstream and thus elevate serum ALT levels
most ALT elevations are from liver disease. Therefore, if medications are then metabolized by the liver, this metabolic process will be altered and possibly lead to toxic levels of drugs
What are the normal levels of Gamma-glutamyl transferase (GGT)?
Male/female 45 years of age and older: 8-38 units/L
What is the rational for the gamma-glutamyl transferase (GGT) assessment?
GGT is an enzyme that is present in liver tissue; when there is damage to the liver cells (hepatocytes) that manufacture bile, the enzyme will be released throughout the cell membranes and released into the blood
Individuals of African ancestry have normal values that are double the values of those who are white
What are the normal levels of Aspartate aminotransferase (AST)?
0-35 units/L
What is the rationale for aspartate aminotransferase (AST) assessment?
Formerly called serum glutamic-oxalocetic transaminase (SGOT)
AST is elevated with hepatocellular diseases
With disease or injury of liver cells, the cells lyse and the AST is released and picked up by the blood; the elevation of AST is directly related to the number of cells affected by disease or injury
What are the normal levels of Lactic dehydrogenase (LDH)
100-190 units/L
What is the rationale for lactic dehydrogenase (LDH) assessment?
LDH is found in cells of many body tissues including the heart, liver, red blood cells, kidneys, skeletal muscles, brain, and lungs
Because it is in so many tissues, the total LDH level is not a specific indicator of one disease
If there is disease or injury affecting cell containing LDH, the cells lyse and LDH is released from the cells into the bloodstream, thus increasing LDH levels
This enzyme is just part of the total picture of altered liver function which, if present, will then decrease the breakdown/metabolism of drugs and other chemical compounds, resulting in elevated levels of drugs
What is the generic name for morphine?
Astramorph PF
AVINza
Doloral
Duramorph PF
Embeda
Epimorph
Infumorph
Kadian
M-Eslon
Morphine H.P.
M.O.S.
What is the mechanism of action of morphine sulfate?
Binds to opiate receptors in the CNS
Alters the perception of an response to painful stimuli while producing generalized CNS depression
Decrease in severity of pain
Addition of naltrexone in Embeda product is designed to prevent abuse or misuse by altering the formulation
naltrexone has no effect unless the capsule is crushed or chewed
What is the drug class of morphine sulfate?
therapeutic: opioid analgesic
Pharmacologic: opioid agonist
What are the indications for mophine sulfate?
Morphine is indicated for severe pain and has a high abuse potential
Pulmonary edema
Pain associated with MI
What are the contraindications for morphine sulfate?
Hypersensitivity
Some products contain tartrazine, bisulfites, or alcohol and should be avoided in patients with known hypersensitivity; Acute, mild, intermittent, or postoperative pain; Significant respiratory depression; acute or severe bronchial asthma; paralytic ileus
What are the precautions for morphine sulfate?
Morphine has a potentially toxic metabolite known as morphine-6-glucuronide. Accumulation of this metabolite is more likely to occur in patients with renal impairment
Head trauma; increased intracranial pressure; severe renal, hepatic, or pulmonary disease; hypothyroidism; seizure disorder; adrenal insufficiency
History of substance abuse
Undiagnosed abdominal pain
Prostatic hyperplasia
Patients undergoing procedures that rapidly decrease pain (cordotomy, radiation)
Long-acting agents should be discontinued 24 hr before and replaced with short-acting agents
geriatric or debilitated patients
avoid chronic use in OB or when lactating
What are the adverse effects for morphine sulfate?
CNS: confusion, sedation, dizziness, dysphoria, euphoria, floating feeling, hallucinations, headache, unusual dreams
EENT: bluured vision, diplopia, miosis
Resp: Respiratory depression
CV: hypotension, bradycardia
GI: constipation, nausea, vomiting
GU: urinary retention
Derm: flushing, itching, sweating
Physical dependence, psychological dependence, tolerance
What drugs interact with morpine?
Use with extreme caution in patients receiving MAO inhibitors within 14 days prior
Increased CNS depression with alcohol, sedative/hypnotics, clomipramine, barbiturates, tricyclic antidepressants, and antihistamines
Administration of partial-antagonist opioid analgesics may precipitate opioid withdrawal in physically dependent patients
Buprenorphine, nalbuphine, butorphanol, or pentazocine may decrease analgesia
May increase the anticoagulant effect of warfarin
Cimetidine decreases metabolism and may increase effects
Concurrent use of kava-kava, valerian, or chamomile can increase CNS depression
Patient teaching for morphine sulfate
May cause drowsiness or dizziness
Advise patient to change positions slowly to minimize orthostatic hypotension
Caution patient to avoid concurrent use of alcohol or other CNS depressants with this medication
Encourage patients who are immobilized or on prolonged bedrest to turn, cough, and breathe deeply every 2 hr to prevent atelectasis
Explain to patient and family how and when to administer morphine and how to care for infusion equipment properly
Assessment for morphine sulfate
Assess type, location, and intensity of pain prior to and 1 hr following PO, subcut, IM, and 20 min following IV administration
Patients on a continuous infusion should have additional bolus every 15-30 min (breakthrough pain)
Assess level of consciousness, BP, pulse, and respiration before and periodically during administration. if respiratory rate is < 10/min, assess level of sedation
Prolonged use may lead to physical and psychological dependence and tolerance
Assess bowel function routinely. Institute prevention of constipation with increased intake of fluids and bulk with laxatives to minimize constipating effects
May increase plasma amylase and lipase levels
Administration for morphine sulfate
Available in oral, injectable, and rectal dosage forms
Extended release forms include MS Contin, Kadian, and Avinza
IM:
Onset: rapid
Peak: 30-60 min
Duration: 6-7 hr
Coadministration with nonopioid analgesics may have additive analgesic effects and may permit lower doses
Morphine should be discontinued gradually to prevent withdrawal symptoms after long-term use
Doses may be administered with food or milk to minimize GI irritation
Swallow extended-release tablets whole; do not break, crush, dissolve, or chew
Evaluation of morphine sulfate
Decrease in severity of pain without a significant alteration in level of consciousness or respiratory status
Decrease in symptoms of pulmonary edema
What are opioid tolerant patients?
Those who have been taking at least 60 mg of oral morphine daily or at least 30 mg of oral oxycodone daily or at least 8 mg of oral hydromorphone daily or an equianalgesic dose of another opioid
What is the antidote for opioid overdose?
Naloxone (IV)/Narcan
Naltrexone (PO)/Revia
What is the mechanism of action for acetaminophen (tylenol)?
Blocks peripheral pain impulses by inhibition of prostaglandin synthesis
lowers febrile body temperatures by acting on the hypothalamus, the structure in the brain that regulates body temperature. Heat is dissipated through vasodilation and increased peripheral blood flow
What are the therapeutic effects for acetaminophen (tylenol)?
Indicated for the treatment of mild to moderate pain and fever
The antipyretic (antifever) drug of choice in children and adolescents with flu syndromes, because the use of aspirin in these populations is associated with Reye's syndrome
What are the contraindications for acetaminophen (tylenol)?
Known drug allergy
Severe liver disease
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Management of acetaminophen (tylenol) overdose
Overdose can cause hepatic necrosis
The standard maximum daily dose of acetaminophen for healthy adults is 4000 mg
Acetylcysteine is the recommended antidote for acetaminophen toxicity and works by preventing the hepatotoxic metabolites of acetaminophen from
What are the adverse effects of acetaminophen (tylenol)?
Rash
Nausea
vomiting
Blood disorders or dyscrasias (anemias)
Nephrotoxicities
Hepatotoxicity
what drugs interact with acetaminophen (tylenol)?
Chronic heavy alcohol abusers may be at increased risk of liver toxicity from excessive acetaminophen use
Other hepatotoxic drugs need to be avoided
What is the drug class for acetaminophen (tylenol)?
Nonopioid analgesic
What is the mechanism of action for Benzodiazepines?
The sedative and hypnotic action of benzodiazepines is related to their ability to depress activity in the CNS
GABA is the primary inhibitory neurotransmitter of the brain, and it serves to modulate CNS activity by inhibiting overstimulation. Benzodiazepines are believed to increase the action of GABA
Benzodizepines exert their effects by depressing activity in the areas of the brain called the brainstem and the limbic system
How can you tell if a drug is a benzodiazepine?
-azepam
What are the indications for Benzodiazepines?
Commonly used for sedation, relief of agitation or anxiety, treatment of anxiety-related depression, sleep induction, skeletal muscle relaxation, and treatment of acute seizure disorders
Used in the treatment and prevention of the symptoms of alcohol withdrawal, insomnia and muscle spasms, seizure disorders, and adjuncts in anesthesia
Commonly used in therapy for depression because depressive and anxious symptoms often occur together
What are the contraindications for benzodiazepines?
Known drug allergy
Narrow-angle glaucoma, due to their ability to cause mydriasis
Pregnancy, due to sedative properties and risk for teratogenic effects
Mydriasis
Dilation of the pupil of the eye
Teratogenic effects
Drugs that may disturb the development of the fetus
Management of benzodiazepine overdose
Symptoms include: somnolence, confusion, coma, diminished reflexes, and respiratory depression
Flumazenil can be used to reverse the sedative effects of benzodiazepines. May cause acute withdrawal syndrome, including seizures in patients taking long-term benzodiazepines or those with a history of substance abuse
Rebound disinhibition
An elderly patient experiences marked sedation for 1 to 2 hours, followed by marked agitation and confusion for several hours afterward
What are the adverse effects for benzodiazepines?
CNS: CNS depression, hyperactivity and aggressive behavior (paradoxical excitement or nervousness), rebound disinhibition, amnesia, sedation, dizziness (vertigo), lethargy, fatigue, confusion, drowsiness, ataxia, headache
ENNT: visual changes
GI: anorexia, weight gain or loss, nausea
MS: Weakness
CV: hypotension
Patient teaching for benzodiazepines
Encourage patients to avoid operating heavy machinery and driving
Educate about the development of tolerance to the sedating properties
alcohol and other CNS depressants must be avoided
Advise patients to carry a medical alert or other identification bracelet/necklace with their diagnoses and a list of their drugs and allergies
Assessment for benzodiazepines
When these drugs are used, the HCP may order lab studies, such as CBCs, serum electrolyte levels, and hepatic/renal function studies
Blood pressure readings are important because of drug-related postural hypotension
Perform a baseline neurological examination
Perform a baseline eye examination
Administration for benzodiazepines
Frequent monitoring of vital signs with sepcific attention to blood pressure and postural blood pressures
Encourage the use of SCDs or compression stockings and to change positions slowly to minimize dizziness and falls
What drugs interact with benzodiazepines
Alcohol and CNS depressants, when coadministered, with benzodiazepines, can result in additive CNS depression and even death. More likely to occur in patients with renal and/or hepatic compromise
Oral contraceptives, azole antifungals, SSRIs, verapamil, diltiazem, opioids, and valproic acid enhance benzodizepine effects because of impaired hepatic elimination of benzodiazepine
Rifampin reduces therapeutic effects and enhances benzodiazepine clearance
Theophylline reduces sedative effects
phenytoin causes an increased risk for digoxin toxicity and phenytoin toxicity when given with benzodiazepines
Evaluation for benzodizepines
Improved mental alertness, cognition, and mood
Fewer anxiety and panic attacks
Improved sleep patterns and appetite
What is the mechanism of action of barbiturates?
CNS depressants that act primarily on the brainstem in an area called the reticular formation
Act by reducing the nerve impulses traveling to the area of the brain called the cerebral cortex
What are the indications for barbiturates?ocedures
Can be used as hypnotics, sedatives, and anticonvulsants and also as anesthesia during surgical
What are the contraindications for barbiturates?
Known drug allergy
Pregnancy
Significant respiratory difficulties
Severe kidney or liver disease
What are the precautions of barbiturates?
Must be used with caution in elderly patients due to their sedative properties and increased fall risk
What are the adverse effects of barbiturates?
CNS: Drowsiness, lethargy, vertigo
CV: vasodilation and hypotension, especially if given too rapidly
GI: nausea, vomiting, diarrhea, constipation
Hem: Agranulocytosis, thrombocytopenia
Resp: respiratory depression, cough
Hypersensitivity reactions: urticaria, angioedema, rash, fever, Stevens-Johnson syndrome
What drugs interact with barbiturates?
Stimulate the action of enzymes in the liver that are responsible for the metabolism or breakdown of many drugs
Additive CNS depression occurs with the coadministration of barbiturates with alcohol, antihistamines, benzodiazepines, opioids, and tranquilizers
What is the mechanism of action for Beta-Lactam Antibiotics?
Penicillin and cephalosporin antibiotics are structurally and pharmacologically simimlar. Both contain a beta-lactam ringe, are bactericidal, work by interfering with bacterial cell wall synthesis, and have a broad spectrum of activity.
Where do penicillins come from?
The penicillins are a very large group of chemically related antibiotics derived from a mold fungus often seen on bread and fruit
Where do cephalosporins come from?
Cephalosporins are semisynthetic antibiotic derivatives also derived from mold
What are the Therapeutic effects of Beta-Lactam Antibiotics?
Modifications of the basic chemical structure have given rise to four generations of cephalosporins. Depending on the generation, these drugs may be active against gram-positive, gram-negative, or anaerobic bacteria.
What are Contraindications for Beta-Lactam Antibiotics?
Drug allergy (Cross-sensitivity is probably the result of structural similarity, so penicillins should be used cautiously in patient's allergic to cephalosporin and vice versa)
What Drugs do Beta-Lactam Antibiotics interact with?
Increased effects occur when combined with aminoglycosides and other penicillins
Prolonged effects occur when combined with NSAIDs
Decreased effects occur when combined with neomycin and rifampin (penicillins)
Decreased effectiveness of oral contraceptives occurs with penicillins
Enahanced anticoagulant effects of warfarin occur when penicillins are given with potassium supplements
Increased alcohol intolerance occurs when cephalosporins are given with disulfiram
What are the adverse effects of Beta-Lactam Antibiotics?
CNS: lethargy, hallucinations, anxiety, depression, twitching, coma, and convulsions
GI: nausea, vomiting, diarrhea, increased levels of aspartate aminotransferase and alanine transaminase, abdominal pain, and colitis
Hem: anemia, increased bleeding time, bone marrow depression, and granucolytopenia
Metabolic: hyperkalemia, hypokalemia, and alkalosis
Taste alterations, soreness in mouth, dark discolored or sore tongue, hives, and rash
Nursing implications for Beta-Lactam antibiotics
Assess allergies prior to administration and continue to monitor for hypersensitivity reactions after the assessment phase because immediate reactions may occur within 30 minutes, accelerated reactions occur within 1-72 hours, and delayed responses may occur after 72 hours
Administer around the clock to maintain effective blood levels
Administer oral penicillins with at least 6 ounces of water (versus juice) because of interaction between the drug's antibacterial action and acidic juices
Administer oral cephalosporins with food to decrease gastrointesitnal upset, even though this will delay absorption. Alcohol and alcohol-containing products should be avoided because of the Antabuse-like reactions that are associated with some of the cephalosporins
Patient teaching for Beta-Lactam antibiotics
For penicillins: take the drugs exactly as prescribed and for the full duration, with spacing of doses at regularly scheduled intervals. Take then with water. Oral dosage forms should not be taken with caffeine, citrus fruit, cola beverages, fruit juices, or tomato juice because they will inactivate the drug.
For cephalosporins: It is important to eat dairy products to minimize superinfections. Avoid OTC liquid cold products that contain alcohol so as to avoid an Antabuse-like reaction (with some of the cephalosporins). Report diarrhea, flui-like symptoms, blistering or peeling of the skin, hearing loss, breathing difficulty, or seizures to the HCP immediately. Report immediately the occurrence of foul-smelling, loose, frequent stools or bloody stools.
Consume yogurt, buttermilk, or kefir to help prevent superinfections such as the occurrence of vaginal yeast infections
Oral contraceptives interact with the antibiotic, so use other forms of contraception
What are the signs and symptoms of superinfection?
Fever
Black hairy tongue
Stomatitis
Loose or foul-smelling stools
Vaginal discharge
Cough
What is the mechanism of action for Beta-Agonist (Sympathomimetic) Bronchodilators?
The mechanism of action of beta-agonist bronchodilators begins at the specific receptor stimulated and ends with the dilation of the airways, but many reactions must take place at the cellular level for this bronchodilation to occur.
When a beta2-adrenergic receptor is stimulated by a beta-agonist, adenylate cyclase (an enzyme needed to make cAMP) is activated. The increased levels of cAMP make available by adenylate cyclase cause bronchial smooth muscles to relax, which results in bronchial dilation and increased airflow into and out of the lungs.
Non-selective adrenergic agonist drugs also stimulate alpha-adrenergic receptors, causing constriction within the blood vessels. This vasoconstriction reduces the amount of edema, or swelling, in the mucous membranes and limits the quality of secretions normally secreted by these membranes
What are the therapeutic effects of Beta-agonist (sympathomimetic) Bronchodilators?
The primary therapeutic effects are the relief of bronchospasm related to bronchial asthma, bronchitis, and other pulmonary diseases
The Beta2-stimulants are thought to stimulate the NaK+-adenosine triphosphatase (ATPase) ion pump contained in the cell membranes. This facilitates a temporary shift of potassium ions from the bloodstream into the cells, resulting in a temporary decrease in serum potassium levels
What are the contraindications for Beta-agonist (sympathomimetic) Bronchodilators?
Drug allergy
Uncontrolled cardiac arrhythmias
High risk for stroke
What drugs interact with Beta-Agonist (Sympathomimetic) Bronchodilators?
Non-selective Beta-blockers antagonize bronchodilation
Increased risk for hypertension occurs with monoamine oxidase inhibitors (MAOIs) and other sympathomimetics
Hypokalemia and changes in electrocardiograms are more likely to occur with concurrent use of diuretics
A decreased effectiveness of oral hypoglycemic drugs occurs
What are the adverse effects of Beta-Agonist (Sympathomimetic) Bronchodilators?
Insomnia
Restlessness
Anorexia
Cardiac stimulation
Hyperglycemia
Tremor
Hypotension
Hypertension
Vascular headache
Nursing implications for Beta-Agonist (Sympathomimetic) Bronchodilators
Assess vital signs and breath sounds before and after administration
Monitor for adverse effects, includeing tachyarrhythmias, chest pain, restlessness, agitation, nervousness, and insomnia
Allow 1 minute in between puffs, and use a spacer if necessary to increase the amount of drug delivered
Do not allow crushing or chewing of oral sustained-release tablets. They should be taken with food if gastrointestinal upset occurs
Make sure the patient rinses the mouth with water immediately after inhaling the drug so as to prevent oral dryness and irritation
Patient teaching for Beta-Agonist (Sympathomimetic) Bronchodilators
Participate in healthy living, including health checkups, forcing fluids, eating three balanced meals daily, and engaging in consistent exercise as tolerated and as ordered
In cases of asthma, bronchitis, or COPD: avoid exposure to conditions and situations that may lead to bronchoconstriction or worsening of the condition, such as allergens, stress, smoking, and air pollutants
Avoid excessive fatigue, heat, and extremes of temperature, and avoid consuming caffeinated beverages because they may increase bronchoconstriction
Short-acting beta-agonists are known as rescue drugs and are used for acute attacks of asthma or acute exacerbations of bronchospastic diseases
The proper method of administering the inhaled forms of these drugs is as demonstrated; return the demonstration. Taking more than the prescribed dose of beta-agonists is strongly discouraged because of the excessive cardiac demands and cardiac and CNS stimulation (hypertension and tachycardia) that may occur
What is the mechanism of action of Calcium Channel Blockers (Class IV antiarrhythmics)?
Class IV antiarrhythmics work specifically by blocking the inward flow of calcium ions into the slow (calcium) channels in cardiac conduction tissue
The conduction effects of these drugs are limited to the atria and the atrioventricular (AV) node, where conduction is prolonged and the tissues are made for refractory to stimulation, resulting in negative chronotropic, inotropic, and dromotropic actions
What are the therapeutic effects of Calcium Channel Blockers (Class IV antiarrhythmics)?
These drugs are used to treat paroxysmal supraventricular tachycardia (PSVT), atrial fibrillation, and atrial flutter but have little effect on ventricular arrhythmias
Calcium channel blockers are also effective in the treatment of hypertension and angina because of their ability to cause smooth muscle relaxation by blocking the binding of calcium to its receptors, thereby preventing contraction
Subsequent dilation of peripheral arteries decreases afterload, leading to a decrease in blood pressure and a reduction in myocardial workload and oxygen demand
Coronary arteries also dilate, increasing blood flow to the myocardium
What are the contraindications for Calcium Channel Blockers (Class IV antiarrhythmics)?
Hypersensitivity
Acute myocardial infarction
Pulmonary congestion
Wolff-Parkinson-White syndrome
Severe hypotension
Cardiogenic shock
Sick sinus syndrome
Second- or third-degree AV block
What drugs interact with Calcium Channel Blockers (Class IV antiarrhythmics?
Increased effects occur with other antiarrhythmic drugs, cimetidine, and ranitidine
Decreased effects occur with phenytoin and rifampin
Grapefruit juice may increase serum levels
Possible toxicity occurs when anesthetics, doxorubicin, benzodiazepines, buspirone, carbamazepine, digoxin, statins, steroids, tacrolimus, sirolimus, theophylline, or vincristine are given concurrently
What are the adverse effects of Calcium Channel Blockers (Class IV antiarrhythmics)?
Hypotension
Palpitations
Bradycardia
Heart failure
Constipation
Nausea
Dermatitis
Dyspnea
Rash
Flushing
Peripheral edema
Wheezing
Nursing implications for Calcium Channel Blockers (Class IV antiarrhythmics)
Assess heart rate, blood pressure, and rhythm before administration. Hold dose and notify the HCP if heart rate is < 60 bpm or systolic blood pressure is < 90 mmHg (or according to institutional policy)
Monitor electrocardiogram continuously if intravenous infusion, and initially if oral therapy. Monitor for prolongation of PR interval or AV block. Discontinue medication and notify the HCP if these occur
Use an infusion pump when administering intravenously
Assess for clinical manifestations of toxicity, such as hypotension, bradycardia, heart failure, and conduction disorders
Assess therapeutic effectiveness as evidenced by improved cardiac output and decreased chest discomfort and fatigue; and note improved vital signs, skin color, and urinary output
Patient teaching for Calcium Channel Blockers (Class IV antiarrhythmics)
Take radial pulse before each dose (instructions have been provided). Withhold a dose and notify the HCP according to the parameters provided
Move and change positions slowly and with caution to prevent syncope
Contact the HCP immediately if experiencing cardiac irregularities, pronounced dizziness, nausea, or dyspnea
Monitor daily weights; report a weight gain of 2 pounds in 1 day or 5 pounds or more within 1 week
Avoid concurrent use of antacids and the ingestion or grapefruit juice
What is the mechanism of action of Cardiac Glycosides?
Cardiac glycosides alter the electrochemical properties of the myocardium, affecting the conduction system and cardiac automaticity
What are the therapeutic effects of Cardiac Glycosides?
A positive inotropic effect increases cardiac contractility and cardiac output, making these drugs useful in the treatment of heart failure
A negative chronotropic effect (decreased heart rate) and negative dromotropic effect (decreased conductivity) make these drugs useful in the treatment of supraventricular tachydysrhythmias as well
What are the contraindications for Cardiac Glycosides?
Hypersensitivity
Second- or third-degree heart block
Atrial fibrillation
Ventricular tachycardia or fibrillation
Heart failure resulting from diastolic dysfunction
Subaortic stenosis (obstruction in the left ventricle below the aortic valve)
What drugs interact with Cardiac Glycosides?
Bran may decrease the absorption of oral digitalis drugs
Increased risk for toxicity occurs with loop diuretics, adrenergic drugs, laxatives, thiazide diuretics, quinidine, verapamil, amiodarone, succinylcholine, and amphotericin B
Increased therapeutic effects occur with anticholinergics, calcium channel blockers, and beta-blockers
Decreased therapeutic effects occur with barbiturates, antacids, antidiarrheals, colestipol, cholestyramine, and the herbal supplement hawthorn
What are the adverse effects of Cardiac Glycosides?
Bradycardia or tachycardia
Anorexia
Nausea
Vomiting
Diarrhea
Colored vision (green, yellow, or purple)
Haloed vision
Flickering lights
Headache
Fatigue
Malaise
Confusion
Convulsions
Hypokalemia increases the risk for toxicity
Nursing implications for Cardiac Glycosides
Assess the patient's serum electrolytes and digoxin level prior to administration
Auscultate apical pulse for 1 full minute. Hold dose and notify the health care provider if beats per minute are < 60 or > 120 (or according to institutional policy)
administer intravenous dose undiluted at no more than 0.25 mg/min or according to institutional policy
Assess for clinical manifestations of toxicity
Assess blood pressure, lung sounds, peripheral edema, and energy levels for therapeutic effect
Patient teaching for Cardiac Glycosides
Take radial pulse before each dose according to instructions. Withhold a dose and notify the HCP according to provided parameters
Remember tthe signs and symptoms of digoxin toxicity. Withhold a dose and notify the HCP immediately if they occur
Monitor daily weights, reporting a weight gain or 2 pounds in 1 day or 5 pounds or more within 1 wk
Do not take within 2 hours of ingesting bran, antacids, or dairy products because they decrease absorption of the drug
Know the signs and symptoms of hypokalemia. Maintain a diet high in potassium to prevent toxicity
What is the mechanism of action for HMG-CoA reductase Inhibitors?
HMG-CoA reductase inhibitors are the most potent antilipemic drugs available
Cholesterol production by the liver requires the action of an enzyme called HMG-CoA reductase. Statins competitively inhibit the actions of this enzyme, thus decreasing the actual synthesis of hepatic cholesterol
How do you know if a drug is an HMG-CoA Reductase Inhibitor?
Because the generic name of these medications ends in -statin, they are collectively referred to as the statin drugs
What are the therapeutic effects of HMG-CoA reductase inhibitors?
Decrease in plasma concentration of low-density lipoproteins (LDLs; bad cholesterol) and triglyerides and the increase in plasma concentration of high-density lipoproteins (HDLs; good cholesterol)
What are contraindications for HMG-CoA reductase inhibitors?
Drug allergy
Advanced age
Renal dysfunction
Hepatic dysfunction
What drugs interact with HMG-CoA Reductase Inhibitors?
Increased risk for rhabdomyolysis with erythromycin, gemfibrozil, niacin, and grapefruit juice
Increased risk for bleeding occurs with oral anticoagulants
What are the adverse effects of HMG-CoA Reductase Inhibitors?
Mild, transient GI disturbances
Rash
Headache
Increase in serum liver enzymes and creatinine kinase levels
Rhabdomyolysis (manifested by muscle pain and myoglobinuria)
Nursing implications for HMG-CoA Reductase inhibitors
Assess patient's dietary history and any cultural preferences that may affect taking this drug
Assess client's lipid profile, liver function tests, and renal function tests
Monitor for muscle pain and myoglobinuruia
Monitor for cataract formation
Patient teaching for HMG-CoA Reductase Inhibitors?
Take medication exactly as prescribed. Do not stop taking it abruptly. It may take several weeks for therapeutic effect to occur. Lab tests will be taken for monitoring at 3-6 months
Take with at least 6 ounces of water or with food to minimize gastrointestinal upset
Limit intake of grapefruit juice to less than 1 quart daily
Immediately report signs of toxicity, including muscle soreness, changes in urine color, fever, malaise, nausea, and vomiting
Do not neglect follow-up lab work because it is important to monitor for potential hepatic or renal dysfunction
Do not neglect ophthalmic examinations prior to and during therapy because of the potential development of adverse visual effects