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pharmacology
| Question | Answer |
|---|---|
| Chemical name | Describes the drug’s chemical composition and molecular structure |
| Generic name (nonproprietary name) | Name given by the United States Adopted Names Council |
| Trade name (proprietary name) | The drug has a registered trademark; use of the name is restricted by the drug’s patent owner (usually the manufacturer). |
| Drug classifications: | By structure (ex: beta blocker) Subclass (ex: selective, nonselective) By therapeutic use (ex: antibiotic, antihypertensives) Prototypical drugs-first drug in a class of drugs |
| PHARMACEUTICS | study of how various drug forms influence the way in which the drug affects the body. |
| Dissolution | dissolving of solid dosage forms and their absorption |
| Enteral | tablets, capsules, oral soluble wafers, pills, timed-release capsules, timed-release tablets, elixirs, suspensions, syrups, emulsions, solutions, lozenges or troches, rectal suppositories, sublingual or buccal tablets |
| Parenteral | Injectable forms, solutions, suspensions, emulsions, powders for reconstitution |
| topical | Aerosols, ointments, creams, pastes, powders, solutions, foams, gels, transdermal patches, inhalers, rectal and vaginal suppositories |
| PHARMACOKINETICS | study of what the body does to the drug |
| Absorption | The movement of a drug from its site of administration into the bloodstream for distribution to the tissues |
| Bioavailability | the extent of drug absorption |
| First-pass effect | initial metabolism of a drug in the liver that has been absorbed by the GI tract before the drug reaches the bloodstream |
| Distribution | the transport of a drug by the bloodstream to its site of action Albumin is the most common blood protein and carries the majority of protein- bound drug molecules. |
| Metabolism(biotransformation) | the biochemical alteration of a drug into an active metabolite |
| Excretion | the elimination of drugs from the body (kidney, liver, bowel) |
| See Table 2.3, pages 19 &20 in the textbook for | Routes of Administration and Related Nursing Considerations |
| ENTERAL ROUTE | drug is absorbed into the systemic circulation through the oral or gastric mucosa or the small intestine. Oral Sublingual Buccal Rectal (can also be topical) |
| PARENTERAL ROUTE | intravenous (fastest delivery into the blood circulation) Intramuscular Subcutaneous Intradermal Intraarterial Intrathecal Intraarticular |
| TOPICAL ROUTE | Skin (including transdermal patches) Eyes Ears Nose Lungs (inhalation) Rectum vagina |
| Cytochrome P-450 enzymes (or simply P-450 enzymes), also known as | microsomal enzymes |
| Lipophilic | fat loving |
| Hydrophilic | water loving |
| Renal excretion | the process where the kidneys filter waste, toxins, and excess substances from the blood, eliminating them from the body via urine |
| Biliary excretion | the liver's process of eliminating waste, drugs, and metabolites by actively secreting them into bile, which then travels to the intestines for fecal elimination or reabsorption |
| HALF-LIFE | time required for half (50%) of a given drug to be removed from the body Measures the rate at which the drug is eliminated from the body After approximately five half-lives, most drugs are considered to be effectively removed from the body |
| Steady state | Physiologic state in which the amount of drug removed via elimination is equal to amount of drug absorbed with each dose. |
| Onset of action | time required for a drug to elicit a response |
| Peak effect | time required for a drug to reach maximum therapeutic response |
| Trough level | lowest blood level of a drug |
| PHARMACODYNAMICS | study of what the drug does to the body The mechanism of drug actions in living tissues |
| PHARMACOTHERAPEUTICS | clinical use of drugs to prevent and treat diseases Defines principles of drug actions—the cellular processes that change in response to the presence of drug molecules |
| Contraindications | conditions, situations, or other substances that make a particular treatment or drug unsafe to use, potentially causing harm |
| Acute therapy | involves intensive, short-term rehabilitation (Physical, Occupational, Speech Therapy) in a hospital setting for patients needing immediate stabilization after severe injury, illness, or surgery |
| Maintenance therapy | ongoing treatment to prevent the return of a disease (like cancer) or to stop functional decline in chronic conditions |
| Supplemental (or replacement) therapy | provides substances your body lacks, most commonly hormones , to restore balance, ease symptoms (hot flashes, bone loss), and improve well-being, involving prescription medications, bioidentical hormones, or sometimes plant-based alternatives |
| Supportive therapy | focuses on relieving symptoms, distress, and side effects of serious illnesses, improving quality of life, rather than curing the underlying disease |
| Prophylactic therapy | any medical treatment, medication, or action taken to prevent a disease, infection, or complication from developing, rather than treating it after it occurs |
| Empiric therapy | starting medical treatment, often antibiotics, based on an educated guess or experience before a specific diagnosis is confirmed |
| Therapeutic response | a beneficial or desirable outcome from treatment, such as pain relief from medication or improved coping skills in therapy |
| Therapeutic index | a measure of a drug's safety, representing the ratio between the dose that causes toxicity and the dose that produces a desired therapeutic effect |
| Additive effects | occur when the combined result of two or more agents (like drugs, chemicals, or genetic factors) is equal to the simple sum of their individual effects, often described as 2 + 2 = 4, without interaction |
| Incompatibility | occurs when mixing medications (or drugs with solutions/foods/supplements) causes a chemical or physical reaction, creating an inactive, toxic substance, or changing drug potency/effectiveness |
| Adverse drug event | any harm or injury resulting from a medication, including side effects, allergic reactions, overdoses, or errors |
| Adverse drug withdrawal event | a clinical set of symptoms or worsening of a condition that occurs when a medication is stopped or its dose is reduced |
| Pharmacologic reaction | the body's response to a drug |
| Idiosyncratic reaction | a rare, unpredictable, and often severe adverse response to a drug or substance that isn't a typical side effect |
| Teratogenic | describes agents (like drugs, chemicals, infections, alcohol) that interfere with normal fetal development, causing birth defects or abnormalities, with effects depending on the agent, dose, and timing of exposure during pregnancy |
| Mutagenic | a substance or agent that causes a permanent change (mutation) in the DNA of a cell, altering its genetic material, which can lead to cell damage, disease (like cancer), or altered traits |
| PHARMACOGNOSY | The study of natural (versus synthetic) drug sources |
| Four main sources for drugs | Plants Animals Minerals Laboratory synthesis |
| PHARMACOECONOMICS | Study of the economic factors influencing the cost of drug therapy Cost–benefit analysis Examine treatment outcomes in relation to the comparative total costs |
| TOXICOLOGY | Science of the adverse effects of chemicals on living organisms Clinical toxicology deals specifically with the care of poisoned patients. Poison Control Centers Treatment based on system of priorities |
| These lifespan changes have dramatic effects of the four phases of pharmacokinetics | Pregnancy ◦ Newborn ◦ Pediatric ◦ Older adult |
| Considerations for Older Adult Patients | Decline in organ function occurs with advancing age. ◦ Drug therapy in older adults is most likely to result in adverse effects and toxicity, Polypharmacy ◦ Noncompliance, nonadherence ◦ Increased incidence of chronic illnesses |
| Absorption older adult | gastric pH less acidic ◦ Gastric emptying slowed ◦ Movement through GI tract slowed because of decreased muscle tone and activity ◦ Blood flow to GI tract reduced ◦ Absorptive surface of GI tract reduced |
| Distribution older adult | Lower total body water percentages ◦ Increased fat content ◦ Decreased production of proteins by the liver, resulting in decreased protein bindin of drugs (and increased circulation of free drugs) |
| Metabolism older adult | Aging liver produces fewer microsomal enzymes, affecting drug metabolism. ◦ Reduced blood flow to the liver ◦ Potential for drug toxicity to due decreased metabolism |
| Excretion older adult | Decreased glomerular filtration rate ◦ Decreased number of nephrons ◦ Drugs are cleared less effectively because of decreased excretion |
| NEAR MISS | Event or situation that did not produce patient injury, but only because of chance • Must still be reported so that safety issues can be addressed and future incidents are prevented |
| Never use a | trailing zero” with medication orders. • Do not use 1.0 mg; use 1 mg. |
| Always use a | “leading zero” for decimal dosages. • Do not use .25 mg; use 0.25 mg. |
| REPORTING MEDICATION ERRORS | Report to prescriber and nursing management. • Document error per policy and procedure. • Factual documentation only • Medication administered • Actual dose • Observed changes in patient condition • Prescriber notified and follow-up orders |
| PREVENTING PEDIATRIC MEDICATION ERRORS | Obtain and document accurate weight (kg) • Report all medication errors. • Know the drug thoroughly. • Follow the Rights of medication administration. • Avoid verbal orders in general. • Avoid distractions. |
| MEDICATION RECONCILIATION | • Patients provide a list of all the medications they are currently taking (including herbals and over- the-counter drugs). • Prescriber then assesses the medications and decides if they are to be continued upon hospitalization |
| MEDICATION RECONCILIATION (CONT.) | Should be done at each stage of health care delivery: • Admission • Status change (e.g., from critical to stable) • Patient transfer within or between facilities or provider teams • Discharge |
| Adrenergic Blockers | Bind to adrenergic receptors but inhibit or block stimulation of the sympathetic nervous system (SNS) Have the opposite effect of adrenergic drugs Inhibit—or lyse—sympathetic stimulation |
| Beta Blockers | Block stimulation of beta receptors in the SNS Compete with norepinephrine and epinephrine Can be selective or nonselective Cardioselective beta blockers or beta1-blocking drugs Nonselective beta blockers block both beta1 and beta2 receptors |
| Beta2 receptors are located primarily on the | smooth muscles of the bronchioles and blood vessels. |
| Carvedilol and labetalol: | alpha-receptor– blocking activity, especially at higher dosages |
| Acebutolol, penbutolol, pindolol: not only block beta-adrenergic receptors but also | partially stimulate them |
| Beta 1 Receptors | Located primarily on the heart Beta blockers selective for these receptors are called cardioselective beta blockers. |
| beta 2 receptors | Located primarily on smooth muscle of bronchioles and blood vessels |
| Cardioselective beta blockers (beta 1) | Reduce SNS stimulation of the heart Decrease heart rate Prolong sinoatrial (SA) node recovery Slow conduction rate through the AV node Decrease myocardial contractility, thus reducing myocardial oxygen demand |
| Beta Blockers: Mechanism of Action | Nonselective beta blockers (beta1 and beta2) Cause same effects on heart as cardioselective beta blockers Constrict bronchioles, resulting in narrowing of airways and shortness of breath Produce vasoconstriction |
| Beta Blockers: Indications | Angina Decreases demand for myocardial oxygen Cardioprotective Inhibits stimulation from circulating catecholamines Used in patients who have had a MI Dysrhythmias Class II antidysrhythmic Migraine headache |
| Beta Blockers: Indications (Cont.) | Antihypertensive Ability to reduce SNS stimulation of the heart, reducing heart rate and force of myocardial contraction Heart failure Glaucoma (topical use) |
| Beta Blockers: Contraindications | Known drug allergy Uncompensated heart failure Cardiogenic shock Heart block, bradycardia Pregnancy Severe pulmonary disease Raynaud’s disease |
| Beta Blockers: Adverse Effects | Blood Agranulocytosis, thrombocytopenia Cardiovascular AV block, bradycardia, heart failure CNS Dizziness, depression, unusual dreams, drowsiness, Gastrointestinal Nausea, vomiting, diarrhea, constipation BRONCHOSPASMS |
| Nonselective beta blockers may interfere with | normal responses to hypoglycemia (tremor, tachycardia, nervousness). May mask signs and symptoms of hypoglycemia Use with caution in patients with diabetes mellitus |
| Beta Blockers: Toxicity and Management of Overdose | Symptomatic and supportive care Atropine for bradycardia Cardiac pacing Vasopressors for severe hypotension Hemodialysis |
| Atenolol (Tenormin) | Cardioselective beta blocker Commonly used to prevent future heart attacks in patients who have had one Hypertension and angina Management of thyrotoxicosis to help block the symptoms of excessive thyroid activity |
| Carvedilol (Coreg) | Nonselective beta blocker, an alpha1-blocker, a calcium channel blocker, and possibly an antioxidant Uses: heart failure, hypertension, and angina Slows progression of heart failure |
| Esmolol (Brevibloc) | Very strong short-acting beta1-blocker Primary use: acute situations to provide rapid temporary control of the ventricular rate in patients with supraventricular tachydysrhythmias Administered IV |
| Metoprolol (Lopressor) | Most commonly used beta1 blocker Oral and injectable Monitoring required when giving IV Increased survival rate in patients when taken following an MI |
| Propranolol (Inderal) | Prototypical nonselective beta1 and beta2-blocking drug Multiple uses Tachydysrhythmias Subaortic stenosis Migraine headaches Essential tremor Oral and injectable form |
| Sotalol (Betapace) | Nonselective beta blocker Potent antidysrhythmic properties Indicated for management of difficult-to-treat dysrhythmias Oral use |
| Nonselective Beta Blockers | Carvedilol Labetalol Nadolol Penbutolol Pindolol Propranolol Sotalol Timolol |
| Cardioselective Beta Blockers | Acebutolol (Sectral) Atenolol (Tenormin) Betaxolol (Kerlone) Esmolol (Brevibloc) Nebivolol (Bystolic) Metoprolol |
| Beta-Blocking Drugs: Nursing Implications | hypertension if this medication is discontinued abruptly. Instruct patients to notify their physicians if they become ill and unable to take medication. Inform patients that they may notice a decrease in tolerance for exercise |
| Beta-Blocking Drugs: Nursing Implications (Cont.) | Weight gain of more than 2 lb in 1 day or 5 lb in 1 week Edema of the feet or ankles Shortness of breath Excessive fatigue or weakness Syncope or dizziness |
| Parasympathetic nervous system (PNS): | stimulates smooth muscles, cardiac muscles, glands |
| Sympathetic nervous system | stimulates heart, blood vessels, skeletal muscles • Stimulation is controlled by neurotransmitters. • Acetylcholine • Norepinephrine |
| ACE inhibitors | Currently are 10 ACE inhibitors • Often used as first-line drugs for HF and hypertension • May be combined with a thiazide diuretic or CCB |
| ACE inhibitors meds | PRIL |
| ACE Inhibitors: Mechanism of Action | converts angiotensin I (AI) (formed through the action of renin) to angiotensin II (AII) • AII: potent vasoconstrictors that induce aldosterone secretion by the adrenal glands • Aldosterone: stimulates sodium and water resorption, which can raise BP |
| Primary Effects of the ACE Inhibitors | Cardiovascular and renal • BP: reduce BP by decreasing SVR • HF • Prevent sodium and water resorption by inhibiting aldosterone secretion • Diuresis: decreases blood volume and return to the heart • Decreases preload |
| Cardioprotective Effects of the ACE Inhibitors | ACE inhibitors decrease SVR (a measure of afterload) and preload. • Used to prevent complications after MI • Ventricular remodeling: left ventricular |
| Renal Protective Effects of the ACE Inhibitors | ACE inhibitors: reduce glomerular filtration pressure • Cardiovascular drugs of choice for patients with diabetes • ACE inhibitors reduce proteinuria |
| ACE Inhibitors: Indications | Hypertension • HF (either alone or in combination with diuretics or other drugs) • Slow progression of left ventricular hypertrophy after myocardial infarction |
| ACE Inhibitors: Adverse Effects | Fatigue • Dizziness • Headache • Mood changes • Impaired taste • Possible hyperkalemia • Dry, nonproductive cough, which reverses when therapy is stopped |
| Captopril (Capoten) | Uses: prevention of ventricular remodeling after MI; reduce the risk of HF after MI • Shortest half-life • Must be administered multiple times throughout the day |
| Enalapril (Vasotec) | Only ACE inhibitor available in both oral and parenteral preparations • Enalapril intravenous (IV) does not require cardiac monitoring. • Oral enalapril: prodrug |
| Angiotensin II Receptor Blockers | Also referred to as angiotensin II blockers • Well tolerated • Do not cause a dry cough that is common with ACE inhibitors |
| Angiotensin II Receptor Blockers: Mechanism of Action | ARBs affect primarily vascular smooth muscle and the adrenal gland. • Selectively block the binding of AII to the type 1 AII receptors in these tissues • ARBs block vasoconstriction and the secretion of aldosterone. |
| Comparison of ACE Inhibitors and Angiotensin II Receptor Blocker | ACE inhibitors and ARBs appear to be equally effective for the treatment of hypertension. • Both are well tolerated. • ARBs do not cause cough. |
| Angiotensin II Receptor Blockers: Indications | Hypertension • Adjunctive drugs for the treatment of HF • May be used alone or with other drugs such as diuretics |
| Angiotensin II Receptor Blockers: Adverse Effects | Chest pain • Fatigue • Hypoglycemia • Diarrhea • Urinary tract infection • Anemia • Weakness |
| Angiotensin II Receptor Blockers Nursing Implications | contraindications to specific antihypertensive drugs., not missing a dose, Oral forms should be given with meals, administer iv wt caution, Hot tubs, showers, or baths; hot weather may aggravate low BP |
| ACE Inhibitors and Laboratory Values | ACE inhibitors can cause renal impairment, which can be identified with serum creatinine. • ACE inhibitors can also cause hyperkalemia |
| Angina Pectoris | When the supply of oxygen and nutrients in the blood is insufficient to meet the demands of the heart, the heart muscle “aches.” The heart requires a large supply of oxygen to meet the demands placed on it. |
| Ischemia | Poor blood supply to an organ Ischemic heart disease Poor blood supply to the heart muscle Atherosclerosis Coronary artery disease |
| MI | Necrosis, or death, of cardiac tissue Disabling or fatal |
| Chronic stable angina | predictable, short-lived chest discomfort (pressure, squeezing, or burning) caused by reduced blood flow to the heart, typically due to coronary artery disease |
| Unstable angina | a high-risk acute coronary syndrome (ACS) characterized by unexpected, severe, or resting chest pain, often caused by ruptured plaque and partial coronary artery blockage |
| Vasospastic angina | rare form of chest pain caused by temporary, severe spasms of the coronary arteries that restrict blood flow, often occurring at rest, typically at night or early morning |
| Drugs for Angina | Nitrates or nitrites Beta blockers Calcium channel blockers |
| Nitrates and Nitrites: Mechanism of Action | Cause vasodilation because of relaxation of smooth muscles Potent dilating effect on coronary arteries Result: oxygen to ischemic myocardial tissue |
| Nitrates and Nitrites: Indications | Treat stable, unstable, and vasospastic angina Rapid-acting forms Used to treat acute anginal attacks Sublingual tablets; IV infusion |
| Nitrates: Contraindications | Known drug allergy Severe anemia Closed-angle glaucoma Hypotension Severe head injury Use of the erectile dysfunction |
| Nitrates: Adverse Effects | Headaches Usually diminish in intensity and frequency with continued use Reflex tachycardia Postural hypotension Flushing Weakness Nausea Skin irritation |
| nitrates Tolerance | Occurs in patients taking nitrates around the clock or with long-acting forms Prevented by allowing a regular nitrate-free period to allow enzyme pathways to replenish |
| Isosorbide dinitrate | Organic nitrate Available in rapid-acting sublingual tablets, immediate-release tablets, and long-acting oral dosage forms Produces more consistent, steady, therapeutic response |
| Nitroglycerin | Prototypical nitrate The most important drug used in the symptomatic treatment of ischemic heart conditions such as angina |
| Nitrates | Nitroglycerin Large first-pass effect with oral forms Used for symptomatic treatment of ischemic heart conditions (angina) |
| Calcium Channel Blockers for Chronic Stable Angina | Amlodipine Diltiazem Nicardipine Nifedipine Verapamil |
| Calcium Channel Blockers: Mechanism of Action | Cause coronary artery vasodilation Cause peripheral arterial vasodilation, thus decreasing systemic vascular resistance Reduce the workload of the heart Result: decreased myocardial oxygen demand |
| Calcium Channel Blockers: Indications | Angina Hypertension Supraventricular tachycardia Coronary artery spasms (Prinzmetal angina) Short-term management of atrial fibrillation and flutter Migraine headaches Raynaud’s disease Nimodipine |
| Nimodipine | cerebral artery spasms associated with aneurysm rupture |
| Calcium Channel Blockers: Contraindications | Known drug allergy Acute MI Second- or third-degree AV block (unless the patient has a pacemaker) Hypotension |
| Calcium Channel Blockers: Adverse Effects | Limited Primarily relate to overexpression of their therapeutic effects May cause hypotension, palpitations, tachycardia or bradycardia, constipation, nausea, dyspnea |
| Diltiazem | Very effective for the treatment of angina pectoris resulting from coronary insufficiency and hypertension Used in the treatment of atrial fibrillation and flutter along with paroxysmal supraventricular tachycardia |
| Amlodipine | Indicated for both angina and hypertension Available only for oral use |
| Nursing Implications CCB | baseline vital signs, including respiratory patterns and rate. Assess for drug interactions, should not take any medications, including over-the-counter medications, without checking with their physicians. limit caffeine |
| CCB Patients should report | Blurred vision Persistent headache Dry mouth Edema Fainting episodes Weight gain of 2 lb in 1 day or 5 lb in 1 week Pulse rate less than 60 beats/min |
| Nursing Implications Nitroglycerin | Instruct patients never to chew or swallow the sublingual form. burning sensation felt with sublingual forms indicates that the drug is still potent. |
| Nursing Implications Nitroglycerin pt 2 | medications should be stored in an airtight, dark glass bottle(protect from light) with a metal cap and no cotton filler, take as-needed nitrates at the first hint of anginal pain. Monitor vital signs frequently during acute exacerbations of angina |
| Nitroglycerin—part 4 If anginal pain occurs | Stop activity and sit or lie down and take a sublingual tablet. If there is no relief in 5 minutes, call 911 or emergency services immediately and take a second sublingual tablet. If there is no relief in 5 minutes, take a third sublingual tablet. |
| IV forms of nitroglycerin must be given with | special non-PVC tubing and bags. Discard parenteral solution that is blue, green, or dark red |
| CCBs problems | Constipation is a common problem; instruct patients to take in adequate fluids and eat high-fiber foods. Monitor serum potassium levels Swallow pills whole Do not stop medications abruptly |
| Antianginal drugs monitor | adverse reactions: allergic reactions, headache, lightheadedness, hypotension, dizziness. Monitor for therapeutic effects: relief of angina, decreased BP, or both. |
| Heart Failure | heart is unable to pump blood in sufficient amounts from the ventricles to meet the body’s metabolic needs, dyspnea, fatigue, fluid retention and/or pulmonary edema |
| “Left-sided” heart failure | pulmonary edema, coughing, shortness of breath, and dyspnea |
| Right-sided” HF | systemic venous congestion, pedal edema, jugular venous distension, ascites, and hepatic congestion |
| Heart Failure: Causes | (MI) Coronary artery disease Cardiomyopathy Valvular insufficiency Atrial fibrillation Infection Tamponade ischemia |
| Stages of Heart Failure | Stage A: At high risk for heart failure but no symptoms or structural heart disease Stage B: Structural heat disease but no symptoms Stage C: Structural heart disease with symptoms Stage D: Refractory HF requiring intervention |
| Positive inotropic drugs | increase the force of myocardial contraction |
| Positive chronotropic drugs | increase heart rate |
| Positive dromotropic drugs | accelerate cardiac conduction |
| Drug Therapy for Heart Failure | Positive inotropic drugs Phosphodiesterase inhibitors Cardiac glycosides Sinoatrial modulators Angiotensin receptor-neprilysin inhibitors, ACE, ARBS, Beta blockers Diuretics |
| Drugs of Choice for Early Treatment of Heart Failure | Focus on reducing effects of the renin- angiotensin-aldosterone system and the sympathetic nervous system ACE inhibitors, ARBS, some beta blockers |
| Drugs of Choice for Early Treatment of Heart Failure (Cont.) | Loop diuretics (furosemide) are used to reduce the symptoms of HF secondary to fluid overload. Aldosterone inhibitors (spironolactone, eplerenone) are added as the HF progresses. Only after these drugs are used is digoxin added |
| Drugs of Choice for Early Treatment of Heart Failure (Cont. again) | Dobutamine: positive inotropic drug Hydralazine and isosorbide dinitrate became the first drug approved for a specific ethnic group. Hydralazine/isosorbide dinitrate |
| ACE Inhibitors pt 2 | Inhibit angiotensin-converting enzyme. Responsible for converting angiotensin I to angiotensin II Prevent sodium and water resorption by inhibiting aldosterone secretion. Diuresis results, which decreases preload, |
| Lisinopril | Uses: hypertension, HF, and acute MI Hyperkalemia Common adverse effect: dry cough, hyperkalemia, decreased renal function |
| Angiotensin II Receptor Blockers pt 2 | Potent vasodilators; decrease systemic vascular resistance (afterload) Used alone or in combination with other drugs such as diuretics in the treatment of hypertension or HF |
| Valsartan | Valsartan shares many of the same adverse effects as lisinopril. ARBs are not as likely to cause the cough associated with the ACE inhibitors. ARBs are not as likely to cause hyperkalemia |
| Angiotensin Receptor-Neprilysin Inhibitors | Newer class of drugs Valsartan/sacubitril (Entresto) Blocks the degradation of vasoactive peptides by inhibiting the neprilysin enzyme Common adverse effects: hypotension, hyperkalemia, increased serum creatinine |
| Beta Blockers heart failure | prevent catecholamine-mediated actions on the heart by reducing or blocking sympathetic nervous system stimulation to the heart and the heart’s conduction system, reduced heart rate, delayed AV node conduction, reduced myocardial contractility |
| Aldosterone Antagonists | Useful in severe stages of HF Action: activation of the renin-angiotensin- aldosterone system causes increased levels of aldosterone, which causes retention of sodium and water, leading to edema that can worsen HF |
| Aldosterone Antagonists Spironolactone | potassium-sparing diuretic and aldosterone antagonist shown to reduce the symptoms of HF |
| Aldosterone Antagonists Eplerenone | selective aldosterone blocker, blocking aldosterone at its receptors in the kidney, heart, blood vessels, and brain |
| Hydralazine/isosorbide dinitrate | First drug approved for a specific ethnic group, namely African Americans |
| Dobutamine | Beta1-selective vasoactive adrenergic drug Structurally similar to dopamine |
| Ivabradine | Sinoatrial node modulator Inhibits f-channels within the SA node which ultimately results in reduced heart rate Used in stable, symptomatic HF with ejection fraction of =/< 35% Increase risk of atrial fibrillation, bradycardia, avoid grapefruit |
| B-Type Natriuretic Peptides-Nesiritide | Synthetic version of human B-type natriuretic peptide Vasodilating effects on both arteries and veins Effects of nesiritide Diuresis (urinary fluid loss) Natriuresis (urinary sodium loss) Vasodilation |
| B-Type Natriuretic Peptides: Adverse Effects | Nesiritide is used in the intensive care setting as a final effort to treat severe, life-threatening HF, often in combination with several other cardiostimulatory medications. Hypotension Dysrhythmia Headache |
| Phosphodiesterase Inhibitors (PDIs) | Work by inhibiting the enzyme phosphodiesterase Result in Intracellular increase in cAMP Positive inotropic response Vasodilation Increase in calcium for myocardial muscle contraction. Inodilators (inotropics and dilators) |
| Phosphodiesterase Inhibitors: Indications | Short-term management of HF for patients in the intensive care unit (ICU) AHA and ACC advise against long-term infusions. |
| Milrinone | Only available phosphodiesterase inhibitor-which increases calcium resulting in an increased cardiac contraction positive inotropic response- resulting in vasodilation Milrinone is available only in injectable form. |
| Milrinone adverse effects and Interactions | cardiac dysrhythmias, headache, hypokalemia, tremor, thrombocytopenia, and elevated liver enzyme levels diuretics (additive hypotensive effects) and digoxin (additive inotropic effects) affects electrolytes |
| Cardiac Glycosides | One of the oldest groups of cardiac drugs No longer used as first-line treatment Not been shown to reduce mortality in HF patients Originally obtained from Digitalis plant, foxglove Digoxin is the prototype. Used in HF |
| Cardiac Glycosides: Mechanism of Action | Increase myocardial contractility Change electrical conduction properties of the heart Decrease rate of electrical conduction Prolong the refractory period Area between sinoatrial (SA) node and atrioventricular (AV) node |
| Cardiac Glycosides: Drug Effects | Positive inotropic effect Increased force and velocity of myocardial contraction (without an increase in oxygen consumption) Negative chronotropic effect Reduced heart rate Negative dromotropic effect Decreased automaticity at SA node |
| Cardiac Glycosides: Drug Effects (Cont.) | Increased stroke volume Reduction in heart size during diastole Decrease in venous BP and vein engorgement Increase in coronary circulation Decrease in exertional and paroxysmal nocturnal dyspnea, cough, and cyanosis |
| Cardiac Glycosides: Adverse Effects | Digoxin (Lanoxin) Very narrow therapeutic window Drug levels must be monitored. 0.5 to 2 ng/mL Low potassium levels increase its toxicity |
| Cardiac Glycosides: Adverse Effects (Cont.) | Cardiovascular: dysrhythmias, including bradycardia or tachycardia Central nervous system: headaches, fatigue, malaise, confusion, convulsions Eyes: colored vision (seeing green, yellow, purple), halo vision, flickering light |
| Digoxin Toxicity | Digoxin immune Fab (Digibind) therapy Hyperkalemia (serum potassium greater than 5 mEq/L) in a digitalis-toxic patient Life-threatening cardiac dysrhythmias Life-threatening digoxin overdose |
| Conditions That Predispose to Digoxin Toxicity | Hypokalemia Use of cardiac pacemaker Hepatic dysfunction Hypercalcemia Dysrhythmias Hypothyroid, respiratory, or renal disease |
| Heart Failure Drugs: Nursing Implications | Assess history, drug allergies, and contraindications. Assess clinical parameters, including: BP Apical pulse for 1 full minute Heart sounds, breath sounds |
| Heart Failure Drugs: Nursing Implications (Cont.) | Assess clinical parameters (Cont.) Weight, input, and output measures Electrocardiogram Serum labs: potassium, sodium, magnesium, calcium, renal, and liver function studies |
| Heart Failure Drugs: Nursing Implications (Cont.) AGAIN | Before giving any dose, count apical pulse for 1 full minute. For an apical pulse less than 60 or greater than 100 beats/min: Hold dose. Notify prescribe rAvoid giving digoxin with high-fiber foods (fiber weight gain of 2 lb or more in 1 day |
| Nesiritide or milrinone implications | Use an infusion pump. Monitor input and output, heart rate and rhythm, BP, daily weights, respirations, and so on. |
| Dysrhythmia | Any deviation from the normal rhythm of the heart |
| Antidysrhythmics | Used for the treatment and prevention of disturbances in cardiac rhythm |
| Dysrhythmia Can develop in | association with many conditions After MI, cardiac surgery, or as a result of CAD Usually serious and may require treatment with antidysrhythmic drug or nonpharmacological therapies |
| Cardiac Cell | Inside the resting cardiac cell, there is a net negative charge relative to the outside of the cell. This difference in electronegative charge results from an uneven distribution of ions (sodium, potassium, calcium) across the cell membrane. |
| Resting Membrane Potential | An energy-requiring pump is needed to maintain this uneven distribution of ions. Sodium-potassium ATPase pump The RMP results from an uneven distribution of ions across the cell membrane |
| Action Potential | A change in the distribution of ions causes cardiac cells to become excited. The movement of ions across the cardiac cell’s membrane results in an electrical impulse spreading across the cardiac cells. |
| Action Potential phases 0-1 | Phase 0: upstroke Resting cardiac cell membrane suddenly becomes highly permeable to sodium ions; movement through sodium channels Depolarization Phase 1 Begins a rapid process of repolarization that continues through more phases |
| Action Potential Duration | Interval between Phase 0 and Phase 4 Absolute or effective refractory period Relative refractory period Threshold potential Automaticity or pacemaker activity |
| Aspects of Action Potential | SA node, AV node, and His-Purkinje cells all possess the property of automaticity. SA node is the natural pacemaker of the heart. SA node has an intrinsic rate of 60 to 100 bpm. AV node has an intrinsic rate of 40 to 60 bpm. |
| Supraventricular dysrhythmias | Originate above the ventricles in SA or AV node or atrial myocardium |
| Ventricular dysrhythmias | Originate below the AV node in the His-Purkinje system or ventricular myocardium |
| Ectopic foci | Outside the conduction system |
| Conduction blocks | Dysrhythmias that involve the disruption of impulse conduction between the atria and ventricles |
| Vaughan Williams classification | System commonly used to classify antidysrhythmic drugs Based on the electrophysiologic effect of particular drugs on the action potential |
| Vaughan Williams Classification 1 | Membrane-stabilizing drugs Fast sodium channel blockers Divided into Ia, Ib, and Ic drugs, according to effects |
| Vaughan Williams Classification la | procainamide, quinidine, and disopyramide Block sodium (fast) channels Delay repolarization Increase APD Used for atrial fibrillation, premature atrial contractions, premature ventricular contractions |
| Vaughan Williams Classification lb | phenytoin, lidocaine Block sodium channels Accelerate repolarization Increase or decrease APD Lidocaine is used for ventricular dysrhythmias only. Phenytoin is used for atrial and ventricular tachydysrhythmias caused by digitalis toxicity |
| Vaughan Williams Classification lc | flecainide, propafenone Block sodium channels (more pronounced effect) Little effect on APD or repolarization Used for severe ventricular dysrhythmias May be used in atrial fibrillation or flutter, Wolff-Parkinson-White syndrome |
| Vaughan Williams Classification II | beta blockers Reduce or block sympathetic nervous system stimulation, thus reducing transmission of impulses in the heart’s conduction system Depress Phase 4 depolarization |
| Vaughan Williams Classification III | amiodarone, dronedarone, dofetilide, sotalol, ibutilide Increase APD Prolong repolarization in Phase 3 Used for dysrhythmias that are difficult to treat Life-threatening ventricular tachycardia or fibrillation, atrial fibrillation or flutter |
| Vaughan Williams Classification IV | Calcium channel blockers Inhibit slow-channel (calcium-dependent) pathways Depress Phase 4 depolarization Reduce AV node conduction Used for paroxysmal supraventricular tachycardia |
| Contraindications to the Use of Antidysrhythmic Drugs | Known drug allergy Second- or third-degree AV block, bundle branch block, cardiogenic shock, sick sinus syndrome, and any other ECG changes |
| Antidysrhythmics: Adverse Effects | ALL antidysrhythmics can cause dysrhythmias! Hypersensitivity reactions Nausea, vomiting, and diarrhea Dizziness Headache and blurred vision Prolongation of the QT interval |
| Antidysrhythmics: Drug Interactions | Coumadin: monitor international normalized ratio Grapefruit juice: amiodarone, disopyramide, and quinidine |
| Procainamide (Pronestyl) | Class Ia Uses: atrial and ventricular tachydysrhythmias Significant adverse effects: include ventricular dysrhythmias, blood disorders, systemic lupus erythematosus (SLE)–like syndrome |
| Procainamide (Pronestyl) contradictions | known hypersensitivity, heart block, and SLE |
| Quinidine (Quinidex) | Class Ia Both direction action on the electrical activity of the heart and indirect (anticholinergic) effect Significant adverse effects: cardiac asystole and ventricular ectopic beats Others: cinchonism |
| Lidocaine (Xylocaine) | Class Ib, raises the ventricular fibrillation threshold twitching, convulsions, confusion, respiratory depression or arrest, hypotension, bradycardia, and dysrhythmias hypersensitive,Stokes-Adams or Wolff-Parkinson- White syndrome |
| Flecainide (Tambocor) | Class Ic First-line drug in the treatment of atrial fibrillation Negative inotropic effect and depresses left ventricular function Adverse effects: dizziness, visual disturbances, and dyspnea Contraindications: hypersensitivity, cardiog |
| Propafenone (Rythmol) | Class Ib Similar action to flecainamide Mild beta-blocking effects Use: life-threatening ventricular dysrhythmias, atrial fibrillation Most common reported adverse reaction: dizziness Others: metallic taste, constipation |
| Atenolol (Tenormin) | Class II Cardioselective beta blocker; preferentially blocks the beta1-adrenergic receptors that are located primarily in the heart. Noncardioselective beta blockers block not only the beta1- adrenergic receptors in the heart but also the beta2- |
| Esmolol (Brevibloc) | Ultrashort-acting beta blocker Cardioselective, blocks beta1-adrenergic receptors Use: acute treatment of supraventricular tachydysrhythmias; hypertension; post-MI tachydysrhythmias |
| Metoprolol (Lopressor) | Class II Another cardioselective beta blocker commonly given after an MI to reduce risk of sudden cardiac death Treatment of hypertension and angina |
| Amiodarone | Class III Markedly prolongs the action potential duration and the effective refractory period in all cardiac tissues Blocks both the alpha- and beta-adrenergic receptors of the sympathetic nervous system |
| Amiodarone uses/indications | Uses: one of the most effective antidysrhythmic drugs for controlling supraventricular and ventricular dysrhythmias Indications: management of sustained ventricular tachycardia, ventricular fibrillation, and nonsustained ventricular tachycardia |
| Amiodarone effects | corneal microdeposits, which may cause visual halos, photophobia, and dry eyes; photosensitivity; pulmonary toxicity |
| Amiodarone contraindications | Drug interactions: digoxin and warfarin Contraindications: hypersensitivity, severe sinus bradycardia or second- or third-degree heart block |
| Ibutilide (Corvert) | Class III Indicated for atrial dysrhythmias Dosed based on body weight Can cause ventricular dysrhythmias |
| Dofetilide (Tikosyn) | Class III Only physicians who have received special training are allowed to prescribe. Must be initiated in the hospital and patient have continuous ECG monitoring for first 3 days torsades de pointes, supraventricular dysrhythmias,chest pain |
| Sotalol (Betapace) | Class III Selective beta blocker Similar antidysrhythmic properties similar to class III while exerting beta blocker or class II effects on conduction For life-threatening ventricular dysrhythmias |
| Diltiazem (Cardizem, Others) | Class IV Temporary control of a rapid ventricular response in patients with atrial fibrillation hypersensitivity, acute myocardial infarction, pulmonary congestion, Wolff-Parkinson-White syndrome, severe hypotension, cardiogenic shock |
| Verapamil (Calan) | Class IV Inhibits calcium ion influx across the slow calcium channels in cardiac conduction time Results in dramatic effects on the AV node Used to prevent and convert recurrent PSVT and control ventricular response |
| Unclassified Antidysrhythmic | Adenosine (Adenocard) Slows conduction through the AV node Used to convert PSVT to sinus rhythm Very short half-life—less than 10 seconds Only administered as fast intravenous (IV) push May cause asystole |
| Adenosine considerations | Measure baseline blood pressure (BP), pulse, input and output, and cardiac rhythm. Measure serum potassium, Assess plasma drug levels as indicated.Instruct patients not to crush or chew oral preps |
| Solutions of lidocaine that contain epinephrine should not be | given IV; they are to be used ONLY as local anesthetics. |
| Teach patients taking beta blockers, digoxin, and other drugs how to | take their own radial pulse for 1 full minute and to notify their physicians before taking the next dose if the pulse is less than 60 beats/min. |
| HEMOSTASIS | term for any process that stops bleeding Coagulation is hemostasis that occurs because of the physiologic clotting of blood. |
| COAGULATION SYSTEM | Cascade” Each activated factor serves as a catalyst that amplifies the next reaction. Result is fibrin, a clot-forming substance. Intrinsic pathway and extrinsic pathway |
| FIBRINOLYTIC SYSTEM | Initiates the breakdown of clots and serves to balance the clotting process Fibrinolysis: mechanism by which formed thrombi are lysed to prevent excessive clot formation |
| Fibrin in the clot binds to | circulating protein known as plasminogen. This binding converts plasminogen to plasmin. Plasmin is the enzymatic protein that eventually breaks down the fibrin thrombus into fibrin degradation products |
| HEMOPHILIA | Natural coagulation and hemostasis factors are limited or absent. Patients with hemophilia can bleed to death if coagulation factors are not given. Two types inhibit platelet aggregation Factor VII deficiency Factor VIII and/or factor IX |
| Anticoagulants | Inhibit the action or formation of clotting factors Prevent clot formation, no direct effect on a blood clot that is already formed Prevent intravascular thrombosis by decreasing blood coagulability |
| Antiplatelet drugs | Inhibit platelet aggregation Prevent platelet plugs |
| Hemorheologic drugs | Alter platelet function without preventing the platelets from working |
| Thrombolytic drugs | Lyse (break down) existing clots |
| Antifibrinolytic or hemostatic | Promote blood coagulation |
| Thromboembolic events | Myocardial infarction (MI): embolus lodges in a coronary artery Stroke: embolus obstructs a brain vessel Pulmonary emboli: embolus in the pulmonary circulation |
| Heparins—part 1 | Action: inhibit clotting factors IIa (thrombin) and Xa Unfractionated heparin: “heparin” Low–molecular-weight heparins (LMWHs) Enoxaparin (Lovenox) Dalteparin |
| Heparins—part 2 | Unfractionated heparin (heparin) Relatively large molecule that is derived from animal sources Frequent laboratory monitoring for bleeding times such as aPTT |
| Heparins—part 3 | LMWHs Enoxaparin (Lovenox) and dalteparin (Fragmin) Synthetic smaller molecular structure More predictable anticoagulant response Frequent laboratory monitoring of bleeding times not needed |
| Coumarins | Action: inhibit vitamin K–dependent clotting factors II, VII, IX, and X Warfarin (Coumadin) |
| Warfarin (Coumadin) | inhibits vitamin K synthesis by bacteria in the gastrointestinal tract Inhibits production of vitamin K–dependent clotting factors II, VII, IX, and X, which are normally synthesized in the liver Final effect prevention of clot formation |
| Direct thrombin inhibitors | Action: inhibit thrombin (factor IIa) Human antithrombin III (Thrombate) Lepirudin (Refludan) Argatroban (Argatroban) Bivalirudin (Angiomax) Dabigatran (Pradaxa) |
| ANTICOAGULANTS: INDICATIONS | prevent clot formation in certain settings in which clot formation is likely MI Unstable angina Atrial fibrillation Indwelling devices, such as mechanical heart valves Major orthopedic surgery |
| ANTICOAGULANTS: CONTRAINDICATIONS | Drug allergy Any acute bleeding process or high risk for such an occurrence. Warfarin is strongly contraindicated in pregnancy. Other anticoagulants are rated in lower pregnancy categories (B or C). |
| ANTICOAGULANTS: ADVERSE EFFECTS | Bleeding Risk increases with increased dosages. May be localized or systemic May also cause: Heparin-induced thrombocytopenia Nausea, vomiting, abdominal cramps, thrombocytopeni |
| HEPARIN-INDUCED THROMBOCYTOPENIA | Type I Gradual reduction in platelets Heparin therapy can generally be continued. Type II Acute fall in the number of platelets (more than 50% reduction from baseline) Discontinue heparin |
| HEPARIN-INDUCED THROMBOCYTOPENIA manifestations | Thrombosis that can be fatal Treatment: thrombin inhibitors lepirudin and argatroban Use of warfarin: can cause skin necrosis and “purple toes” syndrome |
| TOXIC EFFECTS OF HEPARIN | Symptoms: hematuria, melena (blood in the stool), petechiae, ecchymoses, and gum or mucous membrane bleeding Stop drug immediately. Intravenous (IV) protamine sulfate: 1 mg of protamine can reverse the effects of 100 units of heparin |
| TOXIC EFFECTS OF WARFARIN | Discontinue the warfarin. May take 36 to 42 hours before the liver can resynthesize enough clotting factors to reverse the warfarin effects Vitamin K1 (phytonadione) can hasten the return to normal coagulation. |
| TOXIC EFFECTS OF WARFARIN (CONT.) | Caution: when vitamin K is given, warfarin resistance will occur for up to 7 days. Severe bleeding: transfusions of human plasma or clotting factor concentrates. Life-threatening bleeding from warfarin: Kcentra |
| IDARUCIZUMAB (PRAXBIND) | Specific dabigatran antidote Reverses the anticoagulant effects for dabigatran for emergency surgery or in life-threatening or uncontrolled bleeding |
| DRUG INTERACTIONS: ANTICOAGULANTS | Enzyme inhibition of metabolism Displacement of the drug from inactive protein- binding sites Decrease in vitamin K absorption or synthesis by the bacterial flora of the large intestines |
| ARGATROBAN | Synthetic direct thrombin inhibitor Used for active HIT and percutaneous coronary intervention procedures in patients at risk for HIT Only given IV |
| DABIGATRAN (PRADAXA) | Prodrug that becomes activated in the liver Specifically and reversibly binds to both free and clot- bound thrombin Dose dependent on renal function Adverse effects: bleeding, GI bleeding |
| ENOXAPARIN (LOVENOX) | Prototypical LMWH Greater affinity for factor Xa than for factor Iia Higher degree of bioavailability and longer elimination half-life Lab monitoring is not necessary. Injectable form |
| FONDAPARINUX (ARIXTRA) | treatment of DVT or PE Bleeding is most common and serious adverse reaction. Anemia, wound drainage, hematoma, confusion, UTI, hypotension, dizziness, hypokalemia Thrombocytopenia can occur not be given for at least 6 to 8 hours after surgery |
| HEPARIN | Natural anticoagulant obtained from the lungs or intestinal mucosa of pigs 10 to 40,000 units/mL DVT prophylaxis: 5000 units subcutaneously two or three times a day; does not need to be monitored when used for prophylaxis |
| RIVAROXABAN (XARELTO) | First oral factor Xa inhibitor Used for prevention of strokes in patients with a- fib; post-op thromboprophylaxis with ortho surgeries; treatment of DVT and PE Adverse reactions: Peripheral edema, dizziness, headache, bruising, diarrhea, hematuria |
| COUMADIN | Most commonly prescribed oral anticoagulant Careful monitoring of the prothrombin time/international normalized ratio (PT/INR) A normal INR (without warfarin) is 1.0, but a therapeutic INR (with warfarin) ranges from 2 to 3.5 |
| ANTIPLATELET DRUGS | Work to prevent platelet adhesion at the site of blood vessel injury Platelets normally flow through blood vessels without adhering to their surfaces Collagen from damaged vessels stimulate platelet adhesion |
| ASPIRIN | many combinations with other prescription and nonprescription drugs Contraindicated for flulike symptoms in children and teenagers Reye’s syndrome Aspiring and dipyridamole (Aggrenox) Used for antiplatelet purposes |
| CLOPIDOGREL (PLAVIX) | Most widely used ADP inhibitor Oral use Prasugrel (Effient), ticagrelor (Brilinta) Similar to clopidogrel |
| EPTIFIBATIDE (INTEGRILIN) | GP Iib/IIIa inhibitor Usually administered in an ICU or cardiac catheterization lab setting IV use |
| THROMBOLYTIC DRUGS | break down, or lyse, preformed clots Older drugs Streptokinase and urokinase Current drugs Alteplase (Activase, Cathflo Activase) |
| THROMBOLYTIC DRUGS: MECHANISM OF ACTION | Activate the fibrinolytic system to break down the clot in the blood vessel quickly Activate plasminogen and convert it to plasmin, which can digest fibrin Reestablish blood flow to the heart muscle via coronary arteries |
| THROMBOLYTIC DRUGS: INDICATIONS | Acute MI Arterial thrombolysis DVT Occlusion of shunts or catheters Pulmonary embolu |
| THROMBOLYTIC DRUGS: ADVERSE EFFECTS | Bleeding Internal Intracranial Superficial Other effects Nausea, vomiting, hypotension, anaphylactoid reactions |
| ALTEPLASE (ACTIVASE) | t-PA made through recombinant DNA techniques Fibrin specific so does not produce a systemic lytic state Present in the body in a natural state Very short half-life (5 minutes) Indications: MI, strokes Smaller doses to flush clogged IV |
| ANTIFIBRINOLYTIC DRUGS | Prevent the lysis of fibrin Result in promoting clot formation Used for prevention and treatment of excessive bleeding resulting from hyperfibrinolysis or surgical complications Treatment of hemophilia or von Willebrand’s disease |
| ANTIFIBRINOLYTIC DRUGS: ADVERSE EFFECTS | Uncommon and mild Rare reports of thrombotic events Others include Dysrhythmia, orthostatic hypotension, bradycardia, headache, dizziness, fatigue, nausea, vomiting, abdominal cramps |
| AMINOCAPROIC ACID (AMICAR) | Synthetic antifibrinolytic drug Prevents and controls excessive bleeding that result from surgery or overactivity of fibrinolytic system Oral or parenteral |
| DESMOPRESSIN (DDAVP) | Synthetic polypeptide Similar to vasopressin, which is an antidiuretic hormone Indications: diabetes insipidus; hemophilia Nasal spray: used for nocturnal enuresis |
| TRANEXAMIC ACID | Antifibrinolytic drug that forms a reversible complex that displaces plasminogen from fibrin resulting in inhibition of fibrinolysis Used IV prior to surgery Adverse reaction: hypotension with rapid IV injection |
| HEPARIN NURSING IMPLICATIONS | IV doses are usually double checked with another nurse. Ensure that subcutaneous doses are given subcutaneously, not intramuscularly. Subcutaneous doses should be given in areas of deep subcutaneous fat |
| LWMHS: NURSING IMPLICATIONS | Given subcutaneously in the abdomen Rotate injection sites. Protamine sulfate can be given as an antidote in case of excessive anticoagulation. |
| WARFARIN (COUMADIN): NURSING IMPLICATIONS | started while the patient is still on heparin until PT/INR levels indicate adequate anticoagulation Full therapeutic effect takes several days. Monitor PT/INR regularly; keep follow-up appointments. Antidote is vitamin K |
| WARFAN Many herbal products have potential interactions; increased bleeding may occur | Capsicum pepper Garlic Ginger Ginkgo St. John’s wort Feverfew |
| ANTICOAGULANTS: PATIENT EDUCATION | Importance of regular laboratory testing Signs of abnormal bleeding Measures to prevent bruising, bleeding, and tissue injury Wearing a medical alert bracelet Avoiding foods high in vitamin K |
| ANTIPLATELET DRUGS: NURSING IMPLICATIONS | Concerns and teaching tips same as for anticoagulants Drug-drug interactions Adverse reactions to report Monitoring for abnormal bleedin |
| THROMBOLYTIC DRUGS: NURSING IMPLICATIONS | Follow strict manufacturer’s guidelines for preparation and administration. Monitor IV sites for bleeding, redness, and pain. Monitor for bleeding from gums, mucous membranes, nose, and injection sites. Observe for signs of internal bleeding |
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