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156 Cards in this Set

  • Front
  • Back
Manifestations of Anthrax
pain, swelling, and restriction of activity. Clinical manifestations of cutaneous anthrax are small skin lesions that turn into black scabs. Clinical manifestations of gastrointestinal anthrax are sore throat, difficulty swallowing, cramping, diarrhea, and abdominal swelling. Clinical manifestations of inhalation anthrax are initially fever and fatigue, followed by persistent cough and shortness of breath.
treatment of anthrax exposure.
2. Ciprofloxacin (Cipro) is used for anthrax prophylaxis and treatment. For prophylaxis, the usual dosage is 500 mg PO, every 12 hours for 60 days. For confirmed cases, the dosage is 400 mg IV, every 12 hours. Other antibiotics that are effective are penicillin, vancomycin, ampicillin, erythromycin, tetracycline, and doxycycline. In inhalation anthrax, the FDA has approved the use of ciprofloxacin and doxycycline in combination for treatment.
Treatments of nerve agents are GA (tabun) (liquid), GB (sarin) (gaseous, liquid), GD (soman) (liquid), and VX (gaseous, liquid)
injection of atropine, flushing eyes with water, applying sodium bicarbonate or 5 percent liquid bleach solution to the skin, and no induction of vomiting.
Treatments of blood agents are hydrogen cyanide (liquid) and cyanogens chloride (gas)
flushing the eyes and washing the skin with water; if inhaled as a mist, oxygen and amyl nitrate may be given; if ingested, 1 percent sodium thiosulfate may be given to induce vomiting. Treatment for cyanogens chloride involves giving oxygen and amyl nitrate; give milk or water but do not induce vomiting.
Treatment acute radiation exposure
A single 130-mg dose of potassium iodide (KI), if taken prior to or immediately following a nuclear incident, can prevent radioactive iodine (I-131) from entering the thyroid gland and damaging thyroid cells.
morphine
Opiod analgesic
naloxone (Narcan)
Opiod antagonist
acetaminophen (Tylenol)
Nonopiod analgesic
ibuprofen (Motrin).
NSAID
aspirin
Salicylate
tramadol (Ultram).
Centrally acting agents
celecoxib (Celebrex).
Selective Cox-2 inhibitors:
sumatriptan (Imitrex
4. Antimigraine agents: Tripans
Opiod analgesics: adverse effects
respiratory depression, sedation, nausea, and vomiting
2. Opioid antagonists: adverse effects
pain
NSAIDS; adverse effects
include GI upset, such as gastric ulcers and bleeding and acute renal failure
Antimigrain agents: adverse effects
GI upset
: latanoprost (Xalatan).
2. Drugs for glaucoma—Prostaglandins
2. Drugs for glaucoma—Prostaglandins: Mechanism of action
reduce IOP by increasing the outflow of aqueous humor
Prostaglandins: adverse effects
conjunctival edema, tearing, dryness, burning, pain, irritation, itching, a sensation of a foreign body in the eye, photophobia, and visual disturbancesThe eyelashes on the treated eye may grow thicker and/or darker. Changes may occur in the pigmentation of the iris of the treated eye and in the periocular skin.
timolol (Betimol, Istalol, Timoptic).
3. Drugs for glaucoma—Beta-adrenergic blocker.
3. Drugs for glaucoma—Beta-adrenergic blocker: mechanism of action
reduces the formation of aqueous humor.
4. Pharmacotherapy for ear disorders
antibiotics to treat infections, topical medication (eardrops) for the external ear, and systemic antibiotics for middle and inner ear infections and also for extensive outer ear infections. Other otic medications are glucocorticoids, which are used when inflammation is present, and cerumen (earwax) softeners to remove accumulated earwax buildup.
atorvastatin (Lipitor)
1. HMG-CoA reductase inhibitors/statins
1. HMG-CoA reductase inhibitors/statins; mechanism of action
inhibit HMG-CoA reductase, which results in less cholesterol biosynthesis
HMG-CoA reductase inhibitors/statins; adverse effects
headache, fatigue, muscle or joint pain, and heartburn
cholestyramine (Questran
2. Bile-acid resins
2. Bile-acid resins: adverse effects
are more frequent than those with statins and are limited to the GI tract, such as bloating and constipation. These agents can also bind other drugs, such as digoxin and warfarin, thus increasing the potential for drug-drug interactions.
3. Nicotinic acid. Prototype drug: Niacin: adverse effects
Adverse effects are more pronounced. Flushing and hot flashes occur in almost every patient. A variety of uncomfortable intestinal effects such as nausea, excess gas, and diarrhea are commonly reported.
gemfibrozil (Lopid)
4. Fibric-acid agents
4. Fibric-acid agents; adverse effects
GI distress, and if patient is on anticoagulant therapy, watch for signs of bleeding.
nurse’s role:2. Statins
Monitor the side effects, as they can be serious. Liver dysfunction can occur, monitor liver-function tests before and during the first few months of therapy. Do not use with those who wish to be pregnant or are pregnant or breast-feeding. Watch for signs of GI upset, as this is a common but less serious side effect.
nurse’s role; 3. Bile-acid resins
Monitor for the significant GI effects such as constipation, abdominal pain, bloating, nausea, vomiting, diarrhea, and steatorrhea. Take a careful history for past GI disorders such as peptic ulcer disease, hemorrhoids, inflammatory bowel disease, or chronic constipation. Bile-acid resins may worsen these conditions.
nurse’s role; 4. Nicotinic acid (niacin
Monitor carefully the patient’s liver function prior to and during therapy for risk of liver toxicity. Patients with a history of liver disease, elevated liver enzymes, or peptic ulcer disease should not take niacin. In patients predisposed to gout, nicotinic acid may increase uric-acid levels and precipitate acute gout. If a diabetic, monitor blood-sugar levels. Nicotinic acid can affect glycemic control.
nurse’s role; 5. Fibric-acid agents
Assess the patient for complaints of abdominal pain, nausea, and vomiting. These are common side effects of the medication, so knowing baseline complaints will enable you to determine if later complaints are a result of drug therapy or an underlying problem. Using these agents with warfarin (Coumadin) may potentiate the effects of the anticoagulant, so lower warfarin doses may be needed. Monitor prothrombin time and international normalized ration (PT/INR).
1. Primary antihypertensive agents: Diuretics; primary use
These are the first drug of choice; they have few side effects and are effective in treating mild and moderate hypertension as well as heart failure.
1. Primary antihypertensive agents:
Angiotensin-converting enzyme (ACE) inhibitors
These medications, with the angiotensin II receptor blockers, assist the body’s own mechanism to control blood pressure and fluid balance. ACE inhibitors cause intense vasodilation and lower the blood pressure.
1. Primary antihypertensive agents:
Angiotensin II receptor blockers:
This class of medication also affects the hormone aldosterone from the adrenal cortex. This increases sodium reabsorption in the kidneys and aids in retention of fluid in the blood vessels, thereby increasing blood pressure.
1. Primary antihypertensive agents:
Beta-adrenergic antagonists:
These affect the vasomotor center and the sympathetic nervous system to control blood pressure.
Primary antihypertensive agents:
Calcium channel blockers; primary use
These drugs have emerged as a primary choice in the treatment of hypertension and other cardiovascular diseases. They are used for individuals who do not respond well to other pharmacological choices.
2. Secondary antihypertensive agents: Alpha1-adrenergic antagonists
These affect the sympathetic nervous system’s control of the blood pressure by blocking the sympathetic receptors in the arterioles, thereby causing the vessels to dilate.
2. Secondary antihypertensive agents: Alpha2-adrenergic agonists:
drugs decrease the outflow of sympathetic nerve impulses from the central nervous system to the heart and arterioles. This has the same effect as the alpha1.
2. Secondary antihypertensive agents: Direct-acting vasodilators:
These directly affect vascular smooth muscle, which lowers blood pressure. This class has many side effects and is used for the hypertensive crisis.
the nurse’s role;2. Diuretics
Key areas for the nurse to monitor with the use of nonpotassium-sparing diuretics include orthostatic hypotension; laboratory electrolyte values and daily weights; potassium levels; increased weight of more than two pounds in 24 hours; intake and output assessment of edema and heart and lung sounds for signs of fluid overload. The patient’s ability to safely ambulate to the bathroom should be assessed, since diuretics increase urination. The patient should also be aware of the side effect of photosensitivity and of the possible need to increase potassium in the diet or with supplements.
For a potassium-sparing diuretic, teach the patient to limit the use of salt substitutes and potassium-rich foods. Also, pregnant and lactating women should not take these types of diuretics. Patients with a history of gout and kidney stones should be monitored closely. Key areas for the nurse to monitor include uric acid levels and gynecomastia and hirsutism for spironolactone (Aldactone).With the use of thiazide-like diuretics, key areas to monitor include laboratory values (potassium, sodium, calcium, magnesium, CBC, BUN, creatinine, and serum lipids); blood-glucose levels in diabetics, since these drugs may cause hyperglycemia; uric-acid levels. Patients should increase potassium because these are not potassium-sparing drugs. The nurse should assess the patient for pregnancy and lactation, systemic lupus erythematosus, and the use of digoxin; these medications should be avoided in patients with these conditions, or patients should be monitored more closely. For loop diuretics, the nurse should monitor these key areas: severe potassium loss; hypovolemia; hypotension; hearing loss (these drugs are ototoxic); glucose and uric acid levels.
the nurse’s role;3. Calcium channel blockers (CCBs
Key areas for the nurse to assess include the following: ECG, heart rate, and blood pressure prior to therapy, since CCBs affect the coronary arteries and myocardial contractility; during therapy the nurse should monitor heart rate and blood pressure regularly; health history specific for heart dysrhythmias, because these drugs are contraindicated with some dysrhythmias; assess for signs of CHF and reflex tachycardia since some CCBs reduce myocardial contractility; with IV administration, tachycardia and hypotension are more pronounced; assess for pregnancy since CCBs are a category C for pregnancy; dizziness, headache, and flushing are minor side effects. The nurse should teach the patient to avoid drinking grapefruit juice because it increases the absorption of these drugs.
the nurse’s role;
4. Renin-angiotensins: (ACE inhibitors)
Key areas for the nurse to assess and monitor include the following: baseline vital signs; hypotension, because ACE inhibitors given for the first time or by the IV route can cause a severe drop in blood pressure; angiodema, a serious side effect of ACE inhibitors, which can cause laryngeal swelling, leading to asphyxia; lab values and signs of infection for the serious side effect of neutropenia or agranulocytosis; potassium levels for hypokalemia, especially in patients with CHF, impaired kidney function, and diabetes. Less serious side effects to monitor for include dizziness, light-headedness, headache, and a tickling nonproductive cough; pregnancy-risk category D.
the nurse’s role; 5. Adrenergic antagonists
Key areas for the nurse to assess and monitor include the following: baseline vital signs and blood pressure response; hold the medication for pulse below 60 beats per minute and B/P below 90/60; monitor cardiac response through ECG, heart rate, and rhythm; assess for bradycardia, which may be an indication of heart block; orthostatic hypertension and other minor side effects, such as dizziness, nausea, and dry mouth. In order to avoid the complication of rebound hypertension, administration of adrenergic antagonists should not be stopped abruptly. Diabetic patients taking these drugs may experience hypoglycemia without exhibiting signs or symptoms, so fingerstick blood-sugar levels should be assessed regularly. Patients taking alpha1 drugs should be monitored specifically for GI complaints, and elderly patients should be assessed for hypothermic effects related to the vasodilation of these drugs. The pregnancy-risk categories for these drugs are B and C. Patients with hypertension that is not controlled by other medications are candidates for alpha2 therapy, since these drugs are centrally acting and have multiple side effects. The nurse should assess these patients for the following: orthostatic hypotension; sedation; decreased libido; impotence; sodium/water retention and dry mouth; pregnancy-risk category C. Specific nursing considerations for beta-adrenergic drugs include monitoring for effects of vasoconstriction, evidenced by any respiratory distress, including wheezing and shortness of breath.
the nurse’s role; 6. Direct vasodilators:
Key areas for the nurse to assess and monitor include the following: Since these drugs are used primarily for emergency situations to reduce blood pressure quickly, the vital signs, ECG, and pulse oximetry should be continuously monitored; assess the health history specifically for hypersensitivity, coronary artery disease, rheumatic mitral-valve disease, cerebrovascular disease, renal insufficiency, and systemic lupus erythematosus, since these conditions are contraindicated with these drugs. Additional nursing considerations are monitoring for priapism; signs of fluid retention with repeated IV diazoxide (Hyperstat); body-hair changes and orthohypotension with administration of minoxidil (Loniten) that reverse when drug is stopped. Nurses should only mix nitroprusside IV administration with 5% dextrose in water, and know that this drug is extremely light sensitive (container should be wrapped in an opaque substance), is brown in color, and is only stable for 24 hours. This drug can be used for hypertensive emergencies during labor and delivery.
hydrochlorothiazide (HydroDiuril)
1. Diuretics
1. Diuretics: Mech of action
decrease blood pressure by increasing the amount of urine produced and excreted
1. Diuretics: adverse effects
electrolyte imbalances, especially loss of potassium.
nifedipine (Procardia)
2. Calcium channel blockers
2. Calcium channel blockers; mechanism of action
cause vasodilation in the arteriole, which decreases blood pressure by blocking calcium channels in the plasma membrane
2. Calcium channel blockers: adverse effects
dizziness, headache, and flushing.
enalapril (Vasotec)
Angiotensin- converting enzyme (ACE) inhibitors
Angiotensin- converting enzyme (ACE) inhibitors: mechanism of action
to decrease blood pressure by decreasing blood volume through blocking of the angiotensin- converting enzyme (ACE). This blocks formation of angiotensin II, causing vasodilation and decreased reabsorption of sodium by the kidneys with increased urine excretion.
Angiotensin- converting enzyme (ACE) inhibitors; adverse effects
being persistent cough and hypotension
doxazosin (Cardura)
alpha-adrenergic blocker
beta and alpha-adrenergic blocker: mech of action (hypertension)
decrease blood pressure by blocking alpha and beta receptors or stimulation of alpha2 in the vasomotor center (brain stem), which blocks effects of the sympathetic nervous system leading to vasodilation
beta and alpha-adrenergic blocker; adverse effects (hypertension)
orthostatic hypotension, dizziness, nausea, bradycardia, and dry mouth.
metoprolol (Lopressor).
beta-adrenergic blocker
hydralazine (Apresoline
5. Direct vasodilators:
5. Direct vasodilators: mechanism of action
decrease blood pressure through direct relaxation of arterial smooth muscle, causing vasodilation
5. Direct vasodilators: adverse effects
reflex tachycardia and sodium and fluid retention.
Explain how preload affect cardiac function.
1. Cardiac output is affected by preload; that is, the degree to which the myocardial fibers in the heart are stretched prior to contraction. This occurs just before the chambers of the heart contract as they are filling to their maximum capacity with blood.
Explain how afterload affect cardiac function.
2. Cardiac output is also affected by afterload, or the degree of pressure in the aorta that must be overcome for blood to be ejected from the left ventricle.
Heart failure:nurse’s role ;ACE-inhibitor therapy
monitoring the CBC, since these drugs can cause neutropenia; assessing for severe hypotension (especially with initial doses); and using with caution in patients who have impaired kidney function, hyperkalemia, and autoimmune diseases. Patient teaching should include notifying the patient that it may take weeks or months for the maximum therapeutic response, noting sodium and potassium restrictions, and cautioning patient to not take any other medications, OTCs, herbals, or vitamins without notifying the prescriber.
Heart failure:nurse’s role diuretic therapy
for HF includes assessing renal function, because these drugs are contraindicated for kidney diseases, and monitoring electrolyte levels and for weakness, hypotension, and confusion. Additionally, the nurse should monitor vital signs, intake and output, and blood glucose and blood-urea nitrogen (BUN). Patient teaching includes instructing patients to monitor their sodium intake in order to not exceed 4,000 mg daily; to report a weight loss of more than two pounds per week and any fatigue or muscle cramping; and to change position slowly to avoid dizziness.
Heart failure:nurse’s role beta-adrenergic blockers
includes monitoring for worsening of symptoms, hepatic toxicity, and liver function. These drugs are contraindicated in patients with chronic obstructive pulmonary disease (COPD), bradycardia, heart block, and decompensated heart failure. Patient teaching should include monitoring for blood pressure and pulse (notify health care provider if the pulse is below 50 beats/minute); reporting signs and symptoms of worsening HF, such as shortness of breath, edema, and chest pain; and being warned to not stop taking the drug without notifying the prescriber.
Heart failure:nurse’s role cardiac glycoside
evaluating the patient for ventricular dysrhythmias not associated with HF and assessing renal function, since this drug is excreted by the kidneys. Monitor for drug interactions, and do not give the medication within two hours of giving antidiarrheal medications or antacids, because this decreases the absorption of digoxin. Patient teaching includes having lab tests to monitor therapeutic range, knowing the signs and symptoms of toxicity (nausea, vomiting, anorexia, and visual disturbances), and counting the pulse for one full minute and notifying the prescriber if the pulse is below 60 or above 100. The patient should report a weight gain of two or more pounds per day and should eat foods high in potassium.
Heart failure: 6. The nurse’s role in phosphodiesterase inhibitors and other inotropic agents
assessment of potassium levels for hypokalemia, monitoring for hypotension, and assessing for renal impairment and dysrhythmias. If given an IV, the patient should be continuously monitored for ventricular dysrhythmias, such as premature ventricular contractions (PVCs), ectopic beats, ventricular tachycardia, and fibrillation. Patient teaching includes ensuring the patient immediately reports irregular or rapid heart rate, a fever of 101 degrees or higher, or an increase in chest pain. If given an IV, the patient should be monitored for a fever of 101 degrees or higher or pain or swelling at the infusion site.
lisinopril (Prinivil, Zestril).
1. ACE inhibitors
Heart failure:1. ACE inhibitors Mechanism of action
the afterload on the heart and lower blood pressure by enhancing the excretion of sodium and water, which lowers peripheral resistance and reduces blood volume
Heart failure: 1. ACE inhibitors adverse effects
first-dose hypotension, cough, hyperkalemia, and renal failure.
Heart failure:2. Diuretics: mechanism of action
increases urine flow, which reduces blood volume and cardiac workload and also reduces edema and pulmonary congestion
Heart failure:2. Diuretics: adverse effects
dehydration, electrolyte imbalances, hypotension, and ototoxicity.
furosemide (Lasix)
2. Diuretics:
Heart failure; 3. Beta-adrenergic blocker mechanism of action
slowing the heart and reducing blood pressure, which reduces the workload of the heart by exhibiting a negative inotropic effect
Heart failure; 3. Beta-adrenergic blocker adverse effects
fluid retention and worsening of HF, fatigue, hypotension, bradycardia, and heart block.
carvedilol (Coreg).
Beta-adrenergic blocker
digoxin (Lanoxin).
5. Cardiac glycosides
5. Cardiac glycosides; mechanism of action
cause the heart to beat more forcefully and more slowly, which improves cardiac output.
5. Cardiac glycosides; adverse effects
neutropenia, dysrhythmias, and digitalis toxicity.
milrinone (Primacor).
6. Phosphodiesterase inhibitors and other inotropic agents:
6. Phosphodiesterase inhibitors and other inotropic agents: mech of action
block the enzyme phosphodiesterase in cardiac and smooth muscle, which increases the amount of calcium available for myocardial contraction. This causes a positive inotropic response and vasodilation, thus increasing cardiac output by increasing the contractility and decreasing afterload.
6. Phosphodiesterase inhibitors and other inotropic agents: adverse effects
hypokalemia, hypotension, and ventricular dysrhythmias.
nitroglycerin (Nitrostat).
1. Organic nitrates
1. Organic nitrates; mechanism of action
a potent vasodilator in vascular smooth muscle
1. Organic nitrates; adverse effects
: severe hypotension, dizziness, blurred vision, dry mouth, or severe headache.
atenolol (Tenormin
2. Beta-adrenergic blockers
MI; Beta-adrenergic blockers; mechanism of action
to reduce the cardiac workload by slowing the heart rate and reducing contractility.
MI; Beta-adrenergic blockers; adverse effects
hypotension, dizziness, fatigue during exercise
diltiazem (Cardizem)
3. Calcium channel blockers
MI: Calcium channel blockers mechanism of action
is similar to the beta blockers: reducing the cardiac workload
MI: Calcium channel blockers; adverse effects
hypotension, bradycardia, heart failure, and constipation.
reteplase (Retavase).
4. Thrombolytics:
MI; Thrombolytics: mechanism of action
dissolve clots obstructing the coronary arteries
MI; Thrombolytics: adverse effects
excessive bleeding due to interference with the normal clotting process.
procainamide (Pronestyl).
1. Sodium-ion-channel blockers (Class I):
Sodium-ion-channel blockers (Class I): mechanism of action;
block the sodium-ion channels, which slow the rate of impulse conduction across the heart.
Sodium-ion-channel blockers (Class I): primary use
correct many types of atrial and ventricular dysrhythmias
Sodium-ion-channel blockers (Class I):adverse effects
creation of new dysrhythmias or worsening of existing ones, lupus effect, nausea, vomiting, abdominal pain, and headache. High doses can produce CNS effects.
dsyrhythmias: Beta-adrenergic blockers; primary use
treatment of atrial dysrhythmias associated with heart failure
propranolol (Inderal).
dsyrhythmias: Beta-adrenergic blockers
dsyrhythmias: Beta-adrenergic blockers; mechanism of action
block beta receptors, which reduces automaticity and slows conduction velocity across the myocardium.
dsyrhythmias: Beta-adrenergic blockers; adverse effects
bradycardia, hypotension with dizziness and fainting, bronchospasms, hypoglycemia, and diminished libido.
amiodarone (Cordarone).
Potassium-ion-channel blockers
Potassium-ion-channel blockers; primary use
treat resistant ventricular tachycardia and atrial dysrhythmias with heart failure.
Potassium-ion-channel blockers ; mechanism of action
block potassium-ion channels in myocardial cells, which prolongs the refractory period of the heart.
Potassium-ion-channel blockers ; adverse effects
blurred vision, pneumonia-like syndrome, bradycardia, and hypotension. Potassium-ion-channel blockers can create new dysrhythmias or worsen existing ones.
verapamil (Calan).
4. Calcium-ion-channel blockers
Calcium-ion-channel blockers; mechanism of action
block calcium channels, which reduces automaticity and slows myocardial (AV) conduction velocity
Calcium-ion-channel blockers ; primary use
is treatment of supraventricular tachycardia
Calcium-ion-channel blockers ; adverse effects
include bradycardia, hypotension, and headache.
a. Anaphylactic shock
an acute allergic reaction caused by a severe reaction to an allergen such as penicillin, nuts, shellfish, or animal proteins
b. Cardiogenic shock
failure of the heart to pump sufficient blood to tissues caused by left heart failure, myocardial ischemia, MI, dysrhythmias, pulmonary embolism, myocardial or pericardial infection.
c. Hypovolemic shock
due to loss of blood volume from hemorrhage, burns, excessive diuresis, severe vomiting or diarrhea.
d. Neurogenic shock
there is vasodilation due to overstimulation of the parasympathetic or understimulation of the sympathetic nervous systems due to trauma to spinal cord or medulla, severe emotional stress or pain, drugs that depress the central nervous system.
e. Septic shock
multiple organ dysfunction as a result of pathogenic organisms in the blood; it is often a precursor to acute respiratory distress syndrome and disseminated intravascular coagulation caused by widespread inflammatory response to bacterial, fungal, or parasitic infection. (See Table 29.1 for common of types of shock.)
initial treatment priorities for a patient who is in shock.
1. Shock is treated as a medical emergency, and the first goal is to provide basic life support. Rapid identification of the underlying cause, followed by aggressive treatment, is essential, because the patient’s condition may deteriorate rapidly without specific emergency measures. The initial nursing interventions of maintaining the ABCs of life support—airway, breathing, and circulation—to sustain normal blood pressure are critical. The patient is immediately connected to a cardiac monitor, and a pulse oximeter is applied. More invasive monitoring (e.g., arterial line monitoring of blood pressure and pulse rate) is often required and should be started as soon as feasible. Unless contraindicated, oxygen is administered at 15 L/min via a nonrebreather mask. Neurological status and level of consciousness are carefully monitored. Additional nursing interventions consist of keeping the patient quiet and warm and offering psychological support and reassurance.
normal serum albumin (Albuminar, Albutein).
1. Fluid-replacement agent/colloid
Fluid-replacement agent/colloid; mechanism of action
maintain plasma osmotic pressure and transport substances through the blood
Fluid-replacement agent/colloid; primary use
restoration of plasma volume and blood proteins
Fluid-replacement agent/colloid; adverse effects
include allergies and protein overload.
norepinephrine (Levaterenol, Levophed).
Vasoconstrictors/sympathomimetics
Vasoconstrictors/sympathomimetics; mechanism of action
act directly on alpha-adrenergic receptors to raise blood pressure; they also have positive inotropic effects.
Vasoconstrictors/sympathomimetics; primary use
treat acute shock and cardiac arrest
Vasoconstrictors/sympathomimetics; adverse effects
tachycardia, bradycardia, and hypertension.
dopamine (Dopastat, Inotropin).
3. Inotropic agents
Inotropic agents; mechanism of action
Low doses have a dopaminergic effect; high doses have a beta-adrenergic effect.
Inotropic agents; primary use
hypervolemic and cardiogenic shock.
Inotropic agents; adverse effects
include dysrhythmias, hypertension, and gangrene.
epinephrine (Adrenalin)
4. Sympathomimetic/anaphylaxis
Sympathomimetic/anaphylaxis; mechanism of action
The mechanism of action is as a nonselective adrenergic agonist (sympathomimetic)
Sympathomimetic/anaphylaxis; primary use
treatment of anaphylaxis, shock, and cardiac arrest
Sympathomimetic/anaphylaxis; adverse effects
hypertension and dysrhythmias.
1. The role of the nurse in the pharmacological management of renal failure and in diuretic
careful monitoring of a patient’s condition and providing education as it relates to the prescribed drug treatment. The nurse obtains a medical, drug, dietary, and lifestyle history from each patient. Assessment of weight, intake and output, skin turgor and moisture, vital signs (check blood pressure lying, sitting, and standing), breath sounds, and the presence of edema will indicate the effectiveness of the diuretic.
The role of the nurse in the pharmacological management;Loop (high-ceiling) diuretics:
Obtain baseline, and monitor periodically during drug therapy the patient’s lab values, weight, and current level of urine output. It is critical to measure the patient’s electrolytes, especially potassium, sodium, and chloride, prior to loop diuretic therapy. Monitor the patient’s blood urea nitrogen (BUN), serum creatinine, uric acid, and blood-glucose levels. Assess for adverse effects such as circulatory collapse (due to loss of fluid), dysrhythmias, hearing loss, renal failure, and anemia. Orthostatic hypotension, hypokalemia, hyponatremia, and polyuria are additional common side effects. Observe for a rash or pruritis, which can indicate hypersensitivity to loop diuretics. Teach patients to take diuretics in the morning, change positions slowly, and to monitor weight. Patients should take potassium supplements, if ordered, and consume potassium-rich foods.
The role of the nurse in the pharmacological management; Thiazide and thiazide-like diuretics
Obtain baseline, and monitor periodically during drug therapy the patient’s lab values, weight, and current level of urine output. It is critical to measure the patient’s electrolytes, especially potassium, sodium, and chloride, prior to loop-diuretic therapy. Monitor the patient’s blood urea nitrogen (BUN), serum creatinine, uric acid, and blood-glucose levels. Increased potassium loss may occur when used with digoxin. Patients taking lithium have an increased risk of toxicity when taking thiazide diuretics. Hypersensitivity reactions may occur more frequently in patients who are allergic to sulfa-based medications. These reactions often present as rashes. Use with caution in pregnant women. Do not administer thiazide diuretics to lactating women. Teach patients to use sunscreen to decrease photosensitivity. Patients should take potassium supplements, if ordered, and consume potassium-rich foods, report any tenderness or pain in joints, which may indicate gout.
The role of the nurse in the pharmacological management; Potassium-sparing diuretics
The advantage of these medications is that the patient will not experience hypokalemia. It is critical to assess electrolytes, especially potassium and sodium levels, prior to administering potassium-sparing diuretics. Monitor the patient’s BUN and serum creatinine. Be alert for adverse effects that may include hyperkalemia and GI bleeding, confusion, dizziness, muscle weakness, blurred vision, impotence, amenorrhea, or gynecomastia. Spironolactone may also decrease the effectiveness of anticoagulants. Patients taking digoxin or lithium may be at increased risk for toxicity when taking potassium-sparing diuretics. Do not use triameterene in lactating women. Teach patients to immediately report signs and symptoms of hyperkalemia, such as irritability, anxiety, abdominal cramping, or irregular heartbeat. Avoid use of potassium-based salt substitutes. When in direct sunlight, use sunscreen to decrease photosensitivity. Avoid performing tasks that require mental alertness until the effects of the medication are known. Do not eat excess amounts of foods high in potassium.
furesomide (Lasix);
loop or high-ceiling agents
loop or high-ceiling diuretics agents; mechanism of action
: to block reabsorption of sodium in loop of Henle.
loop or high-ceiling diuretics agents; primary use;
to treat hypertension and reduce edema associated with heart failure, hepatic cirrhosis, and renal failure.
loop or high-ceiling diuretics agents; adverse effects;
rapid excretion of large amounts of water dehydration, electrolyte imbalances, and ototoxicity.
chlorothiazide (Diuril)
thiazide diuretic

the most widely prescribed class of diuretics
thiazide diuretic; mechanism of action
by blocking sodium absorption in the distal tubule of the nephron
thiazide diuretic; primary use
mild to moderate hypertension or in combination with other antihypertensives for severe hypertension
thiazide diuretic; adverse effects
are dehydration, orthostatic hypotension, and hypokalemia.
spironolactone (Aldactone).
potassium-sparing diuretics
potassium-sparing diuretics; mechanism of action
to block the action of aldosterone
potassium-sparing diuretics ; primary use
to significantly reduce mortality in heart failure.
potassium-sparing diuretics ; adverse effects
is hyperkalemia.
action of Beta 1 adrenergic receptors
heart muscle contraction
action of beta 2 adrenergic receptors
smooth muscle relaxation
Action of alpha 1 adrenergic receptors
smooth muscle contraction
Action of alpha 2 adrenergic receptors
Smooth muscle contraction and neurotransmitter inhibition & Cardiac muscle relaxation