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Pharmacology Cardiovascular Drugs :: Nursing Pharmacology :: Review For Nursing Licensure Examination Slide Transcript
Slide 1: Cardiovascular drugs
Slide 2: Cardiac Drugs • Used in Hypertension • Used in Angina Pectoris and MI • Used in Shock • Used in Arrhythmias • Used in CHF
Slide 3: Antihypertensive drugs The Drugs employed to control hypertension can be classified as: • Diuretics • Beta-blockers • Alpha adrenergic blockers • Calcium channel blockers • Angiotensin-converting enzyme inhibitors • Angiotensin II receptor blockers • Peripheral vasodilators
Slide 4: Common Drugs in HPN IN Evaluating the effectiveness of these drugs is simply to monitor the BP if it becomes NORMAL
Slide 5: The “olol”s The Beta-Blockers (B1) • These agents are antagonist of the beta- receptors of the sympathetic nervous system. • They reduce cardiac output by diminishing the sympathetic nervous system response and sympathetic tone.
Slide 6: The “olol”s The Beta-Blockers • Vascular resistance and heart rate decrease causing reduced blood pressure. Beta-blockers can either block the beta- receptor, beta 2 receptor or BOTH. • The selective beta-blockers (B1) are specific to one type of receptor only.
Slide 7: The “olol”s The following are the common beta-blockers- the ‘-OLOL’ • Non-selective (B1 and B2) – Propranolol – Carteolol – Nadolol – Penbutolol – Pindolol – Timolol • Selective and Specific (B1) – Acebutolol – Atenolol – Betaxolol – Bisoprolol – Metoprolol
Slide 8: The “olol”s Pharmacodynamics: the mechanism of action of the beta-blockers • These agents block the beta-adrenergic receptors in the body, thereby decreasing the heart rate and in turn, the blood pressure.
Slide 9: The “olol”s Pharmacodynamics: the mechanism of action of the beta-blockers. • The non-selective agents block both Beta1 and 2 receptors causing bronchial constriction. • The onset of action is 30 minutes and the duration may range from 6-12 hours.
Slide 10: The “olol”s Clinical Indications of the beta-blockers • Hypertension • Angina pectoris • Myocardial infarction
Slide 11: The “olol”s Contraindications and precautions These agents are not given to patients with: • Heart blocks • Bradycardia • Congestive heart failure • Chronic obstructive pulmonary disease • Diabetes
Slide 12: The “olol”s • Pharmacodynamics- Side effects and adverse effects • CVS- Bradycardia, Hypotension, rebound hypertension when abruptly stopped • Respi- Bronchoconstriction, bronchospasms • Others- insomnia, depression, nightmares, constipation • Impaired ability of the liver to convert glycogen to glucose causing HYPOGLYCEMIA!
Slide 13: The “olol”s Implementation • Monitor patient’s vital signs. Take the heart rate before giving the drug • Instruct the patient to take the drug as prescribed. Warn not to abruptly stop the medication • Suggest to avoid over-the-counter medications • Give health teaching as to name of drug, dosages and side effects.
Slide 14: The “olol”s Implementation • Remind client NOT to change position abruptly as to avoid orthostatic Hypotension • Alert diabetic clients of the possible hypoglycemic effect • Inform that this can cause sexual dysfunction
Slide 15: The “olol”s Implementation • Advise client to utilize other means to control blood pressure such as diet modification, exercise, lifestyle changes, etc • Advise to eat high fiber foods to counter- act constipation
Slide 16: The Prils The Angiotensin Converting Enzyme Inhibitors • These are commonly called ACE inhibitors because the agents BLOCK the conversion of AI to AII in the LUNGS. • These agents alter one of the mechanisms of blood pressure control- the RAAS or renin- angiotensin-aldosterone system. • Angiotensin II is a very powerful vasoconstrictor and stimulus for the release of aldosterone.
Slide 17: The Prils The Angiotensin Converting Enzyme Inhibitors “—Pril” • Benazepril • Captopril- prototype • Enalapril • Enalaprilat • Fosinopril • Lisinopril • Moexipril • Quinapril • Ramipril • Trandorapril
Slide 18: The Prils Pharmacodynamics: The mechanism of action of the ACE inhibitors • These agents prevent the conversion of angiotensin I to angiotensin II by inhibiting the enzyme in the lungs- the angiotensin converting enzyme. • The action leads to decreased AII and decreased aldosterone level leading to a decrease in blood pressure.
Slide 19: The Prils Pharmacodynamics: The mechanism of action of the ACE inhibitors • The effect of lowering the blood pressure is attributed to the decrease in cardiac workload and decrease peripheral resistance and blood volume.
Slide 20: The Prils Clinical indications of the ACE inhibitors • Hypertension, either alone or in combination with other agents. • Congestive heart failure, left ventricular dysfunction • Diabetes
Slide 21: The Prils Contraindications and Precautions in the Use of ACE inhibitors • Presence of allergy is a clear contraindication. • The ACE inhibitors are NOT given to patients with renal dysfunction because these drugs may cause further decrease in renal blood flow. • If given to pregnant women, the drugs cross the placenta and produce renal abnormalities in the fetus.
Slide 22: ACE inhibitors Pharmacodynamics: the adverse effects • CVS- reflex tachycardia, chest pain, angina, cardiac arrhythmias • CNS- dizziness, drowsiness, and lightheadedness • GIT- GI irritation, nausea, vomiting, peptic ulcer, constipation and liver damage • Renal- renal insufficiency, proteinuria • Others- rash, photosensitivity, dermatitis and alopecia, sodium excretion and potassium retention, fatal pancytopenia. • COUGH- this cough is really unrelenting and bothersome.
Slide 23: ACE inhibitors Implementation • The nurse should encourage the patient to implement lifestyle changes such as weight reduction, smoking cessation, decreased intake of alcohol, dietary restriction of salt/fats and increased exercise. • Give the drug on an empty stomach, either 1 hour before or 2 hours after meals to ensure proper drug absorption
Slide 24: ACE inhibitors Implementation • Monitor the patient who is at risk of developing fluid volume alteration • Provide comfort measures like safety Precaution, environmental control, skin care, oral care and symptomatic relief of cough.
Slide 25: ACE inhibitors Implementation • Provide patient teaching including the name of drug, dosage, measure to handle adverse effects and the warning signs to report. Stress the importance of NOT abruptly stopping the medication if symptoms are improving. • Caution the patient to change position slowly and to avoid hazardous or delicate tasks and driving if drowsiness is a problem
Slide 26: The “sartans” • The Angiotensin II Receptor Blockers These are SELECTIVE agents that specifically bind to the angiotensin II receptors in the blood vessels and adrenal cortex to prevent the release of aldosterone and to prevent vasoconstriction.
Slide 27: The “sartans” Prototype: Losartan • Candesartan • Irbesartan • Losartan • Telmisartan • Valsartan
Slide 28: The “sartans” Pharmacodynamics- The mechanism of action of the A-R-B • These agents work by attaching to the Angiotensin II receptors in the vascular smooth muscles and in the adrenal gland. • The action results in VASODILATION because AII action (constriction) is inhibited and BLOCKAGE of aldosterone release
Slide 29: The “sartans” Clinical Use of the A-R-B • Hypertension, either alone or in combination. • These agents are also used if the patient cannot tolerate the unrelenting cough associated with ACE inhibitors.
Slide 30: The “sartans” Contraindications and precautions associated with the A-R-B • These agents are contraindicated in the presence of allergy. • It is NOT GIVEN to pregnant mothers because of the associated FETAL DEATH and severe fetal abnormalities. Lactating women should also avoid these drugs because they can affect the neonate.
Slide 31: The “sartans” Pharmacodynamics: the adverse effects • CNS- headache, dizziness, weakness, syncope and orthostatic Hypotension • GIT- Diarrhea, abdominal pain, nausea, dry mouth and tooth pain • Respiratory- mild cough • Skin- rash, dry skin and alopecia.
Slide 32: The “sartans” Implementation • Encourage the patient to implement lifestyle changes, including weight loss, smoking cessation, decrease in alcohol and salt in the diet, and increased exercise, to increase the effectiveness of anti-hypertensive therapy. • Administer without regard to meals; give with food to decrease GI distress if needed.
Slide 33: The “sartans” Implementation • Alert the surgeon and mark the patient's chart prominently if the patient is to undergo surgery to alert medical personnel that the blockage of compensatory angiotensin II could result in hypotension following surgery that needs to be reversed with volume expansion.
Slide 34: The “sartans” Implementation • Ensure that the patient is not pregnant before beginning therapy and suggest the use of barrier contraceptives while on this drug to avert potential fetal death or abnormalities that have been associated the these drugs. • Find an alternative method of feeding the baby if patient is nursing to prevent the potentially danger- block of the renin- angiotensin system in the neonate.
Slide 35: The “sartans” Implementation • Monitor the patient carefully in any situation that might lead to a drop in fluid volume (e. g., excessive eating, and vomiting diarrhea, dehydration) to detect treat excessive hypotension that may occur. • Provide comfort measures to help the patient tolerate drug effects (e.g., small, frequent meals; access to bathroom facilities; safety precautions if CNS effects occur environmental control; appropriate skin care needed; analgesics as needed).
Slide 36: Calcium channel blockers • These agents prevent the movement of calcium into the cardiac and smooth muscle cells when the cells are stimulated.
Slide 37: Calcium channel blockers • This blocking of calcium will interfere with the muscle cell's ability to contract, leading to a loss of smooth muscle tone, vasodilation, and a decrease in peripheral resistance. • These effects will decrease blood pressure, cardiac workload, and myocardial oxygen consumption.
Slide 38: Calcium channel blockers • Calcium channel blockers are very effective in the treatment of angina because they decrease the cardiac workload.
Slide 39: Calcium channel blockers Pharmacodynamics: Mechanism of action • Calcium channel blockers inhibit the movement of calcium ions across the membranes of myocardial and arterial muscle cells, altering the action potential and blocking muscle cell contraction. • This effect will depress myocardial contractility, slow cardiac impulse formation in the conductive tissues, and relax and dilate arteries, causing a fall in blood pressure and a decrease in venous return.
Slide 40: Calcium channel blockers The calcium channel blockers that are used in the treatment of hypertension include the following: The “-dipine” and others • Diltiazem (Cardizem, Tiamate) • Verapamil • Amlodipine (Norvasc) • Felodipine (Plendil) • Isredipine (DynaCirc) • Nicardipine(Cardene) • Nifedipine (CALCIBLOC, Procardia XL)- prototype! • Nisoldipine (Sular)
Slide 41: Calcium channel blockers CONTRAINDICATION and PRECAUTIONS • These drugs are contraindicated in the presence of allergy to any of these drugs • With heart block or sick sinus syndrome because these could be exacerbated by the conduction-slowing effects of these drugs • With renal and hepatic dysfunction, which could alter the metabolism and excretion of these drugs; and with pregnancy and lactation because of the potential for adverse effects on the fetus and neonate.
Slide 42: Calcium channel blockers Pharmacodynamics: the ADVERSE EFFECTS • The adverse effects associated with these drugs are related to their effects on cardiac output and on smooth muscle. – CNS effects include dizziness, lightheadedness, headache, and fatigue. – GI problems can include nausea and hepatic injury related to direct toxic effects hepatic cells. – Cardiovascular effects include hypotension, bradycardia, peripheral edema, and heart block. Skin flushing and rash may also occur
Slide 43: Calcium channel blockers Pharmacodynamics: The main use of calcium channel blockers is the treatment of angina Also in hypertension Also in vascular spasm= Raynauds
Slide 44: Calcium channel blockers IMPLEMENTATION • Monitor blood pressure carefully while patient is on therapy because of increased hypotensive episodes • If possible, obtain serial ECG tracing • Provide comfort measures to help patient tolerate drug effects- includes serving small frequent feedings and safety precaution due to hypotension and dizziness
Slide 45: Calcium channel blockers IMPLEMENTATION • Provide health teaching as to drug name, dosage, administration, side effects and warning manifestations to report
Slide 46: The Vasodilators • Vasodilators produce relaxation of the vascular smooth muscle, decreasing peripheral resistance and reducing blood pressure. • They cause the reflex tachycardia that occurs when blood pressure drops
Slide 47: The Vasodilators • The vasodilators are used to treat severe hypertension
Slide 48: Vasodilators • Diazoxide (Hyperstat) • Hydralazine (Apresoline) • Minoxidil (Loniten) • Sodium Nitroprusside (Nitropress) • Tolazoline (Priscoline)
Slide 49: Vasodilators Pharmacodynamics: mechanism of action of the vasodilators • The vasodilators act directly on vascular smooth muscle to cause muscle relaxation, leading to vasodilation and drop in blood pressure. • They are indicated for the treatment of severe hypertension that has not responded to other therapy.
Slide 50: Vasodilators Contraindications and Precautions • The vasodilators are contraindicated in the presence of known allergy to the drug; with pregnancy and lactation because of the potential for adverse effects on the fetus and neonate; and with any condition that could be exacerbated by a sudden fall in blood pressure, such as cerebral insufficiency.
Slide 51: Vasodilators Pharmacodynamics: the adverse effects of the vasodilators • CNS- dizziness, anxiety, headache • CVS- reflex tachycardia, CHF, chest pain, edema; skin rash, lesions (abnormal hair growth with minoxidil), hypotension • GI upset, nausea, and vomiting
Slide 52: Vasodilators Pharmacodynamics: the adverse effects of the vasodilators • Cyanide toxicity (dyspnea, headache, vomiting, dizziness, ataxia, loss of consciousness, imperceptible pulse, absent reflexes, dilated pupils, pink color, distant heart sounds, shallow breathing) may occur with nitroprusside, which is metabolized to cyanide and which also suppresses iodine uptake and can cause hypothyroidism.
Slide 53: Vasodilators IMPLEMENTATION • Encourage the patient to implement lifestyle changes, including weight loss, smoking cessation, decrease in alcohol and salt in the diet, and increased exercise, to increase the effectiveness of antihypertensive therapy. • Monitor blood pressure closely during administration to evaluate for effectiveness and to ensure quick response if blood pressure falls rapidly or too much.
Slide 54: Vasodilators IMPLEMENTATION • Monitor blood glucose and serum electrolytes to avoid potentially serious adverse effects. • Monitor the patient carefully in any situation that might lead to a drop in fluid volume (e.g., excessive sweating, vomiting, diarrhea, dehydration) to detect and treat excessive hypotension that may occur.
Slide 55: Vasodilators IMPLEMENTATION • Provide comfort measures to help the patient tolerate drug effects (e.g., small, frequent meals, access to bathroom facilities safety precaution if CNS effects occur, environmental control, appropriate skin care as needed, analgesic as needed). • Provide thorough patient teaching • Offer support and encouragement to deal with the diagnosis drug regimen.
Slide 56: Drugs for the Treatment of Congestive Heart Failure • Vasodilators- Nitrates that act to directly relax vascular muscle tone and cause decrease in blood pressure with pooling of blood in the veins. The preload and afterload will be decreased • ACE inhibitors- are agents that block the conversion of angiotensin I to angiotensin II. The result is blockage of the vasoconstriction and decreased blood volume. The afterload will be decreased. • Diuretics are employed to decrease the blood volume, which decreases the venous return and the blood pressure. The results are decreased preload and decreased afterload.
Slide 57: Drugs for the Treatment of Congestive Heart Failure • Beta stimulators will stimulate the beta receptors in the sympathetic nervous system, increasing the myocardial contraction- called positive inotropic effect. • Cardiotonic drugs- these agents affect the INTRACELLULAR calcium levels in the heart muscles leading to increased contractility . The result is increased cardiac output, increased renal blood flow, increased perfusion and increased urine formation. The cardiotonic drugs are: the cardiac glycosides and the phosphodiesterase inhibitors.
Slide 58: The cardiac glycosides • These are agents extracted from the foxglove plant. They are available in oral and parenteral preparations. The following are the cardiac glycosides: • Digoxin (Lanoxin) • Digitoxin (Crystodigin) • Ouabain
Slide 59: The cardiac glycosides Pharmacodynamics: the Mechanism of action • They increase the level of CALCIUM inside the cell by inhibiting the Sodium- Potassium pump. • More calcium will accumulate inside the cell during cellular depolarization.
Slide 60: The cardiac glycosides • Positive inotropic Effect- the myocardium will contract forcefully – Increased cardiac output – Increased blood flow to the body organs like the kidney and liver • Negative chronotropic effect- the heart rate is slowed due to decreased rate of cellular repolarization – Bradycardia • Decreased conduction velocity through the AV node
Slide 61: The cardiac glycosides Clinical Use of the cardiac glycosides • Treatment of congestive heart failure • Treatment of dysrhythmias like atrial flutter, atrial fibrillation and paroxysmal atrial tachycardia
Slide 62: The cardiac glycosides Contraindications and Precautions • Contraindicated in the presence of allergy to any cardiac glycoside. • They are NOT given to patients with ventricular dysrhythmias, heart block or sick sinus syndrome, aortic stenosis, acute MI, electrolyte imbalances (HYPOKALEMIA, HYPOMAGNESEMIA and HYPERCALCEMIA) and renal failure (may cause accumulation of drug)
Slide 63: The cardiac glycosides Pharmacodynamics: the Adverse Effects of the Cardiac glycosides • CNS- Headache, weakness , seizures and drowsiness • CVS- arrhythmias • If digitalis toxicity is developing- the nurse must assess the following adverse effects: Anorexia, nausea and vomiting, visual changes- YELLOW halo around an object, and palpitations or very slow heart rate
Slide 64: The cardiac glycosides Drug-Drug Interactions • If taken with Verapamil, Amniodarone, quinidine, quinine, erythromycin and tetracyclines- can increase the risk of INCREASED effects of digitalis. • If taken with potassium-losing diuretics like furosemide- can INCREASE the risk of toxicity and arrhythmias. Potassium replacement must be given. • If given with cholestyramine, charcoal and colestipol- can cause impaired absorption of digitalis
Slide 65: The cardiac glycosides Implementation • Administer the initial rapid digitalization and loading dose as ordered intravenously • Monitor the APICAL pulse rate for ONE full minute before administering the drug. Withhold the drug if – Less than 60 in adults – Less than 90 in infants – More than 110 in adults • Retake pulse in one hour, if pulses remain abnormal, refer!
Slide 66: The cardiac glycosides Implementation • Check the spelling of the drug- DIGOXIN is different from DIGITOXIN! • Check the dosage preparation and the level of digitalis in the blood. (Therapeutic level is 0.5 to 2.0 nanograms/mL) • Administer intravenous drug VERY slow IV over 5 minutes to avoid arrhythmias. Do NOT administer intramuscularly because it can cause severe pain
Slide 67: The cardiac glycosides Implementation • Administer the drug without food if possible to avoid delayed absorption. Weight patient daily to determine fluid retention • Maintain emergency equipment and drugs= Potassium salts, Lidocaine for arrhythmias, phenytoin for seizures, atropine for bradycardia. • Provide comfort measures- small, frequent meals, adequate lighting, comfortable position, rest periods and safety precautions
Slide 68: The cardiac glycosides Implementation • Provide health teaching- drug name, action, dosage and side effects. Advise the patient to report any of the following: Visual changes, rapid weight gain, unusually low heart rate, persistent nausea, vomiting and anorexia • Monitor serum potassium level
Slide 69: The cardiac glycosides Evaluation Evaluate effectiveness of the drug: Increased urine output Normal heart rate in arrhythmia
Slide 70: The Antianginal drugs • In the treatment of angina, three agents are commonly employed- – Organic nitrates – Beta-blockers and – Calcium-channel blockers. • The benefits of the drugs lie in their different mode of action.
Slide 71: The Antianginal drugs • The nitrates can cause vasodilatation of the veins and to some extent, coronary artery
Slide 72: The Antianginal drugs • Beta-blockers will decrease the heart rate
Slide 73: The Antianginal drugs • Calcium-channel blockers will decrease force of contraction leading to a decreased myocardial workload and demand. • They can also produce vasodilation
Slide 74: The Antianginal drugs • Anti anginal drugs are effective if the chest pain is relieved
Slide 75: The Organic nitrates • These agents are simple nitric and nitrous acid esters of alcohols. Being alcohol, they differ in their volatility. The following are the nitrates commonly used: • Nitroglycerin- A moderately volatile nitrate • Isosorbide Dinitrate (Isordil) or mononitrate • Amyl nitrate- an extremely volatile nitrate
Slide 76: The Organic nitrates Nitroglycerin • This agent is supplied in oral, spray, transdermal and ointment preparations.
Slide 77: The Organic nitrates Pharmacodynamics: the mechanism of action • Nitroglycerin relaxes the smooth muscles in the vascular system by its conversion to nitric oxide, a chemical mediator in the body that relaxes smooth muscles.
Slide 78: The Organic nitrates Administered nitrates Increased nitrates in the blood increased formation of nitric oxide increased cGMP formation increased dephosphorylation of myosin Vascular smooth muscle relaxation vasodilatation
Slide 79: The Organic nitrates Pharmacokinetics- absorption to excretion • It can be given orally, parenterally and topically. • The onset of action of nitroglycerin is more than 1 hour. • Because significant first-pass hepatic effect, Nitroglycerin is given SUBLINGUALY.
Slide 80: The Organic nitrates Pharmacodynamics: Side effects and adverse effects • HEADACHE is the most common effect of nitroglycerin. • CVS- postural Hypotension, facial flushing, tachycardia • TOLERANCE- the tolerance to the actions of nitrates develop rapidly. This can be managed by providing a day of abstinence.
Slide 81: The Nitrates Implementation • Monitor vital signs, especially watchful for hypotensive episodes • Advise patient to remain supine or sit on a chair when taking the nitroglycerin for the first time. Emphasize that he should change his position slowly or rise from bed slowly to avoid orthostatic Hypotension • Offer sips of water before giving sublingual nitroglycerin because dryness may inhibit drug absorption
Slide 82: The Nitrates Implementation • Apply nitroglycerin ointment to the designated mark on paper. • The nurse should remove any excess ointment on the skin from the previous dose. • She should NEVER USE her bare fingers because the drug can be absorbed, utilize gloves or tongue blades instead.
Slide 83: The Nitrates Implementation • Apply nitroglycerin patch to an area with few hairs. Never touch the medication portion. • The patch and the ointment should NOT be applied near the area for defibrillation because explosion and skin burns may result
Slide 84: The Nitrates IMPLEMENTATION • Emphasize that tolerance to the nitroglycerin can occur. • If the medication cannot relieve the pain, report to the hospital immediately.
Slide 85: The Nitrates IMPLEMENTATION • Provide client health teaching- the sublingual nitroglycerin tablet is USED if chest pain occurs • The dose may be repeated if pain is unrelieved within 5 minutes. • Repeat the medication administration if the pain has not yet subsided. • DO NOT give more than 3 tablets!!! If chest pain persists for more than 15 minutes, hospital consult should be done immediately.
Slide 86: The Nitrates IMPLEMENTATION • Instruct the client to avoid alcohol while taking nitroglycerin to avoid potentiating the hypotensive effect of the medication • If beta blockers and calcium-channel blockers are given, instruct the patients to consult the physician before discontinuing the medication
Slide 87: The Nitrates IMPLEMENTATION • Other components of health teaching for home self-administration: – If taking Sublingual Nitroglycerin, the patient should be instructed to place the tablet under the tongue for quick absorption. – A burning sensation/biting/stinging sensation may indicate that the tablet is FRESH! – Store the tablet in a dark container, keep it away from heat and direct sunlight to avoid lessening the potency
Slide 88: The Nitrates IMPLEMENTATION • Other components of health teaching for home self-administration: – HEADACHES are common in the initial period of nitroglycerin therapy. Advise patient to take PARACETAMOL for relief – The nitroglycerin patch is applied once a day, usually in the morning. The sites should be rotated, in the chest, arms and thighs avoiding hairy areas.
Slide 89: The Nitrates IMPLEMENTATION • Other components of health teaching for home self-administration: – Position supine with elevated legs to manage Hypotension. – Nitroglycerin tablet can be taken prophylactically in situations where chest pain is anticipated- Sex, exercise, etc.. – If patient is taking beta blockers, instruct how to obtain heart rate in a minute
Slide 90: Drugs for Shock Dopamine • This is a sympathomimetic drug often used to treat Hypotension in shock states that are not caused by Hypovolemia. • This drug is an immediate precursor of nor-epinephrine, occurs naturally in the CNS basal ganglia where it functions as a neurotransmitter.
Slide 91: Drugs for Shock Dopamine • Pharmacodynamics: It can activate the alpha and beta adrenergic receptor depending upon the concentration. It stimulates receptors to cause cardiac stimulation and renal vasodilation. • The dose range is 1-20 micrograms/kg/min
Slide 92: Drugs for Shock Dopamine • Pharmacokinetics: Dopamine is administered IV, excreted in the urine. • At low dose (1-2 micrograms), dopamine DILATES the renal and mesenteric blood vessels producing an increase output (dopaminergic effect)
Slide 93: Drugs for Shock Dopamine • At moderate dose of 2-10 micrograms, dopamine enhance cardiac output by increasing heart rate (beta 1-adrenergic effect) and elevates blood pressure through peripheral vasoconstriction (alpha adrenergic effect)
Slide 94: Drugs for Shock Dopamine • At higher doses of more than 10 micrograms- vasoconstriction of all vessels will predominate that can lead to diminished tissue perfusion
Slide 95: Drugs for Shock Dopamine • Dopamine is indicated to treat Hypotension, to increase heart rate and to increase urine output (given less than 5 mg/kg/min) • The nurse typically prepares the dopamine drip- dopamine (at a concentration of 400-800 mg) is mixed in 250 mL D5W and administered as drip via an infusion pump for precise dosage administration. • Sodium bicarbonate will inactivate the dopamine
Slide 96: Drugs for Shock Dopamine • Pharmacodynamics: side effects- Tachycardia hypertension ectopic beats, angina dysrhythmias, myocardial ischemia, nausea and vomiting.
Slide 97: Drugs for Shock Dopamine: Nursing consideration – Check the IV site hourly for signs of drug infiltration of dopamine, which can cause severe tissue necrosis. – Phentolamine should be infiltrated in multiple areas to reduce tissue damage. – Drug is effective if Urine output is increased and BP is increased
Slide 98: Anti-Arrhythmias • Arrhythmias (sometimes called Dysrhythmias) are conduction dysfunctions caused by abnormalities in impulse generation or impaired transmission of the impulses. • They are simply deviations from the normal rate or pattern of the heartbeat.
Slide 99: Anti-Arrhythmias Four things may happen during arrhythmias: • The heart will beat too FAST (tachycardia, either the atrium or the ventricle) • The heart will beat too slow (bradycardia) • The heart will respond to other impulses generated by the cardiac cells (other than the SA node) • The heat will respond to impulses traveling along extra pathways
Slide 100: Anti-Arrhythmias • Anti-arrhythmic agents are given to modify impulse generation and conduction. • The desired action of these antidysrhythmics is to restore the cardiac rhythm to normal. • They affect the action potential of the cardiac cells, altering their automaticity, conductivity, or BOTH
Slide 101: Anti-Arrhythmias • Because the anti-arrhythmic drugs affect the conduction system, they also can produce ARRHYTHMIAS! • They are also Pro-Arrhythmics!
Slide 102: Anti-Arrhythmias The classes of anti-arrhythmic agents: • Class 1 agents - are fast SODIUM channel blockers that affects the depolarization phase. • Class 2 agents- are BETA blockers that affect the depolarization. • Class 3 agents- are POTASSIUM channel blockers that diminish the outward potassium current during repolarization of cardiac cells. • Class 4 agents- are calcium channel blockers that decrease the calcium influx into the specialized cardiac muscle cells causing slowed conduction
Slide 103: Anti-Arrhythmias The classes of anti-arrhythmic agents: • Class 1 agents - – Class 1 A- Quinidine, Procainamide, Disopyramide, Moricizine – Class 1 B- Lidocaine, Mexiletine, Tocainide – Class 1 C- Encainide, Flecainide, propafenone
Slide 104: Anti-Arrhythmias • The classes of anti-arrhythmic agents: • Class 2 agents- are BETA blockers that affect the depolarization. They decrease the conduction velocity, automaticity and recovery time. Examples are: Propranolol, Metoprolol, pindolol, acebutol and esmolol
Slide 105: Anti-Arrhythmias • The classes of anti-arrhythmic agents: • Class 3 agents- are POTASSIUM channel blockers that diminish the outward potassium current during repolarization of cardiac cells. • They increase the refractory period and prolong the action potential. Examples are: sotalol, bretylium, amniodarone
Slide 106: Anti-Arrhythmias • Class 4 agents- are calcium channel blockers that decrease the calcium influx into the specialized cardiac muscle cells causing slowed conduction. They increase the refractory period of the AV node, which decreases the ventricular response. • The examples of calcium channel blockers are diltiazem and verapamil
Slide 107: Anti-Arrhythmias • Miscellaneous- digoxin and adenosine
Slide 108: Anti-Arrhythmias General Nursing Process for Anti-arrhythmics Assessment • Patient History- the nurse obtains health and drug histories. She should elicit symptoms of shortness of breath, heart palpitations, coughing, chest pain, previous angina or dysrhythmias, and the current medications. • Physical Examination- the nurse performs assessment and baseline monitoring • Laboratory exams- the nurse obtains ECG results and cardiac markers- CK-MB, AST and LDH)
Slide 109: Anti-Arrhythmias Nursing Diagnoses • Alteration on perfusion: decreased cardiac output • Alteration in thought processes and sensory- perceptual alteration • Anxiety related to irregular heartbeat • Risk for activity intolerance • Risk for injury related to CNS effects • Knowledge deficit regarding drug therapy
Slide 110: Anti-Arrhythmias Planning • The client will no longer experience abnormal cardiac rhythm • The client will comply with the drug regimen
Slide 111: Anti-Arrhythmias Implementation • Monitor Vital signs especially BP and HR. Patient can develop Hypotension • Administer the parenteral drugs slow IV for a period of 2-3 minutes • Monitor ECG for abnormal patterns and report findings. • Instruct to report palpitations and abnormal cardiac rate • Maintain life support equipment on stand by to treat severe adverse reactions that might occur
Slide 112: Anti-Arrhythmias Implementation • Establish safety precautions- side rails, lighting, and noise control. • Provide client teaching. Instruct the client to take the prescribed drug as ordered. Emphasize the client to avoid alcohol, caffeine and tobacco. • Alcohol can intensify the hypotensive effects, caffeine increases the cathecolamine levels and tobacco can promote vasoconstriction. • Instruct the client to report side effects including dizziness, faintness, and nausea and vomiting.
Slide 113: Anti-Arrhythmias Evaluation • Evaluate the effectiveness of the prescribed anti-dysrhythmic by comparing heart rates with baseline heart rate. • Assess the client’s response to the drug. • Monitor for adverse effect- sedation, Hypotension, cardiac arrhythmias, respiratory depression, CNS effect. • Evaluate the effectiveness of the teaching plan. Monitor the effectiveness of comfort measures and compliance to regimen.
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