Cardio Vascular Drugs PDF
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Jomark P. Guevara BSN, RN, USRN
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Summary
This presentation covers various cardiovascular drugs, going into detail on topics like hypertension, diuretics, and more important elements related to treating these conditions. The summary notes different types of drugs used for managing these conditions and important details related to their mechanism, usage, and side effects.
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Cardio Vascular Drugs Jomark P. Guevara BSN, RN, USRN Hypertension Hypertension (HTN) is defined as the consistent elevation of systemic arterial blood pressure. patient is said to have chronic HTN if he or she presents with a sustained systolic blood pressure of grea...
Cardio Vascular Drugs Jomark P. Guevara BSN, RN, USRN Hypertension Hypertension (HTN) is defined as the consistent elevation of systemic arterial blood pressure. patient is said to have chronic HTN if he or she presents with a sustained systolic blood pressure of greater than 140 mmHg or diastolic pressure of greater than 90 to 99 mmHg after multiple measurements are made over several clinic visits Classification of HTN Factors Responsible for Blood Pressure Important nonpharmacologic methods for controlling hypertension Limit intake of alcohol. Restrict sodium consumption. Reduce intake of saturated fat and cholesterol and increase consumption of fresh fruits and vegetables. Increase aerobic physical activity. Discontinue use of tobacco products. Reduce sources of stress and learn to implement coping strategies. Maintain optimum weight. Pharmacologic Treatment for Hypertension Diuretics Thiazide and thiazide-like diuretics The thiazide diuretics are inexpensive, and most are available in generic formulations. They are safe drugs, with urinary potassium loss being the primary adverse effect. The most frequently prescribed thiazide diuretic, hydrochlorothiazide Potassium-sparing diuretics - produce only a modest diuresis, their primary advantage is that they do not cause potassium depletion. Thus, they are beneficial when patients are at risk of developing hypokalemia due to their medical condition or the use of thiazide or loop diuretics. - Concurrent use with an ACE inhibitor or angiotensin II receptor blocker significantly increases the potential for the development of hyperkalemia. Loop Diuretics - cause greater diuresis, and thus a greater reduction in blood pressure, than the thiazides or potassium sparing diuretics. Although this makes them very effective at reducing blood pressure, they are not ideal drugs for HTN maintenance therapy - cause greater diuresis, and thus a greater reduction in blood pressure, than the thiazides or potassiumsparing diuretics. Although this makes them very effective at reducing blood pressure, they are not ideal drugs for HTN maintenance therapy ACE INHIBITORS AND ANGIOTENSIN RECEPTOR BLOCKERS ACE Inhibitor(Pril) – bayaw ni sir makaNanay (MUDRA KO) MI –Myocardial Infacrtion Unang dose phenomenom(1st dose phenomenom) Dry Cough/ Dizziness Rash Angioedema K+=increase K+ Orthostatic Hypotension ANGIOTENSIN II RECEPTOR BLOCKER(ARB) (SARTAN) SI ARBIE na Satanas(ARUY DUDE) Angioedema Renal Failure/Rash Unang Dose phenomenon Y –toxicitY and mortalitY to the babY Dizziness Orthostatic hypotension Diarrhea Sakit mo sa Ulo (Headache) CALCIUM CHANNEL BLOCKERS - Muscular contraction occurs when calcium enters the cell through channels in the plasma membrane. CCBs block these channels and inhibit Ca+ from entering the cell, limiting muscular contraction. At low doses, CCBs relax arterial smooth muscle, thus lowering peripheral resistance and decreasing blood pressure. - CCB are also know as the “valium” of the heart Calcium Channel Blockers(Pine) CC ka ng CC ede Pine(BAD HEAD) Body Pain(myalgia and arthralgia)/Weakness Bradycardia Angioedema Dizziness Dysfunction in sex Happy and sad(mood swing) Headache ADRENERGIC ANTAGONISTS Beta-Adrenergic Blockers/Beta Blocker( OLOL ) (SALAD DIC MI) S – Steven Jonhson’s D- Dysrythmias A- Agranulocytosis I – Impotence L- Libido Decrease C – Confusion A – Anaphylaxis M - Myocardial D – Dizziness I - Infarction Alpha1-Adrenergic Blockers – (ZOSIN) ( TUDO HeadDik) T- Tachycardia Head – HeadAche U- Unang Dose(1st Dose Phenom) Dik - Dyspnea D- Dizzieness O- Othostatic Hypotension Alpha2-Adrenergic Agonists(BIDA SI BATMAN) (PASAD HAG) P- Peripheral Edema H- Hepatotoxic A- Anticholinergic(Dry Mouth) A- Ache(Head) S- Sedation G- Granulocytopenia A- Anemia D- Decrease Libido Drugs for Heart Failure Heart failure (HF) is the inability of the ventricles to pump enough blood to meet the body’s metabolic demands. HF can be caused by any disorder that affects the heart’s ability to receive or eject blood. What can cause or accelerate HF Coronary artery disease (CAD). Mitral stenosis. MI. Chronic HTN. Diabetes mellitus. Hyperthyroidism or hypothyroidism Drugs for Heart Failure CARDIAC GLYCOSIDES Digoxin (Lanoxin) cause the heart to beat more forcefully (positive inotropic effect) and more slowly, thus improving cardiac output. The reduced heart rate, combined with more forceful contractions, allows for much greater efficiency of the heart The reduced heart rate, combined with more forceful contractions, allows for much greater efficiency of the heart primarily used for more advanced stages of HF VASODILATORS hydralazine (Apresoline) and isosorbide dinitrate (Isordil) act directly to relax blood vessels and lower blood pressure. Because the two drugs act synergistically, isosorbide dinitrate is combined with hydralazine in the treatment of HF 20 mg of isosorbide dinitrate with 37.5 mg of hydralazine. adverse effects, including reflex tachycardia and orthostatic hypotension limits their use to patients who cannot tolerate ACE inhibitors PHOSPHODIESTERASE INHIBITORS AND OTHER INOTROPIC DRUGS The two primary classes of inotropic agents used for decompensated HF are phosphodiesterase inhibitors and beta-adrenergic agonist. Blocking phosphodiesterase has the effect of increasing the amount of calcium available for myocardial contraction. Blocking phosphodiesterase has the effect of increasing the amount of calcium available for myocardial contraction. Phosphodiesterase inhibitors have serious toxicity that limits their use to patients with resistant HF who have not responded to ACE inhibitors, digoxin, or other therapies(2 to 3 days) If the patient presents with hypokalemia, it should be corrected before administering phosphodiesterase inhibitors because it can increase the likelihood of dysrhythmias. ANGINA PECTORIS Angina When angina occurrences are fairly predictable as to frequency, intensity, and duration, the condition is described as stable angina. The pain associated with stable angina is typically relieved by rest. When episodes of angina arise more frequently, become more intense, or occur during periods of rest, the condition is called unstable angina. When episodes of angina arise more frequently, become more intense, or occur during periods of rest, the condition is called unstable angina. Silent angina is a form of the disease that occurs in the absence of chest pain. One or more coronary arteries are occluded, but the patient remains asymptomatic. Although the mechanisms underlying silent angina are not completely understood, the condition is associated with a high risk for acute MI and sudden death. Nonpharmacologic Management of Angina Limit alcohol consumption to small amounts. Eliminate foods high in cholesterol or saturated fats. Keep blood cholesterol and other lipid indicators within the normal ranges. Do not use tobacco. Keep blood pressure within the normal range. Exercise regularly and maintain optimum weight. Keep blood glucose levels within normal range. Limit salt (sodium) intake. Surgery Percutaneous coronary intervention (PCI)- PCI may include atherectomy (removing the plaque) or angioplasty (compressing the plaque against the vessel wall). Coronary artery bypass graft (CABG) surgery is reserved for severe cases of coronary obstruction that cannot be effectively removed by PCI. A portion of a vein from the leg or chest is used to create a “bypass artery.” One end of the graft is sewn to the aorta and the other end to the coronary artery beyond the narrowed area Pharmacologic Management of Angina Antianginal drugs reduces the myocardial demand for oxygen by the following mechanisms: Slowing the heart rate. Dilating veins so the heart receives less blood (reduced preload). Causing the heart to contract with less force (reduced contractility). Lowering blood pressure, thus offering the heart less resistance when ejecting blood from its chambers (reduced afterload). ORGANIC NITRATES The primary therapeutic action of the organic nitrates is their ability to relax both arterial and venous smooth muscle. With less blood for the ventricles to pump, cardiac output is reduced and the workload on the heart is decreased, thereby lowering myocardial oxygen demand. The therapeutic outcome is that chest pain is alleviated and episodes of angina become less frequent(Stable Angina) This action, however, is crucial in treating vasospastic angina, in which the chest pain is caused by coronary artery spasm. MISCELLANEOUS DRUGS(Ranolazine) newer drug for angina that is believed to act by shifting the metabolism of cardiac muscle cells so that they use glucose as the primary energy source rather than fatty acids. This decreases the metabolic rate and oxygen demands of myocardial cells. Thus, this is the only antianginal that acts through its metabolic effects, rather than hemodynamic effects. Ranolazine does not change heart rate or blood pressure. dizziness, nausea, constipation, and headache being the most frequently reported adverse effects MYOCARDIAL INFARCTION The pharmacologic goals for treating a patient with an acute MI are as follows: Restore blood supply (reperfusion) to the damaged myocardium as quickly as possible through the use of thrombolytics or PCI. Reduce myocardial oxygen demand with organic nitrates, beta blockers, or CCBs to prevent additional infarctions. Control or prevent MI-associated dysrhythmias with beta blockers or other antidysrhythmics. Reduce post-MI mortality with aspirin, beta blockers, and angiotensin- converting enzyme (ACE) inhibitors. Manage severe MI pain and associated anxiety with narcotic analgesics. Prevent enlargement of the thrombus with anticoagulants and antiplatelet drugs. Pharmacologic treatment Nitrates Beta-Adrenergic Blocker Angiotensin-Converting Enzyme (ACE) Inhibitors Pain Management Coagulant Drugs THROMBOLYTICS Thrombolytics are most effective when administered from 20 minutes to 12 hours after the onset of MI symptoms. If administered after 24 hours, the drugs are mostly ineffective. In addition, research has suggested that patients older than age 75 do not experience reduced mortality from these drugs. Reteplase (Retavase) The most serious adverse effect of reteplase is abnormal bleeding. Bleeding may be prolonged at injection sites and catheter insertion sites. Dysrhythmias may occur during myocardial reperfusion. Antiplatelet and Anticoagulant Drugs Aspirin - use in the weeks following an acute MI dramatically reduces mortality, probably due to its antiplatelet action. The low doses used in maintenance therapy (75–150 mg/day) rarely cause GI bleeding. Unless contraindicated, 160 to 325 mg of aspirin is given as soon as an MI is suspected Clopidogrel (Plavix) - adenosine diphosphate (ADP)–receptor blocker. Is an effective antiplatelet medication approved for the prevention of thrombotic stroke and MI. For high-risk patients, a loading dose of clopidogrel is administered as soon as the diagnosis of acute coronary syndrome is confirmed and prior to PCI. Abciximab (ReoPro) - Glycoprotein IIb/IIIa inhibitors are antiplatelet drugs with a mechanism of action distinct from that of aspirin. These medications are sometimes indicated for unstable angina or MI, or for patients undergoing PCI(Percutaneous Coronary Intervention) Heparin and Warparin Heparin - On diagnosis of MI in the emergency department, patients are immediately placed on the anticoagulant heparin to prevent additional thrombi from forming. Heparin therapy is generally continued for 48 hours, or until PCI is completed. Warparin/Enoxaparin– Being use for maintenance Hemostatics also called antifibrinolytics, have an action opposite that of anticoagulants: They shorten bleeding time The class name hemostatics comes from the drugs’ ability to slow blood flow. They are used to prevent excessive bleeding following surgical procedures. Shock Treating Shock with IV Fluid Therapy VASOCONSTRICTORS/ VASOPRESSORS drugs for maintaining blood pressure when vasodilation has caused hypotension but fluids have not been lost (i.e., anaphylactic shock) and when aggressive fluid replacement therapy has been unsuccessful. Vasopressors used to treat shock include dopamine (Dopastat, Intropin), norepinephrine (Levophed), phenylephrine (Neo-Synephrine), and epinephrine. Because dopamine also affects the strength of myocardial contraction, it is considered both a vasopressor and an inotropic drug. INOTROPIC DRUGS also called cardiotonic drugs, increase the force of contraction of the heart. In the treatment of shock, they are used to increase the cardiac output. have the potential to reverse the cardiac symptoms of shock by increasing the strength of myocardial contraction. For example, digoxin (Lanoxin, Lanoxicaps) increases myocardial contractility and cardiac output, thus quickly bringing critical tissues their essential oxygen. Dobutamine (Dobutrex) is a selective beta1-adrenergic drug that has value in the short-term treatment of certain types of shock, due to its ability to cause the heart to beat more forcefully. Dopamine (Dopastat, Intropin) activates both beta- and alpha-adrenergic receptors. It is primarily used in shock conditions to increase BP by causing peripheral vasoconstriction (alpha1 activation) and increasing the force of myocardial contraction (beta1 activation). ANAPHYLAXIS Anaphylaxis is a potentially fatal condition in which body defenses produce a hyperresponse to a foreign substance known as an antigen or allergen. Epinephrine, 1:1000, given subcutaneously or intramuscularly (IM), is an initial drug of choice because it causes vasoconstriction and can rapidly relieve symptoms of bronchoconstriction. If necessary, the dose may be repeated up to three times at 10- to 15-minute intervals. Antihistamines such as diphenhydramine (Benadryl) may be administered IM or IV to prevent further release of histamine. Drugs for Dysrhythmias END