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Description : Angina is caused by reduced blood flow to the heart muscle. When the heart muscle isn't getting enough oxygen, it causes a condition called ischemia

Tags : cardiology,angina,organic nitrates,mechanism of action,nitroglycerin

Published on : Nov 06, 2022 | Views : 1189 | Downloads : 4

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Presented by: Mawaddah Olaimat Anti Anginal Medications
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In this section : Brief overview of Angina. Drug of Choice for Angina and as Family How it work. Drugs Uses and mechanism of action. Adverse reaction and drug interaction. Nursing Management and intervention. Outlines:
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At the end of this Section the student will be able to: Understand how Anti- anginal Medications Work Able to know indication of drugs Able to understand adverse interaction and contraindication. Objectives:
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1 Causes Angina is caused by reduced blood flow to the heart muscle. When the heart muscle isn't getting enough oxygen, it causes a condition called ischemia 2 Angina most common cause reduced blood flow to the heart muscle is coronary artery disease (CAD). The heart (coronary) arteries can become narrowed by fatty deposits called plaques. This is called atherosclerosis
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Organic Nitrates 1.direct relaxant effect on vascular smooth muscles. 2.the dilation of coronary vessels improves oxygen supply to the myocardium. 3.The dilation of peripheral veins, and in higher doses peripheral arteries, reduces preload and after load. 4. lowers myocardial oxygen consumption. 5. Inhibition of platelet aggregation
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1.Nitric oxide (NO) is a molecule produced by many cells in the body that serves several functions. 2.NO is primarily produced by vascular endothelial cells in the cardiovascular system. 3.Endothelial-derived NO performs a variety of important functions, including relaxing vascular smooth muscle (vasodilatation), inhibiting platelet aggregation (anti-thrombotic), and inhibiting leukocyte-endothelial interactions (anti-inflammatory). 4.NO-stimulated CGMP formation is involved in these actions. 5. Nitrodilators are medications that act similarly to endogenous NO by releasing or forming NO within tissues. 6.These medications relax the vascular smooth muscle directly, making them endothelial-independent vasodilators. Mechanism Of Action
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Primary Cardiovascular Actions of Nitrodilators Systemic Vasculature: 1.Venous dilation more than arteries dilation at small doses. 2. Decrease venous pressure and arterial pressure. Cardiac: reduced preload and after load (decreased wall stress); decreased oxygen demand Coronary prevents/reverses vasospasm vasodilatation (primarily epicardial vessels) improves subendocardial perfusion increased oxygen delivery
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is a nitrate vasodilator used to treat or prevent angina, heart failure, hypertension, and anal fissures. 1 Nitroglycerin
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Nitroglycerin  converted by mitochondrial aldehyde dehydrogenase in smooth muscle cells  nitric oxide (NO) a potent vasodilator activates the enzyme guanylate cyclase  converts guanosine triphosphate (GTP)  cyclic guanosine -monophosphate (cGMP) in vascular smooth muscle and other tissues. cGMP endogenous vasodilator of vascular smooth muscle causes protein kinase-dependent phosphorylation and activates downstream cascades  promote relaxation and increased blood flow in veins, arteries and cardiac tissue (in vitro ) aorta nitric oxide active metabolite of nitroglycerin  targets the natriuretic peptide receptors
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1.Sublingual nitroglycerin :is indicated for the acute relief of an attack or acute prophylaxis of angina pectoris due to coronary artery disease 2.Transdermal nitroglycerin :is indicated for the prevention of angina pectoris due to coronary artery disease. 3.Intravenous nitroglycerin: is indicated for the treatment of perioperative hypertension; for control of congestive heart failure in the setting of acute myocardial infarction; for treatment of angina pectoris in patients who have not responded to sublingual nitroglycerin and beta (β)-blockers; and for induction of intraoperative hypotension. 4. Topical nitroglycerin ointment: is used to treat moderate to severe pain associated with chronic anal fissure Indications & Route Nitroglycerin
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Dosage For Each Route:
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Management and prophylaxis of angina pectoris: 1. acute angina attack 0.3 to 0.6 mg S.L., repeated q 5 minutes for 15 minutes PRN. 2.one to two translingual sprays  repeated q 5 minutes for 15 minutes PRN. 3.For long-term or prophylactic use 1-mg extended-release buccal tablet q 5 hours, frequency increased PRN. 4. P.O 2.5 to 9 mg (extended-release tablets). q 8 to 12 hours; 5. P.O1.3 to 6.5 mg (extended-release capsules) . q 8 to 12 hours. -Hypertension during surgery; adjunct in heart failure: 5 mcg/minute I.V. increased by 5 mcg/minute q 3 to 5 minutes up to 20 mcg/minute. then increased by 10 to 20 mcg/minute q 3 to 5 minutes (dosage based on hemodynamic parameters)
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Heart failure associated with acute myocardial infarction (MI): 12.5 to 25 mcg I.V.then a continuous infusion of 10 to 20 mcg/minute q 5 to 10 minutes increase by 5 to 10 mcg/minute q 5 to 10 minutes as needed to a maximum of 200 mcg/minute.
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Contraindications Hypersensitivity to drug, other organic nitrates, nitrites, or adhesive (transdermal form) Angle-closure glaucoma, Orthostatic hypotension, Early MI (S.L. form), Severe anemia, Concurrent sildenafil therapy Pericardial tamponade or constrictive pericarditis, Hypotension or uncorrected hypovolemia (I.V. form), Increased intracranial pressure (as from head trauma or cerebral hemorrhage)
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1. severe renal or hepatic impairment, glaucoma, hypertrophic cardiomyopathy 2.hypovolemia, normal or decreased pulmonary capillary wedge pressure with I.V. use 3.alcohol intolerance (with large I.V. doses) 4.pregnant or breastfeeding patients 5.children (safety not established). Precautions
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Adverse reactions
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Interactions: 1.Drug-drug: Anti-hypertensives ,beta adrenergic blockers, calcium channel blockers, haloperidol, phenothiazines: additive hypotension Drugs with anti-cholinergic properties (antihistamines, phenothiazines, tri-cyclic antidepressants): decreased absorption of lingual, S.L., or buccal nitroglycerin Sildenafil: increased risk of potentially fatal hypotension 2.Drug-diagnostic tests Cholesterolfalse elevation Methemoglobin:significant levels (with excessive doses) Urine catecholamines, urine vanillyl-mandelic acid increased levels 3.Drug behaviors Alcohol use, acute alcohol ingestionincreased risk of potentially fatal hypotension
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1.Patient monitoring Nursing Management and intervention: 1. With IV: Monitor V\S with Titrate the Dosage . 2. With transdermal check for skin rash or irritation. 3.Pt Anginal relief There is no antidote for nitroglycerin
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2.Teaching Patient 1.Instruct patient to place S.L. dissolves Caution him not to chew or swallow tablet. 2.Tell patient to use drug before physical activities that may cause angina. 3.Tell patient not to chew or crush sustained-release tablets. 4. Instruct the patient to take the medication at the onset of pain and to repeat every 5 minutes for three doses. 5. Advise him to seek medical attention if the pain does not subside. 6. Instruct the patient on how to apply the appropriate amount of ointment with an applicator. Warn him not to rub the area. 7. Instruct him to wrap and tape the ointment, to wash his hands after application, and to rotate sites. 8. Advise the patient to consult with their prescriber or pharmacist before switching transdermal system brands.
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(Lopressor, Toprol):Its Beta-blockers affect heart and circulation. (Cardio selective Beta-Blockers(β1). 2 Metoprolol
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Mechanism of Action Metoprolol cardio selective beta-1-adrenergic receptor inhibitor that competitively blocks beta1-receptors with minimal or no effects on beta-2 receptors at oral doses of less than 100 mg in adults  It decreases cardiac output by negative inotropic and chronotropic effects.
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Hypertension Indications : Tachycardia Angina and HF Ventricular Arrhythmias Tremors & Anxiety
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1.dizziness or lightheadedness 2.tiredness 3.depression 4.nausea 5.dry mouth 6.stomach pain 7.vomiting 8.gas or bloating 9.Heartburn 10.constipation Adverse Affect: 11.rash or itching 12.cold hands and feet 13.runny nose 14.shortness of breath 15.wheezing 16.swelling of the hands, feet, 17.ankles, or lower legs 18.weight gain 19.fainting 20.rapid, pounding, or irregular heartbeat
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Dosage, Routes :
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Precautions and contraindications: Do not use with: 1. bradycardia. 2.second or third-degree heart blocks. 3.systolic blood pressure below 100 mm Hg. 4.caution in patients with renal or liver impairment. 5.Not for use in children.
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1.alpha-adrenergics ( amphetamines, epinephrine, and pseudoephedrine) can cause excessive hypertension with bradycardia 2.Digoxin  can cause severe bradycardia 3.Insulin or oral hypoglycemic  can alter the efficiency of each other 4. MAOIs can cause hypertension 5. antihypertensive can have severe hypotensive effects Drug interactions:
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1.Patient monitoring Nursing Management and intervention: 1. Monitor V\S. 2.Assess level of pain. 3.Signes of CHF. 4.Assess Signs of adverse reaction. In Cases of Bradycardia &Hypotension with symptomatic β-Blocker Poisoning High Dose of glucagon
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2.Teaching Patient 1.Instruct patients on the side effect of orthostatic hypotension. 2.Teach Patients particularly the elderly, should transition from a lying to a sitting or standing position slowly to prevent a drop in blood pressure and subsequent syncope . 3.Monitor for signs of worsening heart failure such as a sudden weight gain or shortness of breath. 4.Extended-release tablets are scored and can be divided but the dosage prescribed should not be crushed or chewed. 5.Alcohol use with metoprolol may increase hypotensive effects. 6.Do not stop abruptly without the guidance of a healthcare provider as withdrawal could occur and result in angina or heart attack.
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Calcium Channel Blockers 1. inhibits the entry of calcium into cells of the cardiac and peripheral vascular smooth muscles. 2. Calcium entry into L-type channels of cardiac and peripheral vascular cells is needed for them to contract or constrict more strongly. _blocking calcium entry, calcium channel blockers cause: peripheral vascular smooth muscle relaxation (decreases blood pressure) decreased myocardial contractility (decrease myocardial demand making them effective in angina) decrease heart rate and conduction velocity (useful in arrhythmias).
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Calcium channel blockers (CCBs) are used in the treatment of many cardiovascular conditions including hypertension and angina. _They are divided into subclasses:- non-dihydropyridines Dihydropyridines. differ by their pharmacokinetic properties, clinical uses, response, and selectivity Calcium Channel Blockers
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Is a non-dihydropyridine CCBs use to treat Hypertension and arrhythmias 3 Verapamil
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Indication 1.control rapid heartbeats or abnormal heart rhythms. 2. affects the movement of calcium into the cells of the heart and blood vessels. 3. result, the heart beats slower  the blood vessels relax, thus, increasing the supply of blood and oxygen to the heart while reducing its workload .
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Verapamil Dosage:- Oral: Initial dose 180 mg orally (once a day at bedtime); if adequate response is not obtained with 180 mg, the dose may be titrated upward. Maximum dose: 480 mg/day Immediate release tablets: Initial dose 80 to 120 mg orally 3 times a day; alternatively 40 mg orally 3 times a day may be warranted in patients who may have an increased response to verapamil (e.g., renal/hepatic impairment, elderly) Maintenance dose Upward titration should be based on therapeutic efficacy and safety evaluated about 8 hours after dosing Dosage may be increased daily (e.g., patients with unstable angina) or weekly until optimum clinical response is obtained. Maximum dose 480 mg/day
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Adverse reaction 1.blurred vision 2.chest pain or discomfort 3.confusion 4.dizziness, faintness, or lightheadedness when getting up from a lying or sitting position suddenly 5.fast, slow, pounding, or irregular heartbeat or pulse 6.lightheadedness, dizziness, or fainting 7.shortness of breath 8.sweating 9.unusual tiredness or weakness
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Drug interaction 1.aspirin, imatinib, lithium, nefazodone. 2.all other heart or blood pressure medicines, especially clonidine, digoxin. 3.an antibiotic - clarithromycin, telithromycin; 4.antifungal medicine. 5.antiviral medicine to treat hepatitis or HIV/AIDS 6. beta blocker . 7.cholesterol lowering medicine 8.drugs to treat high blood pressure or a prostate disorder. 9. seizure medicine - carbamazepine, phenobarbital, phenytoin. 10. tuberculosis medicine - isoniazid, rifampin.
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1.Patient monitoring and Assessment Nursing Management and intervention: 1. Monitor V\S. 2. Obtain full Hx for any allergy 3.Assess KFT; LFT and U\A. 4.Assess for any underlying medication or Diseases. 5.Protect IV solution from light Anti-Dote is Insulin
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2.Teaching Patient 1.Take sustained-release form in the morning with food; swallow it whole, do not cut, crush, or chew it. 2.Do not drink grapefruit juice while using this drug. 3. may experience these side effects Nausea, vomiting (eat frequent small meals); headache (adjust lighting, noise, and temperature; request medication); dizziness, sleepiness (avoid driving or operating dangerous equipment); emotional depression (reversible); constipation (request aid). 4.Report irregular heartbeat, shortness of breath, swelling of the hands or feet, pronounced dizziness, nausea, constipation.
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Is Piperazine acetamide, Antianginalused to treat chronic angina (chest pain). not for use during an acute (emergency) attack of angina 4 Ranolazine
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Indication 1.chronic angina(used alone or in conjunction with others). 2. Anti-ischemic ( effects dependent on reductions in heart rate or blood pressure). 3. At therapeutic levels can inhibit the cardiac late sodium current (INa) and the delayed rectifier K current (IKr ). 4. Two distinct hypotheses regarding the MOA of ranolazine have been proposed: inhibition of (INa) Inhibition and of partial fatty acid oxidation (pFOX)
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1.mechanism underlying ranolazine's anti-anginal and anti-ischemic effects is unknown. 2.It inhibits the late phase of inward sodium channels in ischemic cardiac myocytes. 3. lowering intracellular sodium concentration . 4.intracellular calcium influx via the Na-Ca channel Reduced intracellular calcium. 5. lowers ventricular wall tension  as a result, oxygen consumption.(It has no impact on blood pressure or heart rate) Mechanism of Action
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Mechanism of Action
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1. light-headed feeling . 2.fast or pounding heartbeats, fluttering. 3.kidney problems--little or no urination painful or difficult urination, swelling in feet or ankles, feeling tired or short of breath. 4. nausea. 5.constipation. 6.headache. 7.dizziness. Side effects:
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Orally 500 mg twice a day increase to 1000 mg orally twice a day as neededMaximum dose1000 mg orally twice a day Dosage & Route
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Drug interaction 1.any other medicine to treat heart disease. 2.an antibiotic or antifungal medicine 3.cholesterol-lowering medicine. 4.oral diabetes medicine. 5.medicine to prevent organ transplant rejection. 6.medicine to treat a mental illness. 7.medicine to treat or prevent nausea and vomiting caused by chemotherapy or radiation.
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1.Patient monitoring and Assessment Nursing Management and intervention: 1. Monitor V\S. 2. Obtain full Hx for any allergy 3.Assess ECG (QT –interval Prolongation) 4.Assess for any underlying medication or Diseases. 5.Assess KFT, LFT, Respiratory Evaluation
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2.Teaching Patient 1.Take this drug twice a day Swallow the tablet whole; do not cut, crush, or chew it. 2.If you miss a dose of the daily medication take it as soon as you remember and then return to your usual routine.( Do not take more than two doses in one day). 3.Do not take this drug for an acute anginal attack this drug helps chronic chest pain. (Continue to use your other angina drugs as prescribed). 4.You may be asked to have periodic ECGs and blood tests to monitor the effects of this drug on your body. 5.Do not consume grapefruit juice or grapefruit products while taking this drug. 6.You may experience these side effects if this occurs, avoid driving a car or operating dangerous machinery. 7.Report palpitations, fainting spells, severe constipation.