Client with Angina: A 68 yr old woman arrives in the emergency department stating, "I think I had a heart attack".

She states that she had an episode of chest pain that lasted a couple of minutes during her daily 3-mile walk; the pain was relieved by rest. ECG rhythm is normal sinus rhythm. She has no abnormal heart sounds or laboratory values. V/S are stable. PO2 by pulse oximetry is 97% on room air. She is diagnosed with angina. 1. How would the client's clinical manifestations be different if she had a MI? Angina vs Myocardial Infarction Angina and Myocardial Infarction is something majority of people are not aware of. It is common to see people becoming confused when they or someone who is dear to them suffers a situation when he experiences pain in his chest. Though both are closely related and tell tale signs of problem as far as health of heart is concerned, there is urgent need to make people aware of the difference between the two problems so as to take necessary action and medical help. Angina Literally meaning choking pain, Angina pectoris refers to a situation where a person feels pain or uncomfortable sensation in his chest. It takes place when part of the heart does not receive enough oxygen because of either blocked arteries or some disease in coronary arteries. This lack of blood means heart muscles get deficient in oxygen and other nutrients. It is a condition that can occur when your heart has to work harder and at a faster rate and there could be many reasons for this condition including physical exertion, smoking, emotional stress or heredity. Those who have experienced Angina know how terrible it feels and the possible reasons that trigger the sensation. Usually, angina lasts for a few minutes only and as soon as the blood supply to the heart is normalized, the person gets relief and he is back to normal. Angina is of two types, the stable one and the unstable one. It is the unstable angina that can lead to Myocardial Infarction. Myocardial Infarction Myocardial Infraction is the condition when blood supply to the heart is stopped because of blood vessels carrying blood to the heart. When heart does not get enough oxygen, heart muscles die or get permanently damaged. MI is also called heart attack in common parlance and normally occurs when coronary artery is blocked as plaque surrounding arteries gets ruptured. This plaque is an unstable collection of fatty acids on the wall of the artery. The lack of blood supply and oxygen results in death of heart muscle tissue. In medical terms this death of muscle tissue is called infarction. Sudden and acute chest pain, nausea, shortness of breath, anxiety, palpitations and sweating are some of the common symptoms of MI. When a person suffers MI, he needs immediate medical attention and the extent of damage to his heart tissues is ascertained using Electro Cardiogram and Echocardiography. Immediate help is given through oxygen supply and aspirin. Talking of differences, while angina is temporary, and as soon as blood supply to the heart is resumed, it starts to function normally. On the other hand, in the case of MI, the heart gets damaged and needs medications. There is no permanent damage in case of angina. Summary Both angina and myocardial infarction are problems related with heart. In both cases, blood supply to heart is blocked. While angina is temporary, MI is permanent. Angina is less severe health problem but MI can even cause death.

Read more: http://www.differencebetween.com/difference-between-angina-and-vs-myocardialinfarction/#ixzz1TIQFBgKf

2. How would you explain to the client the diagnosis of angina? 3. What instructions should this client have received regarding managing her chest pain at home? The client is seen by cardiologist who prescribed nitroglycerin tablets, nifedipine, and one aspirin per day. After 6 months the client returns to the cardiologist with additional complains regarding her chest pain. A cardiac catheterization reveals the following result: 50% blockage of the circumflex artery, 60 % blockage of the anterior descending (LAD), AND 90% blockage of the right coronary artery. On this clients return appointment, indicate the assessment findings that indicate to the cardiologist that her angina is now unstable. 4. Nifedipine was prescribed for this client. Identify the drug classification of this medication and the pertinent information that a client needs to know about it. Indication & Dosage Oral Hypertension Adult: Long-acting preparation: 10-40 mg bid, or 20-90 mg once daily. Child: 1 mth-12 yr: 200-300 mcg/kg tid (max: 3 mg/kg daily or 90 mg daily); 12-18 yr: 5-20 mg tid (max: 90 mg daily). Dose frequency may vary based on the preparation used. For hypertensive crisis: 1 mth-18 yr: 250-500 mcg/kg as a single dose. Elderly: Dose reduction may be necessary. Hepatic impairment: Reduce dose by 50%-60% in patients with cirrhosis. Oral Angina pectoris Adult: Long-acting preparation: 10-40 mg bid or 30-90 mg once daily. Liquid-filled capsules: 5-20 mg tid. Child: Angina in Kawasaki disease or progeria: 1 mth-18 yr: 200-300 mcg/kg tid (max: 3 mg/kg/day or 90 mg/day). Dose frequency may vary based on the preparation used. Elderly: Dose reduction may be necessary. Hepatic impairment: Reduce dose by 50%-60% in patients with cirrhosis. Oral Raynaud's syndrome Adult: Liquid-filled capsules: 5-20 mg tid. Child: 2-18 yr: 2.5-10 mg 2-4 times daily; intiate with low doses at night. Increase slowly to prevent posturalhypotension. Dose frequency may vary based on the preparation used. Elderly: Dose reduction may be necessary. Hepatic impairment: Reduce dose by 50%-60% in patients with cirrhosis Immediate-release: May be taken with or without food. (Avoid grapefruit juice.) Retard, GITS & OROS: May be taken with or without food. (Avoid grapefruit juice. Swallow whole, do not chew/crush.) Hypotension and bradycardia; hyperglycaemia, metabolic acidosis, coma. Management is mainly supportive and symptomatic. Acute MI, cardiogenic shock, acute unstable angina, treatment of anginal attack in chronic stable angina. Hypotension, poor cardiac reserve, heart failure (deterioration has been noted), severe aortic stenosis, hepatic impairment, DM, porphyric patients, pregnancy. Avoid abrupt withdrawal (associated with exacerbation of angina). Discontinue if with ischaemic pain following administration. Peripheral oedema, hypotension, palpitations, tachycardia, flushing, dizziness,

Administration

Overdosage Contraindications Special Precautions

Adverse Drug

Reactions

Drug Interactions

Food Interaction

Lab Interference Mechanism of Action

MIMS Class ATC Classification

headache, nausea, increased micturition frequency, lethargy, eye pain, mental depression, visual disturbances, gingival hyperplasia, myalgia, tremor, impotence, fever, paradoxical increase in ischaemic chest pain during initiation of treatment, rashes, abnormalities in liver function (including cholestasis), GI obstruction in some tablets covered in indigestable membrane. Potentiates antihypertensives. Increases the effects of neuromuscular-blocking agents and CYP1A2 substrates (e.g. theophylline, aminophylline). Enhances toxic effects of magnesium. Enhanced antihypertensive effects with alpha 1-blockers, aldesleukin, and antipsychotics. Reduced effects with calcium. With concurrent use with quinidine, serum concentration is increased while reduced in quinidine. Decreased levels/effects with CYP3A4 inducers (e.g. carbamazepine, nafcillin, phenobarbital, phenytoin, and rifampicin). Increased levels/effects with CYP3A4 inhibitors (e.g. azole antifungals, cimetidine, erythromycin, and HIVprotease inhibitors). Serum levels may be decreased with food, St John's wort. Increased levels/effects with grapefruit juice, ethanol, garlic. Avoid ephedra, yohimbe, ginseng (may worsen hypertension). Falsely elevated spectrophotometric values of urinary vanillylmandelic acid. Nifedipine blocks the slow calcium channels thus preventing the flow of calcium ions into the cell. It produces peripheral and coronary vasodilatation, reduces afterload, peripheral resistance and BP, increases coronary blood flow and causes reflex tachycardia. It has little or no effect on cardiac conduction and rarely has negative inotropic activity. Absorption: Rapidly and completely absorbed from the GI tract (oral); peak plasma concentrations after 30 min (as liquid-filled capsules). Distribution: Enters breast milk. Protein-binding: 92-98%. Metabolism: Extensive hepatic first-pass metabolism. Excretion: Via urine (70-80% as inactive metabolites); 2 hr(elimination half-life). Anti-Anginal Drugs / Calcium Antagonists C08CA05 - Nifedipine ; Belongs to the class of dihydropyridine derivative selective calcium-channel blockers with mainly vascular effects. Used in the treatment of cardiovascular diseases.