Care of Patients with Acute Coronary Syndromes Coronary

Care of Patients with Acute Coronary Syndromes

Coronary Artery Disease (CAD) • Coronary artery disease (CAD) is a broad term that includes chronic stable angina and acute coronary syndromes. It affects the arteries that provide blood, oxygen, and nutrients to the myocardium. When blood flow through the coronary arteries is partially or completely blocked, ischemia and infarction of the myocardium may result. • Ischemia occurs when insufficient oxygen is supplied to meet the requirements of the myocardium. • Infarction (necrosis, or cell death) occurs when severe ischemia is prolonged and decreased perfusion causes irreversible damage to tissue

Angina pectoris • This is a syndrome usually characterized by episodes or paroxysms of pain, or of pressure in the anterior chest. • The cause is insufficient coronary blood flow • the need for O 2 exceeds the supply.

Types of Angina • Stable: consistent pain occurs with exertion and is relieved with rest. • Unstable: symptoms occur more frequently and last longer. The pain may occur at rest and can even wake patients out of sleep. • New Onset: 1 st symptoms • Variant: Prinzmetal’s angina is pain at rest with reversible ST segment elevation, thought to be caused by spasm. • Pre-Infarction: pain occurs days or weeks prior to MI • Intractable or refractory: severe incapacitating chest pain. • Silent: EKG changes are seen but the patient is asymptomatic.

Pathophysiology • Caused by • atherosclerosis, hypertension, coronary artery spasm, hypertrophic cardiomyopathy • Factors associated with typical angina pain: 1. physical exertion 2. exposure to cold 3. eating a heavy meal 4. stress or emotion provoking situation.

Clinical manifestations • Pain varies from a feeling of indigestion to a choking or heavy sensation in the upper chest that ranges from discomfort to agonizing pain accompanied by severe apprehension and a feeling of impending doom. • A feeling of weakness, or numbness in the arms, wrists, and hands may accompany the pain, dypsnea, tachycardia, palpitations, sob, pallor, diaphoresis, dizziness/ syncope, or lightheadedness, nausea or vomiting and anxiety. • An important manifestation of angina is that it abates or subsides with rest or nitro.

Geriatric consideration & Risks • Note: they often do not have the typical pains and pressure because of diminished responses of neurotransmitters that occur in the aging process. Often their complaint is dyspnea, it can also be severe fatigue, or dizziness. • RISK FACTORS: • Non-modifiable • Modifiable • HDL is INVERSELY related to risk for developing CAD

Medical management & assessment • The objectives of the medical management are to decrease the O 2 demand of the myocardium and to increase the O 2 supply. Medically these objectives are met through pharmacologic therapy and control of risk factors. • Diagnostics: • ECG • Exercise Stress Test • Stress Echocardiogram • Coronary Angiogram • Cardiac Catherization

Pharmacologic therapy • Nitrates are the mainstay for treatment of angina. • Nitrostat or nitroglycerin is a vasoactive agent and it is administered to reduce myocardial oxygen consumption, which decreaes ischemia and relieves pain. • Usual routes are sublingual, as a spray, topical or I. V. • For anginal pain the patient is instructed to take 1 tablet under the tongue every 5 minutes up to 3 tabs for relief of pain- if no relief call 911. • Note: before giving a patient a nitrate ASK if they have taken Viagra or Cialis in past 24 hrs. Both have vasodilating effects resulting in SEVERE HYPOTENSION.

Pharm cont’d • Heparin- this prevents the formation of new blood clots. The use of heparin alone in patients with unstable angina reduces the occurrence of MI. Heparin therapy is considered therapeutic when the PTT/INR is 1. 5 to 2. 0 times the normal. • Sometimes a LMWH (low molecular weight heparin) Lovenox is given s/q. This med provides more effective and stable anticoagulation, potentially reducing rebound ischemia and it does not need to be monitored with a. PTT.

Pharm cont’d • Because Heparin and Lovenox increase the risk of bleeding, the patient needs to be monitored closely. • Bleeding precautions include: applying pressure to the site of any needle puncture for a longer time than usual. avoid I. M. injections if possible avoid tissue injury and bruising from trauma or use of constrictive devices.

Oxygen • Is usually administered at the onset of chest pain in an attempt to increase the amount of O 2 delivered to the myocardium and decrease pain. • Normal pulse ox is greater than 93%.

Myocardial Infarction • Causes: • Atherosclerosis of a coronary artery • Rupture of the plaque > thrombosis • Occlusion of blood flow • Other: clotting: platelet aggregation Shock or hemorrhage

Pathophysiology • One or more coronary arteries become occluded • If coronary occlusion lasts longer than 30 -45 minutes, irreversible myocardial cell damage and muscle death occur • Every MI has a central area of necrosis surrounded by an area of hypoxic injury. This injured area is potentially viable is circulation is restored, or it may progress to necrosis.

Signs and symptoms • Extreme anxiety and restlessness • Dyspnea • Nausea or vomiting • Diaphoresis • Tachycardia • Hypertension • Bradycardia and hypotension if inferior MI • An S 4 or. S 3 and paradoxical splitting of S 2 with ventricular dysfunction • Systolic murmur of mitral insufficiency • Pericardial friction rub • Low grade fever within 24 hrs

Assessment • Patient history • 12 lead EKG • Echocardiogram • Labs: • Cardiac markers are intracellular proteins and enzymes released from dead or damaged cells. • CK-creatine Kinase • is the cardiac specific isoenzyme • found mainly in cardiac cells and therefore only rises when there has been damage to these cells. • level starts to increase within a few hours (3 -12) and peaks 1224 hrs of an MI. Returns to normal within 2 -3 days

Assessment cont’d Myoglobin-heme protein that helps transport O 2. -found in cardiac and skeletal muscle. -starts to increase within 1 -3 hours after the onset of symptoms. Peaks 4 -8 hours. Returns to normal: 24 hours -Takes only a few minutes to run. Troponin-a protein found in the myocardium, regulates the myocardial contractile processused to identify myocardial injury. -elevates as early as 1 hour post- injury or about the same as the CK. Peaks 10 -24 hours but remains elevated for a longer period of time 20 days (Normally 5 -14 days). -It is considered the gold standard for identifying MI and cardiac injury. -It can identify small infarcts, which have been undetectable by conventional diagnostic methods, in 3 -6 hours after injury LDH (Lactic dehydrognease) an old test not used anymore.

Nursing interventions • Check B/P before and after Nitro • 12 lead EKG • Don’t overexert patient • Low cholesterol, low sodium diet no caffeine • Use of bedside commode • Daily weights and Intake and output • Cardiac enzymes and coagulation studies

Medical management • The goal of medical management is to minimize myocardial damage, preserve myocardial function, and prevent complications. • goals are achieved by reperfusing the area with the emergency use of thrombolytic agents or PTCA. • Minimizing myocardial damage is also accomplished by reducing myocardial oxygen demand increasing blood supply with meds, O 2 and bedrest.

Pharmacologic therapy • The patient with an MI receives the same meds as a patient with unstable angina with the additions of a thrombolytic agent and angiotensin-converting enzyme inhibitors. • Thrombolytic agents are usually given within 30 minutes of arriving at the ER. • Their purpose is to dissolve and lyse thrombus in a coronary artery, allowing blood to flow through the artery again, minimizing the size of the infarction, and preserving ventricular function. • Although they may dissolve thrombus, they do not affect the underlying atherosclerotic lesion. • The pt may be referred for cardiac cath and other invasive interventions.

Pharm cont’d • Thrombolytic agents- the first was streptokinase not used as often. The t-PA or Alteplase is a type of tissue plasminogen activator. Because it does not decrease the clotting factors as much as streptokinase, a low molecular heparin is used to prevent another clot from forming at the same site. Allergic reactions are less, however, it is more costly.

Medications • M. O. N. A. Oxygen, Nitro, Aspirin, and if no relief Morphine I. V. Other meds: Thrombolytic Therapy: t-PA, activase, retavase, Tenecteplase (TNK) Beta adrenergic blockers Lopressor/Toprol, Coreg Angiotension-converting inhibitors give within 48 hours of MI CCB: Verapamil, Procardia, Norvasc/Cardizem Antiarrhythmics: amiodarone, lidocaine, magnesium for VF/VT Heparin I. V. Stool softeners

Surgical or invasive management • Percutaneous transluminal coronary angioplasty. (PTCA) • The balloon is placed in the affected coronary artery, inflated in the area of the plaque. It is then deflated and the atheroma is cracked, and blood flow improves. • Coronary artery stent- • a woven mesh that provides structural support to the vessel. • Atherectomy- the removal of the plaque • Brachytherapy- • radiation to the area with the stent.

Invasive cont’d • CABG- coronary artery bypass graft. this is a common but complex surgery. -The surgeon uses the saphenous veins of the legs to create a bypass of the coronary arteries with occlusion. -The patient is on a heart lung machine, which bypasses the heart while the surgery is taking place.

Normal ECG

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