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CAD
| Question | Answer |
|---|---|
| Coronary Artery Disease Defined | Blood vessel disorder, category of ATHEROSCLEROSIS May affect the heart’s arteries: reduces the flow of oxygen and nutrients to the myocardium |
| Atherosclerosis | athere “fatty mush” and skleros “hard” Soft deposits of fat (atheroma's) that harden with age • Preference for coronary arteries |
| Coronary Artery Disease Pathophysiology | Deposits of lipids within the intima of the artery • Endothelial injury/inflammation= atherosclerosis Damage to endothelial lining results in inflammation • C-reactive protein (CRP) produced by the liver – inflammatory marker |
| Factors that damage endothelial lining | Tobacco, hyperlipidemia, hypertension, toxins, diabetes, infection cause damage |
| CAD Developmental Stages | • Progressive disease that develops over many years • Disease process is well advanced by the time symptoms develop 1. Fatty streak 2. Fibrous plaque 3. Complicated lesion |
| Fatty Streak | Lipids accumulate and migrate into smooth muscle cells |
| Fibrous Plaque | -Collagen covers fatty streak -Vessel lumen is narrowed -Blood flow is reduced - Fissures can develop |
| Complicated lesion | - Plaque rupture - Thrombus formation - Further narrowing or total occlusion of vessel |
| Collateral Circulation | Arterial connections within coronary circulation Slower developing occlusion= chance that adequate collateral circulation will develop (myocardium can receive blood and oxygen) |
| Extent of collateral circulation depends on | • Inherited predisposition to develop new blood vessels (angiogenesis) • Presence of chronic ischemia |
| Risk Factors for Coronary Artery Disease Non-modifiable | Non-modifiable risk factors • Age • Sex • Ethnicity |
| Risk Factors for Coronary Artery Disease Modifiable | • Elevated serum lipids • Hypertension • Tobacco use • Physical inactivity • Obesity Modifiable contributing risk factors • Diabetes mellitus • Metabolic syndrome • Psychological states • Homocysteine • Substance use |
| Chronic Stable Angina | Demand for myocardial oxygen exceeds the ability of coronary arteries to supply the heart with oxygen (myocardial ischemia) Narrowing of coronary arteries by atherosclerosis is primary reason for insufficient blood flow |
| Health Promotion CAD | Risk and management Physical activity Nutritional therapy Medications • Cholesterol-lowering medications • Antiplatelet therapy |
| Angina | chest pain that is reversible • Increased demand for oxygen • Decreased supply of oxygen LACTIC ACID BUILD UP FROM ANAREOBIC METABOLISM |
| Time it takes for myocardium to become hypoxic | within 10 seconds of coronary occlusion |
| Time it takes for contractility to cease | With total occlusion of coronary arteries: contractility ceases after several minutes Myocardial cells deprived of oxygen and glucose for aerobic metabolism (ANAEROBIC METABOLISM STARTS) |
| Time that cardiac cells are viable for | 20 minutes in ischemic conditions. Afterwards necrosis can occur |
| Chronic Stable Angina Factors Precipitating | • Physical exertion • Temperature extremes • Strong emotions • Consumption of heavy meal • Tobacco use • Sexual activity • Stimulants • Circadian rhythm patterns |
| Chronic Stable Angina Clinical Manifestations | Intermittent chest pain (3-5 minutes) Same pattern Aching, constricting, squeezing, heavy, choking, suffocating Indigestion/burning sensation in epigastric region SUBSIDES when precipitating factor is relieved ECG: ST-segment DEPRESSION (ischemia) |
| Chronic Stable Angina Interprofessional Management (ABCDEF) | • Decrease oxygen demand • Increase oxygen supply • Reduction of risk factors Antiplatelet Antianginal Beta-adrenergic blocker Blood pressure Cigarette smoking Cholesterol Diet Diabetes Education Exercise Flu vaccination |
| Chronic Stable Angina Medication therapy | • Antiplatelets • Cholesterol-lowering medications • Short- and long-acting nitrates • Beta adrenergic blockers • Calcium channel blockers • Angiotensin-converting enzyme inhibitors |
| Chronic Stable Angina Nursing Implementation | • Administer supplemental oxygen • Measure vital signs • Request 12-lead ECG • Prompt pain relief first with a nitrate and if necessary, an opioid analgesic • Auscultation of heart sounds • Comfortable positioning • PQRST assessment of the pain |
| Prinzmetal’s Angina (variant angina) | Occurs during rest in response to spasm of a major coronary artery • Strong contraction of smooth muscle in the coronary artery caused by an increase in intracellular calcium |
| Prinzmetal’s Angina Clinical Manifestations & Management | Angina when spasm occurs ST-segment ELEVATION May occur during sleep (specifically REM sleep when myocardial oxygen consumption increases) Relieved by moderate exercise or disappear spontaneously Treated with calcium channel blockers, nitrates |
| Acute Coronary Syndrome Defined | Myocardial ischemia is prolonged and not immediately reversible • Unstable angina • Non-ST elevation myocardial infarction • ST-elevation myocardial infarction |
| Acute Coronary Syndrome Pathophysiology | Deterioration of an atherosclerotic plaque that was once stable • Plaque ruptures, exposing the intima to blood, stimulating platelet aggregation and local vasoconstriction with thrombus formation |
| NSTEMI | UNSTABLE ANGINA Partially occluded by a thrombus NON-ST Segment elevation |
| STEMI | (Unstable lesion) Totally occluded by a thrombus ST segment ELEVATION |
| Unstable Angina | • Chest pain that is new in onset, occurs at rest, or has a worsening pattern • Chronic stable angina may lead to unstable angina • Unpredictable, represents a medical emergency |
| Myocardial Infarction | Sustained ischemia causing irreversible myocardial cell death Thrombus develops: perfusion to myocardium distal to the occlusion is halted (necrosis) Loss of contractile function |
| Time taken for entire thickness of the heart muscle to become necrotic | If ischemia persists 5-6 hours |
| Clinical Manifestations of Myocardial Infarction (1) | Severe, immobilizing chest pain (no relief) Heaviness, pressure, tightness, burning, constricting, crushing Activity or at rest Lasts > 20 minutes Discomfort, weakness, shortness of breath, fatigue |
| Clinical Manifestations of Myocardial Infarction (2) | Ashen, clammy and cool to touch (catecholamines) Elevated BP to diminished BP Decreased renal perfusion and decreased UOP Crackles, JVD Abnormal heart sounds Nausea and vomiting due to pain Fever (inflammation) |
| Myocardial Infarction Healing Process | Leukocytes (24 hrs) Enzymes released (dead cardiac cells) Necrotic tissue removed (thin muscle wall) Collagen matrix form scar tissue 10-14 days after MI vulnerable to stress 6 weeks post-MI scar tissue replaces necrotic tissue (Less malleable) |
| Complications of Myocardial Infarction | Dysrhythmias • Heart failure • Cardiogenic shock • Papillary muscle dysfunction • Ventricular aneurysm • Pericarditis • Dressler’s syndrome |
| Coronary Artery Disease Diagnostic Studies | History and physical exam ECG (12-lead) Chest radiograph Exercise stress tests Echocardiogram Nuclear imaging studies CT scan PET scan Coronary angiography •Labs: Troponin, myoglobin, lipid panel, CBC, C-reactive protein, homocysteine |
| Electrocardiographic Changes Ischemia | • ST-segment depression (>1 mm below isoelectric line) • T-wave inversion |
| Electrocardiographic Changes Injury | • ST-segment elevation (>1 mm above isoelectric line) • Avoidance of infarction determined by absence of serum cardiac markers |
| Electrocardiographic Changes Infarction – necrosis | • ST-segment elevation • Pathological Q wave (indicates at least ½ heart wall is involved) • T-wave inversion within hours and may persist for months |
| Diagnostic Studies Serum Cardiac Markers | • Released into the blood in large quantities from necrotic heart muscle • Indicate whether cardiac damage is present and the approximate extent of the damage • CK-MB, Troponin, Myoglobin |
| CK-MB | Rise 3-12 hours after an MI • Peak in 24 hours • Return to normal within 2-3 days |
| Troponin | Myocardial muscle protein • More accurate at determining myocardial injury than CK-MB • Increase 3-12 hours after the onset of MI • Peak at 24-48 hours • Return to baseline over 5-14 days |
| Myoglobin | • Released into circulation within a few hours after an MI • Lacks cardiac specificity • Rapidly excreted in urine so that blood levels return to normal within 24 hours after an MI |
| Coronary Angiography | • Evaluate the extent of the disease • Determine the most appropriate therapeutic treatment • Percutaneous coronary intervention may be performed • Conservative medical management |
| Interprofessional Care MI | Diagnosis, airway, vitals, O2, ECG, IV catheters, PQRST, blood tests, chest x-ray, Medication |
| Interprofessional Care Medications MI | IV nitroglycerin Morphine ASA Beta-adrenergic blockers Systemic anticoagulation (LMWH or IV heparin) ACE inhibitors for some patients post-MI Calcium channel blockers Antidyrhthmic medications Cholseterol-lowering medications Stool softeners |
| Emergent Percutaneous Coronary Intervention (PCI) | First line of treatment Open affected artery within 90 minutes Stents may be deployed Aggressive anticoagulation preventing occlusion of the stents by thrombus formation Depending on severity of blockage(s)- medical management/surgery |
| Advantage of PCI | • Alternative to surgical intervention • Performed with local anesthetic • Patient is ambulatory 24 hours after the procedure • Length of hospital stay is 1-3 days • Patient can return to work faster (5-7 days post PCI) |
| Complications of PCI | Dissection of newly dilated coronary artery • Coronary artery could rupture resulting in cardiac tamponade, ischemia, infarction, decreased CO and possibly death Re-stenosis |
| Fibrinolytic Therapy | Without an interventional cardiac catheterization lab/patient unstable to safely transfer Dissolve the thrombus and re-perfuse the myocardium Given STAT Can cause major bleeding or re-occlusion (IV heparin + antiplatelet therapy) |
| Nutritional Therapy MI | NPO initially • Sips of water until stable • Diet advanced to as tolerated • Low salt • Low saturated fat • Low cholesterol |
| Coronary Surgical Revascularization | Coronary artery bypass graft (CABG) FOR: Symptoms despite medical management Lt main coronary artery or 3-vessel disease Can't PCI (ex. Lesion is long or difficult to access) Chest pain despite PCI LV failure Longer-term benefits with CABG vs PCI |
| Phases of Rehabilitation after ACS | Hospital, Early Recovery, Late recovery |
| Phase I: Hospital | Activity level varies with severity of MI Initially can sit up in bed, chair, perform ROM and self- care, and progress to ambulation in hallway and limited stair climbing • Attention focused on management of pain, anxiety, dysrhythmias, complications |
| Phase II: Early Recovery | Discharged 2-12 weeks and conducted in an outpatient facility Activity level gradually increases under supervision with ECG monitoring Physical activity may be resumed at home (recommended by HCP) Information regarding risk- factor reduction provided |
| Phase III: Late Recovery | Long-term maintenance program is followed Individual physical activity programs designed and implemented at home Patient and family may restructure lifestyles/roles Lifestyle changes= lifelong habits Medical supervision is still recommended |
Created by:
selenay15
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