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Patho
Imbalance between myocardial supply and demand
| Question | Answer |
|---|---|
| What are the layers of the heart? | P-pericardium E-epicardium M-myocardium E-endocardium |
| what are cardiac chambers? | A-Atria V-ventricles |
| what are the Cardiac valves? | 1. Atrioventricular valves tricuspid and mitral 2. Semilunar valves Pulmonic and aortic |
| conduction system of Atria? | sinoatrial node internodal pathways intraatrial bundle |
| conduction system of ventricles? | R and L bundle branches and purkinjie fibers |
| coronary blood supply of the coronary arteties? | L coronary artery divides into L anterior descending and L circumflex. R coronary artery perfuses the R side of the heart and in most people the SA and AV nodes. In 70% of the population the R CA perfuses the posterior coronary artery |
| Venus return from the heart by what? | cononary sinus, thebesian vessels drain directly into the chambers of the heart and produce physiologic shunt |
| Systemic circulation is by what? | arterial system of resistance vessels, capillary bed: tissue perfusion, and venous system of capacitance vessels |
| proterties of cardiac tissue? | excitability, conductivity, automaticity, rhythmnicity, contractility, refractoriness |
| Cardiac cycle? | ventricular systole, ventricular diastole, cardiac output |
| Regulation of heartbeat? | nervous control, and intrinsic regulation |
| control of peripheral circulation? | intrinsic control, extrinsic control |
| Ejection fraction? | Normal is 50% or higher. Low is less than 40% |
| 4 things occur in ejection fraction? | 1. MUGA (multiple-gated acquisition) scan 2. Echocardiogram 3. Cardiac Catheterization 4. Nuclear tests |
| how many people are affected by CAD in USA? and how many people died of it each year? | 13 million of people in the USA. causes 500,000 deaths each year. |
| what is coronary artery disease? | 1. inside of diameter arteries that give blood to the heart become small. 2. lots of plaque that highly increases the risk of having a heart attack or myocardial infarction |
| what are Modifiable risk factors in pathophysiologic factors and life style factors? | 1. Pathophysiologic factors are Hypertension, diabetes, hyperlipidemia, dyslipidemia. 2. Lifestyles factors are smoking, obesity,physical inactivity,stress |
| Nonmodifiable risk factors of CAD are? | Age, gender after menopause, race/ethnic background, heredity, family history |
| Emerging risk factors of CAD are? | Homocysteine blocks NO production which leads to less elastic blood vessels and produce permit plaque formation. 2. TTT is B complex Flolic acid, niacin a) LDL-C mechanical injury b) prothrombotic state (e.g., high fibrinogen or plasminogen activ |
| Five majors risk factors of CAD? | Smoking hypertension high cholesterol diabetes family history |
| what is the effects of smoking in CAD? | rough effet of the inside diameter of the arterial wall leads toformation of plaque, constriction of arteries and hypertension. Increases heart rate and irregular heart beats, clots, stroke. decrease of HDL levels and increase risk CAD |
| Management of smoking are? | Quit smoking, avoid secondary smoke, and tertiary smoke |
| what is Hypertension? | 1. High PB= SBP is less than 120 mmhg, while DBP is less than mmhg. 2. indicates that there is a problem in the mechanism that regulates blood pressure in the circulatory system. 3. hyper=too much, tension=pressure |
| Effects of Hypertension? | mechanical injury causes thickening r hardening of walls off arteries causing narrowing n decreases blood flow to coronary arteries which leads to MI.thickening of L ventricle decrease cardiac output n cause CHF, kidney damage, renal dialysis. |
| Effects of Hypertension in diabetes PT? | HPN leads to retinal damage (retinopathy) and blindness |
| what are some key features of HTN? | for persons over age 50, SBP is more important than DBP as CVD risk factor. Starting at 115/75 mmhg, CVD risk doubles w/ each increment of 20/10 mmhg throughout BP range. persons who are nomotensive at age 55 have 90% lifetime risk of developing HTN. |
| what are other some key features of HTN? | those with SBP 120-139 mmhg or DBP 80-89 mmhg should be considered prehypertensive who require health promoting lifestyle modifications to prevent CVD. |
| what kind of diuretic drug use for HTN? | Thiazide-type diuretics should b initial drug therapy for most,either alone or combine w/other drug classes.certain high risk conditions are compelling indication for other drugs classes.most pt will requir 2 r mor antihypertensive drug fornormal BP goa |
| what kind of diuretic drug use for HTN?(cont'd) | If BP is less that 20/10 mmhg above goal, initiate therapy with two agents, one usually should be thiazide-type diuretics. |
| what is normal BP? | SBP is less than 120, DBP is less than 80 |
| Prehypertension is what? | SBP is 120-139, DBP is 80-89 |
| Stage 1 HTN is what? | SBP=140-159, DBP=90-99 |
| Stage 2 HTN is what? | SBP=greater than 160, DBP=less than 100 |
| Benefits of lowering BP are? | reducing stroke incidence (35-40%) myocardial infarction (20-25%) heart failure (50%) |
| treatmeant overview of therapy goals? | lifestyle modification, pharmacologic treatment: algorithm for treatment of hypertension, classification and management of BP for adults, and follow-up monitoring |
| Ways of managing HTN? | Exercise proper stress management quit smoking healthy diet decrease sodium intake anti-HPN medication |
| Lifestyle Change: What Difference Does it Make ? | Weight loss.(decreases SBP*1.6 mm Hg for each kg lost).Dietary Approaches to Stop Hypertension:DASH diet:decreases systolic BP 8-14 mmHg.Reducing salt in the diet(decreasesSBP2-8 mmHg)30-45 minutes daily aerobic exercise(decreases systolic BP 4-9 mmHg). |
| Lifestyle Change: What Difference Does it Make ? | Limit alcohol.(decreases SBP* 2-4 mm Hg)Avoidance of tobacco products.(*SBP = systolic blood pressure) |
| Medications for HPN? | Diuretics Beta-Blockers Calcium channel Blockers ACEI Vasodilators |
| what does diabetes causes? | Causes vasoconstriction of coronary arteries >decrease blood flow > decrease oxygen supply >increase risk of heart attack or MI |
| Management of Diabetes? | Healthy diet Exercise Stress Management Medications Check Blood sugar regularly |
| Effects of Increased Cholesterol levels? | Causes plaguing of the coronary walls,narrows coronary arteries,creates blockage of coronary arteries less blood flow to heart cells >MI |
| types of cholesteroles? | LDL cholesterol HDL cholesterol Total cholesterol Triglycerides |
| Serum cholesterol levels of LDL? | LDL Cholesterol –Primary Target of therapy <100=Optimal 100-129= Near optimal/above optimal 130-159= Borderline high 160-189= High 190 > = Very High |
| Serum cholesterol levels of total cholesterol? | Total cholesterol < 200=Desirable 200 - 239=Borderline 240> =High |
| Serum cholesterol levels of HDL? | HDL <40=Low >60=High |
| Management of cholesterol levels are? | Diet, medication, non-smoking, exercise |
| family history of CAD? | Parent or sibling that died of CAD less than 60 years of age... |
| Medications for CAD? | [1] Anti-platelet medications [2] Medications for dyslipidemia [3] Anti-anginal medications |
| Anti-platelet medications are?(CAD) | [1] Aspirin [2]Clopidogrel (Plavix) |
| Medications for dyslipidemia are?(CAD) | HMG CoA-reductase inhibitors (statins)and NursingInterventions 1.Rosuvastatin=No grapefruit 2.Simvastatin= monitor liver enzymes 3.Atorvastatin=Instruct pts. mm tenderness 4.Pravastatin=Take at night |
| Medications for dyslipidemia are? (CAD | Niacin and nursing interventionsa 1.Niaspan,Niacin=With meals/Flushing/?med Fibric Acid Derivatives [1] Lopid=30 minutes before or with meals [2] Zetia |
| Anti- anginal medications for CAD are? | [1] NTG preparations [2]Beta-blockers [3] Calcium channel blockers |
| what is Coronary Artery Disease (CAD)? | CAD is a broad term that includes stable angina pectoris and acute coronary syndromes. When blood flow through the coronary arteries is blocked, ischemia or infarction of the myocardium may result |
| what is ischemia? | Ischemia occurs when insufficient oxygen is supplied to meet the requirements of the myocardium |
| what is infarction? | Infarction (necrosis of the cells, cell death) occurs when sever ischemia is prolonged and irreversible damage to tissue results |
| Acute Coronary Syndromes? | Angina-coronary ischemia-temporary imbalance between the coronary arteries ability to supply oxygen and the cardiac muscle’s demand for oxygen (no permanent damage to myocardial tissue).Stable Angina- predictable; fixed lesions. |
| Acute Coronary Syndromes? (contd') | Unstable Angina- more intense, may occur at rest or with exertion and causes marked limitations of activity. Attacks increase in intensity and pain. Includes new-onset angina, variant (Prinzmental’s) angina, pre-infarction angina and crescendo angina |
| what should you look for on angina? | Location Duration Quality Radiation Precipitating Factors Medication Relief |
| what is Myocardial Infarction? | Irreversible necrosis due to an abrupt decrease or total cessation of coronary blood flow. ex:Plaque rupture,New thrombus in coronary artery |
| what are the process of infarction? | Tissue Ischemia Hypoxemia Autonomic Nervous System Influences Metabolic Derangement Acid-base imbalances Hemodynamic disturbances Electrolyte disturbances Fiber stretch |
| the zone of infarction depends on what? | Dependent on Three Factors: Collateral circulation Anaerobic metabolism Workload demands |
| what are the zone of infarction? | Zone of Ischemia = T-wave inversion Zone of Injury = ST elevation Zone of Necrosis = Abnormal Q wave |
| what is the 1st type of infarction? | 1. Subendocardial Infarction (non-Q wave)(multifocal areas of necrosis confined to the inner 1/3-1/2 of the left ventricular wall. These do not show the same evolution of changes seen in a transmural MI.) |
| what is the 2nd type of infarction? | Transmural Infarction (Q wave) (involving the entire thickness of the left ventricular wall from endocardium to epicardium, usually the anterior free wall and posterior free wall and septum with extension into the RV wall in 15-30%). |
| what is the 2rd type of infarction? | Physiologic response = ventricular remodeling (change in shape and size of L ventricle causing decrease L V F leading to HF) |
| Classification of MI by Location are?(1) | Inferior: Abnormalities that appear in leads II, III, and F (called the inferior leads) indicate pathology on the inferior or diaphragmatic surface of the heart. |
| Classification of MI by Location are?(2) | Lateral: Leads I, F, and V5-V6 are called lateral leads. Abnormality in these leads indicates pathology on the lateral, upper surface of the heart. |
| Classification of MI by Location are?(3) | Anterior: Anterior pathology is seen in leads V1-V4, and often in lead I. |
| Classification of MI by Location are?(4) | Posterior: Problems on the posterior surface of the heart are difficult to diagnose using the standard 12 ECG leads. The pathology may be seen as “reflected” through V1 and V2. |
| Classification of MI by Location are?(5) | Combination: Abnormalities may not be limited to one of the four areas above. Inferolateral damage will show up in a combination of the inferior and lateral leads. Anterolateral damage will be seen in both the anterior and the lateral leads. |
| Identify which coronary artery is affected? | [1] severe crushing chest pressure/pain/radiating to neck [2] chest pressure/pain with radiation to L arm [3] chest pressure radiating to the back/scapula. |
| Differences in Heart Attack Symptoms in men? | Sub-sternal chest pain or pressure Rest pain Pain down left arm and shoulder Weakness |
| Differences in Heart Attack Symptoms in women? | Pain in chest, upper back, jaw or neck Shortness of breath Flu-like symptoms: nausea or vomiting, cold sweats Fatigue or weakness Feelings of anxiety, loss of appetite, malaise |
| Postmenopausal Hormone Therapy (HT)? | 1. Postmenopausal HT is no longer recommended as a strategy to prevent heart disease. 2. Hormone therapy, generally short term, may still be used to treat symptoms of menopause - this is a decision between a woman and her healthcare provider. |
| Collaborative Management of heart attack/cad? | History Pain Assessment Cardiovascular Assessment Psychosocial Assessment Laboratory Assessment Radiographic Assessment Other Diagnostic Assessments |
| History/ Pain Assessment of heart attac/cad? | 1.Historical data 2.If chest pain present, describe and find out for how long (time is muscle) 3. Attempt to differentiate between angina pain and infarction pain 3.Associated symptoms patient describes i.e. N/V, diaphoresis |
| Cardiovascular and Physical Assessment? | Vital signs Monitor for dysrhythmias Distal peripheral pulses Heart and Lung sounds |
| Psychosocial Assessment? | Denial Fear Anxiety Anger |
| Laboratory Assessment of heart attack/CAD?(1) | 1.Troponin T and I- myocardial muscle protein released into the bloodstream with injury to the myocardial muscle (not found in healthy clients. |
| Laboratory Assessment of heart attack/CAD?(2) | Creatine kinase-MB(CK-MB) is enzyme specific to cells of brain,myocardium n skeletal muscle.Indicates tissue necrosis or injury,Cardiac specificity is determined by measuring isoenzyme activity CK-MB is found in myocardial muscle CK-MM=skeletal/CK-BB-brai |
| Laboratory Assessment of heart attack/CAD?(3) | Myoglobin early marker of MI is a low-molecular-weight heme protein found in cardiac and skeletal muscle, appears as early as 2 hours after an MI with rapid decline after 7 hours |
| Laboratory Assessment of heart attack/CAD?(4) | C-Reactive Protein is a marker of inflammation. Any inflammatory process can increase CRP in the blood |
| Additional Laboratory Tests | Homocysteine Serum Lipids PT, PTT, INR Arterial Blood Gases Serum Electrolytes CBC |
| Radiographic and Other Diagnostic Tests ? | Chest X-ray ECG- what are we looking for? Stress Tests- exercise tolerance testing with or without pharmacologic agents Myocardial Perfusion Imaging- Thallium scans Cardiac Catherization |
| Cardiac Catherization? | This procedure is performed to determine the extent and exact location of obstruction of the coronary arteries. Helps to identify course of therapy for patients i.e. PTCA/stent or CABG |
| Nursing Diagnoses and Collaborative Problems? | Acute pain related to biologic injury agents Ineffective tissue perfusion related to interruption of arterial blood flow Activity intolerance related to fatigue Ineffective coping related to effects of acute illness and major changes in lifestyle |
| NICs/NOCs? | NIC Pain Management Drug Therapy NOC Ineffective Tissue Perfusion- expect to have adequate blood flow to maintain heart function Ejection fraction Pulmonary wedge pressure Apical heart rate Systolic and diastolic blood pressure |
| Collaborative Management? | MONA- M=morphine O= oxygen N= nitroglycerine A= aspirin Thrombolytic Therapy Beta Blockers or Calcium Channel Blocker) ACE Inhibitors Antiplatelet Agents- ASA, Plavix, Ticlid |
| Potential Complications and Interventions? | Dysrhythmias- ventricular in origin Ventricular Failure- Class I- IV Cardiogenic Shock- Intra-Aortic Balloon Pump (IABP) Thrombolytic Therapy- Fibrinolytics and/ or Glycoprotein IIb/IIIa inhibitors PTCA |
| other Nursing Diagnoses and Collaborative Problems? | Potential for dysrhythmias Potential for heart failure Potential for recurrent symptoms and extension of injury |
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