The Client with Altered Cardiac Output

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*Coronary Artery Disease (CAD)


*LEARNING OBJECTIVE 1 Discuss the epidemiological factors of coronary artery disease (CAD) and define the risk factors.


*CAD Is Leading Cause of Death in the USCauses one-fifth of all deaths in the US, making it the single largest killer Incidence of CAD increases with age


*Coronary Artery Disease (CAD) progressive disease resulting in coronary artery narrowing or total occlusion. Atherosclerosis Most common cause of CAD The abnormal accumulation of plaques on the vessel wall Causes narrowing then eventually blockages in the coronary arteries that reduces myocardial blood flow = CAD Asymptomatic until 75% occlusion of coronary artery lumen.


*CAD: Risk Factors Modifiable smoking Hypertension Hyperlipidema Physical inactivity Diabetes Mellitus Obesity Stress / Anxiety DietNon-Modifiable Increasing Age Males >45 years old Females >55 years old Gender Affects both men and women; #1 killer is U.S. Genetics Strong genetic component Ethnicity Non-whites increased incidences versus whites


*LEARNING OBJECTIVE 2Define pathophysiology of CAD/ischemic heart disease and explain the interventions used when evaluating a patient with angina pectoris.


*Angina Pectoris As CAD progresses the atherosclerotic plagues become significant, reducing blood flow to portions of the myocardium = Ischemia. ischemia clinically manifests most often as angina (chest pain). Angina pectoris is =myocardial ischemia without cellular death.


*O2Myocardial Oxygen Supply and Demand BalanceDemandSupplyO2Arterial Oxygen ContentPreloadAfterloadCoronary Artery Blood flowContractilityHeart Rate


*Precipitating Factors of Angina Any situation where oxygen demands are increased: Physical exertion Tachycardia Dysrhythmias Cold weather Eating a heavy meal Stress or emotional states


*Angina Pectoris Signs and Symptoms Chest Pain Can occur anywhere in chest; commonly retrosternal. Pain may radiate to the back, arms (left most common), shoulder, neck or jaw. Described as pressure, tightness or burning sensation Often precipitated by physical exertion or stress Maybe associated with: SOB, weakness, anxiety, diaphoresis, N/V, dizziness or numbness in upper extremities


*Types of Angina1)Stable Angina Predictable, consistent pain with physical exertion & relieved with rest; “my usual chest pain” 2)Unstable Angina Last longer increased frequency / intensity of symptoms pain at rest 3) Preinfarction Angina Lasting longer than 15 minutes /unrelieved by NTG x3 is a medical emergency! Pt need hospitalization for management


*imad thultheen critical care nursing ksu *Management of Unstable AnginaDemandO2Beta Blockers Ca Channel Blockers ACE I PreloadNTG ACE I MorphineSupply Blood FlowNTG Ca Channel Blockers ASA Anticoagulants MorphineOpen Occluded ArteriesO2PCIContractility HR  Afterload


*Management: Unstable Angina Goal is to Increase O2 supply & decrease O2 demand to prevent myocardium death. ECG Laboratory Tests Electrolytes Cardiac Enzyme Panel Rule-out MI: every 8 hours x 3 / 6 hours x4


*Management: Unstable AnginaRelief of Chest Pain: “MONA” Morphine (drug of choice) Oxygen Nitroglycerine Increase Coronary Artery Blood Flow Antiplatelet medications ASA Glycoprotein (GP) IIb/IIIa Inhibitors Heparin Percutaneous Coronary Intervention (PCI)


*Pharmacologic Therapies For AnginaNitrates Dilate veins – decreases preload Dilate arteries – decreases afterload dilates coronary arteries Administer- spray, sublingually, PO, IV, topically Side effects – hypotension Ex: Nitrostat SL or Tridil (nitroglycerin), Need a nitrate free interval


*Beta blockers Reduce myocardial oxygen consumption by decreasing heart rate, contractility Side effects – hypotension, bradycardia, bronchial spasm, Ex: Lopressor or Toprol (metoprolol),Inderal


*Calcium channel blockers Dilate arteries – decreases vascular resistance Decrease heart rate and myocardial contractility decreases O2 consumption Side effects - hypotension, bradycardia, Ex: Adalat or Procardia (nifedipine), Cardene (nicardipine), Cardizem (diltiazem)


*Antiplatelet medications Prevent platelet aggregation on atheroma or thrombus ASA ( Aspirin) – side effects: GI irritation, bleeding, increased bruising Ticlid (ticlopidine) Plavix (clopidogrel)


*Anticoagulants Heparin Given IV in acute situations or subcutaneous in non-acute situations Monitor partial thromboplastin time (PTT) Antidote – Protamine Sulfate Observe bleeding precautions Monitor for signs and symptoms of bleeding Half-life of 1-2 hrs


*Anticoagulants Coumadin (warfarin) Used long term; given PO Effects do not occur for 3-5 days Monitor Prothrombin time (PT) or International Normalized Ratio (INR) Antidote – Vitamin K Contraindicated in pregnancy, clients with liver dysfunction or those at risk for bleeding


*Oxygen therapy Oxygen therapy Administered usually at 2 L/min per nasal cannula Increases amount of O2 delivered to myocardium


*Acute Coronary Syndromes (ACS) Coronary artery diseases are two types 1) chronic unstable angina 2) acute coronary syndrome The acute coronary syndrome is an Umbrella describes a wide range of CAD from unstable angina to acute myocardial infarction (MI).


*Myocardial Infarction (MI) MI is defined as irreversible death of myocardial tissue, resulting from decrease or total lack of coronary blood supply and O2 to the myocardium. Causes: Coronary artery thrombosis (most common) Coronary artery spasm Trauma Severe and abrupt hypotension


*Myocardial Infarction (MI) Cont.,Signs and Symptoms: Chest Pain Severe and unrelenting substernal chest pain; often radiating to the back, left arm or jaw. Lasting for 30 minutes or more Only relieved by opioids Occurs without a know precipitating event; usually occurring in the morning Associated Symptoms SOB, weakness, anxiety, diaphoresis, N/V, dizziness or numbness in upper extremities.


*Myocardial Infarction Cont.,Pathophysiology Irreversible cell death within 20-40 minutes of cessation of blood flow. EKG changes associated with an MI: Ischemia: T wave inversion Injury: ST segment elevation Infarction: Pathological Q waves


*Ischemic changes on the ECG

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Last Updated: 8th March 2018

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