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the last set of cards for wvc cardiac year1

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Acute Coronary Syndromes   Stable Angina Unstable Angina Non-Q wave MI Q-wave MI All have a common cause, atherosclerosis within the vascular system  
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Diagnostics & Interventions Chest Pain   12-lead EKG Cardiac markers - CK, CK-MB, Troponin, isoenzymes Cardiac Catheterization Physical assessment MONA  
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Diagnostics for Cardiac Function   EKG Chest x-ray Electrolytes, CBC, UA, ABG, BNP Echocardiogram Thalium or T-phos scans MUGA - gives ejection fraction Pulmonary Wedge Pressure  
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Stable Angina Pectoris   Temporary lack of oxygen Causes pain with exertion Usually associated with stable atherosclerotic plaque  
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Unstable Angina   One of the Acute Coronary Syndromes Occurs with rest or minimal exertion Increase in intensity, duration and frequency. Plaque rupture, thrombus formation  
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Myocardial Infarction   Myocardial tissue is deprived of oxygen Occlusion of blood flow to area of the heart Process of infarction occurs Time is muscle  
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Symptoms of Angina   Substernal chest discomfort Can radiate to the left arm Precipitated by exertion or stress Relieved by NTG or rest Lasting < 15 minutes Few associated symptoms  
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Diagnostics for Angina   12-lead EKG Cardiac Stress Test Echocardiogram Transesophageal Echocardiogram (TEE)  
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Standard Cardiac Markers   Tissue damage releases some intracellular enzymes. Measurement of these enzymes can give a good indication of time & extent of damage  
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Standard Cardiac Markers cont.   CK-MB – rises in 4-6 hrs after MI, peaks at 12-24 hrs Troponin- More specific to heart muscle. Rises 4-6 hrs after MI, peaks at 12-14 hrs and returns to normal in 5 to 9 days Measured on admission, in 6 hrs and 12 hrs after admission.  
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Cardiac Catheterization   Done to determine where the obstruction is in emergent situations Done to look at the coronary arteries to determine need for bypass  
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Stents   Placed during heart cath Mesh that opens the vessel Keeps the unstable plaques secured Drug-eluting stents  
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Balloon Angioplasty   Balloon is placed in the area of narrowing during cardiac cath. Inflated and pushes the plaque against the vessel wall Opens the vessel  
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Risks of Cardiac Catheterization   Acute myocardial infarction Stroke Arterial bleeding Thromboembolus Lethal dysrhythmias Death  
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Manifestations of Successful Reperfusion of Heart Muscle   Cessation of chest pain Onset of ventricular arrhythmias Resolution of ST depression A peak of 12 hours for cardiac markers  
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Bradycardia   A pulse rate of less than 60 bpm How is the patient tolerating the rhythm? Are there medications causing the rhythm? Is there an underlying medical condition causing the rhythm?  
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Sinus Bradycardia   Heart rate less than 60 beats per minute May or may not be symptomatic Treat for symptoms Treat underlying cause  
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Hemodynamics of Bradycardia   Myocardial oxygen demand is reduced Coronary perfusion time is adequate because of prolonged diastole If the rate is too slow, cardiac output and blood pressure may drop and this will decrease coronary perfusion causing symptoms  
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Causes of Bradycardia   Athlete’s normal rate Excessive vagal stimulation Hypoxia Inferior MI Beta-adrenergic blockers Calcium channel blockers Digitalis  
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Symptoms of bradycardia   Dizziness, syncope Weakness Confusion Hypotension Dyspnea Ventricular ectopy Angina  
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Interventions   Treat only if symptomatic Atropine 0.5 mg – 1.0 mg IV push, end point is 0.04mg/kg Treat hypotension with fluid replacement or vasopressors Withhold medications that cause bradycardia Pacemaker  
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Tachycardia   Heart rate of >100 Dominant sympathetic stimulation Normal response to increased oxygen demand Compensatory response to decreased cardiac output  
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Sinus Tachycardia   Rate > 100 bpm Regular rhythm P-wave for every QRS QRS complex is narrow and upright in Lead II  
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Hemodynamics of Tachycardia   Increased oxygen demand by the heart muscle Decreased filling time with shorter diastole Blood is moved through the lungs more rapidly to get oxygen out to the body quickly in stress situations Can trigger angina pain in CAD  
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