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WVCCardiac 2011 3

the last set of cards for wvc cardiac year1

Acute Coronary Syndromes Stable Angina Unstable Angina Non-Q wave MI Q-wave MI All have a common cause, atherosclerosis within the vascular system
Diagnostics & Interventions Chest Pain 12-lead EKG Cardiac markers - CK, CK-MB, Troponin, isoenzymes Cardiac Catheterization Physical assessment MONA
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
Stable Angina Pectoris Temporary lack of oxygen Causes pain with exertion Usually associated with stable atherosclerotic plaque
Unstable Angina One of the Acute Coronary Syndromes Occurs with rest or minimal exertion Increase in intensity, duration and frequency. Plaque rupture, thrombus formation
Myocardial Infarction Myocardial tissue is deprived of oxygen Occlusion of blood flow to area of the heart Process of infarction occurs Time is muscle
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
Diagnostics for Angina 12-lead EKG Cardiac Stress Test Echocardiogram Transesophageal Echocardiogram (TEE)
Standard Cardiac Markers Tissue damage releases some intracellular enzymes. Measurement of these enzymes can give a good indication of time & extent of damage
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.
Cardiac Catheterization Done to determine where the obstruction is in emergent situations Done to look at the coronary arteries to determine need for bypass
Stents Placed during heart cath Mesh that opens the vessel Keeps the unstable plaques secured Drug-eluting stents
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
Risks of Cardiac Catheterization Acute myocardial infarction Stroke Arterial bleeding Thromboembolus Lethal dysrhythmias Death
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
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?
Sinus Bradycardia Heart rate less than 60 beats per minute May or may not be symptomatic Treat for symptoms Treat underlying cause
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
Causes of Bradycardia Athlete’s normal rate Excessive vagal stimulation Hypoxia Inferior MI Beta-adrenergic blockers Calcium channel blockers Digitalis
Symptoms of bradycardia Dizziness, syncope Weakness Confusion Hypotension Dyspnea Ventricular ectopy Angina
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
Tachycardia Heart rate of >100 Dominant sympathetic stimulation Normal response to increased oxygen demand Compensatory response to decreased cardiac output
Sinus Tachycardia Rate > 100 bpm Regular rhythm P-wave for every QRS QRS complex is narrow and upright in Lead II
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
Created by: jsilvestri9720