* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download 280208.ppt
Survey
Document related concepts
Heart failure wikipedia , lookup
Cardiac contractility modulation wikipedia , lookup
Hypertrophic cardiomyopathy wikipedia , lookup
Cardiac surgery wikipedia , lookup
Quantium Medical Cardiac Output wikipedia , lookup
Coronary artery disease wikipedia , lookup
Electrocardiography wikipedia , lookup
Jatene procedure wikipedia , lookup
Heart arrhythmia wikipedia , lookup
Dextro-Transposition of the great arteries wikipedia , lookup
Ventricular fibrillation wikipedia , lookup
Management of acute coronary syndrome wikipedia , lookup
Arrhythmogenic right ventricular dysplasia wikipedia , lookup
Transcript
Complex Cardiac Diagnoses Often Missed Sandra M. Miller, MD Independent Consultant Palm Beach Gardens, FL Objectives • The participant will be able to: – Indentify the types of acute coronary syndromes – Identify common complications of acute myocardial infarction – Identify clues in the medical record – Identify evidence in the medical record – Generate evidence-based query Acute Coronary Syndrome • What does it mean? • To physicians and clinicians: – 411.1, Unstable angina – 410.7, Non-ST-segment elevation MI (NSTEMI) – 410.xx, ST-segment elevation MI (STEMI) • To coders: – 411.89, Other acute and subacute form of ischemic heart disease Definitions • Unstable angina – Rest angina usually > 20 minutes – New-onset exertional angina – Preexisting angina with increase in frequency, duration, or with less than usual exertion Definitions • Non-ST-segment elevation MI – Similar to unstable angina BUT may have elevated cardiac enzymes, and/or EKG changes: • ST-segment depression • T-wave inversions • Other nonspecific ST-T wave changes Definitions • STEMI: – Elevated cardiac enzymes – ST-segment elevation on EKG – New or presumed new left bundle branch block (LBBB) STEMI EKG Actual patient EKG Common Complications of Myocardial Infarction • • • • • Bradyarrhythmias Bundle branch blocks Ventricular tachycardia Right ventricular infarct Pericarditis Cardiac Conduction System Source: Wikipedia Commons - http://en.wikipedia.org/wiki/File:ConductionsystemoftheheartwithouttheHeart.png Bradyarrhythmias • Second-degree heart blocks – Mobitz type I (Wenckebach) • AV nodal block • Progressive P-R prolongation prior to block of atrioventricular impulse • Frequently within first 24–48 hours of MI • Usually seen with inferior wall MI Mobitz I (Wenckebach) Actual patient tracing Bradyarrhythmias • Mobitz type II – Infranodal – Conduction fails suddenly and unexpectedly – No preceding P-R interval change – Usually with anterior wall MI – Can progress to complete heart block – May need temporary pacemaker Mobitz Type II Note p-r interval remains constant with dropped ventricular beat Actual patient tracing Bradyarrhythmias • Third degree – Complete heart block – Can be seen with anterior or inferior wall MI – No P-wave associations – Needs permanent pacemaker if anterior wall – May resolve if inferior wall Complete Heart Block Note lack of relationship of p waves to ventricular contractions. Actual patient tracing Bundle Branch Blocks • • • • Associated with higher mortality Bifascicular or trifascicular Left or right Associated with anterior wall MI within the first 24–48 hours • Temporary pacemaker may be indicated if bundle branch blocks are alternating between left and right Bundle Branch Blocks Source: Wikipedia Commons - http://en.wikipedia.org/wiki/File:Right_bundle_branch_block_ECG_characteristics.png and http://en.wikipedia.org/wiki/File:Left_bundle_branch_block_ECG_characteristics.png Ventricular Tachycardia • • • • • Can occur with any myocardial infarction Most commonly with anterior wall May be transient within the first 48 hours Late VT may indicate ongoing ischemia Most ventricular fibrillation occurs within the first 48 hours Right Ventricular Infarct • Inferior wall • ST-segment elevation in V4, seen with rightsided lead placement • Classic triad – Increased jugular venous pressure – Clear lungs – Hypotension Pericarditis • Anterior or inferior wall MI • 2–14 days after MI • Diffuse ST-segment elevation and P-R depression • Pericardial friction rub in 85%* • Dressler’s syndrome – Occurs weeks to months after MI – Consists of fever, malaise, serositis, pulmonary infiltrates and pleural effusion in addition to pericardial effusion Pericarditis Cardiogenic Shock • Clinical presentation – Hypotension – Tachycardia – Peripheral hypoperfusion – Oliguria – Encephalopathy • Definition of shock – Inadequate end-organ perfusion Cardiogenic Shock • Leading cause of death in patients hospitalized with MI • Typically associated with STEMI • Left ventricular failure is the most frequent cause of cardiogenic shock • Factors associated with increased risk of CS with acute MI – Older age – Female – Prior MI – Diabetes – Anterior MI location Cardiac Tamponade • Occurs in 15% of acute pericarditis cases • Occurs when pericardial fluid increases intrapericardial pressures, and that exceeds intracardiac pressures • Results in compression of the cardiac chambers – Limits diastolic filling – Results in decreased: • Stroke volume • Cardiac output • Systemic blood pressure and elevated venous pressures Cor Pulmonale • Enlargement of the right ventricle secondary to abnormalities of the lungs, thorax, pulmonary ventilation, or circulation • Can result in right heart failure • EKG shows P pulmonale, RV hypertrophy, and right axis deviation • Common underlying causes: – COPD – Pulmonary embolism – Pulmonary interstitial fibrosis Cor Pulmonale P pulmonale seen in leads II, III and aVF (copy of actual patient EKG) General Query Tips • • • • • Review record for evidence Identify key clinical information Include specific information in query Make the clinical case to support your question Remember: – Non-leading – Nonthreatening – Professional Case Study • 57-year-old male presented to the ED with chest • • • • pain radiating to the neck. His history is significant for CAD, s/p DES to RCA, and hypertension. Vitals are stable. EKG shows normal sinus rhythm, rate 86 and nonspecific ST-T wave changes. Initial troponin is elevated. What are the questions you should be thinking about? Thought Process • Detailed description of the characteristics of the • • • • • chest pain Changes in pattern or intensity Prior EKG for comparison Troponin trend Treatment and response to treatment Physician documents “acute coronary syndrome, admit to telemetry” What Could It Be? • • • • Stable angina Unstable angina NSTEMI Noncardiac chest pain • Look for the clues needed to develop the question to the physician for clarification of the diagnosis. Questions? In order to receive your continuing education certificate for this program, you must complete the online evaluation which can be found in the continuing education section at the front of the workbook.