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Presentation on theme: "ADULT CARDIOLOGY IN PRIMARY CARE"— Presentation transcript:

Mary I. Jones, FNP-C, MSN, MHSA Piedmont Heart Institute

2 OUTLINE Adult heart murmurs and abnormal heart sounds
Primary prevention of cardiovascular disease Evaluation and management of the patient with angina Pathophysiology of unstable plaque Evaluation and management of the patient with heart failure Secondary prevention of cardiovascular disease Evaluation and management of the patient with Atrial Fibrillation

3 Recommendations and Level of Evidence: Definitions
Classification of Recommendations Class I: Conditions for which there is evidence for and/or general agreement that treatment is beneficial, useful, and effective Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the efficacy of a treatment Class IIa: Weight of evidence/opinion favors usefulness/efficacy Class IIb: Usefulness/efficacy is less well established by evidence/opinion Class III: Conditions for which there is evidence and/or general agreement that a treatment is not useful/effective and in some cases may be harmful Level of Evidence A: Data derived from multiple randomized clinical trials or meta-analyses B: Data derived from a single randomized trial or from nonrandomized studies C: Only consensus opinion of experts, case studies, or standard of care

4 Adult Heart Murmurs and Abnormal Heart Sounds: The Basics

5 Location of Heart Murmurs

6 Location of Heart Murmurs
Aortic Pulmonic Erbs Triscupic Mitral All People Eventually Take Money

7 Heart Murmurs In general, heart mumurs may be classified as:
systolic or diastolic benign or pathologic Systolic murmurs may be either benign or pathologic. All diastolic murmurs are pathologic.

8 Timing of Heart Murmurs: Systolic Murmurs
Mr. Pass MVP Mitral Regurgitation Physiologic (functional) Aortic Stenosis Systolic Mitral Valve Prolapse

9 Timing of Heart Murmurs: Diastolic Murmurs
Ms. Ard Mitral Stenosis Aortic Regurgitation Diastolic

10 Heart Sounds Normal heart sounds: S1 S2 Abnormal heart sounds: S3 S4

11 Heart Sounds: Normal S1 Closure of AV (mitral and tricuspid) valves
Onset of systole/ventricular emptying S2 Closure of semilunar (aortic and pulmonic) valves Onset of diastole/ventricular filling

12 Heart Sounds: Abnormal
S3 Low pitched (best heard with bell) Occurs in association with (after) S2 Sign of heart failure S4 Low pitched (best heard with bell) Occurs in association with (before) S1 Sign of hypertension or acute MI S1 and S4 occur close to each other in time. Note: 1 and 4 are both straight line figures. S2 and S3 occur close to each other in time. Note: 2 and 3 are both curved line figures.

13 Primary Prevention of Cardiovascular Disease

14 Prevention of Coronary Heart Disease (CHD) Campaigns and Statements
National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP) III LDL goals, CHD risk equivalent, metabolic syndrome Joint National Committee (JNC)-7 Hypertension management World Heart Federation (WHF), World Health Organization (WHO) Cigarette smoking National Heart, Lung, and Blood Institute (NHLBI), Food and Drug Administration (FDA), Centers for Disease Control (CDC) Obesity AHA/NHLBI Go Red for Women, AHA Guidelines on Prevention of Cardiovascular Disease (CVD) in Women Women and CVD STEMI: ACC/AHA guidelines at

15 Evaluation and Management of the Patient with Ischemic Heart Disease

16 Definitions New-onset angina – recently developed symptoms of less than 3 months duration Chronic stable angina – a predictable pattern and presentation of symptoms (sustained > 3 months) that occurs with activity and is relieved quickly by rest and/or NTG Unstable angina – Sustained pain (20-30 minutes) or pain with occurs with increased frequency or duration and/or with lesser exertion Anginal equivalents – angina surrogates such as dyspnea, fatigue, abdominal pain, syncope, and diaphoresis Syndrome X or microvascular angina – angina with normal coronary arteries Prinzmetal/variant angina – symptoms related to coronary artery spasm

17 More Definitions Acute Coronary Syndromes
acute myocardial ischemia with two subtypes (unstable angina and NSTEMI) similar pathophysiology (severe narrowing and/or transient occlusion of a coronary artery) Non-ST-elevation MI (NSTEMI) – chemical evidence of myocardial necrosis without characteristic EKG changes (formerly called non-Q-wave MI) ST-elevation MI (STEMI) – complete and prolonged occlusion of a coronary artery demonstrated by chemical and EKG evidence of necrosis (formerly called Q-wave MI)

18 Thrombus Formation and ACS
UA NQMI STE-MI Plaque Disruption/Fissure/Erosion Thrombus Formation Non-ST-Segment Elevation Acute Coronary Syndrome (ACS) ST-Segment Elevation Acute Coronary Syndrome (ACS) Old Terminology: New It is now recognized that unstable angina (UA), non-Q-wave myocardial infarction (NQMI), and ST-segment elevation myocardial infarction (STE-MI) are all parts of the spectrum of clinical manifestations of acute coronary syndrome (ACS). The older terminology has now been replaced with terminology that divides ACS into non-ST-elevation ACS (NSTE-ACS) and ST-segment-elevation. All the slides in this teaching set deal with NSTE-ACS.

19 Thin, vulnerable, fibrous cap
The Vulnerable Plaque Thin, vulnerable, fibrous cap Large lipid core A cross-section of a coronary artery demonstrating the vulnerable plaque, with its large lipid core and thin fibrous cap Reproduced with permission from Falk E, et al. Circulation. 1998;92:

20 Ruptured Plaque with Occlusive Thrombus Formation
Cross-section of a coronary artery showing the site of plaque rupture (yellow arrow) and thrombus formation, outlined in white, occluding the coronary artery. Plaque rupture Reproduced with permission from Falk E, et al. Circulation. 1998;92:

21 Ruptured Plaque & Occlusive Thrombus

22 Pathogenesis of Acute Coronary Syndromes: The integral role of platelets
Plaque Fissure or Rupture Platelet Adhesion Platelet Activation Platelet Aggregation Platelets are recognized to play an integral role in acute coronary syndromes and arterial thrombosis. After plaque fissure or rupture, there is platelet adhesion and activation. This leads to platelet aggregation within the coronary artery, and ultimately partial or complete occlusion of the coronary artery. Thrombotic Occlusion


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