1. ADULT CARDIOLOGY IN PRIMARY CARE
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 ACSUA
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