3.1 Coronary Artery Disease, Myocardial Infarction & Revascularization (PCI/CABG)

ACSM Certified Clinical Exercise Physiologist ACSM-CEP

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1 Introduction & Exam Overview

1.1 The ACSM-CEP Role, Job Definition & Scope of Practice 1.2 Exam Format, Domain Weights & Scoring 1.3 Eligibility, Study Planning & Test-Day Strategy

2 Applied Exercise Physiology & Metabolic Calculations

Bioenergetics & Energy Systems (ATP-PC, glycolytic, oxidative) Acute Cardiorespiratory & Metabolic Responses to Aerobic Exercise Responses to Resistance Exercise & Chronic Training Adaptations ACSM Metabolic Equations, METs & Interpreting VO₂ / RER / Ventilatory Threshold

3 Pathophysiology of Clinical Populations

3.1 Coronary Artery Disease, Myocardial Infarction & Revascularization (PCI/CABG) 3.2 Heart Failure, Valvular Disease & Cardiac Rhythm Disorders 3.3 Hypertension, Dyslipidemia & Peripheral Artery Disease 3.4 Pulmonary Disease: COPD, Asthma & Restrictive/Interstitial Disorders 3.5 Diabetes, Metabolic Syndrome & Obesity 3.6 Renal Disease & Musculoskeletal/Orthopedic Conditions 3.7 Neuromuscular, Neurological & Cognitive Conditions (stroke, MS, Parkinson's, SCI) 3.8 Neoplastic, Immunologic & Hematologic Disorders (cancer, HIV/AIDS, anemia)

4 Clinical ECG Interpretation

4.1 ECG Leads, Waveforms, Rate & Rhythm Determination 4.2 Arrhythmias & Conduction Blocks 4.3 Ischemia, Injury & Infarction (ST changes, exercise-induced) 4.4 Drug & Electrolyte ECG Effects; Resting/Exercise Monitoring Setup & Lead Placement

5 Pharmacology for the Clinical Exercise Physiologist

5.1 Beta-Blockers, Calcium-Channel Blockers & Nitrates 5.2 RAAS Agents, Diuretics, Antiarrhythmics, Lipid-Lowering & Antithrombotic Drugs 5.3 Bronchodilators, Corticosteroids, Insulin & Oral Antidiabetic Agents 5.4 Medication Effects on HR/BP & Exercise Response; Dose/Meal/Dialysis Timing

6 Patient Assessment (Domain I, 18%)

6.1 Medical Records, HIPAA/HITRUST, Charting & Physician Referral 6.2 Patient Interview, Medical History & Medication Reconciliation 6.3 Resting Vital Signs, Body Composition & Resting ECG 6.4 Preparticipation Health Screening & Level of Monitoring (PAR-Q+, ACSM algorithm, ACC/AHA · GOLD · ADA · AACVPR) 6.5 Assessing Patient Goals, Readiness & Psychosocial Status

7 Clinical Exercise Testing (Domain II, 18%)

Submaximal Aerobic Tests (treadmill, cycle, step, 6-minute walk) Musculoskeletal Fitness, Mobility & Balance Testing Maximal Symptom-Limited GXT: Protocols, Contraindications & ECG Prep Test Termination: Relative & Absolute Indications Interpreting & Reporting Results (ECG response, RPP, claudication, Duke Treadmill Score, VO₂/RER/AT)

8 Exercise Prescription for Clinical Populations (Domain III, 22%)

FITT-VP Principles, Progression & Prescription Foundations Ex Rx for Cardiovascular Disease (CAD, HF, HTN, PAD, post-revascularization) Ex Rx for Pulmonary Disease (COPD, asthma; breathing techniques, supplemental O2) Ex Rx for Diabetes, Metabolic Syndrome & Obesity Ex Rx for Musculoskeletal, Neuromuscular, Neoplastic & Other Conditions Communicating Intensity (THR, RPE, talk test), Monitoring & Modifying the Prescription

9 Exercise Training & Leadership (Domain IV, 24%)

9.1 Discussing the Training Plan, Clinician & Patient Expectations/Goals 9.2 Instructing & Modifying Exercise Modes (cardiorespiratory, strength/endurance, flexibility, coordination, agility) 9.3 Patient Monitoring & Supervision During Exercise (telemetry, oximetry, glucometry, ECG) 9.4 Contraindications to Training & Modifying Recommendations 9.5 Documenting Clinical Status, Reporting Adverse Events & Interdisciplinary Coordination

10 Education & Behavior Change (Domain V, 13%)

10.1 Behavioral-Health Screening & Recognizing Distress (PHQ-9, Beck, SF-36; referral) 10.2 Patient Education, Health Literacy & Disease Self-Management 10.3 Motivational Interviewing & Behavior-Change Theories (Transtheoretical, HBM, Social Cognitive, Five-A's) 10.4 Promoting Adherence, Self-Efficacy, Relapse Prevention & Social Support

11 Legal, Professional & Emergency Management (Domain VI, 5%)

11.1 Emergency Equipment, Crash Cart Inspection & Emergency Procedures 11.2 CPR/AED/BLS/ACLS, Universal Precautions & EMS Activation 11.3 Scope of Practice, Legal/Ethical Standards, Liability/Negligence, Informed Consent & Professional Organizations (ACSM/AACVPR/AHA)

3.1 Coronary Artery Disease, Myocardial Infarction & Revascularization (PCI/CABG)

Key Takeaways Explain This Topic AI

Atherosclerosis begins with endothelial injury and LDL infiltration, progressing to a lipid-rich plaque with a fibrous cap that can rupture and trigger thrombus formation.

The acute coronary syndrome spectrum runs from stable angina (fixed stenosis, no biomarker rise) through unstable angina, NSTEMI, and STEMI (rising myocardial necrosis and ECG severity).

The rate-pressure product (heart rate x systolic BP) estimates myocardial oxygen demand and helps identify a reproducible ischemic threshold during exercise testing.

PCI restores flow with a stent via a percutaneous approach; CABG bypasses obstructions with a vein or arterial graft and is preferred for multivessel or left-main disease.

Post-CABG sternal precautions (no lifting over 5-10 lb, no pushing/pulling, no bilateral overhead work) last approximately 6-8 weeks and must guide early exercise prescription.

Last updated: July 2026

Coronary artery disease (CAD) is the most common cardiovascular disease encountered in clinical exercise settings, and it underlies nearly every cardiac rehabilitation referral. Understanding its pathophysiology, the acute coronary syndrome (ACS) spectrum, and the two revascularization pathways is foundational to safe exercise testing and prescription.

Atherosclerosis: The Underlying Pathophysiology

CAD results from atherosclerosis , a chronic inflammatory process in the coronary artery wall. The sequence begins with endothelial injury from shear stress, hypertension, smoking, or hyperglycemia, which increases endothelial permeability to LDL cholesterol. LDL particles infiltrate the subendothelial space, become oxidized, and attract monocytes that differentiate into macrophages. These macrophages engulf oxidized LDL and become foam cells , forming the visible fatty streak , the earliest lesion. Over years, smooth muscle proliferation and collagen deposition build a fibrous cap over a necrotic lipid core, producing a mature atherosclerotic plaque. A plaque with a thin fibrous cap and large lipid core is vulnerable to rupture or erosion , which exposes thrombogenic material to circulating blood and triggers platelet aggregation and thrombus formation — the event that converts stable CAD into an acute coronary syndrome.

The Acute Coronary Syndrome Spectrum

Condition Mechanism Biomarkers ECG

Stable angina Fixed stenosis (typically >=70%) producing demand ischemia with exertion, relieved by rest/nitroglycerin Negative troponin Normal at rest; may show ST depression with exertion

Unstable angina Non-occlusive thrombus on a disrupted plaque; new, worsening, or rest pain Negative troponin May show transient ST depression/T-wave inversion

NSTEMI Partial/transient occlusion causing subendocardial necrosis Elevated troponin ST depression or T-wave inversion; no ST elevation

STEMI Complete, sustained occlusion causing transmural infarction Elevated troponin (peaks later) ST elevation with reciprocal changes; evolves to Q waves

Risk Factors

Modifiable risk factors — dyslipidemia (elevated LDL, low HDL), hypertension, current tobacco use, diabetes/insulin resistance, obesity, sedentary lifestyle, and poor diet — are the primary targets of exercise-based secondary prevention. Non-modifiable risk factors include age (men >=45, women >=55), male sex or postmenopausal status, and family history of premature CAD (a first-degree male relative affected before age 55 or a female relative before age 65).

Exercise Physiology Implications: Ischemia and the Rate-Pressure Product

Myocardial oxygen demand rises with both heart rate and afterload, so the rate-pressure product (RPP = HR x SBP) is used as a surrogate for myocardial oxygen consumption. Patients with fixed coronary stenoses often demonstrate a reproducible ischemic threshold — a consistent RPP at which angina or ischemic ECG changes appear. Classic ischemic ST-segment depression is horizontal or downsloping depression of at least 1 mm , measured 60-80 ms after the J-point. Because many patients — especially those with diabetic autonomic neuropathy, older adults, and women — experience silent ischemia or anginal equivalents (dyspnea, unusual fatigue, jaw or arm discomfort) rather than classic chest pain, the CEP must monitor symptoms, ECG, and RPP together rather than relying on chest pain alone.

Revascularization: PCI and CABG

Percutaneous coronary intervention (PCI) uses a catheter-delivered balloon and, almost always, a drug-eluting stent to mechanically open a stenosis; access is typically femoral or radial, and patients are placed on dual antiplatelet therapy (DAPT) for 6-12 months to prevent stent thrombosis. Coronary artery bypass graft (CABG) surgery reroutes blood around obstructions using the saphenous vein or, preferentially for durability, the internal mammary (thoracic) artery , accessed through a median sternotomy. CABG is generally favored for extensive multivessel disease, left-main disease, or diabetic patients with complex anatomy, while PCI is favored for single-vessel or focal lesions and offers a faster initial recovery.

Post-Revascularization Precautions and Cardiac Rehabilitation

Post-CABG patients require sternal precautions for roughly 6-8 weeks: no lifting greater than 5-10 lb, no pushing or pulling, and no bilateral overhead or behind-the-back movements that load the healing sternotomy; the CEP should also watch for a sternal click or instability, which signals a possible wound complication. Post-PCI patients need brief precautions at the vascular access site — limiting vigorous lower-body resistance at a femoral site for 24-48 hours and limiting wrist range of motion after a radial approach — plus awareness that DAPT increases bleeding risk with contact or high fall-risk activity. Structured cardiac rehabilitation progresses through Phase I (inpatient, low-level mobility), Phase II (outpatient, ECG-monitored, typically up to 36 sessions), and Phase III/IV (community-based maintenance).

Safety Considerations for the Clinical Exercise Physiologist

Always know the patient's ischemic RPP threshold and symptom pattern from the most recent graded exercise test before prescribing intensity, and remember that beta-blockers blunt the heart-rate response , making RPE and symptom monitoring more reliable than heart-rate-based targets alone. Emergency readiness — recognizing angina equivalents, unstable rhythm changes, and knowing when to stop a session and activate emergency response — is a non-negotiable safety skill in any CAD population.