4.3 Ischemia, Injury & Infarction (ST changes, exercise-induced)

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)

4.3 Ischemia, Injury & Infarction (ST changes, exercise-induced)

Key Takeaways Explain This Topic AI

ST-segment depression indicates myocardial ischemia (inadequate blood flow), while ST-segment elevation indicates acute injury or infarction

Pathologic Q waves indicate a completed or prior myocardial infarction and are typically wide (0.04 sec or more) and deep (25% or more of the following R wave)

MI location can be estimated from which lead groups show ST changes: anterior (V3-V4), septal (V1-V2), lateral (I, aVL, V5-V6), and inferior (II, III, aVF)

The normal exercise ECG response is mild, upsloping ST depression as heart rate rises; an abnormal, ischemic response is horizontal or downsloping ST depression of 1 mm or more

ST elevation of 1 mm or more in leads without diagnostic Q waves during exercise testing is an absolute indication to terminate the test immediately

Last updated: July 2026

Ischemia, Injury & Infarction

Quick Answer: ST-segment depression signals myocardial ischemia, ST-segment elevation signals acute injury or infarction, and pathologic Q waves signal a completed infarction. During exercise testing, mild upsloping ST depression is a normal response to increased heart rate, but horizontal or downsloping ST depression of 1 mm or more indicates ischemia, and any ST elevation of 1 mm or more in leads without pre-existing Q waves is an absolute reason to stop the test immediately.

The ST segment and Q wave are the two ECG features most directly tied to coronary blood flow, and interpreting them correctly is a patient-safety skill central to the CEP's role during both resting evaluation and clinical exercise testing.

The Ischemia-Injury-Infarction Continuum

Finding What It Means ECG Sign

Ischemia Reduced blood flow to a region of myocardium; still viable tissue ST-segment depression (horizontal or downsloping)

Injury Acute, severe reduction in blood flow; tissue at risk but potentially salvageable ST-segment elevation

Infarction Myocardial tissue death (necrosis) Pathologic Q waves — typically 0.04 sec or wider and at least 25% of the height of the following R wave

Think of this as a progression: ongoing ischemia that is not resolved can progress to injury, and unresolved injury can progress to infarction and permanent Q-wave changes. A patient can also present with any one of these findings independently depending on timing and severity.

Localizing the Infarction by Lead Group

Because each lead group views a specific region of the left ventricle, ST elevation (in an acute MI) or Q waves (in a completed MI) can be localized to the likely culprit artery:

Septal: V1-V2 (proximal LAD)
Anterior: V3-V4 (LAD)
Lateral: I, aVL, V5-V6 (left circumflex)
Inferior: II, III, aVF (right coronary artery in most people)

Posterior: No standard lead directly views the posterior wall; suspect it from reciprocal changes in V1-V2 — tall R waves and ST depression that mirror what elevation would look like on a true posterior lead

Recognizing which lead groups are affected helps the care team anticipate complications specific to that territory (for example, inferior MI is more often associated with bradyarrhythmias and AV block due to RCA involvement).

The Normal Exercise ST Response

As heart rate and myocardial oxygen demand rise during a graded exercise test, some downward displacement of the J-point (where the QRS ends and the ST segment begins) is expected. A normal response is:

Mild ST depression that is upsloping — the segment angles back up toward baseline as it moves away from the J-point

Resolves quickly during recovery
The Abnormal (Ischemic) Exercise ST Response

An abnormal, ischemic ST response — the classic positive exercise ECG finding — is defined as:

Horizontal or downsloping ST-segment depression of 1 mm (0.1 mV) or more , measured about 60-80 milliseconds after the J-point, persisting for at least 0.08 seconds

The magnitude, number of leads involved, time of onset (earlier onset at lower workload = more severe), and time to resolve in recovery all add prognostic information (this is the logic behind composite scores such as the Duke Treadmill Score, covered in Chapter 7)

ST elevation of 1 mm or more in leads that do not already have diagnostic Q waves (other than aVR or V1) is far less common but more ominous — it suggests transmural ischemia or acute injury and is an absolute indication to terminate the exercise test immediately.

Exercise-Induced Arrhythmias as a Companion Warning Sign

Ischemia during exercise can also destabilize the ventricles electrically. Increasing frequency of PVCs, multifocal PVCs, couplets, triplets, or runs of ventricular tachycardia appearing as the workload rises should be interpreted alongside any ST changes — the combination of ischemic ST depression and worsening ventricular ectopy is a stronger signal to terminate the test than either finding alone. As covered in Section 4.2, sustained VT during testing is always an absolute indication to stop.

Reciprocal Changes During Acute STEMI

During an evolving ST-elevation MI, leads viewing the opposite wall of the heart often show reciprocal ST depression rather than elevation. For example, an inferior STEMI (ST elevation in II, III, aVF) commonly shows reciprocal ST depression in leads I and aVL, and an anterior STEMI can show reciprocal depression in the inferior leads. Recognizing reciprocal changes increases diagnostic confidence and helps distinguish a true STEMI from other causes of ST elevation, such as early repolarization or pericarditis, which typically lack reciprocal changes.

T-Wave Inversion

Symmetric, deep T-wave inversion is another marker of ischemia and commonly appears as an MI evolves — it can develop alongside or after ST-segment changes and often persists into the recovery period after resolved ischemia. Isolated T-wave inversion without accompanying ST changes is less specific and can also reflect a strain pattern, prior injury, or a normal variant in certain leads, so it should always be interpreted alongside symptoms and the full 12-lead tracing rather than in isolation.