Study guide
4.4 Substance Use Screening: Alcohol, Cannabis, Stimulants & Cardiac Risk
AACVPR CCRP Certified Cardiac Rehab Professional Exam
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1 Chapter 1: Introduction & Cardiac Rehabilitation Foundations
1.1 AACVPR CCRP Credential, Exam Specifications & Core Competencies 1.2 Phases of Cardiac Rehabilitation & Clinical Delivery Models 1.3 Interdisciplinary Team Roles, Clinical Scope of Practice & Safety
2 Chapter 2: Cardiovascular Anatomy, Physiology & Pathology
2.1 Cardiac Anatomy, Coronary Circulation & Hemodynamics 2.2 Atherosclerosis Pathogenesis, Acute Coronary Syndromes (ACS) & Revascularization 2.3 Heart Failure (HFrEF/HFpEF), Cardiomyopathies & Valvular Heart Disease 2.4 Electrical Interventions: Cardioversion, Catheter Ablation & Post-Procedure Rehabilitation
3 Chapter 3: Diagnostic Evaluation, ECG & Clinical Testing
3.1 Baseline Clinical Assessment & AACVPR Risk Stratification 3.2 12-Lead ECG Interpretation: Ischemia, Transmural Infarction & Conduction 3.3 Cardiac Arrhythmias, Conduction Blocks & Device Rhythms (Pacemakers/ICDs) 3.4 Graded Exercise Testing (GXT), Gas Exchange & Termination Criteria
4 Chapter 4: Patient-Centered Assessment: Education, Equity & Social Context
4.1 Learning Readiness: Health Literacy, Learning Styles & Communication Barriers 4.2 Social Determinants of Health, Culture & Spirituality in Cardiac Rehab 4.3 Sex- and Race-Based Differences in Cardiovascular Presentation & Outcomes 4.4 Substance Use Screening: Alcohol, Cannabis, Stimulants & Cardiac Risk
5 Chapter 5: Exercise Prescription & Aerobic Conditioning
5.1 FITT-VP Framework & Aerobic Exercise Intensity Calculation 5.2 Exercise Progression, Environmental Factors & Telemetry Monitoring Guidelines 5.3 High-Intensity Interval Training (HIIT) vs Moderate Continuous Training (MICT) 5.4 Home Exercise Program Design, Prescription & Independent Progression
6 Chapter 6: Exercise Physiology, Monitoring & Session Design
6.1 Health-Related Physical Fitness Components & Functional Capacity Testing 6.2 Acute Cardiovascular Responses to Aerobic Exercise: METs, Rate Pressure Product & VO₂ 6.3 Chronic Training Adaptations in Cardiac Patients 6.4 Structuring the Exercise Session: Warm-Up, Conditioning & Cool-Down 6.5 ECG Telemetry Setup: Skin Preparation, Electrode Placement & Artifact Troubleshooting 6.6 Pulse Oximetry, Exertional Desaturation & Supplemental Oxygen Titration
7 Chapter 7: Resistance, Flexibility & Exercise Safety
7.1 Resistance Training Guidelines, Hemodynamics & Sternal Precautions 7.2 Flexibility, Neuromotor Training & Special CR Populations 7.3 Exercise Contraindications, Adverse Signs/Symptoms & Emergency Protocols
8 Chapter 8: Physical Activity Counseling & Behavior Change
8.1 Physical Activity Guidelines, Sedentary Physiology & NEAT 8.2 Behavioral Change Theories: Transtheoretical Model & Social Cognitive Theory 8.3 Motivational Interviewing Principles & Resolving Ambivalence 8.4 SMART Goal Setting, Activity Tracking & Relapse Prevention
9 Chapter 9: Physical Activity Assessment & Real-World Activity Counseling
9.1 Physical Activity vs Exercise: Assessment Instruments, Logs & Wearables 9.2 Metabolic Requirements of Daily Life: Occupational, Recreational & Sexual Activity 9.3 Environmental & Situational Risk: Heat, Cold, Altitude, Air Quality & High-Risk Activities 9.4 Upper- vs Lower-Body Physiologic Demands & Modality Selection
10 Chapter 10: Hypertension & Blood Pressure Regulation
10.1 2017 ACC/AHA Hypertension Classification & Cardiovascular Risk 10.2 Antihypertensive Pharmacology & Exercise Hemodynamics 10.3 Exertional Blood Pressure Dynamics, Exertional Hypotension & Crisis 10.4 Home Blood Pressure Monitoring, Sodium Restriction & Lifestyle Interventions 10.5 Blood Pressure Measurement Technique, Device Validation & Renal Protection
11 Chapter 11: Diabetes Mellitus & Metabolic Regulation
11.1 Diabetes Pathophysiology, Diagnostic Criteria & Glycemic Targets 11.2 Antidiabetic Pharmacotherapy (Insulin, Sulfonylureas, SGLT2i, GLP-1 RA) 11.3 Exercise-Induced Hypoglycemia Management (Rule of 15) & Hyperglycemia 11.4 Diabetic Complications & Exercise Adaptations (Autonomic & Peripheral Neuropathy) 11.5 Blood Glucose Self-Monitoring, CGM Interpretation & Peri-Exercise Testing 11.6 Diabetic Foot Care, Skin Integrity & Footwear Assessment
12 Chapter 12: Blood Lipid Management & Atherosclerosis Prevention
12.1 Lipid Metabolism, Atherogenic Lipoproteins & Advanced Lipid Testing 12.2 Statin Therapy, Dosing Intensity & Secondary Prevention Targets 12.3 Non-Statin Pharmacotherapies & Statin-Associated Muscle Symptoms (SAMS)
13 Chapter 13: Medical Nutrition Therapy & Dietary Patterns
13.1 Nutritional Assessment & Macronutrient Guidelines in Cardiovascular Disease 13.2 Cardioprotective Dietary Patterns: Mediterranean, DASH & Plant-Based 13.3 Dietary Lipids, Sodium, Soluble Fiber & Plant Stanols/Sterols 13.4 Clinical Scope: CR Professional Counseling Boundaries vs RD/RDN Referral
14 Chapter 14: Body Composition & Weight Management
14.1 Anthropometric Assessment: BMI, Waist Circumference & Obesity Paradox 14.2 Behavioral Weight Management, Energy Balance & Caloric Deficits 14.3 Anti-Obesity Pharmacotherapy (GLP-1/GIP) & Bariatric Surgery Considerations
15 Chapter 15: Tobacco Cessation Interventions
15.1 Cardiovascular Pathophysiology of Tobacco, Nicotine & Secondhand Smoke 15.2 Clinical Cessation Frameworks: The 5 A's & 5 R's Models 15.3 Pharmacotherapy for Nicotine Dependence: NRT, Varenicline & Bupropion 15.4 Behavioral Counseling, Coping Strategies & Relapse Prevention
16 Chapter 16: Psychosocial Health, Screening & Behavioral Support
16.1 Psychosocial Risk Factors & Prognostic Impact in Heart Disease 16.2 Validated Screening Instruments: PHQ-9, GAD-7 & Administration 16.3 Evidence-Based Interventions: Stress Management, CBT Principles & Social Support 16.4 Crisis Protocols, Suicidal Ideation & Mental Health Referral Pathways 16.5 Psychotropic Pharmacology & Cardiac Safety 16.6 Sleep Disturbance, Chronic Pain & Somatic Comorbidity in Psychosocial Management
17 Chapter 17: Regulatory Compliance, Documentation & Program Outcomes
17.1 CMS Coverage Guidelines, Qualifying Diagnoses & Practitioner Supervision 17.2 Individualized Treatment Plan (ITP) Components, 30-Day Updates & Goals 17.3 AACVPR Outcome Domains & Program Certification Performance Measures 17.4 Program Certification, Quality Improvement & Medical Emergency Preparedness
4.4 Substance Use Screening: Alcohol, Cannabis, Stimulants & Cardiac Risk
Key Takeaways Explain This Topic AI
A US standard drink contains 14 grams of pure alcohol: 12 oz of regular beer, 5 oz of wine, or 1.5 oz of distilled spirits.
AUDIT-C is a validated three-item alcohol screen, positive at a score of 4 or higher in men and 3 or higher in women.
Binge drinking precipitates atrial fibrillation in structurally normal hearts — the pattern known as holiday heart syndrome — while sustained heavy intake causes dilated alcoholic cardiomyopathy, hypertension, and hypertriglyceridemia.
Cocaine causes coronary vasospasm and accelerates atherosclerosis; benzodiazepines and nitrates are first-line for cocaine-associated chest pain, and beta-blockers are traditionally avoided because of unopposed alpha-adrenergic stimulation.
SBIRT — Screening, Brief Intervention, and Referral to Treatment — is the framework that converts a positive substance use screen into a documented CR action.
Last updated: September 2026
4.4 Substance Use Screening: Alcohol, Cannabis, Stimulants & Cardiac Risk
Note
Blueprint anchor : Domain 1 (Patient Assessment), task 1.16 — Assess substance use (e.g., alcohol, tobacco, recreational drugs) . Tobacco is developed separately under Domain 7; this section addresses alcohol and other substances.
Substance use is a modifiable contributor to the event that brought the patient to cardiac rehabilitation, and it interacts directly with the exercise prescription, medication management, and psychosocial care. It is also the assessment domain patients are least likely to disclose voluntarily. Structured, non-judgmental screening is therefore an explicit competency.
Alcohol: Definitions and Thresholds
The US standard drink contains 14 grams of pure alcohol :
- Beverage Volume Typical ABV
- Regular beer 12 oz ~5%
- Malt liquor 8-9 oz ~7%
- Table wine 5 oz ~12%
- Distilled spirits (80 proof) 1.5 oz ~40%
Patients systematically underestimate intake because home pours bear little relationship to these volumes. A useful counseling move is to have the patient describe the actual glass and pour, then convert together.
Consumption limits commonly referenced for cardiovascular counseling are no more than 2 standard drinks per day for men and no more than 1 per day for women , with the strong caveat that current guidance does not recommend initiating or increasing alcohol consumption for cardiovascular benefit. The older claim that moderate drinking is cardioprotective has weakened substantially, and any perceived benefit does not offset harms in patients with hypertension, arrhythmia, cardiomyopathy, or hypertriglyceridemia.
Cardiovascular consequences of alcohol
Effect Mechanism and relevance
Hypertension Dose-dependent blood pressure elevation; reduction produces measurable BP lowering and is a first-line lifestyle intervention
Holiday heart syndrome Binge drinking precipitating atrial fibrillation or other atrial arrhythmias, classically in a structurally normal heart
Alcoholic cardiomyopathy Sustained heavy intake causing dilated cardiomyopathy with reduced ejection fraction; partially reversible with abstinence
- Hypertriglyceridemia Alcohol markedly raises triglycerides; a key target when triglycerides are elevated
- Weight ~7 kcal/g with no satiety value, undermining energy-balance goals
Interactions Additive hypotension with antihypertensives and nitrates; hepatotoxicity risk considerations with statins; increased bleeding with anticoagulants; masks and worsens hypoglycemia by impairing gluconeogenesis
Warning
Alcohol impairs hepatic gluconeogenesis and can cause delayed hypoglycemia many hours after intake — a serious risk for patients on insulin or sulfonylureas who drink in the evening and exercise the next morning. This interaction is a frequent exam target.
Screening Instruments
- Tool Format Positive threshold
- AUDIT-C 3 items (frequency, typical quantity, frequency of 6+ drinks) 4 or more in men; 3 or more in women
Single-item NIAAA screen "How many times in the past year have you had 5 (men) / 4 (women) or more drinks in a day?" 1 or more
- CAGE 4 items: Cut down, Annoyed, Guilty, Eye-opener 2 or more suggests problem drinking
- NIDA Quick Screen / DAST-10 Non-alcohol drug use Any positive prompts further assessment
Ask in a normalized, non-judgmental frame: "Many people drink to relax, especially after a health scare. In a typical week, how many days do you have a drink, and how many on those days?" Leading with a presumption of use reduces defensive under-reporting relative to "You don't drink, do you?"
- Stimulants
- Cocaine
Cocaine blocks catecholamine reuptake, producing tachycardia, hypertension, and — most importantly for CR — coronary vasospasm . It also accelerates atherosclerosis, promotes thrombosis, and is associated with left ventricular hypertrophy, aortic dissection, and cardiomyopathy. Myocardial infarction can occur in young patients with minimal atherosclerotic burden.
Important
In cocaine-associated chest pain, benzodiazepines and nitrates are first-line , and beta-blockers are traditionally avoided because beta blockade leaves alpha-adrenergic vasoconstriction unopposed, potentially worsening coronary vasospasm and hypertension. This "unopposed alpha" principle is a classic testable item. Recent ongoing use should prompt discussion with the medical director before high-intensity exercise progression.
Methamphetamine
Methamphetamine causes sustained sympathetic activation and is a recognized cause of methamphetamine-associated cardiomyopathy , often in younger patients with severely reduced ejection fraction, along with pulmonary hypertension, arrhythmia, and accelerated coronary disease. Abstinence can produce meaningful recovery of ventricular function, which makes referral to treatment a genuinely disease-modifying intervention rather than a formality.
Cannabis
Cannabis use is increasingly common in the CR population, including among older adults using it for pain or sleep, and patients frequently do not consider it a drug worth mentioning. Cardiovascular effects include dose-dependent tachycardia , increased myocardial oxygen demand, transient blood pressure changes with orthostatic hypotension, and a documented transient elevation in myocardial infarction risk in the hour following use . Smoked cannabis also delivers combustion products with effects analogous to tobacco smoke. Practical counseling: ask specifically, advise against use within several hours of an exercise session, favor non-smoked routes if the patient continues use, and note that a resting tachycardia at intake may reflect recent use rather than deconditioning.
Anabolic-Androgenic Steroids
More relevant in younger patients and those in fitness settings. Effects include marked HDL suppression with LDL elevation , left ventricular hypertrophy with diastolic dysfunction, hypertension, polycythemia with thrombotic risk, and premature atherosclerosis. Non-prescribed testosterone and supplement products containing undeclared stimulants should be asked about specifically, since patients rarely classify them as drugs.
SBIRT: Converting a Positive Screen Into Action
SBIRT — Screening, Brief Intervention, and Referral to Treatment — is the framework that keeps CR action within scope:
Screening — validated tool at intake, repeated as indicated.
Brief Intervention — a short motivational-interviewing-consistent conversation: give personalized feedback linking the substance to the patient's own cardiac event and lab values, elicit the patient's view, offer clear advice, and negotiate a concrete step. This is squarely within CR scope.
Referral to Treatment — for high-risk scores, dependence, or withdrawal risk, refer to addiction medicine, behavioral health, or the primary physician. CR professionals do not manage withdrawal. Alcohol withdrawal in particular can be life-threatening and requires medical management.
Document the screen, the score, the brief intervention delivered, and the referral in the individualized treatment plan, and re-assess at the 30-day update.
Realistic Clinical Scenario
Scenario : A 52-year-old man enters Phase II after NSTEMI. Resting HR is 96 bpm, triglycerides are 420 mg/dL, and BP runs 148/92 despite lisinopril. He reports "a couple of beers most nights." On AUDIT-C he scores 6. He also mentions using cannabis nightly for sleep. He is on metformin and glipizide.
Assessment : AUDIT-C of 6 is positive. His "couple of beers" is likely a substantial underestimate given a positive screen, and alcohol plausibly contributes to all three of his uncontrolled findings: hypertension, hypertriglyceridemia, and elevated resting heart rate. The glipizide plus evening alcohol combination creates real delayed hypoglycemia risk, particularly before morning sessions. Nightly cannabis may also contribute to the resting tachycardia.
Plan : Deliver a brief intervention linking his own triglyceride value and blood pressure to alcohol intake, clarify standard drink sizes against his actual pour, and negotiate a specific reduction target rather than abstinence-or-nothing. Explicitly teach the delayed hypoglycemia interaction with glipizide and instruct on pre-exercise glucose checking after evenings with alcohol. Ask directly about timing of cannabis use relative to sessions and advise separation from exercise. Communicate the triglyceride level and alcohol history to the prescribing clinician, refer to a registered dietitian, and document the AUDIT-C score, brief intervention, and referrals in the ITP for reassessment at 30 days.