Risk Stratification:
Pre-participation screening is a part of risk assessment and risk management, based on the ACSM guidelines.
Screen for signs/symptoms of disease, known cardiovascular (CV), metabolic, or renal disease, and CVD risk factors.
Identify individuals at risk for acute exercise-related CV events, including sudden cardiac death and myocardial infarction.
Determine the need for medical clearance.
Old ACSM guidelines are referenced.
Clinical Populations:
More likely to have known disease without symptoms or any signs/symptoms suggestive of disease.
Screening Process (ACSM):
Medical clearance is needed.
If cleared, proceed with light to moderate exercise.
Supervision Levels:
Low risk: unsupervised (usually safe to do alone).
Medium risk: HCP with experience in clinical exercise testing.
High risk: HCP with experience in clinical exercise testing, AND a trained doctor immediately available if required.
ILS-trained personnel (at least) for drug administration in case of a CV event.
Safety Considerations:
Safety for both the healthcare provider (YOU) and the participant is key.
Absolute Contraindications (Refer to GP):
Unstable angina.
Unstable or acute heart failure.
Unstable diabetes.
New or uncontrolled arrhythmias.
Resting or uncontrolled tachycardia.
Resting SBP > 180/200 mmHg or Resting DBP > 100/110 mmHg.
Symptomatic hypotension.
Febrile illness/Acute infections.
Assessments Before Exercise:
Ask questions and obtain an ECG.
Check glucose levels.
Measure BP.
Target HR achieved.
Chronotropic incompetence.
Hypertensive responses (>$230 mmHg and/or >110 mmHg).
Drop in SBP (20 mmHg) or failure to increase with intensity.
Verbal and/or physical manifestations of fatigue.
ECG shows arrhythmias or ST depression >1 mm.
Onset of angina/angina-like symptoms.
Participant's request to stop.
Equipment failure.
P wave: Atrial depolarization.
QRS complex: Ventricular depolarization.
PR interval: Atrioventricular conduction time.
T wave: Ventricular repolarization.
Heart Rate Determination.
Rhythm strip: Lead used for rhythm analysis.
Key Intervals & Segments:
PR interval: 0.12-0.22 s
QRS duration: <<0.12 s
Corrected QT duration:
Men: ≤ 0.45 s
Women: ≤ 0.47 s
Reference level for ST-segment deviation: PR segment (isoelectric or baseline level).
P wave: Max 0.12s
PR interval: 0.12 -0.20 s
QRS interval: 0.06-0.1s (max 0.12s)
P wave amplitude: Max 2.5mm
QRS amplitude: Max 30mm
ST segment sets isoelectric line.
T wave review for ischemia.
QTc: < 0.44s (Male); < 0.46s (Female)
Phase 0: Rapid influx of Na^+
Phase 1: K^+ influx
Phase 2: Influx of Ca^{2+ }balanced by K^+ efflux (plateau)
Phase 3: Ca^{2+} channels close, K^+ channels stay open
Phase 4: Na^+ & Ca^{2+} close, K^+ open
Cardiac excitation-contraction coupling.
Wave of depolarization travels toward the positive electrode = positive deflection.
Wave of depolarization travels away from the positive electrode = negative deflection.
Coronary arteries branch off the aorta to supply blood and oxygen to the myocardial cells (cardiomyocytes).
Right Coronary Artery (RCA): Supplies RA, RV, SAN, AVN and posterior LV.
Left Coronary Artery: Splits into LAD and CA, supplying LA and LV.
Coronary blood flow: 250 ml min ^{-1} (0.8 ml min^{-1} g^{-1} of heart muscle) = 5% of resting Q.
Deoxygenated blood leaves myocardial tissue of the LV via veins and collects in the coronary sinus à drains into RA.
High capillary-to-cardiomyocyte ratio & short diffusion distances ensure adequate O2 delivery to cardiomyocytes and removal of metabolic waste (CO2 & H^+).
Very high VO2 and highest a-vO2 difference (extracts 70-80% of O2 from blood).
Sympathetic activation (exercise) à coronary vasodilation via β1-adreno-receptor activation à increased coronary blood flow.
2.5 times more blood flows in coronary vessels during diastole than systole.
Atherosclerosis disrupts/impairs coronary blood flow.
Myocardial ischemia: Lack of blood flow to heart muscle.
Relationship between artery occlusion, ECG leads, and myocardial region:
Inferior: RCA, leads II, III, avF.
Antero-septal or Antero-apical: LAD, leads V1-4.
Antero-lateral: CA, leads V3-6.
Posterior: RCA, no specific leads.
Most common MIs are related to occlusions within the mid-lower section of the LAD.
MI = myocardial infarction.
Sinus tachycardia: Increased HR.
Sinus bradycardia: Decreased HR.
Sinus arrhythmia: Irregular rhythm (often normal).
Sinus = Regular.
Unifocal PVCs: From RV outflow.
Multifocal PVCs: More concerning.
Bigeminy or Trigeminy.
PVC = premature beat arising from an ectopic focus within the ventricles.
More than 3 PVCs = Ventricular Tachycardia (non-sustained).
Sustained VT = impairs Q, reduces myocardial perfusion and could lead to VF.
Ventricular Fibrillation (VF): Chaotic, irregular, varying amplitude, no identifiable waves, Rate 150 to 500/min = DEFIB.
5-10% older adults.
“Irregularly irregular” ventricular rhythm: rapid and chaotic depolarization within atria à erratic transmission of impulses at AV node.
No P waves seen.
QRS rate 170/min (variable).
Fibrillatory waves (often V1): fine <<0.5mm, coarse >0.5mm.
Increases risk of thrombosis/ embolism i.e. 20% of all strokes.
Very short PR intervals (0.08s).
2nd A-V connection in addition to normal conduction via AV node.
Accessory pathway conducts quicker than AV node (pre-excitation).
Sooner depolarization shown by a delta wave.
Can be seen in athletes.
1st, 2nd, 3rd degree.
Prolonged PR interval on the ECG.
3rd degree AV block – A (100bpm), V (40bpm).
Right Bundle Branch Block (RBBB):
Delayed electrical activation of RV as must be depolarized by the LBB.
Distorted QRS shape due to abnormal depolarization pathway.
Wide QRS >3mm (120ms).
RSR’ pattern in V1-3 (‘M-shaped’ QRS complex).
Wide, slurred S wave in the lateral leads (I, aVL, V5-6).
Sometimes ST depression/T wave inversion in the right leads (V1-3).
RBBB is quite common, often seen in athletes and has no major symptoms.
Morro w QRS = M in V1. QRS = W in V6
Left Bundle Branch Block (LBBB)
Do not do an exercise ECG test on someone with LBBB.
RV depolarizes normally and first via RBB.
Delayed electrical activation of LV as must be depolarized by the RBB with septal depolarization from R to L.
Distorted (notched/M) QRS shape due to abnormal depolarization pathway i.e. sequentially R-L and not simultaneously.
Deep S waves in V1-V3 (dominant V1).
Broad R waves in lateral leads (I,aVL,V5- V6).
Wide QRS >3mm (>120ms).
Poor R-wave progression.
Needs attention!
Willia m QRS = W in V1. QRS = M in V6
Can be “Normal” in athletes.
Seen if people have thin chest walls.
Seen with uncontrolled/long-lasting hypertension and aortic stenosis.
LVH = S wave depth V1 + tallest R wave height in V5-V6 > 35 mm PLUS ST depression & T inversion in left-sided leads.
Thickened walls leads to:
Prolonged depolarization (R) and delayed repolarization (ST & T) in lateral leads.
Increased R in I, avL, V4-6.
Increased S in III, avR, V1-3.
ST Depression: ≥1mm$$, most common and useful indication of myocardial ischemia; likely to see during exercise test and in several leads (usually I, II, V4-V6).
T-wave inversion (or flattening) can be seen but not always.
ST Elevation: Most common and useful indication of myocardial infarction (STEMI); location of the ST elevation = region of infarct & likely artery occlusion (e.g., Anterior STEMI (V2-V5) is likely to be occluded in LAD artery).
Varies across countries.
Uncommon in USA.
Refer to the 2018 international recommendations (Sharma et al. 2018).
Dhutia & MacLachlan (2018) reported that the new recommendations have:
Reduced false positive ECG rate to 3%.
Reduced cost of screening by 25%.
Congenital/genetic pathology
Hypertrophic cardiomyopathy
Arrhythmogenic ventricular cardiomyopathy
Dilated cardiomyopathy
Congenital coronary artery anomalies
Premature atheromatous coronary artery disease
Wolff-Parkinson-White syndrome
Right ventricular outflow tachycardia
Mitral valve prolapse
Congenital aortic stenosis
Marfan syndrome
Congenital long QT syndrome
Catecholaminergic polymorphic ventricular tachycardia
Brugada syndrome
Acquired causes
Infections (myocarditis)
Drugs (cocaine, amphetamine)
Electrolyte disturbances (hypokalemia or hyperkalemia)
Hypothermia
Hyperthermia
Trauma (commotio cordis)
*Highlighted causes that can be detected via a resting ECG, per Dhutia & MacLachlan, 2018.
Normal ECG Findings
Increased QRS voltage for LVH or RVH
Incomplete RBBB
Early repolarization/ST segment elevation
T wave inversion V1-V3 < age 16 years
ST elevation followed by T wave inversion V1-V4 in black athletes
Sinus bradycardia or arrhythmia
Ectopic atrial or junctional rhythm
1° AV block
Mobitz Type 12° AV block
Borderline ECG Findings
Left axis deviation
Left atrial enlargement
Right axis deviation
Right atrial enlargement
Complete RBBB
In isolation
2 or more
No further evaluation required in asymptomatic athletes with no family history of inherited cardiac
disease or SCD
Abnormal ECG Findings
T wave inversion
ST segment depression
Pathologic Q waves
Complete LBBB
QRS ≥ 140 ms duration
Epsilon wave
Ventricular pre-excitation
Prolonged QT interval
Brugada Type 1 pattern
Profound sinus bradycardia < 30 bpm
PR interval ≥ 400 ms
Mobitz Type II 2° AV block
3° AV block
≥ 2 PVCs
Atrial tachyarrhythmias
Ventricular arrhythmias
Further evaluation required to investigate for pathologic cardiovascular disorders associated with SCD in athletes