Cardiology in Sport Flashcards
Interpreting ECG
Start at rhythm strip (III)- is there a P wave, followed by a QRS
What is PR interval
Is it followed by normal QT interval and any ST changes
What is sinus rhythm
Number of big squares R wave has
R wave and LVH
If more than 5 big squares, suggestive of LVH
OR if biggest S wave + biggest R wave bigger than 7 big squares
R wave + athletes
R wave>5 big squares common in athletes
Rarely coincides with their acc being LVH at eco
Isolated Sokolow-Lyon voltage criterion for LVH
Common in male athletes and does not warrant further investigation
Early repolarisation pattern accompanied by concave ST segment elevation
Identified in 25-40% of highly trained athletes
More common in males, black athletes and those with sinus bradycardia
T wave inversion in people with chest pain
Think MI
But can be other causes
Bi-phasic T wave inversion in leads V3
Would be considered abnormal ECG and not due to exercise in white athlete
Black athletes + T wave inversion
Higher in prevalence
Thought to be more physiological
Many inverted T waves
Regardless of ethnicity, start thinking about myopathic process, and generally an inherited cardiac myopathy- one of most common is hypertrophic cardiomyopathy
TWI in leads V1-4 present in what percentage of black athletes
12-13%
Usually preceded by J-point and convex ST segment elevation
ESC criteria deem any TWI beyond … as abnormal
V1
If preceding ST segment to TWI is …, suggestive of pathology
Depressed
ST segment depression
Should always be considered pathological
Pathological Q wave
Shouldn’t have this regardless of how much you exercise
Height + length make it pathological
Should be less than a quarter of the R wave
Prevalence of Q waves in athletes
0.7% vs controls 1.2%
Measurement pathological Q wave
> 0.4mV deep in any lead except III, aVR
QT interval
Measured rom beginning of Q wave to end of T wave
Has to be corrected for HR using Bazett formula
Bazzett Formula
QTc=QT/(square root of RR)
When should QT interval be measured
During peak plasma concentration of a QT-prolonging medication
QTc abnormal in males
> 440ms
QTc abnormal in females
> 460ms
QTc interval affected by
Diurnal variations Drugs Clinical history + familial evaluation U waves Subtle T wave changes HR Repolarization abnormalities Decreased K+ Decreased Mg2+ Decreased Ca2+ Increased Ca2+
Problems with measuring QT interval in athletes
Slow HR
Sinus arrhythmia
Slightly wide QRS complexes
T-U complexes
U waves
Common in athletes
Always follow your T wave
Can interfere with measurement of T wave
Are <50% of the height of the preceding T wave
Measuring QT
Summit of T wave to isometric line across that angle
Probability of long QT syndrome factors that give points on ECG
QTC>480- 3 points QTC 460-479- 2 points QTC 450-9 (males)- 1 point QTC >480ms at 4th min of recovery from ETT- 1 point Torsades de pointes- 2 T wave alternans- 1 >3 leads notched T waves-1 Bradycardia for age- 0.5 Syncope with stress-2 Syncope without stress-1 Congenital deafness- 0.5 Family history with definite LQTS- 1 Unexplained sudden death in 1st degree fam member <30
Probability of long QT criterion- <1 point
Low probability
Probability of long QT criterion- 1.5-3 points
Intermediate probability
Probability of long QT criterion- >3.5 points
High probability
Problems with ESC 2010 criteria for QTC
17-32% false positives in white athletes
30-40% false positives in black athletes
Problems with Seattle criteria 2013 WTC
4-9% white athletes false positive
16% black athletes false positive
Over half the people failing ESC and Seattle criteria had following abnormalities
Left or right atrial enlargement Left or right axis deviation RVH Complete RBBB or LBBB RVH with concomitant right axis deviation
Refined 2014 QTC criteria
2.1% false positives white athletes
10% false positives black athletes
Left Axis Deviation
Lead 1 pointing up (leaving page)
Lead III pointing down (leaving page)
Right Axis Deviation
Lead I pointing down
Lead III up (returning)
Left atrial enlargement
Negative potion of P wave in lead V1>0.1mV in depth and >40ms in duration
Right atrial enlargement
P wave amplitude >2.5mm in leads II, III or aVF
RVH
Sum of R in V1 + S in V5 (or V6)>10mm
Sudden cardiac death causes percentage- cardiomyopathy
41%
Sudden cardiac death causes percentage- congenital and anatomic abnormalities
26%
Sudden cardiac death causes percentage- electric disorders
10%
Sudden cardiac death causes percentage- idiopathic hypertrophy
8%
Sudden cardiac death causes percentage- acquired disorders
8%
Sudden cardiac death causes percentage- valvular disorders
6%
Sudden cardiac death causes percentage- coronary artery disease
1%
Sudden cardiac death % below 17 (including)
65%
59% in high school
ATWI
In adult, white, asymptomatic individuals deemed normal if limited to V1-V2
Beyond V2 rare and should be investigated
Preceded by J point depression or ST segment depression should also be investigated further
ST depression
Rare
V bad
Hypokalaemia early changes
Flattening or inversion of T waves
Prominent U waves
ST segment depression
Prolonged QT interval
Hypokalaemia late changes
Prolonged PR interval
Decreased QRS voltage
Widened QRS
Ventricular arrhythmia
Slow HR
Increased vagal tone
Reduced intrinsic sinus pacemaker rate
Reverses on detraining
Slow HR- more likely to exhibit
Sinus bradycardia
Junctional rhythm
1st degree heart block
Mobitz type 1
Mobitz type II and 3rd degree HB are
Rare
Further investigation
