Week 3 - Medical and environmental issues Flashcards
What is over training syndrome (aka unexplained underperformance syndrome)
A neuroendocrine disorder that may result from the process of overtraining and reflects accumulated fatigue during periods of excessive training with inadequate recovery. Leads to impaired performance.
FOR = Functional overreaching
Precipitating factors to OTS
Training:
* Intensive Interval Training
* Large Volume and Monotonous
* Sudden Increases
* Step up in class
* Excessive training load
* Inadequate recovery
* Decreased rest time
Competition stress
* Physical stress
* Glycogen Depletion
* Dehydration
* Psychological stress (monitor POMS)
* Injury or other illness
Symptoms of OTS
- Fatigue, underperformance, heavy muscles,
- Depression,
- Sleep disturbance,
- Frequent minor infections
- Loss of appetite
- Increased anxiety and irritability
- Loss of competitive drive
- Loss of libido
- Excessive Sweating ( ?autonomic response catecholamine mediated)
Pattern persists despite 2/52 rest
Signs of OTS
- HR
Increased resting HR
Increased HRV BJSM Sept 2008 (Likely too small to be of clinical significance)
Slow return of HR after exercise
Decreased maximal HR
Increased HR at sub maximal loads - Postural BP drops
- Performance decrements
- Reduced VO2 Max
- Increase in sub maximal O2 consumption
- Reduced maximal power output
- Reduced lactate conc at max work rate
Assessment of the fatigued athlete
- Exclude organic causes
- Iron deficiency anaemia
- EIA - exercise induced asthma, quite strict TUE for this
- Viral infections Monoculeosis Parvo Toxoplasma
- Diabetes
- Malabsorption probs
- Cardiac issues
- Must not misses (malignancies, cardiac issues, infection Hep A/B HIV, diabetes, pregnancy, post concussion syndrome)
History from a fatigued athlete
Usual and related to symptoms described above
Examination of fatigued athlete
- Pulse / BP
- HS and rhythm / Apex beat
- Lungs ?PFR / Spirometry
- Lymphadenopathy
- Liver / Spleen
- Thyroid
Investigations in the fatigued athlete
- FBC ESR Ferritin Transferrin Sats, CRP, Us+Es, LFT’s, TFT’s Fasting Gluc
- Vit B12 / Folate
- U&E’s
- Viral Titres EBV CMV etc
- Lactate profiling??
- Urinalysis
?CK
What hormonal tests might you test for in the fatigued athlete
Adrenaline and cortisol may be raised, lowTestosterone/cortisol ratio
Glutamine
Serotonin, TSH, GH, trytophan
(this is all pretty hypothetical)d
Assessment of psychological changes in athletes
POMS (profiling of mood states) a validated psychological test
* Daily monitoring used in USA swimmers
* Training decreased when mood deteriorated and increased when mood improved
* Decreased incidence of overtraining and burnout
Management of OTS
- Rest (not total )
- Very low level exercise aids recovery
- Aerobic even few mins daily
- Slow increase over 6-12 weeks
- Programme must be individually designed
- Best avoid own sport
- Increase volume before intensity
- Increase intensity when tolerating 20 mins light exercise Eg 10 second sprints with 3 min recovery
- Reduce stress
- Consider antidepressants no evidence for multivits chromium zinc magnesium selenium etc etc etc
- Beware of performers excelling at 12 weeks
Usually an excellent prognosis
PREVENTION BEST !!!! - Education, good coaching. Non specific - POMS, labs, HR
Discuss cardiac screening
Wilsons criteria - is screening appropriate? E.g. important condition, early detectable, early treatment beneficial, intervals for repeating test determined, risks less than benefits, costs balanced against benefits
“Screening debate” – BJSM 2012 (Asptar hospital in Qatar) highlighted differences between USA and Europe where Europe like investigative but USA likes history and examination, eg echo screening no great for HOCM – unlikely to develop – “optics”. Worry about false positives/false negatives.
Screening would include history, exam, ECG, echo, stress test, holter, cardiac MRI/CT angio
History
* FH of cardiac event
* Diabetic hypertensive valvular disease
* Smoker
* Symptoms of chest pain/palpitations/dizziness/SOB/collapse/syncope
Exam (low sensitivity and low specificity)
* Pulse
* BP
* ?murmers, apex beat
ECGs: have low specificity with a high false positive rate, influence of ethnicity on normal athlete ECG variation. Rely on interpretation.
Echo: wall thickness assessment, heterogeneity of wall thickening, septal thickness, diastolic cavity small in most patients with HOCM - may be used in those with suggestive symptoms or wit abnormal ECG
ESC guidelines help with decision making regarding safety of exercise in those with CVD
Discuss SCD
SCD over 35 years:
IHD commonest cause
Check FH of premature death
Consider predisposing symptoms and need for screening
In those U35
Hypertrophic cardiomyopathy the most common cause, then coronary anomaly, myocarditis
Discuss HCM (hypertrophic cardiomyopathy)
AD inheritance ?genetic testing, with high degree of penetrance
Incidence 1 in 500
Increased prevalence in African Americans
Screening - as above, look for LV hypertrophy (nearly always greater than 15mm)
Symptoms may include chest pain, palpitates, syncope and dyspnoea, inappropriate BP response to exercise
Signs - jerky pulse, double apex beat, fourth heart sound. ESM at left sternal border
Increased risk of death if FH of sudden death, extreme LV wall thickness, predisposition to supra ventricular and ventricular arrhythmias
Echo - hypertrophied non dilated left ventricle with no predisposing cause for LVH, chamber size reduced, impaired diastolic filling
Athletes heart - “Grey zone thickness” between 13 and 15mm, LV cavity >55mm, reduction of LV mass with deconditioning, cardiac MRI would give most detailed.
Change in threshold for “normal” more being referred to cardiology .
Treatment:
* no cure… prevent complications
* B Blockers
* Surgical myomectomy
* Alcohol septal ablation
* ICD devices
Discuss ARVC (Arrhythmogenic right ventricular cardiomyopathy)
- AD pattern of inheritance - strong genetic link to certain parts of Europe (Veneto region north eastern Italy)
- Develops in early adulthood
- Genetic defect in “glue”
- Usually affects small areas of R ventricles
- Repeat testing of family members - more subtle than HOCM so may notice change overtime
What are exercise recommendations based on?
ESC risk score (European society of cardiology)
Low <4%, moderate 4-6%, high >6%
(10 year risk for fatal CVD)
Exercise Recommendations based on:
* Presence of symptoms
* ESC Risk Score
* Presence of resting or inducible LVOT obstruction 9left ventricular outflow tract obstruction)
* BP response to exercise especially hypotension suggesting above
* Presence of resting or inducible arrhythmias (NSVT)
Discuss dilated cardiomyopathy
- Failure of pumping chambers
- Commonest cause IHD but 50% unknown
- Excessive alcohol, persistent high BP, valvular heart disease, viral infections, AI disease
- Possible genetic link in 25%
- Symptoms include SOB, ankle swelling, dizziness, fatigue and palpitations
- Medical management
- Ace inhibitors, diuretics, B blockers, inotropes
- Specialised pacemakers. Resynchronisation therapy
- ICD
- ?Cardiac Transplant –> needed to extend life
Discuss myocarditis
- Inflammation of heart muscle. ?viral, ?SLE, ?drug abuse
Lymphocytic infiltration with focal necrosis leading to cardiac dysfunction and conduction problems - Feverish, flu like, tachycardia
- Blood tests ECG (non specific ST wave change, may show heart block)and Echo (may show chamber dysfunction)
- Athletes with fever and tachycardia should not be exercising
- 75% recover in 2 weeks . 10% go on to develop DCM
Discuss premature CAD
- Atherosclerosis
- Genetic Link
- High BP Smoking Familial Hypercholesterolaemia
- ECG, Exercise ECG, CT angiography
- Interventions aimed at trying to reduce the risk of MI
List ion channelopathies
- Long QT syndrome
- Brugada Syndrome
- Progressive cardiac Conduction defects
- Catecholaminergic PVT
- Short QT syndrome
- Idiopathic VF
Discuss long QT
- 1:2000 genetic testing identify 70%
>0.44s - Most potassium channel defects though some affect sodium channels
- Great variation in severity
- Males more likely pre puberty Females adolescence and early adulthood
- ECG non specific repeated testing exercise ECG and Holter monitoring.
Can lead to VT incl tornadoes de pointes - Provocation testing
- Drugs to avoid, Avoid hypokalaemia. beta blockers may be used, surgical sympathectomy if this fails.
Discuss brugada
- More common men SE Asia
Commonest cause of SD in young men without underlying cardiac disease
AD inheritance - Abnormal function of sodium channels
- ECG changes can come and go
- Genetic testing not useful
- Avoid medications and fevers
- ICD
Discuss WPW
- Accessory pathway 1:300 to 1:500
- Rarely inherited
- Palpitations main symptoms if any
Commonest tachycardia - ECG delta wave, shortened PR interval
- RF ablation
Discuss coronary artery anomalies
- Anomalous coronary origin 1:100
- Small numbers squashing or kinking during exercise
- Chest discomfort ,blackouts with exercise
- Cardiac MRI
- Surgery can be life saving
Discuss MVP
5% population many people have trivial degrees of MV regurgitation
* Dizziness, syncope, palpitations, SOB or significant FH
* If none of above criterion met can be cleared for play
Discuss MVP
5% population many people have trivial degrees of MV regurgitation (ie normal variant)
* Dizziness, syncope, palpitations, SOB or significant FH
* If none of above criterion met can be cleared for play
Describe heat gain and what loss
Heat gain
* Endogenous production - muscle activity other metabolic processes (so a lot to lose when exercising)
* Exogenous - transfer occurs when environmental conditions exceed body temp
Heat loss
* conduction - water
* convection - rest
* radiation - rest
* evaporation - >35 degrees C only method
Humidity –> rapid increase in core temp, loose ability to appropriately regulate, worse in heavier athletes
What is heat stroke
- Metabolic rate function of speed and body mass – bulkier, faster runners more at risk eg 8-21km range
- Rectal temp 41 degrees and above
- Asymptomatic rectal temp at 40.5 degrees not uncommon
- Core temp rises –> cellular damage –> SIRS –> multi organ failure –> death
Rectal temp above 41 degrees
Symptoms and signs of heatsroke
Nausea, headache, confusion, dizziness, aggression, irrational behaviour, drowsiness,
Altered mental state (confusion -> seizures -> coma), tachycardia, hypotension (note sweating no influence on diagnosis), rectal temp >40
Altered glucose, altered Na, weight change
Risk factors for heatstroke
- Men – oestrogen reduces inflammatory response
- Conditions
- Febrile illness
- Dehydration
- Increasing age
- Lack fitness
- Lack sleep or food
- Obesity
- Previous episode
- Skin diseases
- Clothing
- Genetics RyR1 and calsequestran
Drugs
* Alcohol
* Amphetamine
* Antihistamine
* Benzodiazepines
* Beta Blockers
* Cocaine
* Diuretics
* Laxatives
* Thyroid agents
* TCA’s
Management of heat stroke
Rapid cooling to 38 degrees eg ice bath for 5-10 mins (no rationale with going slow)
Note that rectal temp lags core temp (watch for hypothermia)
IV fluids 1-1.5L saline
Complications of heatstroke
Malignant hyperthermia rhabdomylosis
MI/pulmonary oedema
Coma/convulsions/stroke
Liver bleeds/ulcers
DIC
Rhabdomylosis
Acute renal failure
Discuss exercise associated collapse
- Mainly a drop in BP
- Postural hypotension
- Blood pooling in periphery (second heart action stops, splanchnic vein filling)
- Dehydration unlikely to be factor
- Rectal temp not high enough
Mx
* Drink glucose 4-8%
* Trendelenberg
* Spontaneous recovery only 10-20 mins
Discuss hyponatraemia
- Athlete in an ultra endurance event with an altered conscious state and rectal temp below 41`C must have serum sodium measured
- Dehydration does not cause unconsciousness till renal failure
- 50KG athlete run for 10 hours sweating at 1L/hour with no fluids
Signs - altered consciousness, confused, check bracelets and watch straps (tightness), Na <129mmol, 2L-6L overhydrated
Management – catheterise and aim of urine output 500ml/L, NaCL (3-5%) 50-100ml/hr, diuretics, no fluids by mouth, salt containing foods
Consensus is that its due to over drinking >750mls/hour for 4 hours.
Failure to supress ADH
Failure to mobilise osmotically inactive Na stores (Hew Butler et al (2015)
Discuss heat acclimatisation
- Earlier onset sweating
Decreases Na concentration - Increased amount sweating
- Increased dilution sweat
- Greater peripheral sweating
- Heat and Humidity training for at least 2 weeks
- 24 hour exposure
- Sleep only time for AC
Discuss hypothermia
Rectal temp < 35, shivering, quickly depletes energy stores, lessens as glycogen stores fall, loss of muscle coordination
How is heat loss minimised
- Fat
- Peripheral vasoconstriction (you don’t vasoconstrict your head - hat!
- Clothing
- Curling into a ball body position
- Minimising movement
Effects of hypothermia
Cardiovascular:
* Vasoconstriction fluid shift
* Cold diuresis
* Decrease circulatory volume
* Cold myocardium - Decreased HR, J waves, AF, VF
* Warming causes fluid shift
Respiratory
* Hyperventilation
* Heat and water loss
* Bronchospasm
* Increased risk aspiration
Neuromuscular
* Numbness
* Muscle stiffness
* Poor coordination
* Increase in muscle damage
Renal function
Coagulopathies
Clinical features hypothermia
Mild 33-35 Degrees
* Cold
* Shivering
* Tachycardia
* Urinary urgency
* Incoordination
Moderate 31-32 Degrees
* Apathy
* Decreased shivering
* Weakness and clumsiness
* Slurred speech
* Amnesia
* Dehydration
* Increased coordination issues
Severe < 31 Degrees
* Inappropriate behaviour
* Loss of shivering
* Arrythmias
* Oedema
* Decrease in pulse rate and BP
* Decreased conscious level
* Rigidity
Management of hypothermia
–> need gentle rewarming (fluid shift risk makes it far more dangerous than rapid cooling in hyperthermia)
* Remove from wet and windy condition
* Core temp
* Insulate
* Nutritional and fluid support
* Assess for frostbite
* Rewarm
* Transfer to medical facility
Methods of Rewarming
Passive
* Clothing
* Covering body
* Penguin affect
* Little value in space blanket
Active (External)
* Hot air
* Water blankets
* Hot packs
Active (Internal)
* EC blood warming ,full bypass,warm IV infusions
* Needs ITU monitoring
Rx Mild
* Remove from cold
* Insulate where possible
* Warm sweet drink
* Heat to torso axilla and groins
* Mild activity if temp>35
Rx Moderate
* Remove from cold
* Insulate
* In Field No active rewarming till temp 34
* In Hospital active rewarming
* Close monitoring of cardiac status
Severe Hypothermia
* Minimal handling as risk of VF
* Quick transfer to hospital (extra-corneal warming)
* May appear dead
* HR can be as low as 6bpm
* Warm and Dead - warming efforts should continue until the body temp exceeds 35 since a person with hypothermia is not “cold and dead” until they are shown to be “warm and dad”
Also note Vfib is a common compilation of treatment for hypothermia esp during rapid re-warming
Causes of hypothermia
- Accident or Injury
- Exhaustion
- Dehydration
- Immersion
- Cyclists and skiers generate own wind chill
Specific management immersion hypothermia
- Rapid cooling ensues
- Remove in horizontal position – avoiding catastrophic drop in BP
- Temp < 31`C same protocol
- Temp 32`C and in water < 3 hours rapid rewarming can occur (because they’ve cooled so quickly)
Discuss frostbite
- Superficial (skin and sc tissue only)
- Deep (full skin thickness and deeper layers)
- Crystallisation of fluids in skin and tissue
- Peripheral sites (fingers, toes, nose, ears,and cheeks)
- Skiing postponed if temp lower than -20`C
What is athletes heart?
An increase in cardiac mass due to systematic training.
“Grey zone thickness” between 13 and 15mm, LV cavity >55mm, reduction of LV mass with deconditioning, cardiac MRI would give most detailed. Change in threshold for “normal” more being referred to cardiology
