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Transcript
HKCEM College Tutorial
A young man
collapse in
Ruby competition
AUTHOR
DR. TANG KA YUEN
JULY 2013
A 14-year-old boy collapsed during a rugby competition….
IF YOU ARE THE ON-SITE MEDICAL TEAM DOCTOR OR SPECTATOR,
WHAT WOULD YOU DO?
What would be the Onsite immediate management ?
Basic Life Support
▪ Ensure safety
▪ Assess response of the patient
▪ Call for help and get the AED if unconscious
and not breathing
What are the sequences of cardiopulmonary resuscitation (CPR) ?
▪Circulation
▪Airway
▪Breathing
▪2010 AHA Guidelines for BLS
http://www.youtube.com/watch?v=ZjszBXF0l8A
Onsite immediate management
Circulation
▪ Pulse Checking
▪ The rescuer locates the carotid or
femoral pulse and performs the
pulse check. It should take at least
five seconds but no more than ten
seconds.
▪ If there is no pulse or pulse < 60/min,
Chest Compression should be started
immediately.
What is an high quality CPR?
▪ Rate at least 100/min
▪ Compression depth to at least ½ anterior-posterior
diameter of chest, about 1.5 inches (4cm) in infants and
2 inches (5cm) in children
▪ Allow complete chest recoil after each compression
▪ Minimize interruptions in chest compressions
▪ Avoid excessive ventilation
Onsite immediate management
▪ One rescuer: 30 compressions and 2 breaths
▪ Two rescuers: 15 compressions and 2 breaths
Onsite immediate management
Airway
▪Open airway by
head-tilt-chin-lift or
jaw thrust if there is
evidence of C-spine
injury
Onsite immediate management
Breathing
▪ The E-C clamp technique is
recommended for bag-valve-mask
ventilation
▪ Give each breath slowly, over
approximately 1 second, and watch for
chest rise
▪ If the chest does not rise, reopen the
airway, verify that there is a tight seal
between the mask and the face, and
reattempt ventilation.
Onsite immediate management
▪ The rescuer should continue CPR
until ……..
▪ AED/Defibrillator arrives,
▪ Advanced Life Support
Providers take over
or
▪ Victim starts to move.
Automated External Defibrillator
▪ We use AED only when the
victim has no response, no
breathing and no pulse.
▪ Adult pads are available for
victim from age 8 and older. The
child pads are used for victim
from 1 year-old to 8 year-old if
available.
Automated External Defibrillator
1. Power on the AED, this activates
the audio guidance for the
subsequent steps
2. Attach the electrode pads and
connect the cables
3. “ Clear” the victim and analyze the
rhythm
4. If the AED advises a shock, make
sure no one is touching on the
victim before press the shock
button, begin CPR immediately
after the shock
Automated External Defibrillator
5. If no shock is indicated, continue
CPR.
6. After 2 min or 5 cylces of CPR , the
AED will prompt you the Step 3 and
step 4 again.
http://www.youtube.com/watch?v=3trpw_We0UQ
What is your diagnosis?
What are the
differential diagnosis
of VF in young athlete
during competitive
sports?
Cardiovascular causes of VF
▪ Structural & functional abnormalities
▪ Hypertrophic cardiomyopathy (HCM)
▪ Arrhythmogenic right ventricular
cardiomyopathy (ARVC)
▪ Dilated cardiomyopathy (DCM)
▪ Congenital anomalies of coronary arteries
(CCAA)
▪ Acquired
▪
▪
▪
▪
Commotio cordis
Trauma
Artherosclerotic coronary artery disease
Drug abuse
▪ Congenital heart disease
▪ Ebstein’s anomaly, TOF, VSD or cyanotic
heart disease
▪ Myocarditis
▪ Primary electrical abnormalities
▪ Long QT syndrome
▪ Brugada syndrome
▪ WPW syndrome
Non-cardiovascular causes of VF
▪ Respiratory:
▪
▪
▪
▪
▪
▪
Bronchospasm
Aspiration
Sleep apnea
Primary pulmonary HT
Pulmonary embolism
Tension pneumothorax
▪ Metabolic or toxic
▪
▪
▪
▪
Electrolyte disturbance and acidosis
Medication or drug ingestion
Environmental poisoning
Sepsis
▪ Neurologic
▪ Seizure
▪ CVA : ICH
▪ Drowning
Progress
▪ On-site CPR done by coach and St. John First Aid
staff
▪ Ambulance arrived 4 minutes after the incident.
AED detected VF and defibrillation was given once
▪ CPR continued after defibrillation, no more VF
detected afterward
▪ Pulses returned at about 11 minutes
ECG strip from ambulance
HOW WOULD YOU MANAGE
THIS PATIENT IN A&E
DEPARTMENT ?
The patient
remained
unconscious and
was sent to A&E
Department…..
Initial assessment in A&E Department
▪ Unconscious GCS 3/15
▪ Pupils 3mm E&R
▪ Afebrile
▪ BP/P 113/66 130/min
▪ P/E:
▪
▪
▪
▪
No external wound or rash
CVS: HS x 2 no murmur
Chest: normal
CNS: planter <- / ->, jerk not brisk
What other
history would
you ask from
his relative?
Initial assessment in AED
▪ History from relative:
▪ No preceding symptoms
▪ Healthy, no hx of syncope
▪ No hx of drug abuse
▪ No recent URTI
▪ Not on any medication
▪ Family hx: no hx of premature sudden death /
cardiac illness among relatives
Management in A&E department
▪ ABC – Intubated under RSI
▪ Investigations:
▪ Blood tests (including H’stix,CBP, R/LFT, Ca, toxicology,
Cardiac Enzymes, Troponin I, Blood gas)
▪ ECG
▪ CXR- clear
▪ CT brain
1st ECG in AED
Common CVS causes of VF in young athlete during competitive sport
▪ Structural & functional abnormalities
▪ Hypertrophic cardiomyopathy (HCM)
▪ Arrhythmogenic right ventricular
cardiomyopathy (ARVC)
▪ Dilated cardiomyopathy (DCM)
▪ Congenital anomalies of coronary arteries
(CCAA)
▪ Myocarditis
▪ Acquired
▪
▪
▪
▪
Commotio cordis
Trauma
Artherosclerotic coronary artery disease
Drug abuse
▪ Congenital heart disease
▪ Ebstein’s anomaly, TOF, VSD or cyanotic
heart disease (especially with OT done)
▪ Primary electrical abnormalities
▪ Long QT syndrome
▪ Brugada syndrome
▪ WPW syndrome
Hypertrophic Cardiomyopathy
LVH, increased S-wave voltage in V1-5, diffuse ST/T wave changes
Wolf Parkinson White Syndrolme
Shorten PR interval, slurred onset of QRS (delta wave) and increased QRS interval
Brugada Syndrome
ST elevation in leads V1 & V2
(and V3) followed by a
negative T wave
Prolong QT Syndrome
Prolonged QTc = 540ms with board-based T wave
WHAT DO YOU THINK?
Additional hx:
he was hit over chest
wall by another player
before he collapsed!
No convulsion noted.
Progress in AED
▪ Vital signs at AED
▪ GCS 3/15 , BP 133/66, P 130/min, SaO2 99%
▪ Intubated at AED for airway protection
▪ Physical examinations: unremarkable
▪ ECG: sinus tachycardia with no significant ST change
▪ CXR: normal
▪ Consult Pediatrician  transferred to PICU
▪ Extubated soon after admission with good respiratory effort
What are the management of Return of Spontaneous Circulation (ROSC)?
• Use ABCDE approach
• Controlled oxygenation and ventilation
• Investigations
• Treat precipitating cause
• Antiarrhythmic
• Amiodarone
• Therapeutic hypothermia?
http://circ.ahajournals.org/content/122/18_suppl_3/S768.full
What are the uses of Waveform capnography ?
1. Confirming tracheal tube placement
2. Monitoring of the CPR quality
http://acls-algorithms.com/waveform-capnography
Hospital course
▪ Initial echocardiography on day of admission revealed fair right ventricular
contraction, left ventricular apical hypokinesia with ejection fraction of 50%.
Subsequent echocardiography on day 4 did not reveal any evidence of
cardiomyopathy.
▪ Computer tomography of brain was normal. Patient was fully awake on day 3
and neurological examination did not reveal any significant abnormality except
mild intention tremor.
▪ Patient was transferred out from paediatric intensive care unit to general ward
on day 3. Patient recovered well and was assessed by physiotherapist. Mild
deterioration in hand-eye coordination was noted, otherwise patient’s functional
status was back to normal. Patient was discharged on day 7 and followed up by
cardiologist.
Hospital course
▪ All subsequent cardiac investigations were normal.
▪
▪
▪
▪
▪
▪
echocardiography,
24-hour holter monitoring,
exercise treadmill test,
exercise myocardial perfusion test,
computer tomography of coronary angiogram and
cardiac magnetic resonance imaging study
▪ Patient did not have any arrhythmia in all subsequent ECG with normal QTc of
373ms and ST segment. Clinical diagnosis of Commotio Cordis was made by
cardiologist.
▪ Patient returned to school in 2 months later for new semester with satisfactory
performance. He had satisfactory exercise tolerance and continued to play rugby in
school. No major cardiac or neurological sequelae was found.
Commotio cordis
▪ Commotio cordis means ‘disturbance of the heart’ in Latin
▪ Sudden cardiac death as a result of a blunt, often innocent-appearing chest
wall blow.
▪ Ranked as second leading cause of sudden cardiac death in young athletics
▪ The likely cause of death in Commotio Cordis is ventricular fibrillation
Maron, B. J. et al. JAMA 2002;287:1142-1146
Thank You