PICU cardiac guide - PICUDoctor.org

Editor and Author: Dr. Marc Anders
MD (Germany), FRCA (UK), FCICM (Australia), Facharzt Anesthsiology and Intensiv Care (Germany)
WITH MANY THANKS TO ALL WHO CONTRIBUTED TO THIS GUIDE LINE !
Dr. Andreas Schibler, Dr. Bret McVinish, Dr. Chris James, Dr. Clare Nourse, Emma Haisz,
Dr. Jamin Mulvey, Dr. Jason Yates, Dr. Jim Morwood, Dr. Kevin Plumpton, Dr. Mark
Hayden, Dr. Nalini Selveindran, Rachel Teis, Quyen Tu, Dr. Rajshree Trivedi
for K
And special thanks to
Bennett Sheridan - for all the excellent diagrams
Rapsou Rapciewicz and Stephanie Chesneau – for the wonderful drawings
Christian Stocker - for the hard discussions on the TGA chapter and the
excellent Single Ventricle chapter
Vassileios Valntas – for the iPhone app and webpage design
Jubal John – for the webpage hosting
1st
ed May 2011
2nd
ed October 2012
3rd
ed March 2013
4th
ed March 2014
5th
ed December 2014
This is only a guideline and does not substitute local clinical experience, clinical
evaluation and / or judgement of each individual patient!
Any comments / suggestions much appreciated,
email to marcanders@web.de.

TABLE OF CONTENTS
THE BASICS
Cardiac Admission
Patient Discharge from PICU
Initial postoperative care and problems
Capillary Leak Syndrome
Definitions
Formulae
Cardiac Cycle
Frank Starling Mechanisms
Infection
Empiric Antibiotics for general infection
Central Venous Catheters
ANESTHESIA
Analgesia and Sedation
Muscle Relaxation
Tolerance and Withdrawal
Weaning Opiods and Sedation
Intubation in PICU
Inotropes and Vasopressors
Inotropes and Vasodilators
PICU
Fluids
Maintenance Fluids
Nutrition
Feeding Guideline

TABLE OF CONTENTS <CONT>
Blood products
Anticoagulation & Thrombolysis
Chest Drains
Chylothorax
Genetic Syndromes and Cardiac Defects
Low Cardiac Output Syndrome
Open Chest
Arrhythmias
Pacing
Prolonged QT Syndrome
Pulmonary Hypertension
Nitric Oxide
Renal Failure
Renal Failure – Haemofiltration & Dialysis
T3 in cardiac surgery
CARDIAC DEFECTS
Anomalous Left Coronary Artery
Atrial Septal Defect
Atrioventricular Septal Defect
Blalock-Taussig–Shunt
Coarctation of the Aorta
Double Outlet Right Ventricle
Ebstein‘s Anomaly
Fontan Circulation
Glenn Shunt
Heterotaxy

Hypoplastic Left Heart Syndrome
Interrupted Aortic Arch
Left Ventricular Outflow obstruction
Patent Ductus Arteriosus
Pulmonary Atresia with IVS
Single Ventricle Physiology
TAPVD
Transposition of great arteries
Tetralogy of Fallot
Tricuspid Atresia
Truncus arteriosus
Ventricle Septal Defect
HEART FAILURE & ASSIST
Cardiomyopathy
Myocarditis
ECMO
ECMO Antibiotics
Heart Failure and VAD
Berlin Heart VAD EXCOR®
Heart Transplantation
ABO incompatible HTX
Resuscitation Drug Chart
Resuscitation Quick Chart
Neonatal Resuscitaion Guideline USA
Neonatal Resuscitaion Guideline UK
APLS Guideline: Cardiac Arrest Australia

PALS Guideline – Cardiac Arrest AHA

THE BASICS: CARDIAC ADMISSION
General principles: Anticipate the type of patient and potential problems ! Understand
lesion/post correction basic physiology and common postoperative issues ! - Ask if needed !
Admission: Expected admissions should be discussed in the morning ward round. Have a
quick read through the PICU Cardiac Guideline or discuss with fellow or consultant about the
lesion, surgery, expected problems and management. Theatre staff should call with an
expected time of arrival at least 20min in advance. The theatre technician should also write a
cardiac patient transfer report with details of procedure, lines, infusions etc. All patients
returning from cardiac theatre need to get a cardiac surgical admission, even if they‘ve been
in PICU pre-op. If they return to theatre for a second or more procedures they will get
cardiac surgical admissions each time.
• Have cardiac handover sheet ready, write up blood form, CXR form.
• Basic prescription for cardiac patients prior to arrival on the unit:
• Venous Heparin flushes including flushes for intracardiac lines: Heparin infusion @
10U/kg/hr for all babies less than 5kg with CVL
• Arterial Heparin flush infusion & bolus
• Sedation infusion & boluses (usually morphine and midazolam separately)
• Inotropes as per transfer note
• Fluid boluses 5 – 10ml/kg NaCl 0.9% or Albumin 5%
• For ECMO patients prescribe a PRN order for blood, platelets, FFP or Cryo. Also chart the
ECLS Heparin flushes, dialysate order. Blood (packed cells and CMV –ve and irradiated for
all infants less than 4month or if patient is +ve for 22 q11 or any other suspected
immunodeficiency)
• Antibiotics: Cephazolin 25mg/kg q8h for 3 doses plus Mupirocin 2% local application
around nares q12h for 3 days plus Nystatin 100.000U PO q8h as long as on antibiotics in
neonates. In open chest continue antiobiotics until chest closure.
• Paracetamol: < 10kg 7.5mg/kg IV q6h, > 10kg 15mg/kg IV q6h, change to PO/NG as soon
as able, up to 15mg/kg q4h.
• Fluid allowance :
• all non-bypass cases get 50% maintenance if > 10kg and < 10kg 2ml/kg/hr
• for bypass cases > 10kg 30% maintenance and < 10kg 1ml/kg/hr; these fluids are
upgraded with a general rule of increase of 1mL/kg/hr each day but check first i.e.
• Day 1 - 30% maintenance or 1ml/kg/hr
• Day 4 - full maintenance
Cardiac pre op (if patients are going to OT from PICU):
• Ensure 4 units packed cells, 2 units platelet, 2 units FFP, 2 units Cryoprecipitate are ready
for all pre op cardiac patients if in PICU prior – need to liaise with Blood Bank
• Crossmatch is on a separate form and MUST ensure that the sample goes in a EDTA top
tube with an HANDWRITTEN label (blood bank will reject samples with signed labels)
• With neonates make sure pre-op Chromosomes & GN FISH for 22q11 has been sent
especially in outflow obstructive lesions, prior any blood transfusion
• These patients will get a routine medical admission and then cardiac surgical if they have
surgery or a procedure in cathlab.
• Prescribe Mupirocin 2% local application around nares q12h, ideally for 2 days prior to
cardiac procedure.
• Examine the patient just prior to scheduled departure time and hand over to anesthetist.
Transfer of cardiac patient to PICU:
• Phase 1: Pre handover

• approximately 30 min before arrival on PICU, ―Cardiac Patient Transfer Report‖ completed
by anesthetic technician. PICU informed of ETA by phone.
• Phase 2: Equipment and Technology handover
• On arrival on PICU ventilation, monitoring and support pumps are transferred across prior
to handover. Discussion should be kept to a minimum at this point.
• The anesthetist will supervise and direct this transfer with assistance from the anesthetic
technician, OR nurse and PICU team.
• Safety Check: once transfer has occurred the delivery team checks that the patient is
stable and ventilation is occurring and checks that the PICU team is ready for handover.
• At this point the OR nurse may leave if they wish. All activity with the exception of
observing the patient and monitoring ceases.
• Phase 3: Information handover
• The anesthetist and then the surgeon hands over the patient (preferably without
interruption unless a member of the team identifies an urgent issue of stability in which case
handover should pause while it is dealt with). The information will be presented in a standard
order consistent with the Cardiac Surgical admission sheet.
• Safety Check: The PICU team listens and takes notes, they use the Cardiac Surgical
Admission sheet to ensure that they have all necessary information and ask any relevant
questions.
• Phase 4: Discussion and Plan
The team discusses the case, anticipate problems and agree on a documented plan.
The ICU team now assumes responsibility for the patient and commence routine
observations and management.
Notes:
• The chief operating surgeon, anesthetist and admitting intensivist should all be present at
the handover.
• In the event of an arrest during handover - the anesthetist will run things until the PICU
consultant feels they have enough information to do so, or to take over. The person in
charge should say something along the lines of "I will run this" so it's clear for all. The
handover sheet "Cardiac Surgical Admission" - may be filled out by the anesthetist in theatre
if there is adequate time.
Important details to remember:
• Operation performed and the duration of CPB and aortic cross clamping (latter being time
of ‗cardioplegia‘)?
• Check if there are any concerns regarding anatomy or repair (e.g. coronaries, size of
shunt, etc.) or pulmonary hypertension?
• Note pressures (RAP/CVP/PA, LAP and MAP), cerebral saturations, cardiac rhythm and
oxygen saturations in theatre.
• Note intra-operative problems and any complications encountered – during induction,
arrhythmia, pacemaker use, coming off CPB problems, bleeding and blood products given,
and medications given.
• Ask what blood products are available (unused from theatre).
• Discuss with consultant about plan/desired parameters and expected problems and their
management.
Initial Assessment:
Quick assessment focusing on cardiovascular stability and adequate ventilation (vital signs
and chest movement) as patient arrives from theatre.
• Review current support drugs – inotropes and/or vasodilators
• Review with nurses that the patient is safely connected to ICU support and monitoring
equipment. Check ventilator settings
• Review anesthetic, CPB charts and operation or any intra-operative TOE notes. Look for
difficult airway, anesthetic medications given, heart function, and residual lesions
• Detailed physical examination

• Request: ABG / VBG / FBC / U&E / Calcium, Mg, PO4 / Coagulation profile, TEG / CXR
• Document clinical findings and plan in the cardiac surgical admission
• Review as soon as possible CXR (check position of ETT, temperature probe, lines, drains,
any pneumothorax/effusion), and first set of blood results – ventilation settings may need
adjustment according to ABG
• Check baseline ECG
Ongoing Management:
• Adequate Opiate Analgesia. Titrate other sedatives as required
• IV infusion of Muscle relaxant if cardiovascular unstable
• Support the circulation - see lesion specific modules
• Treat @ Arrhythmia
• Bleeding > 3ml/kg/hr investigate (@ Chest Drains). If > 10ml/kg/hour or a sudden stop in
drainage needs urgent surgical & cardiology review. A quick bedside scan with the ultra-
sound machine in the unit maybe useful.
• Fluid resuscitate, send FBC and coagulation profile. Consider TEG & replace factors as
indicated (most likely to need cryoprecipitate and platelets)
• Watch for @ Tamponade ! If suspected quick bedside scan with the ultra-sound machine
in the unit maybe useful
• Packed cells 4 ml/kg raises Hb by 1g/dl
• Follow unit antibiotic policy
• Investigations: FBC, U&E, LFT, Ca /Mg / PO4. Coagulation for post-op on first few days or
when lines/drains coming out. CRP if previous high value or if suspicion of sepsis
• If intracardiac lines going to be removed the next day then needs coagulation profile (plus
crossmatch with blood available in theatre fridge – important to check that the blood is
physically in the theatre fridge, not back in Blood Bank, the bedside nurse will usually do
this, just confirm)
Cardiac handover:
Keep it short/simple & sweet. Please SPEAK UP!
• Name, age and day post-op
• Lesion & procedure done
• Cardiovascular – HR, rhythm, BP, +/- pacing required, trends
• Blood products if any given
• Ventilations: Adequate gas exchange or mention issues if any
• Gases – include lactates and mixed venous, trends
• Fluids balance and urine output / PD for last 24 hrs
• Drain losses – type eg. blood, serous, serosanguineous.
• Trend of last 6 - 8hrs
• Mention bloods if something grossly abnormal
• If CXR done & seen mention briefly.
• ECMO - flow, sweep, inlet and outlet pressures, ACT‘s, blood products given, bleeding,
circuit (i.e. clots), arterial line trace (pulsatile or non pulsatile)
The seven vital causes to remember of postoperative Tachycardia:
• CNS: fever, pain, inappropriate sedation and analgesia, seizures
• CVS: low cardiac output
• CVS: Tachyarrhythmia
• Respiratory: hypoxia, hypercarbia
• Pulmonary Hypertension
• Drugs: catecholamines
• Residual defects

THE BASICS: DISCHARGE FROM PICU
Patients in the PICU will be evaluated and considered for discharge based on the reversal of
the disease process or resolution of the physiological instability that prompted admission to
the unit, and it is determined that the need for complex intervention exceeding ward
capabilities is no longer needed.
Transfer and / or discharge will be based on the following criteria:
• Neurologically stable
• stable hemodynamic parameters
• intravenous inotropic support, vasodilators, and anti-arrhythmic drugs are no longer
required (minimum for 4hours post ceasing)
• haemodynamic monitoring catheters removed or capped and well secured. Once the line
has been capped it is NOT to be flushed or re-used.
• cardiac dysrhythmias are controlled
• Pacing wires are generally removed after 24hours if there is no evidence of arrhythmia
• stable respiratory status (patient extubated with stable arterial blood gases) and airway
patency (minimum 4hours post extubation)
• minimal oxygen requirements that do not exceed patient care unit guidelines
• Approval for and timing of discharges must be by the Consultant or Fellow !
PICU registrar discharge checklist:
• enter a brief discharge note in the patients record before discharge, summarizing final
diagnosis, main PICU therapies, current problems, current medications, and current
management plan
• complete the computer discharge summary
• all notes and discharge summary need to be printed out and signed by registrar / fellow
• complete ward drug chart, double check with pharmacist during duty hours for completion
and correctness
• Notify the cardiologist, surgeon and ward registrar, if not already advised
• Generic PICU to Ward shared Handover to be filled in and signed: Handover given to ward
physician, acute pain service informed or ward pain medication written up, plan of care and
outstanding issues, blood results reviewed and / or actioned, timing and frequency on
medical review, names of registrar / fellow, completed the discharge summary, name of the
ward physician, name of the pain team
• immediately prior to discharge examine the patient, collate investigations including that
days x-ray and blood tests, review IV orders and drugs and check the medications and fluids
for the ward are written
• The patient's relatives must be aware of the discharge plan and notified when their child is
moved

THE BASICS: INITIAL POSTOPERATIVE CARE AND PROBLEMS
Abdominal distension
• Causes: air in stomach or bowel (usually from mask ventilation at induction of anesthesia)
or tension pneumothorax; fluid in bowel or in peritoneal cavity (usually capillary leak, high RA
pressure or PD fluid; rarely fluid overload or peritoneal hematoma). Exclude NEC, especially
in neonates with parallel circulations or long cross-clamp time.
• Investigation and management: examine chest and abdomen: percussion; examine fluid
drainage from PD catheter and chest drains (amount and redness - measure Hb); aspirate
NG tube; repeat CXR (compare with previous, air in stomach or bowel, pneumothorax);
monitor abdominal girth; check coagulation and platelets (correct if abnormal and bleeding);
abdominal ultrasound if suspect retroperitoneal hemorrhage (femoral line). If capillary leak is
the problem, lasts up to 2days (longer in neonates, after long operations, in sepsis and when
the cardiac output is low); during this time, fluid restriction doesn't prevent edema or ascites,
but only leads to hypovolaemia. Adjust ventilation if necessary to compensate for reduced
abdominal compliance.
Atelectasis
• Causes: tracheal intubation, thick secretions, inadequate humidification (check humidifier
tank and tubing temperatures), inadequate tracheal suction, airway compression or collapse
(eg malacia), paralysed hemidiaphragm while spontaneous ventilation
• Signs: decreasing SaO2, rising PaCO2, may be reduced ipsilateral chest movement,
usually involves RUL and LLL.
• Management: hand-ventilation, instill normal saline (0.25 - 0.5ml) into trachea before
suction, physiotherapy, culture tracheal aspirate, X-ray screen diaphragm if clinical suspicion
of paralysis, bronchogram if other signs suggest malacia (hyperinflation, wheezing,
prolonged expiration).
Atrial pressure increasing
• Examine patient; check BP, heart rate, RAP, LAP. AV valve regurgitation. Look for V
wave in atrial trace (AV regurgitation or malposition of atrial catheter through AV valve).
Over-filling. In aortic or pulmonary stenosis, non-compliant ventricles cause atrial pressures
to rise with small increases in volume. Treat by careful diuretics and / or GTN (filling
pressures !). Tamponade. Associated with tachycardia and falling BP and cardiac output.
Notify surgeons and immediate Echo, but do not delay chest opening if situation serious. In
infants, myocardial edema without pericardial fluid can cause tamponade that may be
immediately relieved by opening the chest. Deteriorating myocardial performance.
Arrhythmia. Pneumothorax.
• Management: re-calibrate transducers. Examine chest and abdomen; check blood gas,
electrolytes and lactate; hand-ventilate and suction ETT; check ECG rhythm; obtain a CXR;
notify surgeons if tamponade suspected; trial of vasodilators, diuretics and inotropes.
Cardiac Tamponade
• Signs: rising HR; increasing lactate and metabolic acidosis; falling BP with low pulse
pressure and narrowing of systolic and diastolic BP; both atrial pressures rise (especially
RA); chest drainage may increase (if due to increased bleeding) or (usually) decrease
(drainage blocked); heart sounds may be muffled; QRS complexes may be smaller. Milk
drains (are they on adequate suction, are the drain reservoirs full). If there is the slightest
suspicion of tamponade, notify the surgeon ! (do not delay for investigations).
• Management: obtain CXR (may show increase in heart size; more globular heart shape;
increased distance from pacing wires or LA/PA lines to heart border); obtain Echo; check

blood gases and clotting (PT, PTT, fibrinogen, platelets); milk the chest drains; stop
vasodilators; give blood or saline 10 ml/kg; maintain the coronary perfusion pressure using
inotropes; consider clotting factors or platelets; if ACT >100 sec, give protamine 0.5 mg/kg
and re-check ACT; consider aspirating LA or PA lines to check position of their tips (? in
pericardial cavity); may need urgent chest opening.to prevent further detoriation.
Convulsions
In a paralysed child, a seizure may consist only of increases in HR, BP, PA or atrial
pressures or spontaneous variations in pupil size. Review history: pre-op; intra-op and post-
op events; check blood glucose, gases and electrolytes (including Ca++
and Mg++
); cease
muscle relaxants; check autonomic response to IV midazolam bolus; neurological
examination when muscle power returns; consider consulting neurologist (is this a fit?
prognosis? follow-up ?); monitor EEG during autonomic changes to confirm seizure present;
consider CT scan; load with phenobarbitone up to 30mg/kg IV in 5 - 10mg/kg increments
(beware hypotension); continue phenobarbitone if fits continue; avoid IV phenytoin
(myocardial depressant) after cardiac surgery. Consider Keppra 10mg/kg IV.
Fever
All children become febrile after open heart surgery, and most become febrile after any
thoracotomy. The fever appears as soon as the child re-warms after the operation, and lasts
24 – 48 hours. During this time, the child can still become septic, but the diagnosis of sepsis
depends on other signs. A secondary increase in temperature (after the normal post-op fever
has settled) means sepsis until proven otherwise (CRP, PCT, WCC, ITR). High post-
operative fever may be associated with marked tachycardia, and an increase in VO2 (11%
increase in VO2 per 1o
C increase in temperature). Regular Paracetamol (single dose
30mg/kg post-op) to keep core temperature < 37.5o
C. If the temperature is > 39o
C despite
paracetamol and the child is still paralysed, consider using cool peritoneal dialysis (1.5%
solution at room temperature in 30minutes cycles, each of 10ml/kg) or surface cooling to
normothermia, using a cooling blanket.
Haemorrhage
• Causes: thrombocytopenia; poor platelet function; dilution or consumption of clotting
factors; residual heparin (usually in the first 4hours post-op); surgical problem.
• Signs: losses from chest drains remain bright red and increase in amount or fail to
decrease normally; tamponade; hypoventilation and / or poor unilateral chest movement;
increasing abdominal distension.
• Investigation and Management: notify surgeon early; measure Hb of chest drain fluid;
repeat CXR if suspect tamponade or pneumothorax; check ACT, TEG, coagulation and
platelets; give protamine 0.5mg/kg IV and repeat ACT; give platelets 10ml/kg; give FFP
10ml/kg if ACT, PT or APTT remain prolonged despite protamine; give cryoprecipitate if
fibrinogen low; consider giving aprotinin if major bleeding persists despite the above; urgent
Echo if tamponade is suspected.
If Aspirin stopped within 4days of surgery, give DDAVP if post-op bleeding is a problem.
Hypertension
Common after repair of coarctation beyond the newborn period and after heart transplant.
Other causes are pain, awareness, fits, full bladder, hypercarbia, vasoconstriction.
Examine chest, abdomen, pupils and fontanelle. Check blood gases and glucose. Give a
morphine bolus and reassess. Give a midazolam bolus and reassess. Start infusion of
sodium-nitroprusside (SNP): start with 0.1mcg/kg/min and increase gradually to 2 -
3mcg/kg/min if required (beware of cyanide toxicity and methaemoglobinaemia, especially

rising lactate). In a child > 1year of age, if HR > 100 and still hypertensive, give an IV beta
blocker (esmolol) – cave: negative inotropic effect - or alpha blocker (phentolamine). Convert
to bolus drugs when stable (atenolol, phenoxybenzamine, captopril). Avoid giving a calcium
channel blocker plus a beta blocker.
Hypotension
• Causes: hypovolaemia; low cardiac output; excessive peripheral vasodilatation in the face
of inadequate or limited cardiac output; has the child received a bolus of vasodilator
(intermittently blocked CVC, sudden increase in flow of other fluid through the same line as
the vasodilator); anaphylaxis; low-resistance pathway from the aorta (eg central shunt,
MAPCAs, AV fistula).
• Exclude all the causes of inadequate cardiac output. If hypotension is profound, raise
the legs. Give a fluid bolus 10ml/kg and repeat if necessary (monitor RAP / LAP, may need >
10mmHg in the early postoperative Phase). If MAP < 25mmHg in a neonate or < 40mmHg in
an older child, start external cardiac massage. Notify the cardiac surgeon. Give adrenaline
bolus: 0.1ml/kg of 1:10.000; repeat if necessary and start an adrenaline infusion. If there is
aorto-pulmonary runoff and a high saturation, reduce the FiO2 to 0.21, increase PaCO2 to
45 - 55mmHg and Hb to 140.
Hypoventilation
• Cardinal sign: rising PaCO2.
• Causes: drugs, brain injury in theatre or post-operative, tracheal secretions, atelectasis,
pneumothorax, pulmonary oedema or chest wall oedema, large leak around ETT or in
ventilator circuit, changed ventilator settings, gas in stomach or recently started PD, muscle
relaxant ceased (reduced chest wall compliance)
• Signs: tachycardia and sweating, falling saturation and rising PaCO2, rising PA pressure,
BP may rise (hypercarbia) or fall (impaired myocardial performance)
• Management: examine chest and abdomen, blood gas, hand-ventilate, listen to chest,
suction ETT yourself; obtain CXR, check ETT and ventilator circuit for leaks, check ventilator
settings, increase ventilation or change ventilation mode if necessary, aspirate NG tube,
drain ascites, hand ventilate and suction with saline for atelectasis.
Hypoxaemia
Falling PaO2 or falling saturation. Causes: any of the causes of hypoventilation; right-to-left
shunt: intracardiac or intrapulmonary; parenchymal lung disease; pulmonary oedema;
atelectasis; pneumonia; intrapulmonary haemorrhage.
• Investigation: Is it real? If SpO2 falling, rapidly check the oximeter pulse wave, try the
probe on yourself, change probe site. Take a blood gas sample immediately (noting the
oximeter reading at the time) and monitor the patient closely for signs of cyanosis,
hypotension and low cardiac output. Examine the chest. Manually ventilate and suction the
trachea yourself. CXR. Investigate hypoventilation if PaCO2 raised. Take blood from LA and
arterial lines and measure saturation to look for intracardiac right-to-left shunt. Bubble-
contrast echocardiograph to locate intracardiac R-to-L shunt.
Pulmonary Hypertension
Usually occurs on a background of high pulmonary blood flow or left heart obstruction. Acute
rises in PA pressure usually occur in response to hypoxia, hypercarbia, acidosis or handling
but may also occur with transfusion of platelets or FFP or infusion of Protamine. It can also
occur without stimulus or warning. High risk patients:
• keep well sedated & paralysed for first 4-8 hours. Fentanyl 1 – 2mcg/kg pre suction and
handling

• minimize handling
• aim for PaCO2 30-35, PaO2 >120 mmHg, pH >7.4
• dobutamine plus milrinone is a good combination for systemic cardiac output and
pulmonary vasodilation
• start NO (10ppm) if increasing PA pressure causes tachycardia, hypotension, desaturation
and signs of poor cardiac output or if mean PA pressure > half mean systemic BP
In patients without a PA line, pulmonary hypertension may be indicated by acute
desaturation, decreased lung compliance, wheeze and hypotension. @ Pulmonary
Hypertension)
ETT Suction
Tracheal stimulation can cause severe increases in PA pressure. When suction is
considered necessary, pre-medicate with fentanyl (1 - 2mcg/kg) to ablate airway
responsiveness. Suction the ETT cautiously and quickly.
Sepsis
Increase in temperature (@ Fever and @ Infection); decrease in cardiac output; increase in
pulmonary artery pressure; warm skin, bounding pulses and reduced aortic diastolic
pressure; oliguria; decline in conscious state; increasing lactate and metabolic acidosis;
unexplained increase or decrease in blood glucose; increased CRP or PCT; decreased
platelet count.
• Investigation: examine the child for evidence that sepsis is present and for a septic focus:
wound, lungs, cannulation sites (including signs of caval thrombosis), meningitis,
endocarditis (new murmurs, skin infarcts, fundi, splenomegaly, urinalysis), ears, paranasal
sinuses (especially with prolonged nasal intubation), bones, joints, urinary tract. Repeat FBE
and CRP. Blood cultures: percutaneous, arterial line and central venous cannula. Do not
culture arterial line tip. Consider formal non-bronchoscopic bronchoalveolar lavage if there
are lung opacities on chest x-ray. Culture drain fluid. Culture any pus and send a pus smear
on a microscope slide for Gram stain. Culture urine from suprapubic aspirate or catheter (not
from a bag specimen). Think of fungal sepsis: examine skin, mouth, larynx, fundi. Arrange
ultrasound examination of kidneys.
• Management: consider antibiotics (choice depends on probable organism: flucloxacillin (or
similar Staphylococcus sensitive Penicillin or vancomycin) plus gentamicin usually
appropriate when the organism is unknown; monitor drug levels carefully; add oral nystatin).
Review culture results and CRP daily. Cease antibiotics after 48 hours if culture results
remain negative and clinical evidence of sepsis gone. Otherwise, continue antibiotics for
5days (longer for severe and intractable infections such as mediastinitis and endocarditis).
Sweating
• Causes: pain, awareness, high PaCO2 (inadequate alveolar ventilation), hypovolaemia,
low cardiac output, hypoglycaemia, heart failure, drug withdrawal. Examine child (hydration,
vein status, response to voice, passive movement and tracheal suction; other signs of
sympathetic stimulation (such as pupils); review chart (change in pressures, HR, respiratory
rate, temperature and ventilation); hand-ventilate and suction trachea; check gas and
glucose; trial of fluid bolus 5 - 10ml/kg; trial of morphine bolus 50mcg/kg, repeat if necessary;
try IV midazolam.
Tachycardia
An important sign that something is wrong. You must identify the cause: arrhythmia, low
cardiac output, pulmonary hypertensive crisis, hypoventilation or hypoxaemia,

hypoglycaemia, central (fits, fever, pain or full bladder), drugs (pancuronium or inotropes),
anatomy (eg small LV).
Examine the child: chest, abdomen, pupils, fontanelle. Check the heart pressures, temp,
urine output, ECG, atrial electrogram. Check blood gases and electrolytes and glucose.
Echo.
Tachypnea
If the respiratory rate rises progressively, a cause must be found.
• Causes: pain or other distress; restrictive lung disease (pulmonary oedema, atelectasis,
pulmonary haemorrhage, pneumonia); pneumothorax or pleural effusion; fever; sepsis;
metabolic acidosis; pulmonary hypertension; neuromuscular weakness (residual relaxants or
other cause).
• Investigation: examine (chest, abdomen, pupils, muscle power, autonomic signs of
distress, response to voice, passive limb movement and tracheal suction); review chart (PA
and LA pressure, BP, temperature, urine output); blood gas; hand-ventilate and personally
suction trachea; repeat CXR; consider trial bolus of morphine or midazolam; CRP; platelet
count; culture blood, urine, tracheal aspirate and drain fluid; observe pattern of ventilation
(shallow tachypnoea versus hyperpnoea; coordination with the ventilator). Increase
ventilation (mandatory rate or support pressure) if muscle weakness present.
Ventilator dependence
A high pCO2 may be appropriate if there is metabolic alkalosis caused by hypochloraemia
from diuretic use. Respiratory depression. Drugs or encephalopathy. Irregular, shallow
breaths; high PaCO2; sleepy; may be other evidence of encephalopathy (eg fits); often
prolonged or high-dose morphine or midazolam infusion; wait (days) for sedatives to be
excreted; neurological examination; check fontanelle; cerebral ultrasound (insensitive) ± CT
scan (wait several days). Phrenic nerve palsy. Unilateral or (rarely) bilateral; often transient
(weeks); no ipsilateral inspiratory movement of abdomen. Diagnosis: ultrasound and / or X-
ray image intensifier (screening) – both give false negatives. Plication should be considered
early in a small infant with unilateral palsy who has failed extubation, and after a week of
failed attempts in an older child (especially in palliative repair).
Neuromuscular weakness. Residual muscle relaxants; previous period of poor cardiac
output; impaired liver or kidney function; edema or ascites fluid store relaxant drugs;
prolonged or high dose relaxants (especially if doses given before child moves). Diagnosis:
train of four. Management: wait until movement returns (can lift legs off bed) before giving
neostigmine-atropine; don't rely on neostigmine-atropine to reverse a profoundly paralysed
child. ICU myopathy (prolonged IPPV + relaxants ± steroids ± sepsis; severely ill with normal
train of 4); EMG and consult neurologists if suspected; pressure support ventilation + good
nutrition + wait (avoid steroids and muscle relaxants)
Pleural effusion. If drainage required (after discussion), send fluid for culture, cell count,
triglycerides. Triglyceride >1.1 mmol/L (if fed) and cells > 1000/microL with lymphocytes >
80% suggests chylothorax; Echo and Ultrasound (exclude SVC obstruction), change to
Monogen, or stop feeds and give TPN (77% respond at a mean of 12 days, 45 days if MCT
given); if no response by 14 days, consider trial of octreotide 5 mcg/kg/hr IV @ Chylothorax
Tracheobronchomalacia. Wheeze, prolonged expiration, and active use of expiratory
muscles; gas trapping clinically and on CXR; bronchogram and / or bronchoscopy; use high
CPAP (10 - 15 cmH2O); wean CPAP using deep sedation (morphine ± chloral ± diazepam ±
chlorpromazine); anticipate days to weeks of repeated attempts to wean.
Residual cardiac abnormality. Left-to-right shunt; obstruction in left heart or pulmonary veins;
left-sided AV valve dysfunction; hypoplastic LV; PA stenosis or distortion in BCPS or Fontan
patients. Cardiac catheter ± re-operation.
[1] Pediatr Cardiol. 2013 Feb;34(2):341-7. McDonald ET AL: Impact of 22q11.2 deletion on the postoperative course of children
after cardiac surgery.

CAPILLARY LEAK SYNDROME
Definition: The use of cardiopulmonary Bypass (CPB) is associated with the activation of
multiple inflammatory pathways involving both cellular elements (RBCs, platelets, and white
blood cells) and soluble proteins. The activation of complements is triggered in virtually all
surgical procedures, but the response is higher in cardiac surgical procedures under CPB.
The activation of complements leads to Capillary Leak Syndrome (CLS).
All organs are susceptible to increased tissue edema, but the lungs, brain, kidneys, and
myocardium are particularly vulnerable. Post-CPB syndrome can present as noncardiogenic
pulmonary edema, myocardial dysfunction, severe vasoplegia, hemodynamic instability, and
renal dysfunction and, in severe cases, as multiorgan failure.
Physiology: The major problem associated with CPB in newborns and infants is prolonged
inflammation leading to capillary leak syndrome (CLS) and organ dysfunction, resulting in
higher morbidity and mortality.
The inflammatory response is a complex biological and biochemical process involving
cellular processes, the contact system, the complement system and cytokines. The latter
seem to play a key role in the CPB-mediated inflammatory cascade.
Presentation:
• Low filling pressures
• Systemic oedema and tissue oedema
• Pleural effusions and ascites
• increase analgesia and sedation (bolus Fentanyl 1-10mcg/kg iv)
Risk factors:
• Neonates > Infants > Children
• CPB duration
• Deep hypothermic cardiac arrest
Therapy:
There is no specific treatment for CLS. Management is aimed at supporting compromised
systems.
• Cardiovascular: assure appropriate filling pressures
• Respiratory: higher PEEP maybe needed, but ensure low tidal volumes (5 – 7ml/kg) and
low PIP
• Consider PD – this may reduce proinflammatory cytokines
[1] Eur J Cardiothorac Surg. 2013 Aug;44(2):275-81: Kubicki et al: Early prediction of capillary leak syndrome in infants after
cardiopulmonary bypass
[2] Semin Cardiothorac Vasc Anesth. 2014 May 29;18(2):161-176: Esper et al: Pathophysiology of Cardiopulmonary Bypass:
Current Strategies for the Prevention and Treatment of Anemia, Coagulopathy, and Organ Dysfunction

THE BASICS: DEFINITIONS
Aortic cross-clamp time. Duration of clamping of the aorta during bypass. Independent risk
factor for postoperative mortality.
CCF. Congestive Cardiac Failure.
Cardio-pulmonary bypass (CPB). All blood returning to the right atrium is pumped to a
device that adds O2 and removes CO2, and the blood is then returned to aorta.
Circulatory arrest time (arrest time). Duration of total circulatory arrest
(Cox) – Maze Procdure. Surgical procedure with left atrial, right atrial and atrioseptal
incisions to prevent atrial flutter / fibtrillation.
DHCA. Deep Hypothermic Cardiac Arrest.
Extracorporeal membrane oxygenation (ECMO). A form of extracorporal life support, but
without the means of returning blood lost into the thorax back to the circuit.
LVEDP. Left Ventricular enddiastolic pressure.
LVH. Left Ventricular Hypertrophy.
MR or MI. Mitral Regurgitation / Insufficiency.
MS. Mitral Stenosis
PBF. Pulmonary Blood Flow.
Qp. Pulmonary Blood Flow.
Qs. Systemic Blood Flow.
Qp : Qs. Ratio of pulmonary to systemic blood flow. (normal physiology 1 : 1)
RVH. Right ventricular Hypertrophy.
RVOTO. Right-ventricular outflow obstruction.
SmvO2. Mixed Venous Saturation. Indication for oxygen consumption and CO (SaO2 –
SmvO2 < 30%)
TR or TI. Tricuspid Regurgitation / Insufficiency
TS. Tricuspid Stenosis.
Ventricular assist device (VAD). Form of extracorporal life support, where a blood pump
with axial, laminar or pulsatile flow to augment the function of the left ventricle (LVAD), right
ventricle (RVAD), or both (BiVAD - using two pumps).

THE BASICS: FORMULAE
Alveolar Gas Equation = (Patm – PH2O) x FiO2 – paCO2 / RQ
(Patm – 760mmHg atmospheric pressure at sea level, PH2O – 47mmHg water vapour
pressure, FiO2 – inspired oxygen concentration, RQ – respiratory quotient = CO2 eliminated
/ O2 consumed)
Body Surface Index (BSA) =
= ( [Height(cm) x Weight(kg) ] / 3600 )½
Mean Arterial Blood Pressure (MAP) = (SBP + 2 x DBP) / 3
Transpulmonary Gradient (TPG) =
= mPAP – PCWP or in Glenn / Fontan: SVC (CVP) - LAP
Cardiac output (CO) = SV x HR. normal: 2.1 – 3.5 l/min/m2
Cardiac index (CI) = CO / BSA. normal 3.0 – 5.5 l/min/m2
Systemic vascular resistance index (SVRI) =
= 80 x (MAP - CVP) / CI. normal 800 - 1600 dyne*sec/cm5/m2. SVRI / 80 = normal 15 - 30
Wood unit / m2
Pulmonary vascular resistance index (PVRI) =
= 80 x (MPAP - LAP) / CI. normal 80 - 240 dyne*sec/cm5/m2. PVRI / 80 = normal 1 - 3
Wood unit / m2
Stroke Volume (SV) = CO / HR. normal 1 – 1.5 ml/kg
Ejection Fraction (EF) = (EDV – ESV) / EDV. normal 55 – 75 %
Fractional Shortening (FS) = (LVEDD – LVESD) / LVEDD. normal 28 – 45 %
Modified Bernoulli Equation: p1-p2=4 x v2
.
relates the pressure drop (or gradient) across an obstruction
Flow resistance. Poiseuille’s Law: R = 8 x η x L / π x r4
( η = viscosity, L = length, r = radius). laminar flow only
Right ventricular Pressure (RVP) = 4 x (TR Vmax)2
+ RAP
Pulmonary to systemic blood (Qp : Qs) =
= (SaO2 - SmvO2) / (SpvO2 - SpaO2). normal 1 : 1
in parallel circulation Qp : Qs ~ 25 : (95 – SaO2)
Oxygen Delivery (DO2) = CI x Hb (g/l) x SaO2 x 1.36 x SaO2 / 100
Oxygen consumption (VO2) =
= CI x Hb (g/l) x 1.36 x ((SaO2 - SmvO2) / 100).
normal: infant 160-180, child 100-130, adult 120-150 ml/min/m2
QT interval. Bazett's formula: QTc = QT (sec) / SqrRt of previous RR interval (sec). normal
approximately < 0.44 sec

THE BASICS: CARDIAC CYCLE
NORMAL VALUES
Threshold
Heart Rate
(bpm)
MAP
(mmHg)
Term Newborn 120 – 180 45
up to 1yr 100 – 180 55
up to 2yrs 80 - 130 60
up to 7yrs 70 - 110 65
up to 16yrs 50 – 100 65
[1] Pediatr Crit Care Med 2009 Vol. 10, No. 3: Bronicki et al: Cardiopulmonary Interaction.

THE BASICS: FRANK STARLING MECHANISMS
Increased Preload
Increased Preload
(A B)
 increased LV Volume
 increased Stroke Volume
Increasing Preload above diastolic
compliance
 Failure (F)
Improved diastolic compliance
Improved diastolic compliance
(A  B)
 increased LV Volume

Increased Inotropy
Increased Inotropy
(A  B)
Decreased Afterload
Decreased Afterload
(A  B)

THE BASICS: INFECTION
Surgical Site Infection (superficial / deep / organ):
• Prevalence 5 - 10%
• within 10 – 14days post surgery
• most common: Staphylococcus aureus
• risk factors: neonate, HLHS, hospitalization prior surgery, TPN, emergency procedures,
long CPB
Blood Stream Infection:
• Prevalence 5 - 10%
• within 10 – 14days post surgery
• most common: gramnegative organism (Pseudomonas, Enterbacter)
• risk factors: surgical complexity, open sternum, low body weight, longer duration of central
line, prolonged ICU stay
Pulmonary Infection:
• Prevalence 10%
• risk factors: prolonged mechanical ventilation, surgical complexity, low cardiac output
syndrome, failed extubation
Current recommendation for antimicrobial Prophylaxis in Cardiac Surgery: Cefazolin up to
72hrs (prolonged use may increase antimicrobial resistance). In the setting of either a
presumed or known Staphylococcal colonization, the institution presence of a high incidence
of MRSA, patients susceptible to colonization, or an operation for a patient having prostethic
valve or vascular graft insertion, it would be reasonable to combine the beta-lactam with a
glycopeptide (Vancomycin) for prophylaxis.
Special considerations in immunodeficient syndromes (DiGeorge Syndrome, @
Chylothorax)
See also @ Sepsis and @ Fever
[1] Am J Infect Control 2010 Nov;38(9):706-710: Sohn et al: Risk factors and risk adjustement for surgical site infections in
pediatric cardiothoracic surgery patients
[2] Pediatr Cardiol 2010 May;31(4): 483-9: Abou Elella et al: Impact of bloodstream infection on the outcome of children
undergoing congenital heart surgery
[3] Am J Health Syst Pharm 2008 Nov 1;65(21): 2008, 2010: Survey of congenital heart surgeons‘ preferences for antimicrobial
prophylaxis for pediatric cardiac surgery patients
[4] Ann Thorac Surg 2007 Apr; 83(4): 1569-76: Engelman et al: The Society of thoracic surgeons practice guideline series:
Antibiotic prophylaxis in cardiac surgery, Part II: Antibiotic Choice

THE BASICS: EMPIRIC ANTIBIOTIC GUIDELINES FOR GENERAL INFECTION
Age if meningitis excluded
if meningitis is NOT
excluded
if Staphylococcus aureus
suspected
< 3 months
Amoxicillin 50mg/kg q6hr
Gentamycin 7.5mg/kg q24hr
Cefotaxime 50mg/kg q6hr
consider especially in infants
Aciclovir 20mg/kg q8hr
Vancomycin 15mg/kg q6hr
Clindamycin 15mg/kg q8hr
> 3 months
Flucloxacillin 50mg/kg q4-6h
(or similar Staphylococcus
sensitive Penicillin)
Flucloxacillin 50mg/kg q4-6hr
(or similar Staphylococcus
sensitive Penicillin)
Clindamycin 15mg/kg q8hr
any age group,
if immuno-
compromised
Meropenem 20mg/kg IV q8hr
if Meningitis is NOT excluded, and suspicion of severe Meningitis (gram stain), replace Flucloxacillin by
Vancomycin 15mg/kg q6hr to cover for Penicillin resistant Pneumococcus Meningitis

THE BASICS: CENTRAL VENOUS CATHETERS
Use of central venous catheters in the acute care setting is an integral approach to deliver
fluids, blood products, nutrients, medications, obtaining blood specimens, maintaining
emergency vascular access, and for haemodynamic monitoring.
Risk factors: mechanical complications (malposition, occlusion, dislodgement, tamponade),
infection, pneumothorax, thrombosis
Insertion:
Ask nurse to complete the checklist and to stop you if you are about to breach the rules !
• maximal sterile barriers for insertion
• use chlorhexidine lollipops – the use of liquid in pot is absolutely forbidden !
• dedicated equipment cart easily accessed
• use of a procedural pause ―stop the line‖ if barrier precautions are breached
• use of chlorhexidine impregnated patch at insertion site
• appropriate dressings used over insertion site
• radiographical confirmation of catheter tip position
• always transduce pressure waveform (with heparin !!)
• details of insertion documented in patient record
Maintenance:
• commence Heparin 10U/kg/hr in patients < 5kg
• daily review of lines with prompt removal of unnecessary lines
• use of closed needless mechanical valve on each lumen
[1] http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5110a1.htm
[2] The Pediatric Infectious Diseases Journal, 2010; Sept 29(9): 812 -815: Prasad et al: Risk Factors for Catheter-associated
Bloodstream Infections in a Pediatric Cardiac Intensive Care Unit.

ANESTHESIA: ANALGESIA AND SEDATION
Basic Pharmacology for PICU
Routes of administration and systemic absorption of drugs:
Rate of systemic absorption determines onset, intensity and duration of action. Drug
solubility and blood flow to the site of absorption are the most important factors:
Oral/enteral:
• most convenient & economic route of administration
• complicated by nausea/emesis & irregularities in absorption
• principle site of absorption is the small intestine
• GI mucosa and the liver contribute to extraction and metabolism of drugs
Oral/nasal transmucosal: drains to the SVC and / or VIJ and bypasses 1st pass hepatic
metabolism
Rectal:
• highly unpredictable and irritant to rectal mucosa
• absorption is slow due to the small available surface area
• distal rectal administration will bypass 1st pass hepatic metabolism
• proximal rectal administration will not bypass 1st pass hepatic metabolism
Parenteral:
• includes subcutaneous, intramuscular and intravenous routes
• absorption is more reliable and complete
• IV administration avoids factors that limit systemic absorption by other routes and is a
more comfortable way to administer irritant drugs
Neuraxial:
• epidural route is used to provide analgesia and anesthesia
• significant systemic absorption may occur through the epidural venous plexus especially
with lipid soluble drugs and continuous infusions (eg. fentanyl)
• intrathecal or spinal administration rarely causes unwanted systemic effects
Distribution of drugs after systemic absorption:
Highly perfused tissues (heart, lungs, brain, kidneys and liver) receive a disproportionate
amount of drug and initially sequester it from the plasma. Once plasma concentration falls
following a bolus dose, drug will redistribute back into the plasma.
Following a bolus dose, plasma concentration first falls rapidly during the distribution phase
and then more gradually during the elimination phase.
Remember that increasing an infusion of a drug to increase its desired effect should
be preceded by a repeat bolus / load otherwise its effect will take ~5 half times !
Repeated large doses and / or prolonged infusions will saturate inactive tissues which will
then act as reservoirs and prolong the duration of action of drugs.
Pharmacokinetic variables:
Volume of distribution (Vd):
• apparent volume a drug is injected into (calculated from dose and initial plasma
concentration before any clearance)
• determinant of elimination half time (t½β)
• depicts the distribution characteristics of a drug in the body
• used to determine loading doses
• mainly influenced by physicochemical characteristics of the drug
Metabolism:
• hepatic microsomal enzymes are responsible for most drug metabolism
• hepatic extraction may be perfusion dependent (affected by hepatic blood flow) or capacity
dependent (affected by ionisation and protein binding)

• lungs (eg. catecholamines), kidneys (eg. morphine) and the GIT have considerable drug
metabolising ability
• Plasma cholinesterase and non-specific esterases are important in drugs containing ester
bonds (eg. Esmolol, Succinylcholin)
• Hoffman elimination is spontaneous non-enzymatic breakdown (eg. cisatracurium)
Clearance (Cl):
• volume of plasma cleared of drug per unit time
• determinant of elimination half time (t½β)
• metabolism, excretion and non-organ clearance (eg. ester hydrolysis) all contribute to
clearance
• may be 1st order (proportional to plasma concentration) or zero-order (constant amount of
drug cleared independent of plasma concentration)
Half times:
• time necessary for the plasma concentration of a drug to decrease by 50% (t½β ~ Vd/Cl)
• can be during distribution ( t½α) or elimination (t½β)
• plasma concentration does not always correlate with the clinical effect of the drug
• elimination half time determines the dosing interval to achieve steady state (~5 half times)
• context sensitive half time (CSHT) is the time necessary for the plasma drug concentration
to decrease by 50% after ceasing a continuous infusion of a specific duration (context =
duration of infusion)
Effect site equilibration time (ESET):
• delay between IV administration and onset of clinical effect reflects the delay in delivery of
the drug to its site of action and subsequent dynamic response
• mainly determined by physicochemical properties of the drug
• important in determining dosing intervals when titrating to effect
Physicochemical properties of drugs:
Ionization: most drugs are present as both ionized and non-ionized molecules / proportion
is determined by the pK of the drug and the pH of the surrounding fluid / only non-ionised
drug is free to diffuse across membranes, be metabolized or be excreted
Protein binding: a variable amount of drug may be bound to various plasma proteins which
affects distribution / clinically significant protein binding is > 90% / acidic and neutral drugs
generally bind to albumin and alkaline drugs generally bind to alpha1-acid glycoprotein / only
unbound drug is free cross membranes, be metabolized or excreted
Molecular size: small molecules diffuse much more readily than large ones.
Lipid solubility: ability to physically diffuse through cell membranes (does not necessarily
correlate with rapid onset of action).
Isomerism: mixtures often contain either inactive isomers or isomers that have different and
/ or adverse clinical effects (racemic and non-enantiopure preparations can be considered
mixtures of different drugs).
Individual variability in dynamic response:
• The response (therapeutic and adverse effects) to many drugs varies widely among
patients.
• There is up to a five-fold range of plasma concentrations required to achieve the same
pharmacologic effect in different individual patients.
• There is up to a two-fold range of plasma concentrations required to achieve the same
pharmacologic effect in the same patient using the same dosing regime.
• Absorption and bioavailability as well as variations in cardiac, renal and hepatic function
contribute to inter- and intra-individual variability.
• Enzyme activity (eg. induction/inhibition) and genetic factors (eg. fast / slow acetylators)
also play a role.

Effects of age and disease:
Renal disease will affect drugs excreted by the kidneys to an extent proportional to the
degree to which the drug depends on renal excretion.
Hepatic disease alters plasma protein levels (decreased binding), increases Vd (ascites),
reduces metabolism and may alter bioavailability (decreased 1st pass metabolism and / or
porto-caval collaterals).
Neonates and Infants:
• proportionally more water, larger intravascular volume and larger highly perfused organs
• immature blood-brain barrier makes them more sensitive to drugs acting in the CNS
• immature and inefficient hepatic metabolizing capacity and lower plasma protein levels
• GFR < 10% of adult values will affect clearance

Sedatives and Analgesics
Intravenous anesthetic agents (see Table):
• classified as barbiturates (Thiopentone) and non-barbiturates (Propofol and Ketamine)
• Thiopentone use is largely limited to induction in status epilepticus and for treatment of
raised ICP; it has no analgesic properties and is in fact anti-analgesic at sedative doses.
• Propofol is suitable for induction (bolus) and maintenance of sedation / anesthesia
(infusion); it is suitable for discrete painful procedures but has only minimal analgesic
properties at sedative doses and so must be combined with a suitable analgesic.
• Propofol is a direct myocardial depressant and so should be used in caution in patients in
(or at risk of) low cardiac-output syndrome (LCOS). It obtunds the normal baroreceptor reflex
and so causes a decrease in blood pressure and heart rate.
• Ketamine is a dissociative anesthetic that is also a potent analgesic; it is suitable for
discrete painful procedures but increases respiratory secretions and is complicated by
psychadelic phenomena. Midazolam is suitable to treat or obviate Ketamine's emergence
phenomena but will prolong recovery time.
• combined Ketamine and Propofol in a ratio ranging from 1:1 to 1:4 (Ketofol) is becoming a
popular awake-sedative to facilitate medical procedures.
Narcotics (see Table):
• Morphine, Fentanyl and Methadone are effective analgesics and sedatives; Oxycodone is
also a popular analgesic but is less sedating.
• Levels of sedation, analgesia and respiratory depression do not correlate (patients may be
well sedated and have respiratory depression but not have adequate analgesia).
• Morphine is not a suitable narcotic for discrete painful procedures due to its long and
unpredictable effect site equilibration time (Fentanyl is more appropriate).
• Fentanyl is often used epidurally and results in significant systemic absorption of drug and
resulting side effects.
• Sufentanil, Alfentanil and Remifentanil are phenylpiperidine narcotics used to provide the
analgesic component of general anesthesia. They are very infrequently used in PICU.
• All have predictable effects which include respiratory depression, cough suppression,
sedation, meiosis, biliary spasm, constipation, nausea and vomiting, urinary retention and
cutaneous flushing (especially about the face).
Benzodiazepines (see Table):
• Midazolam and Diazepam are effective sedative agents commonly used in PICU.
• They are direct myocardial depressants via blockade of voltage-gated calcium channels
(use carefully in patients with LCOS).
• Midazolam is also used to acutely treat seizures in bolus doses and in infusions (up to
1mg/kg/hour).
• They are less likely to produce withdrawal syndromes than barbiturates and narcotics (but
no analgesic effect).
Alpha2 agonists (see Table):
• Clonidine and Dexmedetomidine are sedative / anaesthetic agents employed as sedatives
in PICU; they also treat symptoms of drug withdrawal.
• Their main advantage is lack of respiratory depression which allows quicker weaning of
mechanical ventilation.
• They obtund central (brain and spinal cord) sympathetic outflow resulting in negative
inotropy and chronotropy and so should not be combined with direct myocardial depressants
(Benzodiazepines, Propofol etc.) in patients at risk of (or in established) LCOS.
• They cannot be bloused as this can lead to transient alpha1-agonism and severe
hypertension.

Local anaesthetics:
• Local anaesthetics block voltage gated sodium channels and so prevent conduction along
central and peripheral nerve pathways.
• Lignocaine is commonly locally infiltrated for short painful procedures (eg. suturing,
insertion of chest drains etc).
• Bupivacaine and Ropivacaine are generally used for regional blocks and neuraxial
infusions.
• Levobupivacaine (S-bupivacaine) and Ropivacaine are enantiopure preparations.
Cardiotoxicity is less.
• 0.5% solutions contain 5mg/mL; 1% solutions contain 10mg/mL; 2% solutions contain
20mg/mL etc. (1% = 10mg/ml)
• Onset of effect is related to the pKa of the drug; potency is related to lipid solubility; and
duration of action is related to protein binding.
• Systemic absorption of local anaesthetics depends on site of infiltration: intercostal >
subarachnoid > epidural > brachial plexus > femoral > subcutaneous.
• Vasoconstrictors (Adrenaline) slow systemic absorption and increase the maximum safe
dose
• EMLA is a mixture of 2.5% Lignocaine and 2.5% Prilocaine used for topical anaesthesia
prior to cannulation / incision; Prilocaine can induce Methaemoglobinaemia and application
to mucous membranes will result in rapid systemic absorption of drug.
• CNS toxicity manifests first as excitatory phenomena (circumoral tingling, tinnitus,
dizziness and tremors / seizures) followed by CNS depression (unconsciousness, apnoea
and coma).
• CVS toxicity manifests as systemic hypotension, myocardial depression, ventricular
arrhythmias and cardiovascular collapse.
• Treatment of local anaesthetic toxicity is by supportive therapy (airway management,
treatment of seizures with Benzodiazepines, fluids +/- inotropes / vascoconstrictors) and
administration of 20% lipid emulsion (Intralipid) if in cardiac arrest: 1.5mL/kg over 1 minute
followed by an infusion of 0.25-0.5ml/kg/min; repeat bolus doses every 5 minutes during
CPR.
Non-steroidal anti-inflammatory drugs (NSAIDs):
• Classified as specific (COX-2 eg. Parecoxib) or non-specific (COX-1 and COX-2 eg.
Ibuprofen).
• Adverse GI effects are due to decreased mucosal blood flow and decreased secretion of
mucus and bicarbonate.
• Platelet thromboxane A2 is produced from prostaglandins and so NSAIDs impair platelet
aggregation.
• Prostaglandins are vasodilators involved in physiologic control of vasomotor tone
(especially in the kidneys) and their inhibition leads to unopposed vasoconstriction.
• Inhibition of prostaglandin synthesis leads to shunting of arachnidonic acid to lypoxygenase
which is a bronchoconstrictor.
• Specific COX-2 inhibitors are considered to lack effects on platelets and the GIT but will
still affect vasomotor tone.
• Their use in PICU needs careful consideration due to their wide range of potential side
effects.
• Paracetamol is generally considered a (central) COX-3 inhibitor; it also acts peripherally by
inhibiting bradykinin-chemoreceptor associated pain impulse generation.

Other (see Table):
• Chloral hydrate is a prodrug that produces the halogenated alcohol Chloroethanol; its
mechanism is poorly understood but probably acts in a similar way to the volatile
halogenated gases via central GABA-A receptors.
• First-generation antihistamines (eg. Promethazine, Cyclizine etc.) are also effective
sedatives by virtue of their anticholinergic properties; they are generally only used when
specific antihistaminergic and / or anticholinergic properties are desired (eg. antisialogogue
for secretions, anti-tussive).

Table: intravenous anesthetic agents
Thiopentone Propofol Ketamine
Type/class Barbiturate Isopropylphenol Phencyclidine
Mechanism GABAA & glycine agonist
GABAA & glycine direct
agonist and central
nicotinic antagonist
(Possible 5HT3 blockade)
NMDA non-competitive
antagonist & blocks central
catecholamine reuptake
Oral
bioavailability
- - 25%
Oral dose n/a n/a 5mg/kg
IV Bolus 2-7mg/kg 1.5-2.5mg/kg
0.25-0.5mg/kg (analgesia)
1-5mg/kg (GA)
IV Infusion 1-5mg/kg/hour
1-4mg/kg/hour (sedation)
5-15mg/kg/hour (GA)
10-40mcg/kg/hour
Onset time IV < 30seconds < 30seconds 30-60seconds
ESET 30 seconds < 30 seconds 60seconds
pKa 7.6 11 7.5
UNionised
fraction
60% > 99% 45%
Protein
binding
80% 99% 25%
Vd 2.5L/kg 4L/kg 3L/kg
Clearance 3mL/min/kg 50mL/min/kg 15mL/min/kg
t ½-dist 8minutes 4 minutes 12minutes
t ½-elim 12hours 30-60minutes 2-3hours
Metabolism
Hepatic (may become zero-
order with prolonged infusion)
Some active metabolites
-Hepatic (CYP2C9 & 2B6)
& extrahepatic (site/s
unknown)
Inactive metabolites
Hepatic
Active metabolites
Excretion Urine Urine Urine
Hepatic failure No effect No effect Decreased clearance
Renal failure
Active metabolites will
accumulate
No effect No effect
Pros
Rapid onset
Anticonvulsant
Can produce isoelectric EEG
(maximal decreased cerebral
metabolic O2 demand)
Rapid onset & titratability
Bronchodilator
Will obtund airway reflexes
Anticonvulsant
Antiemetic & antipruritic
properties at low doses
Can produce isoelectric
EEG
Mild analgesic properties
Stable CSHT (< 40mins
even after > 8 hrs infusion)
Intense analgesia at low dose
Favourable haemodynamic
profile due to increased central
sympathetic outflow
Bronchodilator
Prevents & treats opioid
tolerance
No respiratory depression /
apnoea
Cons
Resp depression / apnoea
Antanalgesic
Can produce paradoxical
excitement
Will accumulate with prolonged
infusion (long CSHT)
Tolerance & withdrawal are a
problem
Resp depression / apnoea
Myocardial depressant
Can cause a refractory
bradycardia (need β-
agonist)
Rarely causes propofol-
infusion syndrome
Formulation contains
soybean oil & egg lecithin
Emergence delirium
(especially in older patients –
consider midazolam)
Increased secretions (consider
glycopyrrolate)
BrainZ/BIS inaccurate
Other points
BP (SVR)
HR (reflex)
Wont obtund airway reflexes
Racaemic formulation
BP
(SVR & CO)
HR (obtunded
baroreceptor reflex)
EEG dissociation between
thalamus & cortex
Wont obtund airway reflexes
Typical induction agent in
asthma & sepsis

Table: Benzodiazepines
Midazolam Diazepam Flumazenil
Type/class BDZ BDZ BDZ
Mechanism
GABAA receptor indirect-
agonist
GABAA receptor
indirect-agonist
BDZ receptor competitive antagonist
Oral bioavail 40% 95% 25%
Oral dose 0.5mg/kg up to 20mg 0.05-0.2mg/kg n/a
IV Bolus
0.05-0.2mg/kg
up to 5mg/dose
0.05-0.4mg/kg
up to 10mg/dose
8-15mcg/kg
up to 200mcg/dose
IV Infusion 10-100mcg/kg/hour n/a 2-10mcg/kg/hour
Onset time
IV
1-2mins 1-2mins 1-2mins
ESET 5mins 5mins 5-10mins
pKa 6.2 3.3 1.8
%
UNionised
90% >99% >99%
Protein
binding
95% 95% 50%
Vd 1.5L/kg 1.5L/kg 0.5L/kg
Clearance 10mL/min/kg 1mL/min/kg 20mL/min/kg
t ½-dist 5mins 5mins 5mins
t ½-elim 1-4 hours 24-36 hours 60mins
Metabolism
Hepatic (CYP3A4)
Active metabolites
Hepatic (CYP3A4/5)
Active metabolites
Hepatic
No active metabolites
Excretion Urine Urine
90% urine
10% bile
Hepatic
failure
Decreased clearance Decreased clearance Decreased clearance
Renal failure
Active metabolite may
accumulate
Active metabolites will
accumulate
No effect
Pros
Sedation, amnesia &
anxiolysis
Anticonvulsant
Decreases cerebral
metabolic O2 demand
Effective orally
Sedation, amnesia &
anxiolysis
Anticonvulsant
Decreases cerebral
metabolic O2 demand
Allows specific reversal of BDZ component
of resp depression and / or polypharmacy
overdose
Rarely causes acute anxiety &/or agitation
Cons
Resp depression
Can cause paradoxical
excitement
Resp depression
Can cause paradoxical
excitement
Painful on injection
Can precipitate seizures in epileptics on
maintenance BDZs
Other points
BP
(SVR & CO)
[HR (reflex)]
BP
(SVR & CO)
[HR (reflex)]
Is probably a partial agonist

Table: Narcotics
Morphine Fentanyl Methadone Naloxone
Type/class
Phenanthrene
opiate
Phenylpiperidine
opioid
Diphenyl-propylamine
opioid
Phenanthrene opioid
Mechanism
Non-specific OR
agonist
MOR agonist with
some mild activity at
KORs
MOR agonist (L-
isomer) & NMDA
antagonist (D-isomer)
Non-specific OR
competitive antagonist
Oral
Bioavail.
30% n/a 75% <1%
Oral dose 0.2-0.5mg/kg q4-6h n/a 0.1-0.2mg/kg q6-24h n/a
IV bolus
dose
0.05-0.2mg/kg 1-10mcg/kg 0.1mg/kg 10mcg/kg
IV infusion 5-100 mcg/kg/hr 1-10 mcg/kg/hr n/a 10 mcg/kg/hr
Onset time
IV
15-30mins 1-2mins 10-20mins 1-2mins
ESET 30-90mins 3-6mins 10-20mins 5-10mins
pKa 8.0 8.4 9.2 7.9
%
UNionised
25% 10% 1% 30%
Protein
binding
35% 85% 90% 50%
Vd 3L/kg 4L/kg 3.5L/kg 0.2L/kg
Clearance
25
mL/min/kg
10-20 mL/min/kg 1-3 mL/min/kg 30 mL/min/kg
t ½-dist 2-3mins 1-2mins 1-2 mins -
t ½-elim 2-4hours 2-4hours 18-36 hours 45-60mins
Metabolism
Hepatic & renal
10% to active M6G
Hepatic (CYP3A4)
Hepatic (CYP3A4)
Hepatic
No active metabolite
Excretion
90% urine
10% bile
90% bile
10% urine
50% urine
50% bile
Urine
Hepatic
failure
May precipitate
encephalopathy
No effect reduced clearance reduced clearance
Renal
failure
Morphine & M6G
will accumulate
No effect No effect No effect
Pros
No myocardial
depression
Sedation &
euphoria
Antitussive
No myocardial
depression
Sedation & euphoria
Antitussive
No histamine release
Effective enterally
Helpful in withdrawal
syndromes
Suitable for chronic
pain (NMDA actions)
Acts rapidly & is
titratable
Antiinflammatory
properties
Cons
Respiratory
depression
Histamine release
Nausea & vomiting
Pruritis
Urinary retention
Constipation
Respiratory
depression
Nausea & vomiting
Pruritis
Urinary retention
Constipation
Prolonged CSHT
Respiratory
depression
Nausea & vomiting
Constipation
Histamine release
possible but rare
Prolongs QT interval
Can precipitate acute
withdraw
Rarely may cause
pulmonary oedema &
Arrhythmia
Usually needs repeat
dosing
Other points
Meiosis
 HR & BP (SVR)
Meiosis
Meiosis
1mcg/kg effective for
narcotic pruritis
BP may rise or fall

Table: Alpha2 agonists
Clonidine Dexmedetomidine
Type/class Synthetic imidazoline Synthetic imidazoline
Mechanism α2 adrenoceptor partial agonist α2 adrenoceptor agonist
Oral bioavail >99% 15%
Oral dose 1-5mcg/kg up to 300mcg n/a
IV bolus dose 1-5mcg/kg 1-2mcg/kg
IV infusion
dose
0.5-2mcg/kg/hour
0.2-0.7mcg/kg/hour (sedation)
5-10mcg/kg/hour (GA)
Onset time IV 10-30minutes 10minutes
ESET
20-30minutes 10-20minutes
pKa 8.0 7.1
UNionised % 20% 50%
Protein
binding
20% 95%
Vd 2L/kg 1.5L/kg
Clearance 5mL/min/kg 10mL/min/kg
t ½-dist 30minutes 10 minutes
t ½-elim 12-18hours 2-3hours
Metabolism
50% hepatic
50% excreted unchanged
Hepatic
Excretion Urine (50% unchanged) Urine
Hepatic
failure
No effect Decreased clearance
Renal failure Active drug will accumulate No effect
Pros
Effective sedative
No respiratory depression
Spinal-mediated analgesia (very effective
neuraxially)
Known to be useful in opioid & alcohol
withdrawal syndromes
Raises the shivering threshold
Prolongs regional block by local anaesthetics
Effective sedative
No respiratory depression
Spinal-mediated analgesia
Useful for symptoms of opioid withdrawal
Raises shivering threshold
Prolongs regional block by local
anaesthetics
Short(er) half time
Cons
Rapid IV administration will agonise α1 receptors
(BP)
Negative inotropy & chronotropy
Dry mouth
Rebound hypertension can occur (worse if
patient is on a TCA or β-blocker)
Long half time
Rapid IV administration will agonise α1
receptors (BP)
Negative inotropy & chronotropy
Dry mouth
Cannot be used neuraxially due to glycine in
preparation
Other points
HR & BP
CO
Dry mouth may be used therapeutically if
secretions are an issue
HR & BP
CO
Dry mouth may be used therapeutically if
secretions are an issue

Table: Others
Chloral hydrate Promethazine
Type/class Halogenated alcohol Phenothiazine
Mechanism
Prodrug – below data is for trichloroethanol
(active drug)
Probably a GABAA agonist
H1 receptor antagonist & anticholinergic
(antimuscurinic)
Oral bioavail >99% 25%
Oral dose 10-100mg/kg 0.25-1.5mg/kg
IV bolus dose n/a 0.25-1.5mg/kg
IV infusion
dose
n/a n/a
Onset time IV 15minutes (oral) 30-60minutes
ESET 30-60minutes (oral) 1-3hours
pKa 12.7 9.1
UNionised % >99% <1%
Protein
binding
50% 80%
Vd 1L/kg 7L/kg
Clearance not known 15mL/min/kg
t ½-dist n/a 1-2hours
t ½-elim 4-8hours 12hours
Metabolism
Hepatic
Metabolites of trichloro-ethanol are inactive
Hepatic (CYP2D6)
Inactive metabolites
Excretion Urine Urine
Hepatic
failure
Decreased clearance Decreased clearance
Renal failure No effect No effect
Pros
Effective sedative & anxiolytic
Rapid onset following enteral administration
Mild anticonvulsant
Relatively wide therapeutic index
Minimal interference with REM-sleep
Effective antihistamine & antiemetic at low
doses
Effective sedative/hypnotic at high doses
Antitussive
Effective in motion sickness
Useful in allergic pruritis but not opioid induced
pruritis
Respiratory depression is rare
Cons
Respiratory depression in high doses
Irritant to GI mucosa
Arrhythmias in high doses
Trigger for porphyria
Patients can develop tolerance & withdrawal
Anticholinergic effects (dry mouth, blurred
vision, urinary retention etc)
Central anticholinergic syndrome in overdose
Prolonged QT-interval & AV-block
Paradoxical excitement may occur
Other points
BP (SVR)
HR (reflex)
Actual half time of chloral hydrate is minutes
(metabolised by esterases)
[HR & BP]
Antidopaminergic properties
Local anaesthetic properties

ANESTHESIA: MUSCLE RELAXATION
Definition: Muscle relaxants block transmission at the neuromuscular junction (NMJ) by
interfering with nicotinic cholinergic receptors (AChRs). They are large polar molecules with
small volumes of distribution that are not orally bioavailable and do not cross the placenta or
blood-brain barrier. They have no analgesic, anaesthetic or amnestic properties and so
should never be given without appropriate sedative / anaesthetic drugs.
The clinical indications for muscle relaxation are:
• to facilitate intubation of the trachea
• to improve surgical and / or procedural working conditions
• to facilitate intra-hospital and inter-hospital transfers
• to prevent shivering in patients being therapeutically cooled
• to facilitate mechanical ventilation including using mechanical ventilation to manipulate
PaCO2 and acid-base status
• to improve post-operative stability (especially in high-risk cardiac surgery and laryngo-
tracheal surgery with or without complex / abnormal airway anatomy)
Drugs are classified as depolarising (mimic the actions of ACh) and non-depolarising
(interfere with the actions of ACh).
Suxamethonium is the only depolarising neuromuscular blocking drug still in clinical use.
Non-depolarising neuromuscular blocking drugs are classified as long-acting (pancuronium),
intermediate-acting (rocuronium, vecuronium, atracurium & cisatracurium) and short-acting
(mivacurium).
Drug selection is influenced by desired speed of onset, duration of action and the possibility
of drug induced side effects (see table of drugs).
Among suxamethonium‘s myriad of adverse effects it is also a known trigger for malignant
hyperthermia (genetically abberant muscle sarcoplasmic reticulum calcium channels) – the
treatment is active cooling and Dantrolene 1mg/kg up to 10mg/kg.
Patients with genetically abdnormal pseudocholinesterase will have prolonged
neuromuscular blockade with suxamethonium (choline apnoea) – they need supportive care
until it is cleared (severe cases require dialysis to clear the drug) and an assessment of their
pseudocholinesterase function (dibucaine number).
Suxamethonium and rocuronium (see Table: Muscle relaxans rapid onset) are the only
drugs capable of producing intubating conditions in 60 - 90 seconds and so are the only
drugs used for rapid sequence induction (RSI). Suxamethonium has a brief duration of
action where as an RSI-dose of rocuronium will have a prolonged duration of action.
The duration of action of non-depolarising neuromuscular blocking drugs is prolonged by
hypokalaemia, hypocalcaemia, hypoproteinaemia, hypermagnesaemia, dehydration,
acidosis and hypercapnoea.
Potency of neuromuscular blocking drugs is described by the effective dose (ED) necessary
to depress single-twitch depression by 95% in the adductor pollicis muscle – ED95
(Intubating doses are generally two times the ED95 dose; the RSI-dose for rocuronium is
four times its ED95); potency is Centrally located muscles (larynx, jaw and diaphragm)
develop neuromuscular blockade faster, experience less profound block and recover more
quickly than in more peripherally located muscles (adductor pollicis). Eyelash reflex and
orbicularis inversely related to onset time.

Monitoring of depth of neuromuscular blockade:
Nerve stimulators are used to monitor the depth of neuromuscular blockade.
There is a margin of safety regarding nAChRs at the NMJ and the generation of a myocyte
action potential such that >75% of nAChRs must be occupied by drug before clinically
significant (and detectable) blockade is apparent.
Neuromuscular blocking drugs must occupy at least 75% of nAChRs before there is clinically
significant and detectable blockade (this is the margin of safety with regard to nAChR
numbers and transmission at the NMJ).
The ulnar or radial nerves are commonly used with the negative electrode on the volar
surface of the wrist directly over the nerve to be stimulated and the positive electrode at least
3cm distal where it cannot interfere with the relevant muscle groups.
A current of 60mA (maximum 80mA) is applied for 0.1ms (maximum 0.3ms) per stimulation;
the patterns of stimulation used in PICU are the train-of-four (TOF) count, tetanic (>30Hz)
stimulation and post-tetanic count.
The TOF ratio is the ratio of the height of the first twitch (T1) to the fourth twitch (T4) – this is
not easily interpretable if only using visual and tactile evaluation of the response. The TOF
count (absolute number of twitches) is easier to detect and interpret:
• T4 begins to reduce in height at >70% receptor occupancy;
• T1 starts to reduce in height at >80% occupancy;
• T4 disappears at >90% occupancy;
• T1 disappears at >95% occupancy.
Tetanic stimulation (usually 50Hz) is known to increase subsequent twitch height either by
mobilising ACh stores and / or increasing calcium influx into the nerve ending; When the
TOF count is zero (>95% blockade) then a tetanic stimulation and a post-tetanic (TOF) count
can help define deep neuromuscular blockade.
The effects of tetany last for up to 6 minutes and this must be taken into consideration if
repeat testing occurs.
If the TOF-count is zero and the post-tetanic count is also zero – this signifies either very
deep neuromuscular blockade or a malfunctioning nerve stimulator (test it on yourself).
Reversal of neuromuscular blockade:
Antagonist-assisted reversal of neuromuscular blockade using anticholinesterases
(edrophonium, neostigmine or pyridostigmine) reflects their inhibition of acetylcholinesterase
(AChE) and the resulting increased ACh at the NMJ to compete for nAChR binding sites.
Neostigmine is generally used at a dose of 4 - 7mcg/kg and is more suitable for
reversing deeper levels of block.
Anticholinesterases produce typical and expected muscarinic side effects (mainly
bradycardia, bronchoconstriction, increased secretions & GI hyper-peristalsis) and so should
be given with an antimuscarinic anticholinergic drug such as Atropine (20mcg/kg) or
Glycopyrrolate (10mcg/kg).
Sugammadex is a cyclodextrin that encapsulates rocuronium and vecuronium and
effectively neutralises them; remaining drug diffuses away from the NMJ and its effects are
reversed.
It acts within 2 minutes and has no other effects (as yet). The complex is excreted in the
urine. The dose for routine reversal is 2 - 4mg/kg; the dose for emergent reversal in a cant
intubate-can‘t ventilate scenario is 16mg/kg.

Table: Muscle Relaxans rapid onset
Suxamethonium Rocuronium
Type/class Dicholine ester
Aminosteroid
(intermediate acting)
ED95 0.3mg/kg 0.3mg/kg
Intubating
dose
1mg/kg (adults)
2mg/kg (children)
3mg/kg (neonates)
0.6mg/kg
1.2mg/kg (RSI)
Onset time 30-60seconds 30-90seconds
Recovery
time
3-5minutes 20-35minutes
Infusion
dose
n/a 5-15mcg/kg/min
VD 0.17L/kg 0.3L/kg
Protein
binding
99% 30%
Clearance 40mL/kg/min 4mL/kg/min
t½-elim 3-5minutes 80minutes
Metabolism Plasma pseudocholinesterase No significant metabolism
Excretion
Resulting choline is taken up into nerves
<5% unchanged in urine
Bile (50% unchanged)
Urine (30% unchanged)
Hepatic
failure
No effect t½-elim up to 100 minutes
Renal failure No effect t½-elim up to 100 minutes
Pros Rapid onset & intense paralysis make it suitable for RSI
Suitable for RSI due to shorter onset
time
Minimally affected by renal & hepatic
impairment
May be reversed with sugammadex
Cons
Raised intra-gastric, intra-ocular & intra-cranial pressures
Fasciculations that can lead to severe myalgia & even
rhabdomyolysis
Bradycardia (muscarinic) +/- brady-arrhythmias
Hyperkalaemia (more so with neuromuscular disease &
burns)
Malignant hyperthermia
Choline apnoea
Anaphylaxis
Will accumulate with prolonged
infusions (ensure monitoring of depth
of blockade)
Other points
80% of an administered dose is hydrolysed before
reaching the NMJs
Repeat doses should always be accompanied by an
anticholinergic (consider routine anticholinergic
administration in infants)
There are rare reports of anaphylaxis
It does cause a small increase in
intra-occular pressure

Table: Muscle Relaxans slow onset
Vecuronium Pancuronium Cisatracurium
Type/class
Aminosteroid
Aminosteroid
(long acting)
Benzylisoquinolinine
ED95 0.05mg/kg 0.06mg/kg 0.05mg/kg
Intubating
dose
0.1mg/kg 0.1mg/kg 0.1mg/kg
Onset time 3-5minutes 3-5minutes 3-5minutes
Recovery
time
20-35minutes 60-90minutes 20-35minutes
Infusion
dose
0.5-2mcg/kg/min n/a 1-10mcg/kg/min
VD 0.27L/kg 0.26L/kg 0.2L/kg
Protein
binding
60-90% 15-30% unknown
Clearance 5mL/kg/min 2mL/kg/min 5mL/kg/min
t½-elim 60minutes 132minutes 25minutes
Metabolism
Hepatic with some active
metabolites
Hepatic with some
active metabolites
Hoffman elimination (no active metabolites)
Excretion
Urine
Hepatic
failure
t½-elim up to 3 hours t½-elim up to 6 hours No change
Renal
failure
t½-elim up to 2 hours t½-elim up to 48 hours No change
Pros
Commonly used
medication with
predictable onset &
duration of action
May be reversed with
sugammadex
Long acting
(decreased dosing
requirements)
Non-organ clearance makes it unaffected
by renal and/or hepatic impairment
Stable offset time after prolonged infusions
due to rapid Hoffman elimination
Cons
Will accumulate with
prolonged infusion
(ensure monitoring of
depth of blockade)
Minimally metabolized
so sensitive to effects
on hepatic & renal
function
Risk of arrhythmias in
patients on digoxin
Potent drug with prolonged onset time
Other
points
Large doses may cause
a slight (10-15%) drop in
SVR and BP
10-15% increase in HR
(mainly anticholinergic
effect)
Mild increase in BP
secondary to increased
HR (no inotropy)
Useful for obviating HR
effects of induction
doses of narcotics
It may decrease the PT
and APTT
One of 10 stereoisomers of atracurium
(atracurium is not used often anymore due
to histamine release and has a metabolite
that can cause convulsions).

ANESTHESIA: TOLERANCE AND WITHDRAWAL
Definition: Tolerance is the development of the need to increase the dose of a drug to
achieve the same effect previously achieved with a lower dose.
• Duration of therapy is the major factor associated with onset of tolerance and physical
dependence and continuous infusions induce tolerance more rapidly than intermittent and
enteral therapy.
• Tolerance begins within 48 hours of continuous infusion but typically takes 2 – 3 weeks of
regular intermittent use to develop to a clinically significant extent
• Long-term pharmacodynamic tolerance can persist for months-years in some individuals.
• The mechanisms are poorly understood but probably involve changes in receptor number
(down-regulation) and modulation of intracellular signalling pathways leading to receptor
desensitisation.
• Genetics also play a role in both response to opioids and the development of tolerance and
physical dependence but its clinical importance is still being defined.
• Physical dependence also develops to some degree after only 48 hours of continuous
infusion but requires 4 weeks of regular intermittent use to become established.
• Discontinuing a drug after physical dependence is established will produce a typical
withdrawal abstinence syndrome.

ANESTHESIA: WEANING OPIODS AND SEDATION
Withdrawal from drugs (principally opioids) prolongs hospital admissions and causes
morbidity !
Gradual weaning of drug dosing aims to prevent the onset of withdrawal abstinence
syndromes:
• regime one: 10% reduction in original dose per day weaning over 10days or
• regime two: 20% reduction in original dose per day weaning over 5 days
• regime three: 20% reduction in original dose every 2nd day weaning over 10days
All are equally effective and the shorter 5-day wean is not associated with any
increased withdrawal symptoms requiring reinstitution of drug therapy !
The choice of regime is typically arbitrary based on length of therapy and clinician choice.
DOSE CONVERSION of IV and ENTERAL
Dose escalation and / or opioid rotation are both effective ways to combat tolerance
(although there is an inevitable amount of cross tolerance) but not physical dependence.
Converting between opioids and route of administration involves documenting the total 24-
hour dose being administered and then using the conversion table and calculating a total
daily dose of the new drug via the new route.
Drug IV equivalent IV : morphine ratio enteral equivalent IV : enteral ratio
Morphine 10mg 1 : 1 30 mg 1 : 3
Codeine 100mg 10 : 1 200mg 1 : 2
Oxycodone 10mg 1 : 1 20mg 1 : 2
Fentanyl 100mcg 0.01 : 1 n/a n/a
Methadone 10mg 1 : 1 20mg 1 : 2
DOSE CONVERSION for iv Midazolam INTO oral Diazepam
[Midazolam IV [rate in mcg/kg/min] x weight x 24 ] x 0.5 = Diazepam oral
[1] Brunton, L et al (2010), Goodman and Gillman's the Pharmacological Basis of Therapeutics 12th Edition, McGraw Hill
Medical, New York
[2] Macintyre, PE et al (2010), Acute Pain Management: Scientific Evidence 3rd Edition, Australian and New Zealand College of
Anaesthetists and Faculty of Pain Medicine, Melbourne
[3] Miller, RD et al (2009), Miller's Anesthesia 9th Edition, Churchill Livingstone Elsevier, Philadelphia
[4] Peck, TE & Hill, S (2008), Pharmacology for Anaesthesia and Intensive Care 3rd Edition, Cambridge University Press,
Cambridge
[5] Sasada, M & Smith, S (2003), Drugs in Anaesthesia and Intesive Care 3rd Edition, Oxford University Press, Oxford
[6] Stoelting, RK & Hillier, SE (2005), Pharmacology and Physiology in Anesthetic Practise 4th Edition, Lippincott, Williams and
Wilkins, Philadelphia
[7] Pediatrics 2010 May;125(5):e1208-25: Anand et al: Tolerance and withdrawal from prolonged opioid use in critically ill
children.

ANESTHESIA: INTUBATION IN PICU
Indication:
• to secure the airway: severe airway obstruction / inadequate protective reflexes (coma or
prolonged seizures)
• to facilitate ventilation: hypoxaemic and / or hypercarbic respiratory failure
Intubation should NOT be attempted by the inexperienced if more skilled personnel
are available ! Two doctors always present if possible !
Assessment:
• how urgent is the intubation ?
• anatomical abnormality, which would predict difficult intubation ?
• any evidence of airway obstruction ?
• cardiovascular status – any hypovolaemia / hypotension ?
• is the patient fastened ?
Preperation equipment:
• Intubation drugs
• Volume replacement (10ml/kg NaCl 0.9%)
• ETT (size = age / 4 + 4 – for uncuffed ETT for cuffed ETT size = age / 4 + 3.5), one size
above and one size below calculated ETT
• Styllete, gum elastic bougie
• Laryngoscope with blade (check light bulb and battery)
• Magill‘s forceps
• Face Mask
• Guedel and nasopharyngeal airways
• self inflating bag and anaesthetic circuit
• suction equipment: Yankauer‘s sucker and suction catheters
• connector, cuff inflating syringe, tape
• CO2 detector
Procedure:
• monitor cardiovascular and respiratory status (ECG, SpO2, BP non-invasive / invasive)
• explain to patient / parents
• empty stomach if nasogastic tube is in situ
• position patient: neutral position in neonates, young children – sniffing position in older
children, adolescents
• preoxygenation for minimum two minutes
• consider atropine 20mcg/kg IV
• give analgesic agent
• give sedative agent
• apply gentle pressure to the cricoid
• check for bag and mask ventilation possible with appropriate visual inflation / deflation and
chest wall movement
• give paralysis agent
• continue bag and mask ventilation, while continuing to apply gentle cricoid pressure,
except in circumstances where bag and mask ventilation is contraindicated (see rapid
sequence induction)
• intubate orally, release cricoid pressure
• check ETT position: chest wall rise, auscultation and CO2 detector (@ Resuscitation drug
chart)
• once patient stabilized and appropriate ventilation, consider to change to a nasal ETT
• once ETT position confirmed, tape ETT
• insert nasogastric tube, empty stomach
• CXR to confirm position of ETT and nasogastic tube

• consider ongoing Analgesia and Sedation
• document event
Intubation Drugs:
@ Analgesia and Sedation in PICU
Analgesia Sedation Paralysis
cardiovascular stable, no airway
obstruction > 1 year
Fentanyl
1 – 2mcg/kg
or
Morphine
100mcg/kg
Propofol
1 – 2.5mg/kg
Vecuronium 0.1mg/kg
cardiovascular stable, with airway
obstruction > 1 year
Fentanyl
1mcg/kg
or
Morphine
100mcg/kg
Ketamine
1 – 2mg/kg
Vecuronium 0.1mg/kg
cardiovascular stable, no airway
obstruction < 1year
Fentanyl
1 – 2mcg/kg
or
Morphine
100mcg/kg
Midazolam
50 -100mcg/kg
Vecuronium 0.1mg/kg
cardiovascular stable, with airway
obstruction < 1 year
Always seek senior assistance !
Consider induction with volatile anaesthetic !
cardiovascular unstable, any age
Fentanyl
1 – 2mcg/kg
or
Morphine
100mcg/kg
Vecuronium
0.1mg/kg
Rapid Sequence Induction
Fentanyl
1 – 2mcg/kg
or
Morphine
100mcg/kg
Midazolam
50 -100mcg/kg
Rocuronium
1mg/kg
patients with raised ICP
Fentanyl
1 – 2mcg/kg
or
Morphine
100mcg/kg
Thiopentone
2 – 7mg/kg
Rocuronium
1mg/kg
anticipated difficult airway
Always seek senior assistance !
Consider induction with volatile anaesthetic !
Unexpected difficult intubation:
• call for help !
• restart bag and mask ventilation with gentle cricoid pressure
• optimize patient position
• consider bougie or stylete
• consider different laryngoscope blade
Cannot ventilate – Cannot Intubate:
• call for help !
• consider reposition of head
• jaw thrust
• insert Guedel / nasopharyngeal airway
• use both hands to hold mask
• release cricoid pressure
• consider laryngeal mask (LMA)

ANESTHESIA: INOTROPES AND VASOPRESSORS
Definition:
Inotropes: sympathomimetic agent which act on the sympathetic (or adrenergic) nervous
system (β-receptors) resulting in positive inotropic (increase in contractility), chronotropic
(increase in heart rate), dromotropic (increase in conduction of impulse) and lusitropic effect
(improved diastolic relaxation)
Vasopressors: sympathomimetic agent which act on the sympathetic (or noradrenergic)
nervous system (α-receptors) resulting in vasoconstrictor effect.
The ideal vasoactive support agent: effect on cardiac output / effect on SVR / effect on
myocardial oxygen consumption / no tachyphylaxis does not exist !
a) Sympathomimetics: endogenous catecholamines:
Adrenaline (β1 >> β2 and α1 > α2 agonist) via cAMP
Dose
mcg/kg/min
α1 α2 β1 β2 Clinical effect
- 0.05 ++ ++
▲ HR, SV, CO
(▼) SVR
0.05 – 0.10 +++ ▲ HR, SV, CO
0.10 – 0.20 +++ +++ +++
▲ HR, SV, SVR
(▼) CO
Side effects: increasing myocardial oxygen requirement, Tacharrhythmias, worsening diastolic function,
Tachyphylaxis, Hyperglycaemia, Lactate increase
Noradrenaline (α1 > α2 and β1 >> β2 agonist) via cAMP ?
Dose
mcg/kg/min
- 0.10 +++ ++ +++
▲ SVR, HR
(▼) CO
0.10 – 0.20 ++++ +++ +++
▲ SVR, HR, SV
▼ CO
Side effects: increasing myocardial oxygen requirement, can cause decrease in CO, Tachyphylaxis,
Hyperglycaemia
Dopamine (D1 and D2, higher doses: β1 >> β2 and α1 > α2 agonist) via cAMP. Precursor
of norepinephrine
Dose
mcg/kg/min
0.5 – 2 ▲ increased splanchnic perfusion
2 – 5 ++ ▲ HR, SV, CO
5 – 10 ++ ++
▲ HR, SV, SVR
(▼) CO
> 10 +++
▲ SVR
▼ CO
Side effects: increasing myocardial oxygen requirement, can cause decrease in CO, Tacharrhythmias,
Tachyphylaxis, Hyperglycaemia, immunsuppressive effect, inhibition of thyrotropin releasing hormone
b) Sympathomimetics: synthetic catecholamines
Dobutamine (β1 >> β2)via cAMP
Dose
mcg/kg/min
2.5 – 10 ++ ++
▲ HR, SV, CO
(▼) SVR
> 10 +++ ▲ HR, SV, CO
Tachyphylaxis, Hyperglycaemia

Isoprenaline (β)via cAMP
Dose
mcg/kg/min
0.01 - 1 +++ + ▲ HR, SV, CO
Tachyphylaxis, Hyperglycaemia
c) Sympathomimetics: synthetic noncatecholamines
Phenylephrine (α1 >> α2 agonist) – resuscitation in Fallot spells
Dose
mcg/kg/min
0.1 – 5 +++ ++ +++
▲ SVR
▼ HR (reflex), CO
Side effects: increasing myocardial oxygen requirement, can cause decrease in CO, Tachyphylaxis,
Hyperglycaemia
d) Phosphodiestarase Inhibitors
Milrinone via cAMP
Dose
mcg/kg/min
Clinical effect
Load: 50mcg/kg
0.2 – 1
▲ CO (positive inotropic and lusitropic effect)
▼ PVR, (SVR)
Side effects: arrhythmia, hypotension (ensure appropriate volume load)
e) Myofilament calcium sensitizers
Levosimendan via increasing sensitivity to calcium
Dose
mcg/kg/min
Clinical effect
Load: 1.25mcg/kg
over 10min
Infusion: 0.2 ▲ CO (positive inotropic and lusitropic effect)
Side effects: arrhythmia, hypotension in the first hours
f) vasoregulatory agents
Vasopressin (V1 – arterial and V2 – tubular agonist)
Dose
IU/kg/hr
V1 & V2 Clinical effect
0.01 – 0.06 +++ ▲ SVR
Side effects: increasing myocardial oxygen req irement, can cause decrease in splanchnic perfusion
[1] Am Heart J 2002 Jan; 143(1) : 15-21: Hoffman TM et al: Prophylactic intravenous use of milrinone after cardiac operation in
pediatrics (PRIMACORP) study.
[2] Lancet 2002, 306: 196-202: Follath F et al: Efficacy and Safety of intravenous levosimendan compared with dobutamine in
severe low-output heart failure (the LIDO study); a randomised double-blind trial.
[3] Curr Opin Crit Care. 2010 Oct;16(5):432-41: Parissis et al: Inotropes in cardiac patients: update 2011
[4] Curr Opin Anaesthesiol. 2009 Aug;22(4):496-501: Salmenperä et al: Levosimendan in perioperative and critical care
patients.
[5] Pediatr Cardiol. 2013, Jan34(1):1-29: Severin et al: The pediatric cardiology pharmacopoeia: 2013 update
[6] Pediatr Crit Care Med. 2006 Sep;7(5):445-8: Namachivayam P et al: Early experience with Levosimendan in children with
ventricular dysfunction.
[7] N Engl J Med. 2008 Feb 28;358(9):877-87: Russel et al: Vasopressin versus norepinephrine infusion in patients with septic
shock

ANESTHESIA: INOTROPES AND VASODILATORS
Vasodilators: decreasing the pressures against which the heart works (systemic and
pulmonary afterload) decreases the work of the heart hence myocardial O2 demand. Usual
indications for vasodilator therapy are: systemic vasodilation (LV afterload reduction),
pulmonary vasodilatation (RV afterload reduction), systemic hypertension, improving
coronary blood flow. Beware that infants, in response to low CO, increase afterload to
maintain BP. The use of vasodilators leads to increase in vascular capacitance and may
require volume replacement. Avoid or use judiciously with lesions where there is obstruction
to blood flow or fixed stroke volume.
Sodium-nitroprusside (SNP) via release of endogenous NO
Dose
mcg/kg/min
Clinical effect
0.2- 6
Direct smooth muscle cell relaxation
arterial > venous vasodilation
Side effects: severe hypotension (titrate slowly), worsening V/Q mismatch, Cyanide and Thiocyanate
intoxication, Methaemoglobinemia, tachyphylaxis
Glyceryl-trinitrate (GTN) via release of endogenous NO
Dose
mcg/kg/min
Clinical effect
1 - 10
Direct smooth muscle cell relaxation
venous > arterial vasodilation
improved coronary perfusion
Side effects: severe hypotension (titrate slowly)
Phenoxybenzamine via irreversible alpha-blockage
Dose
mcg/kg/min
Clinical effect
Load: 1 mg/kg over 1hr
Vasodilation
TDS or BD:
0.5mg/kg
Side effects: severe hypotension
Hydralazine via direct vasodilation by decreasing intracellular Ca++
Dose
mcg/kg/min
Clinical effect
10 - 50
Vasodilation
Side effects: reactive Tachycardia
Prostacyclin = PGI2 (Epoprostenol) via increase in NO
Dose
ng/kg/min
Clinical effect
2 – 20 (40) Pulmonary vasodilation, treatment of PHT
Side effects: systemic hypotension, haemorrhagic diasthesis due to Platelet aggregation inhibition
Prostaglandine = Alprostadil = PGE1 via release of endogenous NO
Dose
ng/kg/min
Clinical effect
5 - 100
Pulmonary Vasodilation
Maintaining PDA patency
Side effects: systemic hypotension, fever, hypoventilation and apnea, antiplatelet function
Inhaled Nitric Oxide (iNO) @ NO and @ PHT
Sildenafil @ NO and @ PHT

Clonidine via presynaptic alpha 2 adrenergic action
Dose
mcg/kg/hr
Clinical effect
0.5 - 2
Vasodilation
Sedation
Analgesia
Side effects: systemic hypotension, avoid in Porphyria, may decrease CO
Dexmedetomidine via presynaptic alpha 2 adrenergic action
Dose
mcg/kg/hr
Clinical effect
0.2 - 1
Vasodilation
Bradycardia (can be used therapeutically)
Sedation
Analgesia
Side effects: systemic hypotension, decreases CO, avoid in LCOS
Captopril (ACE-I) via angiotensin converting enzyme inhibition
Dose
mcg/kg
Clinical effect
Test dose: 0.1
Vasodilation
Improve in CO
TDS or QID, increase dose by 0.1mg/kg until clinical effect achieved
Side effects: systemic hypotension, renal dysfunction

PICU: ARRHYTHMIA
• prevalence of postoperative arrhythmia: 15 – 48%
• at risk: young age, low body weight, long CPB time, complex surgery, presence of residual
defects
• Prevalence of postoperative arrhythmia is up to 50%
• Haemodynamic impairment in > 50%
• Aggressive treatment in > 50% required
• Most common is sinus bradycardia with / without junctional escape > premature complexes
> supraventricular tachycardia > AV block > JET
• Mechanisms: Re-entry: on / off, inducible, overdriveable, cardiovertable; automatic /
ectopic: warm up, not inducible, not overdriveable, not cardiovertable
• Prevention and unspecific treatment: strict maintenance of normothermia, avoid triggering
drugs, avoid volume overload, avoid acidosis, Mg++
>1.0, Ca++
>1.0, K+
4.5 – 5mmol/L
Bradyarrhythmia
• Sinusbradycardia: increased vagal tone, elevated ICP, drugs (Digoxin, ß-blocker,
Amiodarone, Dexmedetomidine,…), respiratory (hypoxia), metabolic (Hypoglycaemia, Hyper
/ hypocalcaemia, Hypomagnesiaemia), post-surgical (Fontan Circulation, Mustard / Senning)
 correction of underlying cause, Atropine 0.02mg/kg, Isoprenaline 0.1 – 2mcg/kg/min
infusion, Pacing: AAI, DDD, DDI @ Pacing
• AV Block: congenital, increased vagal tone, drugs, respiratory, metabolic, post-surgical
(VSD, AVSD, ccTGA, TGA, Fontan Circulation)  correction of underlying cause, Pacing:
VVI, DDD, DDI @ Pacing
Tachyarrhythmia
• Sinustachycardia: six causes: central (pain, awake, fever, seizure), cardiovascular
(hypovolaemia, LCOS @ LCOS, PHT @ Pulmonary Hypertension), respiratory (hypoxia,
hypercarbia), heart failure  correction of underlying cause, sedation, fluid bolus, general
prevention and treatment
• Intraatrial Reentry Tachycardia (IART ≈ atypical atrial flutter): causes: post-surgical
(Fontan Circulation, Mustard / Senning, ccTGA, TOF, Ebstein‘s anomaly, VSD, ASD, TGA)
 diagnostic: Adenosine (100mcg/kg iv, increasing up to 300mcg/kg iv), treatment:
overdrive pacing if rate low enough (@ Pacing), Cardioversion (1 J/kg), Amiodarone (loading
25mcg/kg/hr for 4 hours in Guardrail (set VTBI) followed by 5 – 15mcg/kg/min infusion for
rate control or Digoxin (20mcg/kg iv in infants, 30 - 40mcg/kg iv in children). Titrate for effect.
AV reciprocating tachycardia (WPW if preexcitation on baseline ECG). Treatment:
Adenosine (100mcg/kg iv, increasing to 300mcg/kg iv). Consider Overdrive pacing.
Consider Cardioversion 1J/kg. If recurrent/ongoing consider beta-blocker or Digoxin or
Amiodarone if concerned in regards to function.
• Atrial Ectopic Tachycardia (AET ≈ chaotic atrial tachycardia) difficult to control
pharmacologically: ß -blocker: Esmolol (bolus up to 500mcg/kg iv followed by 100 –
1000mcg/kg/min infusion) or Propranolol (bolus 10 – 100mcg/kg slowly iv), Digoxin,
Procainamide, Flecainide (3 – 6mg/kg/day), Sotalol (2 – 6mg/kd/day), Amiodarone,
overdrive-pacing if rate low enough, catheter ablation. Consider sedation if compromised
cardiac output.
• Atrial Fibrillation: preexcitation-syndromes, post-surgical (ASD, Fontan Circulation, AS)
 Amiodarone, overdrive pacing, Cardioversion (1J/kg). Consider anticoagulation if
persistent > 48hrs
• Junctional Ectopic Tachycardia (JET): 180 – 250bpm: congenital, post-surgical (ASD,
VSD, AVSD, TOF, Fontan Circulation)  decrease adrenergic drugs if feasible, electrolyte
correction (Mg++
and K+
), sedation and paralysis, correct acidosis / alkalosis, correct
hypovolemia, correct hypoxemia / hypo – or hypercarbia, overdrive pacing,

pharmacologically: Amiodarone, surface cooling to 35°C to slow heart rate (and allow AV
sequential pacing)
• Premature Ventricular Contraction (PVC): < 1 / min acceptable, otherwise  treatment
of underlying cause. Beta-Blocker if clinically indicated.
• Ventricular Tachycardia: respiratory, metabolic (inborn errors of metabolism), drugs
(Class I, Class III, Digitalis toxicity), anatomical (myocarditis), post-surgical, idiopathic  in
unstable patient: immediate Cardioversion (1 J/kg  4 J/kg) and CPR, correction of
underlying cause, Amiodarone (loading over 20min: 5mg/kg iv) or Procainamide (loading
over 30min: 10 mg/kg iv), catheter ablation, ICD
• Torsade de Pointes (polymorph VT): causes: TCA intoxication, long QT Syndrome,
dyselectrolytaemia, see also VT, MgSO4 (0.2mmol/kg), consider Beta-Blocker or pacing if
recurrent.
• Ventricular Fibrillation: immediate DC and CPR  Resuscitation
[1] Critical Heart Disease in Infants and Children; 2nd ed, Nichols et al: Arrhythmia
[2] Am J Emerg Med. 2008 Mar;26(3):348-58: O'Connor et al: The pediatric electrocardiogram part II: Dysrhythmias
[3] Anaesth Intensive Care. 2009 Sep;37(5):705-19: Skippen et al: Diagnosis of postoperative arrhythmias following paediatric
cardiac surgery
[4] Nat Clin Pract Cardiovasc Med. 2008 Aug;5(8):469-76. Snyder: Postoperative ventricular tachycardia in patients with
congenital heart disease: diagnosis and management
[5] Pacing Clin Electrophysiol. 2008 Feb;31 Suppl 1:S2-6: Roos-Hesselink et al: Significance of postoperative arrhythmias in
congenital heart disease
[6] Circulation. 2007 Jun 26;115(25):3224-34: Walsh: Interventional electrophysiology in patients with congenital heart disease
[7] Circulation. 2007 Jan 30;115(4):534-45: Walsh et al: Arrhythmias in adult patients with congenital heart disease
[8] Z Kardiol. 2004 May;93(5):371-80: Haas et al: Postoperative junctional ectopic tachycardia (JET)
[9] Circ Arrhythm Electrophysiol. 2010 Apr 1;3(2):134-40: Chang et al: Amiodarone versus procainamide for the acute treatment
of recurrent supraventricular tachycardia in pediatric patients
[10] Pediatr Emerg Care. 2007 Mar;23(3):176-85; Manole MD: Emergency department management of the pediatric patient
with supraventricular tachycardia

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