Week 1: Cardiac Arrest

I understand the ethics of starting/stopping resuscitation

 Withholding CPR
o In some circumstances it would be appropriate to withhold the commencement of
cardiopulmonary resuscitation, including the following
 Where the pt is exhibiting obvious signs of death such as:
decomposition/putrefaction, hypostasis or rigor mortis
 Where the patient has sustained injuries that are totally incompatible with
life - decapitation, cranial/cerebral destruction, hemicorporectomy, foetal
maceration
 Where CPR may endanger the life, health, or safety of the paramedic
 Where a lawful direction to withhold CPR has been provided to the
paramedic

 General discontinuation criteria

o CRP is to be administered by the paramedic for a period of no less than 20
continuous minutes after which it may be discontinued or withdrawn if the
following are present
 Pt exhibiting signs of life
 Pt cardiac rhythm is asystole or PEA at a rate <10 per min
o If the pt remains in a shockable rhythm (VF/VT) for a period of 30 continuous
minutes, call consult line

 Rapid discontinuation criteria

o CPR is to be discontinued or withdrawn before the expiration of 20 minutes if the
following is satisfied
 The patient was observed to be unresponsive and pulseless for at leas 10
minutes prior to arrival of paramedic, and;
 No CPR was provided during this period
 The patient is exhibiting signs of life
 The patient’s cardiac rhythm is asystole

 Lawful directions to withhold or withdraw CPR

o Medical Decision (Acute Emergency): a direction is issued by a medical
practitioner in circumstances where the commencement or continuation of CPR
would be inconsistent with good medical practice
o Patient Decision (Advanced Health Directive): for the direction in the
advanced health directive to apply, the following must be satisfied
 The pt has impaired decision making capacity
 There is no reasonable prospect that the patient will regain capacity for
health matters
 The patient is suffering from one of the following conditions:
  Terminal illness which is incurable or irreversible, and the patient
may reasonably be expected to die within one year
 A persistent vegetative state involving severe irreversible brain
damage
 Permanently unconscious and has brain damage so severe that
there is no reasonable prospect of the patient regaining
consciousness
 An illness or injury of such severity that there is no reasonable
prospect of recovery
o Health Attorney or Guardian’s Decision
 If patient's health attorney or tribunal appointed guardian provides consent to
withhold or withdraw life-sustaining measure
I can effectively and safely manage a cardiac arrest
I have comprehensive understanding and application of the ROLE CPG
 ROLE
o No palpable carotid pulse
o No heart sounds heard for 30 continuous seconds
 o No breath sounds heard for 30 continuous seconds
o Fixed dilated pupils; and
o No response to centralized stimuli

I am able to perform CPR to a newborn, neonate, child and adult

 Newborn
o CPG resuscitation applies to infants immediately post-partum
o Clinical features
 No signs of life – absent/poor tone, not breathing normally, no heartbeat or
pulse identified on palpation/auscultation or on umbilical cord
 Signs of inadequate perfusion -> absent/poor tone, failure to establish
regular normal breathing, heart rate <100BPM
o HR <100 – IPPV room air @40-60 until HR >100, reassess after 30 secs
o HR still <100 – IPPV 15L O2 reassess after 30 secs
o HR <60 – CPR 3:1, reassess after 30 secs
o Notes
 Suctioning only in obstruction/meconium
 Bradycardia usually due to hypoxia
 Only attach pads if going to shock as can damage skin
 Pulseless VT/VF unlikely
 IV access preferred
 Shock 4J/kg

 Pediatric
o Clinical features
 No signs of life – unresponsive, not breathing normally, pulse cannot
confidently be palpated in 10 seconds
 Signs of inadequate perfusion – unresponsive, pallor or centrally cyanosed,
pulse <60 (infant), <40 (child)

o CPR 15:2 two officer, 30:2 single officer

 Consider basic airway adjuncts, CPR metronome, corPatch
 Shock 4j/kg
 After 6 mins consider – LMA, IV access, adrenaline, reversible causes,
amiodarone, ETT, sodium bicarbonate 8.4%

 Adult
o CPR 30:2
 First rhythm analysis in AED mode
  Both officers to confirm rhythm every 2 minutes
 Consider basic airway adjuncts, CPR metronome, corPatch
 Shock 200J (corpuls3)
 After 3 x 2 mins CPR = 6 mins consider – LMA, EtCO2 monitoring, IV
access, adrenaline, reversible causes, amiodarone,
 ETT after 10 mins

Reversible causes
 Hypoxia
 Hypothermia
 Hypovolaemia
 Hypo/hyperkalaemia
 Hydrogen ion – acidosis
 Tension pneumothorax
 Tamponade
 Toxins
 Thrombosis

ROSC management
 Support circulation, airway & breathing
 Maintain cerebral perfusion
 Manage cardiac dysrhythmias
 12 lead ECG
 Maintain spo2 >94%
 Consider advanced airway
 Maintain EtCO2 30-40
 Ventilate 8-12
 Aim for SBP > 100 in adults, >80 in children

I know the indications, doses and contraindications for adrenaline administration

in cardiac arrest patient

 Indications: cardiac arrest

 Contraindications: nil
 Adult dose: 1mg IV 3-5min NMD
 Pediatric dose: <1yo 100mcg 3-5min NMD, >1yo 10mcg/kg 3-5min NMD

I can effectively use capnography and identify wave forms

 Filter Closest to patient

 Normal capnography – spontaneously breathing/adequately ventilated, normal
C.O, normal metabolic function

 Endotracheal tube is oesophagus – absence of waveform and EtCO2, small

transient diminishing waveforms

 Reduced EtCO2 levels – shock, pulmonary embolus, effective CPR during cardiac
arrest

 Sudden significant increase in EtCO2 – ROSC

 Absent EtCO2 – no metabolic activity, no CPR, exsanguination/profound shock,
equipment failure, apnea, airway obstruction, oesophageal placement

 Inadequate seal around EtCO2 – leaky or deflated endotracheal cuff, an artificial

airway that is too small for patient
 Increased EtCO2 levels from normal – respiratory depression/failure, inadequate
respiratory rate and or tidal volume, increased CO2 production through increased
metabolic rate or temperature or reperfusion of ischemic tissue

 Decreased EtCO2 levels from normal – inadequate respiratory rate and or tidal
volume, diminishing CO2 production through decreased metabolic rate, falling
cardiac output

 Obstruction in breathing circuit or airway – obstruction in expiratory breathing

circuit, presence of foreign body in upper airway, partially kinked line, bronchospasm
 Increased EtCO2 levels towards normal – restoration of normal respiratory rate
and or tidal volume, cardiac output improved, improved integrity of airway seal

 Curare cleft – inadequate or lightening or paralysis

 Decreasing EtCO2 levels towards normal – restoration of normal

metabolism/CO2 production, normalized respiratory rate and or tidal volume

Week 2: ALOC
I know the physiological groupings and causes of ALOC

 AEIOU-TIPS
o A = acidosis/alcohol
o E = epilepsy/endocrine
o I = infection
o O = overdose/opiates
o U = underdose/uremia
o T = trauma to head
o I = insulin (too much or too little)
o P = psychogenic / poisioning
o S = stroke / seizure / syncope

 2 main categories
1. Intracranial pathology (structural)
 CVA, subarachnoid haemorrhage, intracerebral haemorrhage, diffuse
axonal injury, meningitis, post ictal/status epilepticus, space occupying
injury.
2. Extra-cranial pathology (non-structural)
 Cardiovascular – arrhythmia
 Metabolic – hyper/hypoglycaemia, hepatic or renal failure, disorders of
electrolytes,
 Endocrine – thyroid or pituitary disorders
 Toxins – sedative/ hypnotics, ETOH, TCAs, anticonvulsants, opiates
 Other - hypo/hyperthermia, hypoxia/hypercarbia, infection, psychiatric.

I can quickly diagnose and treat appropriately patient suffering CVA/TIA

 Stroke Clinical features

o Classified as hemorrhagic or non-hemorrhagic
o Symptoms
 Sudden severe headache,
 flushed/warm/ ashen grey,
 unequal pupils,
 weakness or paralysis on one side of body,
 brief loss of consciousness,
 blurred vision,
 absent/slurred speech,
 loss of bowel/bladder control,
 facial droop/salivary drool

 TIA Clinical features Brief episode of neurological dysfunction (<24hrs) resulting

from focal temporary cerebral ischemia
 Modified MASS
 o Presence of >/= 1 abnormal findings
 Facial droop
 One side of face doesn’t move
 Have pat show teeth or smile
 Strength in arms
 Close eyes and extend arms for 10 secs
 One arm drifts down
 Handshake
 Hold both hands and ask pt to squeeze
 Abnormal strength in one hand
 Speech
 Have pt say “the sky is blue in Brisbane”
 Abnormal = slurred or unable to speak.

 Management
o Position pt 45 degrees head up to maximise balance between cerebral
perfusion and minimising cerebral oedema.
o Oxygen
o Antiemetic
o Analgesia
o IV fluid

 Stroke mimics
o Hypoglycemia,
o intracerebral mass/lesion,
o seizures/post ictal states,
o hemiplegic migraine,
o electrolyte imbalance,
o conversion disorder

 Prehospital stroke referral 

o onset of symptoms < 3.5hrs
o one or more symptoms from MASS
o Proximity to ASC < 60 mins transport time
o Contraindications
 Serious systemic disease
 Aged care facility requiring significant assistance with ADL
 Trauma
 Hx of epilepsy
 BGL <2.2 or > 22.1

Hospitals in Brisbane – Not PCH

I can appropriately manage a patient with seizures;

 2 types – focal or generalised

 Focal
o Doesn’t impair awareness or responsiveness
o Limited to one hemisphere of cerebral cortex
o Can become generalised

 Generalised
o Both hemispheres of cerebral cortex
 Absence – brief loss of awareness and responsiveness (<10sec) with no
post-ictal stage
 Atonic – sudden loss of muscle tone (<2secs) that results in a sudden fall
 Tonic – sudden increased muscle tone that most often occurs in clusters
 Myoclonic – a brief sudden jerking action of a muscle or muscle group –
may occur in a series leading to tonic clonic seizure
 Tonic Clonic – an abrupt loss of consciousness that is concurrent with
involuntary muscular contractions (tonic) followed by symmetrical jerking
movements (clonic). Typically, last for 1-3 minutes after which the pt
experiences a post-ictal period.

 Status Epilepticus
o Seizure activity >5 minutes in duration where pt doesn’t recover to GCS 15
prior to another seizure.

 Seizure triggers
o Lack of sleep / stress
o Sudden stopping or changing medications
o Fever/infection
o Diarrhoea and vomiting
o Alcohol/drugs
o Menstruation
o Photosensitivity
o Extreme teps
o Electrolyte disturbances
 Psuedo-seizures  Psychogenic

 Management
o Position away from danger
o Treat reversible causes
o Midazolam
o Oxygen
o IPPV
I know the indications, doses and contraindication for midazolam administration

 Midazolam
o Presentation: Ampoule 5mg/1mL
o Indications: Generalised seizures/focal seizures with GCS <12
o Contraindications: KSAR
o Adult Dosages:
 NAS/IV >70yo 2.5mg rp at 10min max dose 10mg
 NAS/IV <70yo 5.0mg rp at 10min max dose 20mg
o Pediatric Dosages:
 NAS/IM 200mcg/kg not to exceed 5mg
 rp at half initial dose (max 2.5mg) at 10min max dose 10mg

I know my medico-legal responsibilities regarding patients who refuse treatment

and/or transport to hospital

 VIRCA = an assessment of the validity of the decision to be not treated/transported

o V = voluntary – the decision to refuse ambulance treatment and/or transportation

must be a voluntary choice of coercion or influence from another person
o I = informed – the patient is to be informed of the risks or possible consequences
of the decision to reject ambulance treatment and or transportation
o R = relevant – the refusal must be relevant in that it relates to the treatment that
has been recommended
o C = capacity – the patient has the requisite capacity or understands the nature
and consequences of the decision to refuse
o A = advice – if the refusal is deemed to be valid, the patient has been provided
with advice or recommendations to promote comfort and safety if the patient is
to remain at home
Week 3: Dyspnoea

I understand the causes of dyspnoea

 Dyspnoea is a subjective feeling, described as SOB, but also implies a sense of

discomfort, with breathing having become a conscious effort

 There are five main causes of dyspnoea

o Neurological
o Airway obstruction
o Respiratory compromise
o Cardiovascular compromise
o Thoracic musculoskeletal compromise

 Clinical features
o abnormal respiratory rate/pattern,
o difficulty speaking in or change in tone,
o diminished air entry or abnormal respiratory sounds,
o flaring nostrils/accessory muscle use, tripoding
o Obstruction:
 inspiratory stridor,
 snoring due to soft tissue collapse,
 gurgling due to fluids in upper airway,
 drooling or difficulty swallowing due to soft tissue edema
 Signs
o Expiratory or inspiratory wheeze
o Pursing of lips
o Hyperinflated chest
o Silent chest

I can correctly manage a patient with the following respiratory problems

Foreign body airway obstruction FBAO

 Mild airway obstruction is partial obstruction with adequate air exchange

characterized by:
o Patients themselves will optimize position,
o effective cough,
o crying or verbal response,
o able to take breath before coughing,
o fully responsive
 Severe airway obstruction is a partial obstruction with inadequate air exchange or
complete obstruction characterized by
o Ineffective cough,
o unable to vocalize,
o worsening stridor,
o quiet/silent chest,
o unable to breath,
o cyanosis,
o decreased LOC

 In the unconscious apneic patient, FBAO is recognised by inadequate airflow and

poor chest rise during attempted positive pressure ventilation.
If an infant has FBAO  place in head down position prior to delivering
back blows.
Croup

 Viral illness that causes variable airway obstruction due to inflammatory oedema
of the subglottis

 Clinical features:
o URTI,
o hoarse/husky,
o inspiratory stridor,
o barking seal like cough,
o may have wheeze and increased work of breathing

 Generally affects children 6months to 3yrs, duration 3-5 days with symptoms worse
at night

 ALOC, cyanosis and pallor are signs of severe obstruction

Stridor at rest? Yes – oxygen and adrenaline neb 5mg

No stridor at rest, consider oxygen (no adrenaline)
Epiglottitis

 Sore throat, difficulty swallowing

 Fever
 Stridor / respiratory distress
 Drooling
 Hoarse voice
 Any unnecessary disturbance of patient including attempts to lie pt down,
examination of throat or insertion of IV cannula can precipitate a total airway
obstruction.
 Do not visualize airway
 Calm pt
 Allow pt to assume position of comfort
 Avoid IV access attempts unless necessary
Asthma

 Chronic inflammation of the lower airways, characterized by episodes of reversible

partial lower airway obstruction
 Obstruction of the lower airways results from a combination of
o bronchospasm,
o inflammation and oedema of airways,
o mucous plugging
o airway smooth muscle hyperplasia and hypertrophy
 This causes increased airway resistance, increased work of breathing, alterations in
pulmonary blood flow and mismatches between ventilation and perfusion, eventually
causing hypoxia
 Management
o Important info –
 Previous ICU admissions
 Previous intubations
 Allergies
 Triggers
 Cause of current episode
 Medications – management of current episode
APO

 Acute pulmonary oedema refers to rapid buildup of fluid in the alveoli and lung
interstitium that has extravasated out of the pulmonary circulation
 As the fluid accumulates it impairs gas exchange and decreases lung compliance,
producing dyspnoea and hypoxia

 Cardiogenic – occurs when cardiac output drops despite an increased systemic

resistance, so that blood returning to L) atrium exceeds that leaving L) ventricle
o As a result, pulmonary venous pressure increases, causing capillary
hydrostatic pressure in lungs to exceed ontonic pressure of the blood, leading
to a net filtration protein poor fluid out of the capillaries.
o Eg:
 LHF
 Fluid overload
 Renal failure

 Non-cardiogenic
o Pathological processes acting either directly or indirectly on the pulmonary
vascular permeability are thought to cause this form of APO
o As a result, proteins leak out of capillaries increasing the interstitial oncotic
pressure, so that it exceeds that of blood and fluid is subsequently drawn from
the capillaries.
o EG:
 Septicaemia
 DIC
 Burns
 Drowning
 Decompression illness

 Clinical features  dyspnoea + tachycardia

o Sudden onset of extreme breathlessness
o Feeling of drowning
o Profuse diaphoresis
o Crackle – at bases first then to apices as worsens
o Cough
o Pink frothy sputum may be present
o Tachypnoea
o Tachycardia
o hypertension
o Hypotension  severe cardiogenic shock
o Raised jugular venous pressure
 Management
o Cardiogenic
 Primary goal is reduction in preload and afterload with nitrates  GTN
 aspirin,
 oxygen
 12-lead, IPPV, PEEP, CPAP
o Non cardiogenic –
 Respiratory support
 oxygen, 12 lead, IPPV, PEEP, CPAP

 CPAP = continuous positive airway pressure

o Reduces work of breathing & improves pulmonary gas exchange

o Increased intrathoracic pressure leads to reduced venous return (preload),
reduced afterload and improved cardiac function.
o Contraindications:
 <16, GCS <8, inadequate ventilatory drive
 hypotension < 90
o O2 concentrations

O2 L/min Cm H2O O2 %
8 5 45
10 8 50
12 10 55
15 15 65

COPD

 COPD describes a number of pulmonary diseases that are characterized by chronic

airflow limitation that is progressive and not fully reversible

 Chronic bronchitis – is defined as daily sputum production for at least three

months over two or more consecutive years
o Presentation
 cyanosed,
 overweight,
 edematous,
 chronic cough,
 chronic sputum production,
 cor pulmonale
 Emphysema – characterized by dilation and destruction of alveoli. The loss of
elasticity and enlargement of these airspaces leads to hyperinflation of the lungs and
increased work of breathing

o Presentation
 thin, barrel chest,
 dyspnoea,
 tachypnoea,
 pursed lip breathing,
 intercostal or suprasternal recession,
 tripod posture
o Can have features of both

 Episodes of acute exacerbation  usually follows infection.

o URTI
o Increased dyspnoea
o Difficulty in speaking
o Reduced exercise tolerance
o Fatigue
o Increased sputum volume and purulence
o Chest tightness and wheeze
o Increased cough
o Anxiety
o Increased medication use with little or no effect.

 Management –
o oxygen
 Hypoxic drive = reliance on hypoxia to drive respiration rather than
hypercapnia, due to chronically raised CO2 levels. Aim  SpO2 88-
92%
o Salbutamol + ipratropium bromide neb,
o hydrocortisone,
o adrenaline,
o IPPV

Allergic reaction/anaphylaxis
 Anaphylaxis is defined as

o any acute onset illness with typical skin features (uticaria/erythema/flushing,

angioedema),
plus
o involvement of respiratory and or cardiovascular compromise and or persistent
severe gastrointestinal symptoms,
 or
o any acute onset of hypotension or bronchospasm or upper airway obstruction
where anaphylaxis is considered possible, even if typical skin features are not
present

 Clinical signs
o Difficulty/noisy breathing/ stridor
o Swelling of tongue
o Swelling/tightness in throat – difficulty swallowing
o Difficulty talking
o Wheeze or persistent cough
o Dizziness + collapse

o Pale and floppy – young children

 Management – oxygen, adrenaline, IV fluid, salbutamol, ipratropium bromide,
hydrocortisone

Smoke/gas/steam inhalation

 100% O2
 assess airway – look for obstruction
 Salbutamol if bronchospasm is present
I know when to and how to operate all methods of oxygen delivery

 Contraindications for oxygen

o Paraquat poisoning SPO2 >88
o Hx of bleomycin therapy SpO2 >88
I know indications, doses and contraindications for salbutamol

 Presentation:
o nebule 5mg/2.5ml
o nebule 2.5mg/2.5ml
 Indications:
o Bronchospasm
o Suspected hyperkalaemia
 Contraindications: KSAR, pt <1yo
 Adult dose: NEB 5mg rp PRN NMD
 Paediatric dose:
o NEB 1-5 years  2.5mg PRN NMD
o NEB >/= 6 years  5.0mg PRN NMD
 COPD – 6L/min, all other = 8L/min.

Ipratropium bromide  must be with salbutamol, not alone

 Presentation:
o nebule 250mcg/1ml
 Indications:
o Bronchospasm
 Contraindications: KSAR, pt <1yo
 Adult dose: NEB 500mcgm rpt @20 mins, Max 1.5mg
 Paediatric dose:
o NEB 1-5 years  250mcg rpt @20 mins, Max 750mcg
o NEB >/= 6 years  500mcg rpt @20 mins, Max 1.5mg

I know indications, doses and contraindications for administration of adrenaline

to an asthma patient
 Severe life threatening bronchospasm or silent chest
o Adult dose: IM 300mcg rp 5min PRN
o Paediatric dose: IM >6yo 300mcg rp 5min PRN, IM <6yo 150mcg rp 5min PRN

I am able to perform laryngoscopy and use Magill’s forceps

 Laryngoscopy
o Visualization of the glottis for
 Oral endotracheal intubation
 Removal of foreign body
o Hold in L hand, put in R side of pts mouth then sweep tongue to the left and
position midline.
 o Advance to be able to view epiglottis

 Magills Forceps
o For removal of laryngeal foreign bodies
o Perform laryngoscopy first

I understand pulse oximetry and its application to a patient suffering dyspnoea

 Estimates the oxygen saturation in the atrial blood by directing both red and infrared
light from two LEDs through a patient’s translucent fleshy body site
 The absorption of the two wavelengths differs significantly dependent on the level of
haemoglobin oxygenation and the pulse oximeter translates this ratio into a
percentage

Week 4: Shock

I can effectively assess and correctly manage a shocked patient in the context of:

Uncontrolled haemorrhage
 External haemorrhage can result from open wounds, lacerations, peripheral vascular
injuries or amputation
 Internal haemorrhage arises secondary to blunt or penetrating forces due to
concealment, it may be difficult to identify the site and extent of bleeding – it should
always be suspected in a shocked trauma patient is bleeding internally until proven
otherwise

 Management
o Active external haemorrhage – direct pressure, proximal pressure points,
indirect pressure, tourniquet, position, nasal pack, maintain normothermia
o Potential internal haemorrhage – FAST, pelvic binder, fracture reduction,
minimize movement, maintain normothermia
o Consider IV access, IV fluid, analgesia, antiemetic

Absolute and relative hypovolaemia

 Acute haemorrhage secondary to trauma is the major cause of hypovolaemic shock,
however non haemorrhagic causes must be considered
 Blood loss can be hidden and not immediately apparent
 Awareness of clinical features of shock is of paramount importance, as early
recognition of hypovolaemia can be lifesaving
 Clinical features of shock
o Tachycardia
o Hypotension
o ALOC
 o Pale, cool peripheries
o Prolonged capillary refill
 Management
o Traumatic haemorrhage with associated TBI
 control haemorrhage,
 oxygen,
 IV access,
 IV fluid to SBP 100-120,
 maintain normothermia
o Traumatic haemorrhage with NO associated TBI
 control haemorrhage,
 IV access,
 IV fluid to palpable radial pulse,
 maintain normothermia
o Non traumatic haemorrhage – oxygen, IV access, IV fluid, maintain
normothermia

I know the indications, dose and contraindications of fluid administration to a

shocked patient

 Indications – inadequate tissue perfusion/shock, hypovolaemia

 Adult dosages – IV PRN titrate according to the indication and patients physiological
response to treatment
 Paediatric dosages – IV consult 10-20mL/kg TMD 60mL/kg

I can recognize the signs and symptoms of an allergic reaction and adapt my
treatment accordingly

 Defined as – any acute onset illness with typical skin features

(uticaria/erythema/flushing, angioedema), plus involvement of respiratory and or
cardiovascular compromise and or persistent severe gastrointestinal symptoms, or
any acute onset of hypotension or bronchospasm or upper airway obstruction where
anaphylaxis is considered possible, even if typical skin features are not present
 Management – oxygen, adrenaline, IV fluid, salbutamol, ipratropium bromide,
hydrocortisone

I know the indications, doses and contraindications for adrenaline administration

in anaphylaxis
 Adult dosages – Anaphylaxis/SAR
o IM 300mcg rpt 5min NDM
o NEB 5mg SDO

 Paediatric dosages – Anaphylaxis/SAR

 o IM >6yo 300mch rpt 5min NMD,
o <6yo 150mcg rpt 5min NMD
o NEB 5mg SDO
Week 5: Chest Pain

I can accurately diagnose and effectively manage ACS

 ACS refers to the spectrum of conditions resulting from myocardial ischemia. It
encompasses STEMI, non STEMI, and unstable angina. ACS should be clearly
distinguished from stable angina that is typically aggravated by exertion or emotional
stress and is relieved quickly with rest and/or sublingual GTN
 ACS will usually present with chest pain and/or discomfort, however certain groups
of patients may present with atypical symptoms
 Diagnosis of ACS is based on history, 12 lead ECG and changes in cardiac
enzymes
 Complications of ACS include arrhythmia, cardiac failure, acute valvar rupture,
cardiogenic shock and death
 Early diagnosis and aggressive treatment is vital including time-critical reperfusion
therapy for patients with STEMI

 Right ventricular myocardial infarction

o Approx. 1/3 of patients with inferior STEMI will have concurrent RVMI
o Patients with haemodynamically significant RVMI will present with hypotension,
jugular vein distention and clear lung fields
o ST elevation in V4R is indicative of RVMI and correlates closely with occlusion
of the proximal right coronary artery
o In RVMI the maintenance of preload is vital and appropriate volume loading to
maintain cerebral perfusion is indicative if haemodynamic compromise occurs
 will require gentle fluid challenge
o Similarly pharmacological agents which reduce preload should be used with
extreme caution to prevent detrimental side effects

 Management
o 12 lead ECG,
o oxygen,
o aspirin,
o GTN,
o antiemetic,
o fentanyl
o 12 lead ECG consistent with STEMI – pPCI referral, prehospital fibrinolysis
I can diagnose and effectively manage patients presenting with: bradycardia,
broad complex tachycardia, PEA/asystole

Bradycardia
 HR <60 in adults
 Cardiac or non-cardiac
 Cardiac  associated with SA node, AV node or His-purkinje system
 Non- cardiac  environmental, metabolic or endocrine disorders and toxicology.
 Hypoxia common cause  Initial management should focus on improving
oxygenation and ventilation.
 Management
o Atropine
o Transcutaneous pacing
o Adrenaline
o Isoprenaline

Broad complex Tachycardia

 HR > 100 with QRS > 0.12sec
 12 lead
o VT
o SVT
 Pre-existing BBB
o Pre-excitation
 Clinical signs
o Palpitations
o Chest pain/discomfort
o Dyspnoea
o ALOC
o Syncope
 If haemodynamically compromised  synchronized cardioversion
 Otherwise consider amiodarone, magnesium sulphate.

Narrow complex Tachycardia

 HR > 100 with QRS <0.12
 SVT
 Atrial fibrillation/ flutter
 Clinical signs
o Palpitations
o Chest pain/discomfort
o Dyspnoea
o ALOC
 o Haemodynamic instability
 Management
o If haemodynamically compromised  synchronized cardioversion
o Otherwise
 Oxygen, Valsalva manouvre, Aspirin if MI suspected
I know the indications, doses and contraindication for Aspirin, Morphine and GTN

Aspirin
 Indications - suspected ACS, APO (cardiogenic)
 Contraindications
o KSAR,
o chest pain associated with psychostimulant overdose,
o bleeding/clotting disorders,
o current GI bleed/peptic ulcer,
o <18yo
 Adult dose: 300mcg PO SDO

Morphine
 Indications – pain, autonomic dysreflexia SBP >160mmHg
 Contraindications: KSAR, renal failure
 Adult dosages:
o 2.5-5mg rp to 5mg every 5 min max 20mg
o >70 2.5mg, rpt 2.5mg every 5 mins, max 10mg
GTN
 Indications – ACS, ACPO, autonomic dysreflexia SBP >160, Irukandji
syndrome SBP >160
 Contraindications
o KSAR,
o HR<50/>150,
o SBP <100,
o acute CVA/ head trauma,
o erectile dysfunction medication
<24hrs
 Dose – SUBLING 400mcg rp 5 mins
NMD

I am competent in acquiring 12 lead ECG*

Using a 12 lead ECG I can quickly and accurately identify an inferior, anterior and
lateral STEMI*

Week 6: Trauma

I understand the concepts of trauma management and the state trauma plan

 The trauma by-pass CMG is designed to identify trauma patients who require
transport to Major Trauma Service
 Three elements should be considered for the triage of trauma patients in QLD
1. VSS
 2. MOI
o High risk mechanisms
 Ejected from vehicle,
 fall from height >3mtrs,
 involved in an explosion,
 involved in high impact RTC with incursion to occupants compartment,
 involved in vehicle roll over,
 involved in RTC with fatality,
 entrapped for >30 min
3. Patterns of Injury
 Injuries to the head, neck, chest, abdomen, pelvis, axilla or groin that are
penetrating, sustained from blast or involve two or more of those regions
 Limb amputation above wrist or ankle, suspected spinal cord injuries
 Burns in adults >20% or in children >10% or other complicated burn injury
including the hand, face, genitals, airway or respiratory tract
 Serious crush injury, major open fracture or open dislocation with vascular
compromise
 Fractures pelvis, fractures involving two or more of the femur, tibia or humerus

I understand how to manage patients suffering pain

Patients in pain should receive timely, effective and appropriate analgesia, titrated
according to response
 Pain score 1-3 (mild): may not require analgesia, non-pharmacological
approaches, consider non-opioid analgesia, paracetamol/ibuprofen
 Pain score 4 -6 (moderate): consider previous step, consider oral opioid and
non-opioid analgesic, oxycodone, paracetamol, ibuprofen
 Pain score 7-10 (severe): consider previous step, will require IV/IM/IO/NAS
inhalation analgesia, morphine, fentanyl, ketamine, penthrane

Non pharmacological techniques include reassurance and compassion, immobilization

or splinting, ice and elevation, psychological techniques eg distraction

I know the indications, doses and contraindications of Fentanyl, Morphine,

Ondansetron and Methoxyflurane administration for pain management

Fentanyl
 Indications – significant pain
 Contraindications – KSAR
 Doses –
o <70
 IM 25-100mcg rpt up to 50mcg every 10min max 200mcg,
 IV <70 25mcg rp 50mcg every 5 min max 200mcg
o >/= 70
  IM 25-50mcg rpt up to 50mcg every 10min max 100mcg,
 IV 25mcg rpt 25mcg every 5 min max 100mcg
o Paediatric dose - >1yo
 NAS 1.5mcg/kg rpt 1mcg/kg 10mins max 100mcg
 IM 1-2 mcg/kg, single max = 50mcg, total max = 2mcg/kg

Morphine
 Indications – pain, autonomic dysreflexia SBP >160mmHg
 Contraindications: KSAR, renal failure
 Adult dosages:
o 2.5-5mg rp to 5mg every 5 min max 20mg
o >70 2.5mg, rpt 2.5mg every 5 mins, max 10mg

Ondansetron
 Indications – nausea/vomiting, prophylactic in ACS
 Contraindications:
o KSAR,
o congenital long Q-T syndrome
o concurrent apomorphine therapy (parkinsons)
o pt <3 yo
 Doses – IM/IV 4-8mg max dose 8mg

Methoxyflurane
 Indications – pain
 Contraindications –
o KSAR,
o pt<1yo,
o hx of significant renal/hepatic failure,
o hx malignant hypothermia
 Dose IHN 3mL rp once after 20min max dose 6mL

I can effectively assess and manage a patient with

Head injuries

 The goal of prehospital care in TBIs is to reduce secondary brain injury due to
hypoxia, abnormal CO2 levels or hypotension
 Clinical features
o External evidence of head injury
o ALOC/focal neurology – reduced GCS, unilateral weakness, seizure,
unequal/unreactive/dilated pupils
o Abnormal vital signs – bradycardia and hypertension (Cushing’s triad) is sign of
raised ICP and suggests imminent brain herniation
o Excluding hypoglycemia is essential
 Risk assessment
o Any episode of hypoxia of hypotension in the setting of TBI will significantly
increase morbidity and morality
o Hyper or hypoventilation of patients causing abnormal CO2 levels will also
impair brain perfusion – hyperventilation causes hypocapnoeic
vasoconstriction; hypoventilation cause hypercapnoeic vasodilation and
increased ICP

 Management
o C-spine,
o oxygen
o IV access,
o analgesia,
o IV fluid SBP 100-120,
o basic airway adjuncts,
o midazolam,
o hypertonic saline,
o antiemetic,
o RSI ETT

Spinal injuries

 Spinal cord injury is injury of the spine or spinal cord with associated motor, sensory
and/or autonomic deficit
 Can be caused by hyperflexion, hyperextension, rotation, compression or
penetrating mechanisms upon the spinal cord
 The leading causes of SCI include road traffic crash, falls, assaults, sporting injuries
and recreational water activities

 Diagnostic pattern for SCI involves

o MOI
o Pain/tenderness over or adjacent to the spinal vertebra
o Impaired motor or sensory function
o Impaired autonomic function
 Prehospital management of SCI aims to limit neurological deficit and prevent
secondary injury through
o Appropriate spinal immobilization
o Maintaining high index of suspicion of SCI
o Identification and reversal of life threats in primary survey
o Cardiovascular and ventilator support
o Ensuring appropriate thermoregulation

 Management
o NEXUS criteria
 Midline tenderness,
 evidence of intoxication,
 ALOC,
 focal neurological deficit,
 any distracting injury
o Spinal immobilization
o Consider neurogenic shock, FAST, IV fluids, inotropic support, analgesia,
antiemetic

Chest injuries

 Life threatening injuries may not be initially apparent and the mechanism of injury is
important in guiding further investigation, lack of obvious fractures doesn’t exclude
injury especially in a paediatric patient

 Clinical features
o Injuries sustained depends on mechanisms and forces
o Penetrating trauma – entry and exit wound, external bleeding may be evident,
internal bleeding may be occult
o Blunt trauma – contusion/abrasion, haematoma, obvious rib # and or clavicle #

 Signs suggesting life-threatening conditions

o Unequal air entry and/or crackles,
o asymmetrical or paradoxical chest wall movement,
o surgical emphysema,
o chest hypomobility,
o bubbling or sucking wounds,
o extreme tachypnea,
o tracheal shift,
o hypotension,
o ALOC,
o JVD,
o muffled heart sounds,
 o dysrhythmias

 Management
o Signs of tension pneumothorax – consider emergency chest decompression
o Signs of shock – stabilize mechanical injuries and manage as per CPG
hypovolaemic shock
o Consider – oxygen, IV access, analgesia, IV fluid, stabilize mechanical injuries,
FAST

Abdominal injuries

 Blunt abdominal trauma

o Results in compression and sheering force injuries. Compression forces are
those that result in abdominal organs and blood vessels being crushed
between solid objects. Shearing forces cause tearing and rupture of solid
organs and blood vessels at multiple sites

 Penetrating trauma
o Extent of vessel and organ damage, including hemorrhage, due to penetrating
trauma is dependent on mechanism. Small entry wounds may mask significant
internal injury
o Regardless of the mechanism, catastrophic deterioration can develop quickly
and unexpectedly – all penetrating injuries regardless of assessed level of
penetration, or actual size of the wound, should be treated as serious and
potentially life threatening

 Children – due to physique, are particularly susceptible to abdominal trauma

o Relatively large abdomen is poorly protected by lower ribs and pelvis and
children may present with fewer external signs of trauma

 Clinical features
o Unexplained shock may be the only sign of severe abdominal trauma
o ALOC, dyspnea, abdominal pain/discomfort/tenderness on palpation,
hypovolaemic shock, abdominal bruising/distension, shoulder tip pain (Kerr’s
sign)

 Management
o Shocked – IV access, analgesia, antiemetic, FAST, normothermia, manage
other injuries
o Shocked with TBI – IV access, IV fluid to SBP 100-120, pelvic binder, FAST,
blood

Crush injuries
 Crush injuries include simple mechanical crush injury, compartment syndrome and
crush syndrome
o Crush injury – localized tissue injury that occurs when a compressive force is
applied
o Compartment syndrome – compromised perfusion to tissues within an
anatomical compartment due to increased pressure within that compartment
 Left untreated can led to tissue necrosis, permanent impairment and
crush syndrome
o Crush syndrome – a systemic condition that results from injuries sustained by
compressive forces sufficient in duration and pressure to cause widespread
ischemia and necrosis to soft tissue
 Ischemia of the muscle leads to increased permeability of cell membranes
and the release of potassium enzymes and myoglobin into the systemic
circulation
 Crush syndrome is characterized by rhabdomyolysis, lactic acidosis,
hyperkalaemia, renal failure, shock, dysrhythmias and death
 Development of crush syndrome is time and pressure dependent
 Crush syndrome can develop over a short period of time where the
compressive force and muscle mass is large, and conversely, over long
periods where compressive forces are relatively small

 Management
o Hyperkalaemia – manage as per hyperkalaemia CPG
o Compressive force in situ
 Control compressive force release
 Anticipate reperfusion injuries – hyperkalaemia, dysrhythmias, shock
 Consider tourniquet
 Consider analgesia and IV fluid 20ml/kg prior to release
o Consider analgesia, IV fluids, elevate limbs

Eye injuries

 All patients with suspected eye trauma and patients who have ALOC should have
eyes assessed and basic eye precautions implemented

 General management principles

o Irrigation with water or saline for chemical or biological fluid exposure, foreign
body or thermal burns
o Protect eye with shield
o Antiemetic
o Position patient head up

Taser injures
 Probe removal – pull straight out in rapid motion, process usually painless due to
electrocautery effect on surrounding tissue
 Probes should not be removed if embedded in eyes, genitals, face or neck
 Transport is indicated in patients where
o Probes cannot be removed, the patient required a psychiatric evaluation,
assessment of injuries is required, patient is affected by substances other than
alcohol

I can correctly identify when to and competently apply

Cervical collars
 Suspicion of cervical spine or SCI
 Measure between base of chin and suprasternal notch  soft collar chin support

Traction splint
 mid – shaft femur fractures
 C/I – fracture or dislocation of the knee, ankle injury
 In pelvic injury  apply after SAM sling

SAM sling
 Pelvic binders reduce and stabilise pelvic ring fractures with diastasis and
thereby control haemorrhage from the pelvic vasculature.
 Applied at level of greater trochanter or symphysis pubis
 C/I NOF

KED/NEIJ
 The NEANN Immobilisation and Extrication Jacket (NIEJ) is a device used to
minimise spinal movement and assist with extrication from confined spaces
 Maintain MILS
 C-collar immobilisation as well.
 C/I – when pt is time critical and application of NEIJ will delay transport

Spinal Immobilization
o NEXUS criteria
 Midline tenderness,
 evidence of intoxication,
 ALOC,
 focal neurological deficit,
 any distracting injury  spinal immobilisation
I can correctly remove a helmet

 The primary officer provides Manual In-line Stabilisation (MILS) from the front of the
patient by placing one hand on the mandible and the other applying supportive
pressure on the occipital region
 The second officer gently flexes the helmet apart laterally and lifts in a steady
rearward motion avoiding movement of the neck.
 As the helmet is removed, the primary officer may be required to readjust hand
position to provide adequate support below the occiput.
 Once the helmet is removed the responsibility of MILS should be safely transferred
to an officer at the head end of the patient.

Week 7: Endocrine

I can identify the S&S of hypoglycaemia

 Hypoglycemia is defined as BGL <4mmol/L which can occur in any patient

regardless of diabetic hx
 Clinical features
o Autonomic features – diaphoresis, hunger, tingling around mouth, tremor,
tachycardia, pallor, palpitations and anxiety
o Neurological features – lethargy, change in behavior, headache, visual
disturbance, slurred speech, dizziness, ALOC, seizures, coma
o S&S may be masked in beta blocked pts
o Pts may present with S&S mimicking intoxication or stroke

I can identify the S&S of hyperglycaemia

 Hyperglycemia defined as BGL >7mmol/L, can present as

o diabetic ketoacidosis,
o hyperosmolar hyperglycemic syndrome,
o or may be asymptomatic

 DKA and HHS are predominantly caused by acute illness, non-compliance

 DKA is life-threatening complication usually seen in patients with TIDM that is
characterized by
o Hyperglycemia >10mmol/L, ketosis and metabolic acidosis
o It is causes by absolute insulin deficiency or resistance precipitating a number
of physiological changes
o High BGL increased blood osmolality drawing water out of cells causing cellular
dehydration
o High BGL in kidney filtrate results in osmotic diuresis and polyuria leading to
severe dehydration and hypovolemia
 o Alternative food sources eg fatty acids are used producing organic acid
ketones, and accumulation of these ketones leads to metabolic acidosis

 HHS is life-threatening complication of T2DM that is characterized by

o Hyperglycemia > 40mmol/L, hyperosmolarity, severe dehydration
o Caused by relative insulin deficiency whereby there is sufficient insulin to limit
ketone production thus preventing metabolic acidosis
o Elevated BGLs still initiate triad of polyuria, polydipsia and polyphagia
o Has greater mortality due to underlying severity of illness, typically sepsis

 Clinical features
o Neurological – lethargy, ALOC, seizure, coma
o Cardiovascular – signs of hypovolaemia, pale, cool or clamming, flushed, hot if
febrile
o Kussmals respiration is due to severe metabolic acidosis (not usually in HHS)
I can correctly manage a patient with hypoglycemia
 Consider hypoglycaemia in all patients with ALOC
 Consider IV access, glucagon, glucose 10%, oral glucose

I
I can correctly manage a patient with hyperglycemia
 Consider – IV access, IV fluid (correcting fluid deficit too quickly can cause cerebral
edema in children), oxygen, 12-lead ECG, calcium gluconate, sodium bicarbonate,
salbutamol

I know the indications, doses and contraindications for glucagon administration

 Indications – symptomatic hypoglycemia with the inability to administer oral glucose
 Contraindications – KSAR
 Dose – IM 1mg SDO
I know the indications, doses and contraindications for glucose 10%
administration
 Indications – symptomatic hypoglycemia with the inability to self-administer oral
glucose
 Contraindications – Nil
 Dose – IV 15g (150ml) rpt 100ml (10g) boluses every 5 min until BGL >4.0mmol/L

Week 8: Obstetrics

I can effectively assess and correctly manage a normal cephalic delivery

 Normal cephalic delivery is defined as the means by which the newborn, placenta
and membranes are delivered via the birth canal in which
o A single newborn presents via vertex presentation
o Newborn is born vaginally at term between 37-42 weeks
o Birth is spontaneous within 18hrs
o No complications occur  low risk at start of labour

 Clinical features  signs of imminent birth

o Increased frequency and severity of contractions
o Loss of mucous plug
o Memebrane rupture
o Bulging perineum
o Appearance of presenting part at vulva

 Management
o Position mother, prepare equipment, consider analgesia
o Ensure controlled delivery of head,
o control rate of delivery,
o is amniotic fluid clear?
o Baby OK?  HR > 100, breathing, crying?
o Oxytocin
o Conduct post-birth assessment and cares:
 Dry baby
 Maintain warmth
 Provide maternal and baby skin to skin contact
 Clamp and cut the cord, when stops pulsating
 Actively manage third stage of labour
 APGAR score at 1 & 5 mins
 Encourage breastfeeding
I can effectively asses and correctly manage a breech delivery

 A breech birth occurs when the fetus enters the birth canal with the buttocks or feet
first

 Management
o Lovset’s Manoeuvre -used to assist in delivery or arms and shoulders if there
is a delay with the birth or the shoulders and arms, Lovset’s manoeuvre may
be necessary using a sterile dressing towel, hold the baby around the pelvic
girdle (thumbs on bums). Keeping the baby’s back uppermost, rotate on
shoulder towards the mother’s front at the same time. Insert two fingers over
the shoulder and sweep the arm down and exert downwards traction, repeat
this manoeuvre for the other shoulder.
o Body cannot be turned - If the baby’s body cannot be turned to deliver the arm
that is anterior first, deliver the shoulder that is posterior hold and lift the baby
up by the ankles move the baby’s chest towards the woman’s inner leg, the
shoulder that is posterior should deliver free the arm and hand
o lay the baby back down by the ankles and the shoulder that is anterior should
deliver
o Mauriceau-Smellie-Veit manoeuvre - used to deliver head (preferred method)
delivery of the head. lay the baby face down with the length of its body over
your hand and arm place the first and third fingers of this hand on the baby’s
cheek bones and place the second finger in the baby’s mouth or chin to pull the
jaw down and flex the head. Use the other hand to hook the baby’s shoulders
with the index and ring fingers with the middle finger of the hand, gently flex the
baby’s head towards the chest while pulling on the jaw to bring the baby’s head
down until the hairline is visible. pull gently to deliver the head, raise the baby,
still astride the arm, until the mouth and nose are free, deliver the baby onto
the mother’s abdomen for skin to skin contact

I have appropriate knowledge, understand and can correctly manage

Abruptio placenta

 Occurs when a normally situated placenta separates either partially or

completely from the uterine wall, resulting in hemorrhage prior to delivery of the
foetus.
 Clinical features
o Constant pain in abdomino–pelvic region
o Bleeding may range from absent to profuse, occurring in waves as the uterus
contracts
o Tonic muscle spasm uterine contractions
o Uterus feels rigid on palpation
 o Fundal height may increase due to expanding hemorrhage
o Signs of shock

 Management
o IV access
o IV fluid – if shocked
o Analgesia
o Antiemetics
o Time critical Transport

Placenta previa

 Occurs when placenta is situated partially or wholly in the lowr uterine segment
 Eveident during third trimester
 Can cause bleeding
 May physically prevent vaginal delivery

 Clinical features
o Several small warning bleeds
o Bright red blood
o No pain other than contractions
o Soft non-tender uterus
o Significant blood loss which may lead to shock

 Management
o IV access
o IV fluid – if shocked
o Analgesia
o Antiemetic

PPPH

 Occurs within 24h of birth and is bleeding from or into the genital tract of
o >500mL following vaginal delivery
o >1L following C-section
o sufficient to cause deterioration on mother’s condition
o symptoms of mild shock may not manifest until >1L lost

 Risk factors
o Thrombin
o Tone
o Tissue
o Trauma
o Multiparity
 o Previous Hx
o Past C-section
o Prolonged labour
o Multi preganancy
o Polyhydramnios

 Clinical features
o PV bleeding – can be torrential and uncontrolled
o Signs of shock
o Restlessness
o Enlarged and soft uterus on palpation
 Management
SPPH

 defined as bleeding from, or into, the genital tract > 24 hours, or up to six weeks
after delivery
 >500mL  deterioration of mothers condition

 Caused by
o Infection
o Retained placental products
o  failure of uterus to contract = sub-involution.

 Clinical features
o Ongoing PV bleed
o Change in lochia  bright red, increasing amounts
o Pain – lower abdo
o Anaemia
o Pyrexia, rigors
o Shock

 Management
o IV fluid
o Analgesia
o Fundal massage
o  sepsis?

Inversion of the uterus

 Uterine inversion is a rare, but potentially life-threatening, obstetric emergency

where the uterus collapses in on itself to varying degrees:
o Incomplete – fundus reaches cervix
o Complete – fundus passes thru cervix but not vaginal opening
o Prolapsed – fundus extends thru vaginal opening
 Timing
o Acute - <24h post delivery
o Subacute – 24h-4weeks
o Chronic > 4 weeks
 Clinical features
o PPH
o Mass at vulva
o Evidence of shock
o Severe abdo pain
 Management
o Analgesia
 o Assist patient to attain position of comfort
o Protect any exposed uterus with moist sterile dressings

Cord prolapse

 Occurs after membranes have ruptured, umbilical cord slips down in front of the
presenting part of the foetus and protrudes into the vagina
 Visualize cord at vaginal opening
 Becomes an issue if cord is compressed cutting off foetal blood supply  hypoxia
and death
 Principle of pre-hospital care is to monitor the cord for pulsations and position the
mother to prevent compression. If cord stops pulsating then pressure will need to be
alleviated.

 Clinical features
o Cord visible in vaginal opening
o Evidence membranes ruptured
o Change in foetal movement
o Meconium

 Management
o Pulsative cord evident?  Exaggerated Sims position  left lateral with pillow
under hip
 Have mother push cord back into vagina
o Not Pulsative?  Knee – chest position
 Push presenting part off the cord
o Transport in Exaggerated Sims position

Pre-eclampsia

 >20 weeks gestation

 diagnosis
o SBP >/= 140
o DBP >/= 90
o Plus
 Neurological problems
 Proteinuria
 Renal insufficiency
 Lover disease
 Haematological disturbances
 Foetal growth restriction

 Clinical features
 o Neurological
 Headache
 Visual disturbance
 Seizure
 Hyperreflexia
 Clonus
o Respiratory
 APO
o Cardiovascular
 HT
 Generalised oedema
o Jaundice

 Management
o Eclampsia?  IV fluid – conservative
 Magnesium sulphate
o High risk of eclampsia?  CNS dysfunction?
 Maintain quiet environment
 Minimise body motion
 Attain position of comfort

Ectopic pregnancy

 Developing embryo outside uterine cavity  normally fallopian tubes

 Clinical features
o Unruptured ectopic
 Hx of at least one missed period
 Abnormal vaginal bleeding
 Pelvic/abdo pain
 Nausea
 Presyncopal symptoms
o Ruptured ectopic
 Syncope
 Shock
 Acute sever pelvic/abdo pain
 Shoulder tip pain (Kehr’s) – free blood irritation diaphragm when supine
 Abdominal distension
 Rebound tenderness/guarding

 Management
o Shock?
o Analgesia
o Antiemetic
 o IV fluid

Abortion/miscarriage
 In Australia miscarriage is defined as the spontaneous loss of pregnancy before 20
weeks of gestation (or < 400 grams)
 Clinical features
o lower abdominal discomfort
o vaginal bleeding
o hypotension
o tachycardia
o postural symptoms
o infection
 pain, rigidity
 purulent discharge
 fever

 Management
o If possible, all tissue
and large clots
should be retained
and transported to
the receiving
facility.
o Foetus < 20wk may
show signs of life
but resuscitation is
futile
Shoulder dystocia

 Disproportion occurs between the bisacromial diameter of the foetus and the antero-
posterior diameter of the pelvic inlet, resulting in impaction of the foetus behind the
symphysis pubis
 Difficult delivery ensues, requiring the use of additional manoeuvres beyond the
downward traction of the foetal head. It is relatively uncommon, occurring in 1 in 300
births.
 Shoulder dystocia usually becomes obvious after the foetal head emerges and
retracts up against the perineum, failing to undergo external rotation.
 Confirmed when standard delivery manoeuvres fail to deliver the foetus and head to
body delivery interval is prolonged >/= 69 secs.

 Management
o External manoeuvres
 McRoberts  knees to nipples
 Rubin I  suprapubic pressure
 Rotation onto all fours

o Internal manoeuvres
 Rubin II
  While suprapubic pressure is being applied (Rubin I), the fingers
of one hand are inserted into the vagina and used to apply pressure
behind the anterior shoulder, pushing the shoulder towards the
baby’s chest.
 Woodscrew
 Rubin II plus insert fingers of second hand in front of posterior
shoulder and add further pressure to rotate
 Reverse woodscrew – opposite direction
 Delivery of posterior arm  flex at elbow and sweep across foetal chest

I can competently assess the APGAR Score in a newborn

Week 9: Environmental/Sepsis/ Infection

I can quickly and correctly identify the S&S and management of

Hypothermia

 Hypothermia is defined as core body temp <35 degrees and is caused by excessive
cold stress and/or inadequate body heat production
 Early compensation mechanisms include shivering, increase muscle tone, peripheral
vasoconstriction, increased resp rate and cardiac output
 When these mechanisms no longer compensate, body temperature falls
 Causes of hypothermia classified under three broad headings
o Increased heat loss
 vasodilation,
 environmental,
 trauma,
 loss of skin integrity eg burns,
 neuropathy
o Decreased heat production
 age,
 endocrine disorders,
 nutritional deficits,
 immobility
o CNS dysfunction
 trauma,
 CVA,
 hypoxaemia,
 malignancy,
 encephalopathy

 Clinical features
o Mild 35-32 degrees
 vasoconstriction,
 apathy/lethargy,
 ataxia,
 tachycardia,
 tachypnea,
 normotension

o Moderate 32-28 degrees –

 confusion,
 delirium,
 ALOC,
 hypotension,
 bradycardia,
 muscle rigidity

o Severe <28 degrees –

 stupor,
  coma,
 diminished or absent signs of life,
 dilated pupils,
 reduced/absent reflexes and apnoea,
 dysrhythmias including SB,
 slow AF (j wave),
 VF and asystole

 Can also develop blunted catecholamine release, hypo/hyperglycemia,

hypo/hyperkalemia, coagulopathy, disseminated intravascular coagulation,
rhabdomyolysis

 Management
o Minimize patient movement,
o prevent further heat loss (remove we clothes),
o commence rewarming, blankets/warming blankets
o Consider oxygen, LMA ETT, 12 Lead ECG, warm fluid, BGL, serial
temperature monitoring

 Resus
o No drugs until 30 degrees
o 30 degrees standard interval between drugs should be doubled
o 35 degrees normal drug interval
o If patient temp below 30 degrees shock at highest DCCS for three shocks
 After 3 shocks withhold further shocks until temperature >30 degrees

Hyperthermia

 Hyperthermia results from thermoregulation failure and occurs when the body
produces or absorbs more heat than it can dissipate, exceeding the normal limits
required to maintain homeostasis
 Heat is transferred to and from body by radiation, conduction, convection and
evaporation
 Extreme hyperthermia >40 degrees is a medical emergency and requires immediate
treatment to prevent disability or death

 Clinical features
o Heat exhaustion (37-40 degrees) –
  severe headache and or dizziness,
 diaphoresis, nausea, vomiting,
 tachypnea, tachycardia, hypotension,
 muscle pain, fatigue, cramps

o Heat stroke (>40 degrees) –

 CNS dysfunction (ALOC, seizures),
 extreme fatigue, headache, syncope,
 facial flushing, vomiting, diarrhea,
 skin hot and dry, nil diaphoresis,
 dysrhythmias,
 hypotension,
 tachypnea and respiratory distress,
 hypoglycemia and hyperkalaemia

 Management
o Remove patient from heat source, remove clothes
o Consider
 rapid cooling if temp >40, “strip, spray, fan. Ice”
 gentle cooling if temp <40,
 IV fluid,
 analgesia,
 antiemetic,
 paracetamol if infective cause
o Consider oxygen, IPPV, LMA ETT

Burns

 Most burn injuries are the result of flame burns or scalds, with electrical and
chemical burns less common
 Life Threats
o Respiratory compromise
 Facial/oral burns
 Singed nasal hair
 Carbonaceous sputum
 Tachypnoea, stridor, hoarseness
 Trapped  look for CO poisioning
o Circumferential burns  to torso can restrict ventilation, requiring urgent
surgical intervention.

 In the acute setting, airway burns and inhalation injury can lead to respiratory
compromise, as over a number of hours, fluid and electrolyte abnormalities develop
in major burns and can lead to shock

 Depth of burn
 o Superficial – erythema, brisk cap refill, painful
o Superficial dermal – moist, reddened with blisters, brisk cap refill, painful
o Deep dermal – white slough, reddened and mottled, sluggish or absent cap
refill, painful
o Full thickness – dry/charred, whitish, absent cap refill, painless

 Management
o Dedicated burns unit
 Partial thickness >20%
 Or >10% in <10 or > 50
 Full thickness >5%
 Burns involving face, eyes, ears, hands, feet, genital, or overlying a major
joint
 All inhalation burns
 All significant electrical burns
 Burns in people with significant co-morbidities.
o IV fluids should not be administered to pts with facial, neck or upper chest
burns with high potential for airway or ventilation compromise before airway is
secured  can increase oedema and make ETT difficult.
o Avoid hypothermia
o Estimate burn area – rule of nines

o Evidence of airway burn/inhalation injury/circumferential thoracic burn 

  oxygen,
 IPPV,
 early airway assessment and management
o Hemodynamically unstable 
 consider other injuries,
 IV fluid,
 continue to reassess airway
o Pain  active cooling, analgesia, midazolam, ketamine
o Protect against hypothermia, active cooling first 20min only,
o Cling wrap, burn aid only if <10% paed, <20% adult

Near drowning

 Post submersion refers to survival following immersion where potential or actual

respiratory compromise has occurred
 Presentation ranges from asymptomatic to significant respiratory and cardiovascular
compromise deteriorating to cardiac arrest
 Secondary complications include non-cardiogenic pulmonary oedema, aspiration
pneumonia and anoxic encephalopathy

 Clinical features
o Neurological – ALOC, confusion, agitation
o Cardiovascular
 dysrhythmias usually associated with hypotension,
 hypotension,
 cardiac arrest
o Respiratory
 dyspnoea,
 non-cardiogenic pulmonary oedema,
 acute respiratory distress syndrome,
 aspiration pneumonia, r
 respiratory arrest
o Other – spinal injury, vomiting and nausea, hypothermia, diving injury

 Management
o Consider oxygen, CPAP, IPPV, PEEP, IV access, gastric tube, analgesia,
antiemetic, correct reversible causes, maintain normothermia
o Spinal immobilisation for significant MOI

Electric shock
 Extent of injury following electric shock depends on amount of current passed
through body, duration of the current, and the tissues traversed by the current
 Visible injury is not an indicator of severity – there may be serious internal injury to
nerves and vessels as they offer little resistance to electrical energy

 Clinical features
o Neurological – ALOC, seizures, amnesia, dysphagia, motor dysfunction, spinal
cord damage
o Respiratory arrest/dysfunction
o Cardiac arrest or dysfunction – dysrhythmia, palpations, myocardial damage
o Pain
o Vascular damage
o Renal failure
o Trauma – burns, fractures, entry and exit wounds, secondary injuries due to
falls, compartment syndrome

 Management
o Consider c-spine injuries,
o IV access, analgesia, 12 lead ECG, IV fluid, dysrhythmia treatment, burn
management

Sepsis

 Clinical features
o Presumed site of infection plus two or more of
 Temperature >38.3 or <36
 HR >90
 Resp rate >20
 BGL >6.6 (not diabetic)
 ALOC
o Severe sepsis defined as presence of sepsis as evidence of organ
hypoperfusion or dysfunction with one or more of the following
 SBP <90 or MAP <65,
 SpO2 <90%,
 not passed urine for >8hrs,
 prolonged bleeding from minor injury or gums
o should be suspected in any unwell person who is immunosuppressed
o paediatric and elderly may only have slight increase in temp.

 Management
o Antipyretic,
o Oxygen
o IV fluid,
o adrenaline
Meningococcal septicemia

 Life-threatening infection caused by Neisseria meningitides

 Clinical features
o Non blanching rash either petechial or purpuric, myalgia
o Evidence of meningism
 photophobia,
 neck stiffness,
 headache,
 nausea and vomiting
o Severe lethargy, fever,
o clinical evidence of shock
o Signs of serious ill child
 Floppy appearance,
 grunting or head bobbing,
 drowsy and unresponsive,
 bulging or full fontanelles,
 respiratory distress,
 tachypnea,
 hypoxia,
 pale cool mottled skin,
 poor cap refill

 Management
o Ceftriaxone,
o IV fluid

I know the indication, dose and contraindications of Ceftriaxone in

meningococcal septicaemia

 Indications – suspected meningococcal septicaemia with a non-blanching petechial

and/or purpuric rash
 Contraindications – KSAR/hypersensitivity to cephalosporin drugs, known
anaphylaxis or KSAR to penicillin based drugs (isolated minor drug rash does not
apply)
 Adult dose – IM 1g +3.6ml water for injection slow push, IV 1g +9.6ml water for
injection, slow push
 Paediatric dose – IM 50mg/kg
I know the indication, dose and contraindication of fluid administration in burns

 IV fluids should not be administered to patients with significant facial, neck or upper
chest burns with high potential for airway or ventilation compromise before the
airway is formally secured at hospital
 Large amounts of fluids increase the risk of interstitial oedema and tissue swelling
 Burns > 25% partial or full thickness  % x pt wt = volume of normal saline  given
over first 2 hours from time of burn.

Week 10: Poisoning/Overdose

I can identify and manage the S&S of an OD, including

Narcotics

 Opioid Toxidrome
o Constricted pupils, sedation/CNS depression, respiratory depression
o Complications of prolong periods of deep sedation – hypothermia, skin
necrosis, compartment syndrome, aspiration

 Management
o IPPV, oxygen, naloxone

Tricyclics
 TCA agents act on multiple receptor sites – their principle antidepressant action is
mediated by serotonin and noradrenaline re-uptake inhibition
 Myocardial toxicity is via sodium channel blockade
 Toxicity is mediated by inhibitory action at the muscarinic, histamine and adrenergic
receptors
 Clinical effects
o Anticholinergic effects – agitation, delirium, dilated pupils, dry/warm/flushed
skin, hyperthermia, urinary retention
o Neurotoxicity – sedation, seizures, coma
o Cardiotoxicity – tachycardia, hypotension, broad complex arrhythmias,
bradycardia (late sign)
o ECG changes – prolonged PR, QRS, QT interval, large terminal R wave in aVR

 Management
o oxygen,
o IPPV,
o IV access,
o IV fluid,
o 12 Lead ECG,
 o sodium bicarbonate,
o midazolam if agitated

Organophosphates
 Pesticides that inhibit acetylcholinesterase enzyme, increasing the action of the
neurotransmitter acetylcholine at parasympathetic and presynaptic sympathetic
ganglion receptors, which may be fatal
 Clinical features
o Muscarinic (DUMBBELS) – diarrhoea, urination, miosis (constricted pupils),
bronchospasm, bradycardia, emesis, lacrimation, salivation, hypotension
o Nicotinic effects – fasciculation’s, tremor, muscle weakness, respiratory muscle
paralysis
o Central effects – agitation, seizures, coma
 Management
o Oxygen, IV access, antiemetic, atropine, IPPV, IV fluid

Corrosive chemicals

 Corrosive agents cause direct injury to the respiratory and

gastrointestinal tract if ingested. Resultant airway compromise can be lethal
 Acids
o Coagulative necrosis
o Eschar formation limits depth of penetration
o HCL, H2SO4, HF
 Alkali
o Liquefactive necrosis  ongoing deeper penetration
o NaOH, KOH,, ammonium, sodium hypochlorite
 Other
o Disc button batteries

 Clinical features
o Respiratory – hoarse voice, dyspnoea, stridor
o GIT – oral burns, drooling, painful swallowing, vomiting, abdo pain.

 Management
o Rinse pt mouth with water
o Do not encourage vomiting
o Consider
 Oxygen, IPPV, Iv access, analgesia, calcium gluconate neb (HF
inhalation)
 Antiemetic
 IV fluid
Paraquat poisoning

 Is a caustic herbicide, and is usually lethal in overdose and just 15ml of a 20%
solution is fatal

 Clinical features
o Immediate – gastrointestinal upset
o Early hours – oral corrosive injury, metabolic acidosis with large ingestions,
hypotension and respiratory distress
o Delayed – progression of acidosis, multi-organ failure, coma seizures
o Late – pulmonary fibrosis if patient survives

 Management
o oxygen, IPPV, analgesia, antiemetic

I can identify and manage the S&S of the following envenomation’s

Stonefish

 Immediate localized pain and swelling, evidence of single or multiple penetration

wounds, swelling can involve the whole limb in severe cases, sometimes blue tinge
may be seen around envenomation site
 Systemic symptoms are rare but typically associated with pain response,
nausea/vomiting, hypotension, bradycardia, incoherent
 Rarely is the hypotension/bradycardia a direct effect of the specific toxins within the
stonefish Synanceia spp, vascular leakage is direct effect of stonefish venom and in
severe cases can cause hypotension
 Anti-venom available
 Management
o Hot water immersion
o Do not remove spine, stabilise
o Consider
 Analgesia

Puffer fish

 Upon ingesting the fish systemic signs of envenomation can develop as, perioral
numbness and paresthesia, nausea, lingual numbness leading to slurred speech,
ataxia and muscle weakness
o In severe cases it can lead to respiratory arrest, onset and severity of
symptoms can vary greatly depending upon the quantity and parts of the fish
consumed, anywhere from 5 mins to 24hrs
Blue ringed octopus

 Hx of handling or interfering with small octopus, bit is normally painless

 Symptoms are that of the puffer fish with the exception of the development of
systemic symptoms can be rapid to de toxin being delivered via bit rather than
ingestion
 Severe respiratory distress and respiratory arrest can develop within 15 -20 minutes
 Management
o Pressure immobilisation bandage

Box Jellyfish

 Severe localized pain, adherent tentacles and associated lesions, possible

dyspnea, incoherence, ALOC, cardiovascular collapse, in some cases cardiac
arrest within 5 mins of sting
 Antivenom available

 Management
o Copious flushing with vinegar
o No vinegar available use sea water
o Remove tentacles
o Ice, cool packs
o Consider
 Analgesia
 Ice, cool packs
 Box jelly fish antivenom
 Magnesium sulphate

Irukandji syndrome

 Localized sting, often minor and unnoticed, occasionally can be severe

o Delayed onset of symptoms 5-10mins, catecholamine excess leading to
restlessness, anxiety, diaphoresis, nausea, vomiting, hypertension,
tachycardia, back and/or chest/abdominal pain with limb involvement
 Management
o Copious flushing with vinegar
o No vinegar available use sea water
o Remove tentacles
o Ice, cool packs
o Consider
  GTN if hypertensive
 Analgesia
 Magnesium sulphate

Blue bottles

 Typically localized pain, welts, any adhering tentacles will be blue

 Systemic effects are rare but may include nausea, vomiting, sweating, muscle
cramps, headache, systemic symptoms may resemble Irukandji if particular species

 Management
o Remove tentacles
o Wash area with sea water
o Poor hot water over sting (max 45 degrees)
o Consider
 Analgesia
 heat packs

Stingray
 Management
o Hot water immersion
o Do not remove spine, stabilise
o Consider
 Analgesia

Ciguatoxin poisoning from tropical fish ingestion

 Two clinical patterns of ciguatera poisoning, GIT and neurological
o GIT – develops initially, but can be delayed up to 24hrs, diarrhea, nausea and
vomiting, abdo pain
o Neuro – may develop over 24hrs, myalgia, temperature sense reversal,
paresthesia of hands and feet, mouth, lips, dental pain, rare hypotension and
bradycardia

Cones Shells
 Intense sharp stinging pain when handling the shell, followed by local numbness
 In severe cases, localized numbness spreads, which can involve throat and lips,
ataxia, partial paralysis of voluntary muscles and respiratory failure
 Management
o Pressure immobilisation bandage
Spider bites

 Large black OR Funnel-web spider

o Localized severe pain at bite site, puncture/fang marks are often visible
o S&S suggest severe systemic envenomation and may occur within 10mins
 General – agitation, nausea, vomiting, headache
 Neuro – muscular spasm, numbness/tingling around mouth, ALOC
 Autonomic – diaphoretic, salivation, piloerection, lacrimation
 Cardiovascular – hyper/hypotension, tachy/bradycardia, pulmonary
oedema
o Management
 Pressure immobilastion bandage

 Red back spider

o Local and regional signs and symptoms
 Bites are not initially painful, increasing pain radiating from the bite site to
the proximal limb, trunk or local lymph nodes
 Localized or regional diaphoresis
 Less common – piloerection, localized redness, bite marks
o Systemic signs and symptoms
 Nausea/vomiting, headache, malaise and lethargy, potentially generalized
pain
 Less common – hypertension, irritability and agitation, fever,
paranesthesia, muscle spasms

o Management
 ICE pack
 Analgesia
 IV access
 IV fluid

Snake bites
 Nonspecific symptoms in most cases – nausea, vomiting, headache, abdominal
pain, diarrhea and diaphoresis
 Other signs and symptoms that may be present – ALOC, visual disturbances,
seizures, respiratory dysfunction, hypotension, haemorrhage or haematoma at site,
paired or single fang marks, swollen tender glands of affected limb
 Systemic effects
o Neurotoxicity – drooping of eyelids, drooling, paralysis
 o Coagulopathy – bleeding from nose and gums common, major haemorrhage
uncommon
o Myotoxicity – damage to skeletal muscles
o Renal impairment/failure

 Management

I know when to apply a pressure immobilisation bandage;

  Snake bite
 Funnel web spider bite
 Blue ringed octopus
 Cone shells

I know the indications, doses and contraindications for Narcan administration

 Indications
o respiratory depression secondary to the administration of narcotic drugs
 Contraindications - KSAR
 Adult dose – IM 1.6mg SDO,
o IV 50mcg  NMD (CCP only)
 Paediatric dose – IM 20mcg/kg SDO not to exceed 800mcrog

Week 11: Paediatrics and Gerontology

I understand the factors and variables which influence patient care in an elderly
patient
Cardiovascular System
 Myocardium loses contractility– ↓ CO → ↑HR → Mild left hypertrophy
 ↓ Elasticity of blood vessels
o ↑ peripheral resistance
o ↑ SBP
 ↓ CO + ↑ peripheral resistance = ↑ risk of hypoxia
 Higher risk of dysrhythmias

Respiratory System
 Stiffening of trachea and rib cage
 Kyphosis may occur increasing the size of the rib cage
 Muscles of respiration weaken
 Reduction in ventilation, cough and gag reflex
 Hypertrophy of mucous producing cells and loss of cilia action increases the risk
of infection
 Reduced arterial partial pressure of oxygen

Gastrointestinal System
 ↓ GIT motility with age → ↓ gastric emptying
 ↓ GIT absorption
 ↓ Subcutaneous fat deposits around organs affords less protection
 Abdominal pain is twice as common amongst the elderly and 10 times likely to
be something serious

Renal System
 Nephrons decrease in both size and number
 ↓GFP
 Kidney reduces in size by 20%
 Hypotension more likely to cause renal damage
 At higher risk of:
o Metabolic acidosis
o Fluid imbalance – overload versus dehydration

Endocrine System
 ↓ Thyroid activity → Reduced metabolism rate
 ↓ Adrenal gland activity
 ↓ Insulin secretion and ↑ insulin resistance
 Impaired glucose metabolism → Hyperglycaemia

The Senses
 ↓ Sensory function
 o Visual loss
o Reduction in peripheral vision
o Hearing loss
o Reduction in sense of smell
o Reduction in skin sensation e.g. Heat, cold, pressure, pain

Nervous System
 Cognitive function begins to slowly decline after the age 20 although intelligence
is stable to the 9th decade
 The brain’s size decreases by 20% from ages 25 – 95
–  loss of neurons
–  atrophy of the cortex
 Cerebral blood flow is decreased and the BBB becomes less effective
o Narcotic drugs have more of an effect on the CNS
 Nervous system is less able to cope with external temperature changes
 Neurotransmitter function can also be altered slowing mental function

Musculoskeletal System
 Muscle atrophy occurs
o Muscle fibres decrease and are replaced by fibrous tissue
o Decrease in muscle strength and movement
o Muscle tone loss is activity related i.e. sedentary lifestyle has higher
muscle fibre loss
 Tendons shrink and harden
 Bone mass decreases
o ↓ Ca absorption through GIT
o Brittle bones
o ↑ risk of fractures

I understand the considerations regarding the delivery of drugs to geriatric

patients

 An increased volume of distribution may result from the proportional increase in

body fat relative to skeletal muscle with aging.
 Decreased drug clearance may result from the natural decline in renal function with
age, even in the absence of renal disease.
 Larger drug storage reservoirs and decreased clearance prolong drug half-lives and
lead to increased plasma drug concentrations in older people.
 Hepatic function also declines with advancing age, and age-related changes in
hepatic function may account for significant variability in drug metabolism among
older adults. Especially when polypharmacy is a factor, decreasing hepatic function
may lead to adverse drug reactions (ADRs).
I understand the factors and variables which influence patient care in a paediatric
patient particularly in relation to pain management
Anatomical and Physiological Differences and Assessment
Airway
 Infants <6 months are obligate nasal breathers - easily blocked especially in
upper respiratory tract infections, narrow in relation to adult
 3-8yo adenotonsillar hypertrophy may cause problems when inserting airways
and can contribute to airway obstruction
 Head is relatively larger in children which is naturally flexed in the supine
 Due to narrow and more compliant airway obstruction occurs more easily
 Effects of Oedema on Airways: a minor reduction in airway diameter in
paediatrics result in significant airway cross-sectional area
 In laminar flow airway resistance to 16 fold but this can double turbulent flow

OP Airway Insertion
 Due to size of oropharynx, large tongue, possibility of trauma, and tonsils, may
be necessary to use alternative method of inserting OP airway

Breathing
 Increased rate of respiration - infants rely on diaphragmatic breathing and their
muscles tire more easily - leads to respiratory failure
 Increased metabolism and oxygen consumption
 Decreased functional residential capacity (reduced oxygen reserve in lung) -
more prone to hypoxia, oxyhaemoglobin desaturation occurs quickly, fewer
alveoli per surface area
 Increased chest wall compliance - leads to prominent sternal recession and rib
space indrawing when airway is obstructed or lung compliance
 Decreased lung elastic recoil - allows intrathoracic pressure to be less negative
(reduces small airway patency)

Signs of Respiratory Distress

 Tachypnoea - often the first sign of respiratory distress
 Increased respiratory effort (retractions, nasal flaring)
 Grunting - from small airway collapse or alveolar collapse (pneumonia, CHF,
acute respiratory distress syndrome, pulmonary contusion)
 Stridor - sign of extrathoracic obstruction, foreign body, infection, upper airway
obstruction
 Wheezing - intrathoracic lower airway obstruction (commonly due to bronchitis
and asthma - usually expiratory wheeze)
o Isolated inspiratory wheeze may suggest foreign body or other upper
airway obstruction
o Inspiratory and expiratory wheeze - often heard in severe asthma/airway
obstruction worsening

 Seesawing or abdominal breathing - severe chest retractions during inspiration

accompanied by expansion of the abdomen
o Serious sign - upper airway obstruction
o Will lead to fatigue and respiratory failure quickly
  Head bobbing - a sign of markedly increased respiratory failure
o More prominent in newborns

Signs of Imminent Respiratory Failure/Arrest

 Bradypnoea,
 bradycardia,
 periodic apnoea,
 diminished air movement,
 low SPO2,
 decreasing LOC/ stupor/coma,
 poor skeletal muscle tone,
 cyanosis

Circulation
 Stroke volume in infants is relatively fixed (until the age of 2)
 The child’s circulating volume is higher per kg per body weight but actual volume
is small
o Small blood loss can be critical
 Paediatrics (esp >2yo) maintain good systemic vascular resistance (SVR) so
maintain BP for significant period and then decompensate rapidly
o Do not rely on BP as an indicator for developing shock - look for other
clinical signs such a pulse CR skin and LOC
 In infants, the brachial pulse is the preferred site
 The apex of the heart can also be used
 Blood Pressure
 In patients 1-10 yo the following can be used to define hypotension
o <70mmHg + (age in years x 2) mmHg
 BP in paediatrics <3yo can be difficult to obtain
o If unable to obtain rely on presence of a central pulse such as the
carotid
o Adequate BP usually correlates with the presence of a central pulse in
this age group
 Other assessment issues
 The cranial sutures not fully fused until 1.5-2yo
o Sunken fontanelle - dehydration/fluid loss
o Tense fontanelle - increased intracranial pressure
I can quickly and accurately calculate drug dosages for paediatric patients
I can quickly and accurately deliver correct drug dosages IMI, IN

Week 12 Theme Mental Health Aspects of Care

I can quickly identify and correctly manage a patient displaying symptoms of a

psychiatric or behavioural emergency

Patients presenting with Acute Behavioural Disturbances (ABD) pose significant clinical
risk to themselves and the health care professionals treating them. The causes of are
usually multifactorial and include mental illness, intoxication with drugs and/or alcohol
and organic illnesses such as hypoglycaemia.
 ABD can be classified into four general categories:
o Psychiatric disorders – schizophrenia, bipolar, PTSD, psychosis
o Substance related – psychostimulants, cocaine, ketamine, LSD, cannabis,
alcohol
o Organic disorders – hypoglycaemia, sepsis, hypoxia, head injury, dementia
o Situational – grief, overwhelming stress
o
 The main principles, where possible, when managing ABD patients are:
o S - Safety: POP threat assessment, constantly reassess the safety of the patient,
paramedics and others
o A - Aggression: be aware of the common triggers of aggression and violence
o F - Fix: Underlying organic illness, Focus on de-escalation strategies
o E - Evaluate the patient: VSS, PSA, RSA, NSA, SAT score, SAMPLE
o T - Tactical communication: active listening, empathy, rapport, influence,
 o Y - Yes I have the right resources: including QPS, CCP, other QAS resources

 Strategies for de-escalation

o Approach the situation with the right attitude and maintain your self-control
o Non-aggression − ensure that you communicate non-aggression with your voice
and body language
o Match energy levels − respond appropriately, and use ‘voices for occasion’
o Empathise and listen actively − empathy can help to defuse a conflict situation
o Focus on the issue at hand– Help the patient focus on how to solve their problem

 Triggers of sudden aggression include (LIFEMORTS)

1. Life or limb – self defence against a perceived threat
2. Insult – either verbal or physical
3. Family: our instincts tell us to protect our nearest and dearest
4. Environment: when someone encroaches in your personal space
5. Mates: aggressive behaviour can be perceived as attractive
6. Order: anyone who threatens to disrupt an established system of rules
7. Resources: such as money or valuables
8. Tribe: we tend to defend those with whom we identify
9. Stopped: when you feel ‘stopped’ or obstructed by a situation or person.

 Documentation and reporting

Accurate and timely recording of information related to sedation of the acute
behavioural disturbance patient is essential and should include:
 Sedation Assessment Score – SAT score for ABD patients must be
recorded on initial presentation and throughout patient reassessment

 Consent – document patient capacity for appropriate decision making (i.e.

delirium, drug or alcohol intoxication, risk to themselves or others)

 Indication for sedation – consider including what de-escalation

techniques were undertaken prior to sedation ( i.e. verbal and non-verbal
techniques)

 Physical restraint – document why utilisation of restraint was required

(i.e. risk of absconding, patient risk), form of restraint (i.e. handcuffs,
physical), potential risks of using restraints (i.e. restricted breathing,
metabolic disturbance, risk to staff or others), duration of restraint
 Medications administered – document rationale for any medications
administered and any complications

 Observations and assessments undertaken – include patient

positioning during and after sedation (i.e. supine, lateral) and frequency of
observations pre and post sedation (i.e. visual and physical)
I have an appropriate understanding of QLD MH Act particularly EEAs

 An Emergency Examination Authority (EEA) authorises the temporary detention and

transport of a person to a treatment or care place, in circumstances where the
person is acting in a manner that indicates there is a major disturbance in the
person’s mental capacity and that the person is at immediate risk of serious harm as
a result of the disturbance.
 To detain and transport a person under an EEA, paramedics must form the belief
that the following criteria are met

o the persons behaviour, including the way in which the person is

communicating, indicates the person is at immediate risk of serious
harm; and

o the risk appears to be the result of a major disturbance in the person’s

mental capacity (whether caused by illness, disability, injury,
intoxication or another reason); and

o the person appears to require urgent examination or treatment and

care, for the disturbance.

o An example of a disturbance in mental capacity is ‘person is threatening to

commit suicide’.

A paramedic may form the belief that the EEA criteria has been met, by virtue of:
 the clinical assessment;
 observations and discussions with the patient;
 relevant information including past history that has been provided by family
and/or other relevant sources. For example:
 - a police officer or a member of the public that has observed the patient
and his/her relevant behaviour prior to the arrival of the paramedic; or
 information provided by the patient’s health provider.
 Must be transported to a treatment care place, where pt can receive treatment
appropriate to their needs  doesn’t include watch house
 The paramedic must inform the person that he/she is to be detained and explain
how that may affect them.
 Patient consent is not relevant. Irrespective of whether the patient consents or
does not consent, if the EEA criteria is met, the EEA is to be applied and the
patient transported.
 Seek QPS assistance if force is required.
 Can be detained at the facility for 6 hours.
I know when to request CCP backup for sedation, I know when to request
police assistance
I know when to provide physical restrain

 Sedation Assessment Tool (SAT) is a simple, rapid and useful scale used to
measure the degree of agitation or sedation of patients with ABD.
 The purpose of the SAT is to determine the patient’s level of agitation and
response to medication administration and resultant level of sedation.
 >/= 2  verbal de-escalation has failed and risk to pat or others  good
indicator for need for sedation.

 Procedure
o Predict pt risk factors
 Observe VSS
o Assemble and brief sedation team
 CCP and QPS backup
 Prepare resus equipment
o Co-ordinate approach to pt
 QPS for restraint
o Post-sedation care
 Vigilant VSS monitoring
 Repeated SAT score
 EEA