All Topics Flashcards
1
Q
What are the components and purpose of the pre hospital “platinum 10mins”?
A
The first 10 mins on scene when assessing trauma patients with the aim of improving survival rates.
Components include:
Assessment & Management
Every action must have a life saving purpose
Organised, details oriented, selective and rapid
2
Q
What is the golden period. Formally known as the golden hour?
A
The time given from the moment of injury until definitive care at a hospital can be reached for a trauma patient.
Survival rates increase by up to 85% if definitive care is achieved within the golden period.
3
Q
What are the basic mechanisms of injury in trauma?
A
Blunt Force Trauma (incl. Falls)
MVC
Penetrating Injuries
Pedestrian Injuries
Tractor Injuries (incl. crush injuries)
Blast Injuries
4
Q
What are the types of impact that can occur from an MVC?
A
Frontal Impact
Lateral Impact
Rear Impact
Rotational
Roll Over
5
Q
What are the 5 injury causes/classifications that occur with blast injury?
A
Primary - Inital air Blast
Secondary - Material that is propelled
Tertiary - Impact of the body on to surrounding objects
Quaternary - Thermal burns and respiratory injury
Quinary - Contamination from dirty bombs.
6
Q
What are the 5 key components of the scene size up?
A
- Number of Pts
- MOI/Nature of illness
- Resource Determination
- Standard Precautions/PPE
- Scene Safety
7
Q
What trauma related injuries are considered to be load and go situations?
A
Altered Mental Status
Abnormal Respirations
Abnormal Circulation
Abnormal Chext Exam
Tender/Distended Adbomen
Pelvic Instability
Bi-Lateral Femur Fractures
8
Q
What is the FAST assessment in relation to trauma?
A
Focused
Assessment with
Sonography in
Trauma
9
Q
What is the vital sign of ventilation and what does it measure?
A
ETCO2 - End tidal Carbon Dioxide
EtCO2 is the measurement of CO2 that is being exhaled with every breath and informs you to how well a patient is respirating.
10
Q
What procedures are completed on-scene in the treatment of a trauma patient?
A
Protect C-Spine
Control Major Haemorrhage
Manage Airway
Begin CPR - if indicated
Assist Ventilations
Seal Sucking Chest
Stabilise Flail Chest
Decompress Tension Pneumo
Stabilise Impaled Objects
Give O2
11
Q
What injury types would you expect to see in a MVC Frontal Impact (Head-On Collision)?
A
- Head, Face and Neck Injuries
- Chest Injuries as a result of Steering wheel
- Deceleration Injuries
- Pelvic, Hip & Knee
- Lower Leg Injuries
12
Q
What injury types would you expect to see in an MVC Lateral Impact?
A
- Rotational forces and Hyperextension of the neck
- Head and Neck
- Spleenic Rupture (Passenger Side)
- Liver Rupture (Drivers Side)
- Shoulder (Subclavian Rupture)
- Abdo, Pelvic, Leg Injuries
13
Q
What is the Ligamentum Arteriosum and when do injuries occur with this ligament?
A
A small fibrous remnant of the foetal ductus arteriosum, located between the connecting proximal left pulmonary artery and the under surface Junction of the aortic arch and descending aorta.
Commonly injured where there is deceleration forces causing a traumatic aortic rupture at the aortic isthmus and ascending aortic arch.
14
Q
Compare tendons versus ligaments?
A
Tendons bind skeletal muscle to bone whereas ligaments bind bone to bone.
15
Q
What are common types of musculoskeletal injury?
A
Fractures
Dislocations
Neurovascular injury
Sprains & strains
Impaled Objects
Amputations
Compartment Syndrome
Burns
Open & Closed Wounds
16
Q
In relation to the neurovascular bundle what can checking PMS inform you to, and what are the components of PMS?
A
PMS:
- Pulse
- Motor
- Sensation
Checking PMS on distal peripheral limbs can inform you of neurovascular compromise and or issues that might be occurring proximally to the injury site.
17
Q
What are the components of the neurovascular bundle?
A
Artery/s
Vein/s
Nerve/s
Lymph Vessels
18
Q
Compare open and closed fractures?
A
Open fractures:
- Communicate with the outside
- Have a high risk of infection due to contamination risk
- Blood loss occurs outside of the body
Closed Fractures:
- Do not communicate with the outside
- Lower risk of infection
- Blood loss occurs inside the body
19
Q
What are the common fracture types?
A
Transverse
Oblique Non-Displaced
Oblique Displaced
Spiral
Linear
Greenstick
Comminuted
20
Q
Explain what an open book fracture is?
A
A fracture of the pelvis caused by anterior compressive forces that widen the Sacroiliac Joint (SIJ) by 4mm or more and the Pubic Symphsis by 5mm or more.
21
Q
What is a major concern with a displaced fracture?
A
Displaced fractures can lead to bone marrow leaking into circulation resulting in the development of a fat emboli. This results in a widespread inflammatory response, primarily in the lungs causing profound dyspnoea and hypoxia.
22
Q
What are the rules of splinting?
A
- Always adequately visualise the injury
- Check PMS before & after splinting
- Cover & treat open wounds before splinting
- Immobilise one joint above & below fracture
- Never attempt to push bone ends back under the skin
23
Q
What is the Ottawa Ankle/Foot Rule and how is the assessment completed?
A
An assessment used to help identify the likelihood of a fracture in the foot or ankle after trauma as opposed to a sprain or strain. Which helps assess the need for an X-ray and transport to hospital.
Steps to complete assessment:
1 - Palpate the posterior edges of the lateral and medial malleolus starting distally moving upwards by approx 6cm.
2 - Palpate for pain or tenderness over the navicular bone and 5th metatarsal.
3 - Ask the Pt to walk 4 consecutive steps.
NB: if there is any positive result there is a 25%-50% chance of a fracture and an X-ray is recommended. If a negative result there is almost a 100% chance of no fracture.
24
Q
Compare a Sprain and Strain?
A
A sprain is a torn or stretched ligament whereas a strain is a torn or stretched tendon past their natural anatomical range of motion.
25
Compare a Dislocation vs Subluxation?
A Dislocation is a complete displacement of a bone from its normal anatomical position.
A Subluxation is an incomplete or partial dislocation where the bones of the joint remain in contact.
26
Explain the management of dislocation that present with and without neurovascular compromise?
Without Neurovascular Compromise:
- Splint in the position the limb is found.
- Analgesia (Methoxy, Morphine, Fentanyl)
With Neurovascular Compromise:
- Analgesia/Sedation (Ketamine, methoxy, Morphine, fentanyl)
- Apply gentle traction in an effort to straighten approx 5kg of force, STOP IMMEDIATELY if resistance is felt.
- Pad and Splint in the most comfortable position.
27
What are the 6 P's of limb ischaemia that indicate neurovascular compromise?
Pain
Pallor
Pulselessness
Perishing Cold
Paresthesia
Paralysis
28
Explain how TXA (Tranexamic Acid) works?
TXA is an antifibrinolytic which prevents fibrinolysis. It exerts its effect by reversibly binding to plasminogen. This inhibits plasmin activation and inhibits fibrin clot degradation allowing for a mesh like structure to remain that RBC's can attach to promotting clot formation, therefore stopping bleeding.
29
What is the stepwise approach to haemorrhage control?
1. Direct Pressure
2. Elevation
3. Pressure Points
4. Consider; Ice and Torniquet
30
What are the main objectives of wound dressing and bleeding?
Haemorrhage Control
Sterility
Immobilisation
31
Define the term 'Contusion'?
Bruising, caused by a direct blow to the body resulting injury to the vessels causing an accumulation of blood to the affected area.
32
Define the term 'Haematoma'?
A type of contusion that involves damage to large vessel resulting in the separation of tissue and the pooling of blood.
33
Define the term 'Abrasion'?
Abridement of the epidermis that oozes blood rather then significant bleeding. This injury has a high risk of infection associated with it.
34
Define the term 'Laceration'?
A type of cut that penetrates into the dermis and deeper tissues resulting in significant damage to vasculature, nerves, muscles, tendons and ligaments.
35
Define the term 'Avulsion'?
An injury that involves a flap of skin that is torn or cut but still attached to the body.
36
Define the term 'Amputation'?
Partial or complete severance of a limb or digit that comes with the possibility of major haemorrhage but is commonly controlled with direct pressure on the injury site.
37
What are the common complications with IO insertion?
Extravasation
Fracture
Compartment Syndrome
Injury to clinician
38
What insertion sites ate used in IO access?
Proximal Tibia
Distal Tibia
Humeral Head
39
What are the contraindications for IO access?
- Fracture of the target site
- Previous orthopaedic procedures at the target site
- Site infection
- Osteoporosis
- Inability to accurately locate landmarks
- IO access within the last 24-48 hours
40
When/What injuries is IO access indicated?
- Pts who are peripherally shut-down and IV access is not possible.
- Burns Pts
- Paeds in arrest
- Special populations (elderly or bariatric paitents)
- Failed IV access in time critical situations (major trauma)
41
What are the IO needle sizes and who are they indicated for?
- Pink 15mm needle (3 to 39kg pts)
- Blue 25mm needle (40kg+ pts)
- Yellow 45mm needle (> 40kg pt with excessive tissue or muscles eg. Bariatric pts)
42
What are the 5Rs of IO insertion?
- Right Site
- Right Needle size
- Right Pain management (Consider lignocaine 2% @ insertion site)
- Right amount of Pressure (100mmHg - 300mmHg for infusions)
- Right flush (NaCl 0.9%l
43
What catecholamines are released during shock?
Adrenaline
Noradrenaline
Dopamine
44
What signs and symptoms do you see with shock progression as a result of catecholamine release?
- Initial rise in BP due to shunting
- Initial narrowing of pulse pressure
- Tachycardia
- Vasoconstriction
- Diaphoresis
- Compensated shock crashes and BP drops
45
In relation to MAP and keeping vital organs perfused, what pressures need to be maintained?
MAP of 50 is the minimal target
MAP of < 40 causes brain damage
MAP of 65 perfuses the heart
MAP of 65-70 perfusses the kidneys.
46
What is MAP and how is it calculated?
MAP = Mean arterial pressure. This is the average pressure in the arteries after 1 cardiac cycle and is used to indicate organ perfusion.
Calculation = SBP + (2 × DBP) ÷ 3
47
What can taking Serum lactate levels tell you about a patient in shock?
An increase of serum lactate can tell you the level of acidosis and indicates decompensation which increases mortality.
POCTSL of > 4mmol/L indicates shock and acidosis
- Normal range is 0.5-1.0mmol/L
48
Explain hypovolaemic shock and identify some common causes?
Hypovolaemic Shock occurs when there is a decrease in systemic blood/fluid volume needed to maintain systemic perfusion which decreases cardiac output and death of vital organs due to inadequate organ perfusion.
Common causes:
- Bleeding (internal and external)
- Diarrhoea
- Vomiting
- Sweating/Low intake.
49
Explain 'Third Spacing'?
Third spacing is the movement of fluid volume from systemic circulation or vessels into the interstitial spaces where it cannot be utilised by the body.
50
Regarding trauma coagulopathy, what are the main causes that alter it and what %age of trauma pts have altered coagulopathy?
25% of trauma pts have altered coagulopathy and increased the incidence of death by 5 x
Common causes:
Haemodilution, hypoxia, hypoperfusion and tissue damage.
51
When should TXA be given and what is it dosage and preparation?
TXA should be given if there is evidence of bleeding within 3 hours of the incident.
Dose given by IV/IO:
10 - 25mg/kg
Or
1g over 10mins then 1g over 8 hours
Preparation:
500mg in 5ml or 100mg in 1ml
52
Explain Cardiogenic shock and the common causes?
Cardiogenic shock occurs due to a problem with the heart reducing its ability to pump enough blood volume to mainting organ perfusion and often associated with pre-existing heart conditions.
Common causes:
Cardiac Arrest
Myocardial Contusion (injury to the myocardium)
Tachycardia/Bradycardia
Toxicology/Drugs (Beta Blockers/Calcium Channel Blockers)
ACS/Electrocution
53
What is the treatment for cardiogenic shock?
Treatment is given by the administration of vasopressors and inopressors to maintain cardiac output.
Vasopressors:
- Vasopressin & Phenylephrine increase venous and arterial vasoconstriction to increase SVR
Inopresors:
- Adrenaline, Noradrenaline & Dopamine, increase HR, SV, CO & SVR
54
What is the dosage as per NSWA protocols for an Adrenaline infusion used for the treatment of Cardiogenic Shock?
1mg/10ml (1:10000 Adrenaline) diluted in 90mls of NaCl to a dose of 10mcg/ml.
Dose is infused via a microdrip set at a rate of 5mcg/min (30dpm)
Or
Via a syringe driver at a rate of 0.5ml/min
55
Explain obstructive shock and some common traumatic causes?
Obstructive shock occurs when there is a blockage that obstructs blood flow to or through the heart, slowing venous return and decreasing cardiac output.
Common Traumatic Causes:
Tension Pneumothorax
Cardiac Tamponade
56
Explain Distributive shock and give some common causes
Distributive shock occurs as a result of vasodilation, an increase in vascular permeability or both, and can also result in the interruption of SNS transmission function and decreased cardiac output.
Common causes:
Anaphylaxis
Spinal Cord Injuries (neurogenic shock)
Sepsis
57
How does neurogenic shock occur, how does the Pt present and what is the treatment regimen for neurogenic shock?
Neurogenic Shock often occurs as a direct result from a spinal cord injury above T6 resulting in decreased SNS function with no catecholamine release to compensate for the injury.
Pts often present better then they actually are with signs and symptoms of:
- Normal or Bradycardic HR
- Dry, warm, pink skin
- Paralysis or deficit
- No chest movement due to decreased SNS response to activate the diaphragm.
- Hypotension due to increased PNS function resulting in vasodilation.
Treatment given to maintain a MAP of 80-85mmHg:
Atropine
Fluids
Vasopressors
58
What are the basic rules of shock management?
- Predict it where possible
- Maintain Airway
- Maintain oxygenation and ventilation
- Control Bleeding where possible
- Maintain circulation (adequate HR and MAP)
- Consider the correct fix (fluids, vasopressors, obstruction, leak fix)
59
What mechanism that lead to spinal injury?
Hyperextension
Hyperflexsion
Lateral Stress
Compression
Rotation
Axial loading injuries
60
Compare Spinal Shock vs Neruogenic Shock?
Spinal shock is an injury to the spinal cord at any level that results in bleeding, inflammation, catecholamine release and the release of additional chemical and inflammatory mediators resulting in vasoconstriction, spinal cord ischaemia and hypoxia with paralysis or loss of sensation below the level of injury.
Neurogenic shock occurs when there is injury to the spinal cord above T6 that depresses the SNS activation and the loss of catecholamine release leading to hypotension, vasodilation and bradycardia and may have paralysis or sensation loss as well.
61
What are some signs and symptoms of a spinal injury?
- Pain on movement of back or spinal column
- Deformity
- Guarding against movement
- Loss of Sensation
- Weak or flacid muscles
- Loss of bladder/bowels
- Priapism
- Neruogenic Shock
62
What is the SPINAL Acronym and what is it used for?
Spinal is used to determine the need for SMR.
- Suspicious MOI
- Pain or Tenderness around spine
- Intoxication of any sort
- Numbness, tingling, sensory or motor deficit
- Any distracting injuries
- Level of consciousness alterations
63
How does pCO2 affect the blood vessels and what is the normal EtCO2 value to be maintained in pts with head injuries?
High pCO2 causes vasodilation
Low pCO2 causes vasoconstriction
Normal range is 35-40mmHg
64
What are pressures to be maintained of the following for pts with head/brain injuries?
ICP
CPP
MAP
ICP = 5-15mmHg
CPP = 60mmHg
MAP = 65mmHg
65
What are the specific ranges of concern when it comes to ICP and if there are present S&S of an increased ICP what is the assumed ICP said to be?
5-15mmHg Normal
> 15mmHg Dangerous
>25mmHg leading to cerebral herniation syndrome
If S&S present ICP = 20mmHg
66
What are the 3 meninges from the outer to inner most layer?
Dura Mater
Arachnoid Mater
Pia Mater
67
What factors lead to a decreased Cerebral Perfusion Pressure and how is CPP measured?
CPP = MAP - ICP
- If MAP is constant & ICP increases: CPP decreases
- If MAP decrease & ICP increases: CPP decreases
68
What bones make up the base of skull and what bones does bleeding usually go through?
Frontal
Occipital
Sphenoid
Temporal
Ethmoid (Cribiform Plate)
Bleeding commonly occurs through the Cribiform Plate.
69
Explain how Primary and Secondary TBIs occur?
Primary TBI: occurs from the direct impact or force to the head and coup and contra-coup from the movement back and forth of the brain inside the skull.
Secondary TBI: Results from hypoxia or decreased perfusion in response to the primary TBI.
70
What is the response of the brain with a TBI?
Swelling or fluid accumulation of the brain causes initial vasodilation which increases blood volume to the brain resulting in increased ICP.
Decreased blood flow and vasoconstriction occurs in response to the increased ICP to protect the brain resulting in decreased perfusion and cerebral ischemia (hypoxia).
71
What are the specific types of brain injury?
Concussion
Cerebral Contusion
Diffuse Axonal injury
Anoxic brain injury
Subarachnoid Haemorrhage
Intracranial heamatoma
Epidural hematoma
Subdural haematoma
72
Explain how the 'no reflow phenomenen' occurs?
The no reflow phenomenen occurs in an anoxic brain injury which lasts longer 4 - 6 mins in which brain cells continue to die from a lack of oxygen, as a result of spasms from cerebral arteries in the cortex of the brain which stops perfusion to the brain cells after restoring BP and oxygenation.
73
In relation to hypotension in TBIs, what value of SBP is considered to increase mortality and by how much?
A single hypotensive episode of SBP <90mmHg in adults increases mortality by 150%
In children a SBP < age appropriate is worse then 150%
74
What value is aimed for when titrating fluids for a pt with a TBI and why?
A SBP of 110-120mmHg
This value is needed to maintain the minimum CPP of 60mmHg
75
Why do you not hyperventilate a pt with a TBI and what is the ventilation rate needed?
A ventilation rate of 1 breath every 6-8secs
Hyperventilation causes vasoconstriction, resulting in an increase in hypoxia more then it decreases ICP which makes the TBI worse.
76
What is Cushing's reflex?
Physiological changes by the body known as Cushing's triad in response to increased ICP from a TBI that causes oedema, bleeding and swelling around the brain tissue resulting in decreased blood supply and perfusion making it become hypoxic.
77
What are the components of Cushing's triad and why do they occur?
Increased SBP with widening pulse pressures
Pulse rate decreases (Bradycardia)
Irregular Respiratations
- Increased SBP with widening pulse pressure; SNS activation of alpha-1 adrenergic and Beta 1 receptors in an attempt to restore adequate blood flow through increased HR and Vasoconstriction and thus improve CPP that decreases as a result of increased ICP.
- Decreased Pulse Rate; a PNS response and activation of Muscarinic 2 receptors that triggers the baroreceptors in the aortic arch to decrease the HR in response to the increased SBP and intial increase in pulse rate, causing bradycardia, decreased CPP and further increase in ICP.
- Irregular Respiratations; Pressure on the brainstem where the respiratory centre is located causes it to become dysfunctional as a result from the accumulation of blood/fluid/swelling around the brain.
78
Explain Cerebral Herniation Syndrome?
Cerebral Herniation Syndrome is preceded by Cushing's reflex and occurs when the brain is forced downwards due to increased volume in the skull, applying pressure to the brainstem and obstructing CSF forcing the brainstem and spinal cord down through the foramen magnum.
79
What are the S&S of Cerebral Herniation Syndrome?
- Preceded by Cushing's Reflex/Triad
- Decreased LOC with rapid progression to coma
-Ipsilateral pupil dilation
- Decerabrate Posturing
- Contralateral paralysis
- Respiratory Arrest
80
What is the treatment for Cerebral Herniation Syndrome and why is it done?
Maintain EtCO2 at 25-30mmHg and Hyperventilation at a rate of:
Adult - 20bpm
Child - 25bpm
Infant - 30bpm
Hyperventilation is done to remove excess CO2 build up to cause vasoconstriction and reduce the swelling/pressure on the brain as increased ICP outweighs the risk of hypoxia.
81
What is The Babinski reflex/sign?
A test that is done in an unconscious pt to assess for a spinal injury, by stroking the lateral side of the foot in an upward motion and across the ball of the foot.
If the toes flex upwards and fan out the test is positive.
If the toes flex downward the test is negative.
82
Define ventilation?
A mechanical process of moving air in and out of the lungs which is initiated by the CNS and driven by the intercostal muscles and the diaphragm for gas exchange to occur at the alveoli.
83
Define respiration?
The exchange of gases between atmosphere and cells, at the alveoli and semipermeable respiratory membrane in.
84
What are the common causes of tissue hypoxia?
- Inadequate Oxygen Delivery
- Hypovolemia
- VQ mismatch
- Pleural pressure changes (Tension Pneumothorax)
- Pump Failure
85
Explain VQ mismatch?
A VQ mismatch is defined as the ratio of the amount of air reaching the alveoli to the amount of blood reaching the alveolar. V = ventilation/Q = perfusion.
86
What are the primary 'Lethal six' of the deadly dozen?
1. Airway Obstruction
2. Open Pneumothorax (Sucking Chest wound)
3. Flail Chest
4. Tension Pneumothorax
5. Massive Haemothorax
6. Cardiac Tamponade
87
What are the Secondary 'Hidden Six' of the deadly dozen?
7. Myocardial Contusion
8. Traumatic Aortic Rupture
9. Tracheal/Bronchial Tree Injury
10. Diaphragmatic Tear
11. Oesophageal Injury
12. Pulmonary Contusion
88
Compare a Simple Pneumothorax and a Tension Pneumothorax?
A simple pneumothorax occurs when air from the atmosphere enters into the pleural cavity but does not cause any cardiovascular compromise or compression to underlying organs and structure.
A Tension Pneumothorax occurs in a one-way defect to the chest wall or lung tissue that allows air to enter the pleural cavity but cannot be expelled out of the body. Resulting in the accumulation of air and the compression of the lungs, heart and vasculature within the thorax often seen with cardiovascular compromise.
89
Define flail chest?
Flail chest is two or more adjacent ribs with fractures in two or more places and often presents with paradoxical breathing and significant hypoxia.
90
What are the 3 signs of cardiovascular compromise in a patient with a tension pneumothorax?
Distended Neck Veins
Tachycardia
Shock with Hypotension
91
Explain the pathophysiology with distended neck veins as a result of a tension pneumothorax?
Distended neck veins occur as a result of the accumulation of air in the pleural cavity which is significant enough to cause mediastinal shift resulting in the compression of the heart and accompanying vasculature that causing a backflow of blood on the juggular veins from reduced cardiac output.
92
Define a Massive Haemothorax?
The accumulation of at least 1500mls of blood in the pleural cavity which compresses the lungs on the affected side.
93
Explain the pathophysiology of flat neck veins as a result of a massive haemothorax?
Flat neck veins occur due to the pooling of blood in the pleural space that result in decreased arterial blood flow to the brain, poor perfusion and hypotension and therefore flat neck veins due to decreased vascular resistance.
94
What is paradoxical pulse otherwise known as pulsless paradoxus?
A sign commonly seen in cardiac tamponade where there is no palpable peripheral pulse on respiratory inhalation but the palpable peripheral pulse returns on respiratory exhalation.
95
What is a indicative diagnostic test that can be assessed in a diaphragmatic tear?
Auscultating for and hearing bowel sounds in the chest.
96
Compare the retroperitoneum and peritoneum?
The retroperitoneum is there space between the peritoneum and the posterior abdominal wall that contains vital organs and vasculature. Whereas the peritoneum is a smooth transparent membrane that lines the cavity of the abdomen and sits anterior to the retroperitoneum.
97
What signs can indicate intra-abdominal bleeding?
- Kehrs sign
- Cullen's sign
- Seatbelt sign
- Grey Turner's Sign
98
Explain Kehrs sign?
kehrs sign is referred shoulder tip pain on the left or right side which can indicate a splenic or liver rupture due to the accumulation of blood or fluid compressing the phrenic nerve
99
What is the purpose of a needle decompression?
To decompress accumulated trapped air in the pleural cavity that is often seen in a tension pneumothorax.
100
What are the insertion sites for a needle decompression?
1. Anterior Chest
- Mid clavicular line, 2nd intercostal space, inserted over the 3rd rid
2. Lateral Chest
- Mid Axillary Line, 4th or 5th intercostal space, inserted over the 5th or 6th rib
- Anterior Axillary Line, 4th or 5th intercostal space, inserted over the 5th or 6th rib
101
What's the complications of needle decompression?
-High risk of blood/fluid exposure to the clinician
- Dislodgement of catheter on movement
- Blocking of the catheter
- Retensioning of Pneumothorax
- Infection
- Pt injury through mis diagnosis/poor technique
- Insufficient needle length
102
What are some common causes of a tension pneumothorax?
- Spontaneous/Simple Pneumothorax
- Blunt Force Trauma
- Penetrating Trauma
- Complications from a medical procedure.
103
Explain what the 'BURP' manoeuvre is?
Backwards
Upward
Right
Pressure Manoeuvre
This manoeuvre is used in FBAO removal to improve the visualisation of the glottis by a manual manoeuvre and displacement of the larynx with pressure on the thyroid cartilage
104
What are the types of blades used with a laryngoscope in a FBAO removal?
Macintosh Blades
Miller Blades (commonly used in paeds and larger adults with excess fat. Also used in pt with spinal consideration where a normal head tilt cannot be applied (
105
What landmark is used to ensure the correct placement of a laryngoscope in a FBAOR?
The base of the tongue which is called the vallecula
106
When is the use of laryngoscope FBAOR indicated?
Indicated in an unconscious pt who has a life-threatening blockage of the upper airway
107
What are the basic airway manoeuvres when assessing and maintaining a patients airway?
Crossed finger technique
Head tilt jaw lift
Trauma jaw thrust
Recovery position
108
What is the Sellick manoeuvre?
The sellick manoeuvre involves compression of the thyroid cartilage between the thumb and forefinger in a downwards direction. This closes the oesophagus to prevent aspiration during intubation and provides better visualisation of the upper airway.
109
What are the components of the larynx?
Laryngeal prominence
Vocal cords
Thyroid cartilage
Circoid cartilage
Circothyroid membrane
110
How do you confirm the correct placement of an airway adjunct?
Auscultation
EtCO2 monitoring
Chest rise and fall
SpO2
Monitor vitals
111
What are the ventilation ranges for EtCO2 and what do they indicate?
- Normal EtCO2 = 35-45mmHg
- EtCO2 ≥ 45mmHg = Hypoventilation
- EtCO2 ≤ 35mmHg = Hyperventilation
112
What does each section of a capnography waveform indicate?
A-B = Baseline
B-C = Expiratory Upstorke
C-D = Expiratory Plateau
D = EtCO2 value
D-E = Inspiration Begins
113
What does FiO2 refer to and when giving Oxygen how does the FiO2 varry?
FiO2 = Fraction of Inspired O2
For every litre of supplemental O2 given FiO2 increases by 4%.
A normal FiO2 is 21% on RA
114
What are the common sources of burns?
Thermal
Radiation
Chemical
Electrical
115
When do burns have a clinical significance?
When the burn is ≥ 20% on and Adult or ≥ 10% on a child.
116
What methods can be used to classify the extent of a burn?
Rules of nines
Lund and Browder Chart
Palmer method
117
Identify the individual BSA %ages for the rule of 9's in an adult and child?
Adult :
Head = 9% (4.5% front and back)
Chest = 9%
Abdo = 9%
Upper Back = 9%
Lower Back = 9%
L Arm = 9% (4.5% front and back)
R Arm = 9% (4.5% front and back)
L Leg = 18% (9% front and back)
R Leg = 18% (9% front and back)
Genitals = 1%
Child:
Head = 18% (9% front and back)
Chest = 18%
Back = 18%
L Arm = 9% (4.5% front and back)
R Arm = 9% (4.5% front and back)
L Leg = 14% (7% front and back)
R Leg = 14% (7% front and back)
Genitals = 1%
118
What does the HISSCA acronym mean and what does it indicate?
The HISSCA acronym indicates the likelihood of airway involvement in a burns pt.
Hoarse voice
Inspiratory Stridor
See-saw breathing
Singed facial/nose hairs
Carbonaceous Material (on mouth)
Anterior neck burns
119
Early burns deaths occur due to what?
Airway compromise and not the burn injury
120
Explain how carbon monoxide poisoning causes hypoxia and when is it commonly seen?
Carbon monoxide poisoning is commonly seen when there has been smoke inhalation. It causes hypoxia due to carbon monoxide molecules having a higher affinity for haemoglobin than oxygen does. Therefore, it displaces oxygen molecules from the haemoglobin and no oxygen being transported around the body leading hypoxia and subsequent cardiac arrest.
121
When must fluid administration be avoided in a burns patient?
Fluid administration must be avoided when there is airway burns from heat or steam inhalation, as it can increase swelling and airway compromise.
122
What is the common treatment for burns?
- Cool the burn for 20 minutes first
- Analgesia
- Clean & dry burns sheets/dressings
- Cling Wrap
- Fluids if indicated
- Prevent Hypothermia
- Transport to burns centre
123
Explain Burns shock and when does it occur?
Burns shock occurs in burns with ≥ 20% TBSA. Shock occurs when the burn causes a systemic cytokine release that results in a systemic inflammatory response. This systemic inflammatory response causes vasoactive changes that leads to fluid shifts due to increased capillary permeability from intravascular spaces to interstitial spaces and subsequent hypovolemic shock.
124
Explain Parklands formula and how is it calculated?
Parklands formula is used to determine the volume of fluid in mls to be administered for a burns patient with ≥ 20% TBSA within the first 24 hours.
-50% of total fluid is given in the first 8 hours.
- Remaining 50% is given over the following 16 hours.
Calculated using the formula:
4 x % TBSA x Weight (kg).
125
Explain crush injury?
Crush injury refers to the mechanism of injury, when a body part is compressed injuring muscles, blood vessels, bones, nerves and other internal structures.
126
What are some of the associated injuries that occur with a crush?
Fractures
Open/closed soft tissue injury
Neurovascular Compromise
Blunt/Penetrating injury
Dehydration
Hypothermia
127
What is the main consideration that needs to be taken into account in a crush injury?
The greater the body surface area compressed and the longer the entrapment, the greater the risk of developing crush syndrome.
128
Explain the pathophysiology of crush syndrome?
- Crush syndrome occurs when body tissues are subjected to severe and prolonged compressive forces that disrupt a tissues normal state.
- Damaged tissue, vessels or underlying structures become ischaemic and necrotic leading to cell lysis and death, resulting in the release of K+ and other cellular compounds into interstitial spaces and eventually into systemic circulation which alters organ and system function.
129
What are the by products released from cell lysis?
Myoglobin
Phosphate
Potassium
Uric Acid
Lactic Acid
130
What are the signs and symptoms of hyperkalemia? (Use the MURDER acronym)
Muscle Weakness
Ureamia
Respiratory Distress
Decrease cardiac contractility
ECG Changes
Reflexes decreased
131
Explain the pathophysiology of hyperkalemia?
Hyperkalemia is classified when blood K+ levels rise above 5.5mEq/L causing an imbalance in ion equilibrium, early cell depolarization, and makes cell resting membrane potential more positive.
As a result of these changes Na+ voltage gated channels become inactive, preventing Na+ to stimulate cells. This causes the cells to remain in a refractory state which results in the impairment of neuromuscular, cardiac, skeletal, and GI organ systems.
132
Explain how hyperkalemia affects the heart?
Increased K+ levels cause Na+ channels to become inactive. The inactive Na+ channels do not allow Na+ to cross the cell membrane and stimulate the myocardial cells. This results in decreased contractility and excitability of the SA and AV node leading to impairment of electrical conduction pathway of the heart resulting in dysrhythmias such as; bradycardia, heart blocks and cardiac arrest if not treated.
133
What ECG presentations indicate hyperkalemia and it's worsening state?
- Peaked and tall T wave = 5.5 - 6.0mEq/L
- " " + Wide QRS = 7.0 - 7.5mEq/L
- " " + Lost/Flat P waves = 7.0 - 8.0mEq/L
- Sinusoidal Wave = > 9.0mEq/L (pt is peri-arrest)
134
Identify what medications are used to treat hyperkalemia and what specifically each one corrects in its treatment?
1. CSL - used to promote K+ reabsorption in the kidneys and excrete the excess ions out through urine.
2. Sodium Bicarbonate - used to help restore acid-base balance which is initially altered from the effects of acidosis which decreases blood pH.
3. Calcium Gluconate - used as a protective measure on the heart by aiming to restore the threshold potential/resting membrane potential gradient of the cardiac cell membrane. This reducees dysrhythmias and restore normal electrical function.
4. Beta2 agonists (Salbutamol) - used to promote the reuptake of K+ from the blood to the cells through stimulation of the Na+/K+ pump
135
Explain the pathophysiology of compartment syndrome?
Compartment syndrome occurs when the pressure within a fascial compartment increases as a result of injury to the extremities.
This injury causes bleeding inflammation, swelling and the accumulation of oedema within the compartment.
The swelling and oedema disrupts and compresses the neurovascular bundle within the compartment resulting in; decreased arterial blood flow, decreased venous return, tissue ischaemia and decreased function due to compression of the neurovascular bundle.
136
Identify the 6 P's of compartment syndrome?
Pain
Pallor
Paralysis
Paraesthesia
Pulselessness
Pressure
137
What's are the common causes of compartment syndrome?
Fractures (75% of cases)
Burns
Crush Injury
Thrombus
Internal Haemorrhage
Medical Conditions
138
Explain the pathophysiology of Rhabdomyolysis?
Rhabdomyolysis is the breakdown of muscle fibres resulting in the release of myoglobin into the bloodstream that frequently results in acute kidney damage and renal failure.
139
Explain how rhabdomyolysis leads to myglobinuria and acute kidney damage and renal failure?
When the breakdown of muscles occurs myoglobin is released into the circulation and filtered through the kidneys to be excreted in urine. When to much myoglobin is present in urine it causes a condition known as myglobinuria.
Myoglobin is a monomer which binds with other molecules to become larger in size and nephrotoxic, creating an obstruction within the tubules of the nephron. This obstruction is unable to be excreted naturally by the kidney leading to nephron death which presents as acute kidney damage and renal failure.
140
What are the common symptoms with rhabdomyolysis?
Red/Dark Urine
Muscle/General Weakness
Muscle stiffness/Aching
Muscle tenderness
141
What are the mechanisms of heat loss?
Radiation (approx 60% of loss)
Conduction (approx 3% of loss)
Convection (approx 15% of loss)
Evaporation
142
Explain the pathophysiology of heat/muscle cramps?
Caused by an overexertion and dehydration in the presence of high atmospheric temperatures from a loss of ions resulting in subsequent involuntary muscle contractions.
143
Explain Heat Stroke?
Heat stroke is the total failure of thermal regulatory mechanisms which can be rapidly fatal when the body temperature is greater than 40.5ﾟC and has then presence of the heat stroke triad.
144
Explain heat exhaustion?
Heat exhaustion is considered a mild heat illness associated with increased air temperatures and excessive sweating leading to dehydration Na+ loss.
145
What is the Triad of Heat Stroke?
Core temp > 40.5°C
Hot, dry skin
ALOC/Altered mental state
146
What are the 3 classifications of hypothermia and their corresponding temperature ranges?
Mild = 32°C - 35°C
Moderate = 29°C - 32°C
Severe = < 29°C
147
What are the ECG changes seen in Hypothermia?
- Prolongation of the PR interval then the QRS, then the QT interval
- Slow AF is common
- A J wave may be seen in temps < 32.3°C and will increase as temperature decreases.
148
Explain rewarming shock?
Rewarming shock occurs due to reflex vasodilation when rewarming is too quick or not adequate enough. This causes the return of toxins and cold blood from the extremities to vital organs and can lead to VF during the rewarming phase.
149
What are the 2 type of frostbite and how do they present?
Superficial frostbite - presents with freezing of the epidermis which becomes red followed by blistering, swelling and diminished sensation.
Deep frostbite - Presents with freezing to the epidermis and subcutaneous layers with a white waxy like and/or black frozen appearance.
150
What are the signs and symptoms of dehydration?
Tenting/poor skin turgor
Decreased urine output
Vision disturbances
Nausea and Vomiting
Abdominal distress
Signs of hypovolaemic shock
151
Explain the pathophysiology of freshwater drowning?
Fresh water drowning occurs when fresh water makes its way into the alveoli and causes degeneration of aveloar surfactant that is needed to maintain alveolar surface tension. When this degeneration occurs the alveoli collapse and there is no ability for gas exchange to occur, resulting in hypoxia and cell death.
Additionally, freshwater becomes absorbed into circulation and causes hemolysis of the red blood cells leading to dysrhythmias and cardiac arrest.
152
Explain the pathophysiology of Saltwater drowning?
Salt water is a hypertonic solution therefore when salt enters the airways and alveoli there is a shift of Na+ and water from circulation into the interstitial spaces within the alveoli. This fluid shift results in pulmonary oedema and prevents gas exchange from occurring.
153
Explain Boyle's law and how it relates to diving?
Boyle's Law states that when a temperature remains constant, pressure and volume are inversely proportional meaning that when one increases the other decreases.
This relates to diving as when A diver goes deeper into the water the water pressure exerted on them increases and therefore the gas volume pressure within the lungs decreases the reverse happens when they ascend. If a diver ascends to rapidly in the lungs do not adapt to changes in pressure appropriately as the pressure from the water decreases the volume of gas and pressure inside the lungs will increase and potentially cause the lungs to pop.
154
Explain the pathophysiology of HAPE or HAPO?
HAPE is a fluid build-up in the lungs specifically the alveoli a result of high altitudes, decreased O2 pressures and increased CO2 levels causing pulmonary vasoconstriction and hypertension.
The vasoconstruction and pulmonary hypertension causes fluid shifts from pulmonary arterioles to areas where there is less pressure in the pulmonary capillaries, resulting in tearing of the pulmonary membrane, allowing fluid to move freely into the alveoli resulting in pulmonary oedema and decreased gas exchange
155
Explain the pathophysiology of HACE?
HACE is the most severe form of high altitude sickness often at levels above 4000m, that causes an increase in ICP from swelling and oedema accumulation within the brain.
Reduced pO2 results in hypoxia and a compensatory inflammatory response, leading to cerebral vasodilation and increased ICP which causes cerebral hypertension, over perfusion and increased capillary leakage resulting in cerebral oedema.
156
What are the common classes of toxidrome's?
Cholinergic Toxicity
Anti-cholinergic Toxicity
Sympathomimetic Toxicity
Serotonin Toxicity
Opioid Toxicity
157
Explain the pathophysiology of cholinergic toxicity?
Cholinergic Toxicity is common caused by organophosphates and carbamates. They inhibit Acetylcholineesterase enzyme and increase the concentration of acetylcholine resulting in excess cholinergic responses on the muscarinic, nicotinic and peripheral and central nervous systems.
158
Using DUMBBELS & SLUDGE what are the signs and symptoms seen with cholinergic toxicity?
DUMBBELS
Diarrhoea
Urination
Miosis
Bronchospasm
Bradycardia
Emesis
Lacramation
Salivation
SLUDGE
Salivation
Lacramation
Urination
Defecation
GI Cramping
Emesis
159
Explain why Atropine is used as treatment on cholinergic toxicity?
Atropine is an anti-cholinergic. Therefore once administered it will begin to inhibit exocrine gland activity and dry up all secretions. Additionally it increases the SA node firing rate which increases cardiac output
160
What are the CNS and PNS signs and symptoms seen with anti-cholinergic toxicity often referred to as "Mad as a hatter"?
CNS signs and symptoms:
Agitation
Delirium
Visual Hallucinations
Mumbling incoherently
Fluctuating LOC
PNS signs and symptoms:
Dry hot skin (hyperthermia)
Flushed appearance
Tachycardia
Decreased bowel sounds
Urinary retention
161
Explain the pathophysiology of sympathomimetic toxicity
Is often caused by a substance that mimic or modify the action of endogenous catecholamines either by direct or indirect stimulation on Dopamine and adrenergic alpha and beta 1 receptors.
162
What are the causes of indirect stimulation causing sympathomimetic toxicity?
Amphetamines
Methamphetamines
Cocaine
Epedrine
163
What are the causes of direct stimulation causing sympathomimetic toxicity?
Dopamine
Epinephrine
Norepinephrine
Isoproterenol (B1 and B2 agonist)
Dobutamine (heart failure drug)
164
Using the "MATHS" acronym identify the signs and symptoms that indicate sympathomimetic toxicity?
Mydrisis (dilated pupils)
Agitation, arrhythmias, angina
Tachycardia
Hypertension, hyperthermia
Seizures sweating
165
Using "CPR-3H" identify the signs and symptoms often seen with opioid toxicity?
Coma
Pin point pupils
Respiratory depression
Hypotension
Hypothermia
Hyporeflexia
166
Explain the pathophysiology of serotonin syndrome/toxicity?
Serotonin syndrome is a potentially life threatening condition associated with overuse of therapeutic medications, that causes increased serotonergic activity in the CNS and PNS?
167
Using "SHIVERS" what are the signs and symptoms that are seen with serotonin syndrome?
Shivering
Hyperreflexia
Increased temperature > 41°C
Vital sign instability (^HR, ^RR, < BP)
Encephalopathy (ALOC)
Restlessness
Sweating, seizures
168
What are the common medication causes of serotonin syndrome?
SSRIs
SNRIs
Tricyclic Antidepressants (TCAs)
Cocaine
Amphetamines
169
What are the ECG changes that can be seen with a TCA overdose?
- Dysrhythmias (Bradycardia, Tachycardia)
- QRS prolongation and widening
- Terminal R wave seen in lead aVR
170
Explain why sodium bicarbonate is used as the antidote for a TCA overdose?
Sodium Bicarbonate is used to raise blood pH levels and makes it become more alkaline. AS TCAs are a weak base and cause the blood to become more acidic.
It also increase extracellular Na+ levels and provides a protective element on the heart. As TCAs inhibit cardiac fast Na+ channels causing bradycardia.
171
What are the antidotes to treat the following toxic overdoses:
1. Opioid
2. Paracetamol
3. TCAs
4. Organophosphates
5. Insulin
6. Warfarin
7. Benzodiazepines
1. Naloxone
2. N-Acetylcystine
3. Sodium Bicarbonate
4. Atropine
5. Dextrose
6. Vitamin K
7. Flumazenil
172
What are the 3 pathological effects of envenomation?
Coagulopathic
Neurotoxic
Myopathic
173
Explain the pathophysiology of coagulopathic envenomation?
Coagulopathic envenomation commonly occurs with brown, tiger and taipan snake bites. The venom causes venom induced consumptive coagulopathy (VICC). Resulting in procoagulant agglutinis in the snake venom that causes activation of prothrombin and defibrination resulting in clumping of RBCs and and thinning of blood as no fibrin can be formed.
174
Explain the pathophysiology of Neurotoxic envenomation?
Neurotoxic envenomation occurs from snakes and funnel web spider bites. Presynaptically toxins inhibit acetylcholine release and stimulate catecholamines release resulting in sympathetic hyperstimulation seen with hypertension, Tachycardia and pulmonary oedema.
Postsynaptically the toxins Inhibit neuromuscular activation resulting in a progressive, symmetrical descending paralysis which progresses to respiratory failure.
175
Why is GTN and magnesium sulphate used in the treatment of Irukandji strings?
Irukandji stings cause sympathomimetic toxicity and a hypertensive crisis.
GTN is used to treat HTN when the SBP > 160mmHg
Magnesium Sulphate (10 mmol or 2.5g/5ml) is used to promote vasodilation and bronchodilation through inhibiting smooth muscle contraction thus reducing the HTN effects.
176
As per NSWA, what is the dosing of Ketamine for an adult when given IV and IM?
Preparation is 200mg in 2ml diluted to 20mls with 18mls of NaCl
IV dose is 0.25mg/kg (to a max of 200mg)
IM dose = 1mg/kg (to a max of 2mg/kg up to 200mg)
177
What are the components of Beck's Triad?
JVD
Hypotension
Muffled Heart Sounds
178
What are the components of the Trauma Lethal Triad?
Acidosis
Hypothermia
Coagulopathy
