Paramedic practice

Start Studying!

Terms

undefined, object

copy deck

In reagards to MVA and kinetics of trauma what are the three categories of movement?: Vehicle collides with object
Occupant collides with vehicle
Organs collide with persons body
What are five types of MVAs?: Frontal, Lateral, Rear end, Roational and Roll over
What are other areas of road trauma?: motorcyle accidents
pedestrians
What are the facors effecting injury as a result of an exploision?: surrounding environment
delivery method
distances, barriers/hazards
composition/ materials in it
what are the three pahses of an explosion?: 1= Pressure and heat wave
2= Flying debris
3= Pt becomes flying object
Trauma magmt and time citicality What is actual physiological distress?: RR < 8 or > 20
HR <50 > 100
BP < 100 syst
GCS < 13
SpO2 < 90%
What is emergent time critical?: Patient has a PATTERN of injury, having a high probability of deteriorating.
What is potential time critical?: Patient doesnt have a pattern of injury, but does have a MECHANISM of injury that may deteriorate.
What is a Major Inicident?: Event for which the available resources are not adequate to manage the number of casualties or type of emergency.
What are the five major componenets to the Incident Command System?: Command
Fincance
Logistics
Operations
Planning
What are the roles of a commander?: To establish a safe and effective post
to give accurate and timely SITREP
Evaluate & triage
Request resources
control and assign teams
continue until relieved
Why would cold fluids be used?: To help ensure least amount of neuro defecit after recovery. slows metabolsim
When should we not IV?: Pt is in a state to refuse and does so
paramedic not trained
injury/disease to site
dialysis fistular
Name some complications of IV?: Pain
infection
PE/ catheter embolism
Arterial puncture
Local hematoma, thrombosis, cellulitis
tissue damage due to 'blown vein'
what are the ALS fluid resus guidelines?: if HR <100 & BP >100 =No fliud
if HR >100 & BP >100 = 20ml/kg
if BP < 100 = 20ml/kg
What are the modifying factors in IV fluid resus?: Head injured pt, dont > BP
SCI, expect <bp <hr
Penetrating trunk Inj
AAA
PAIN: what is it?: individuals interpretation of noxious stimuli, protective mechanism.(pain is damage)
What are the four aspects to physiological response to pain?: Previous experience
Social training
State of phys health
State of mental health
What are noiciceptors?: Free nerve endings in dermal tissues that detect noxious stimuli
When is pain felt?: When stimulus is strong enough, impulse will be sent up spinal column, if extremely strong, substance P realeased which potentiates the signal
how is it transmitted to the brain?: pain crosses over and is interpreted conta-laterally.
the thalamus then integrates and interprets the stimuli
How is pain interpreted?: Sensory part of cerebrum is notified, assesses intensity and locn of pain and then determines a response
Pain and memory storage: NAd rel increases memory storage
E
ndorphins, oestrogen and oxytocin inhibit memory storage
memory recall: person may remember ++ pain but have patchy event recall due to interference of endorphins
What is the most primitive pain response?: Pain refelxes. occur at spinal cord and thalamus
strong stimuli will activate motor response. at same time cerebrum interprets
What is referred pain and how does it occur?: pain stimuli from one area is so strong that it rises to fequency of another area and brain gets confused
SHOCK definition?: Inability of the cardiovascular system to adequately maintain perfusion. reliant on 3 mechanisms: Heart(pump)
vessels(container) & blood(vol)
What are five types of shock?: HYpovalemic,
Neurogenic
Cardiogenic
Septic
Anaphlyactic
Hypovolaemic: Fluid loss may be relative or absolute, will progress thru all 3 stages. common cause: haemorrhage, burns, dehydrn
Neurogenic: occurs as result of < peripheral vascular resistance, compensation mechs not initiated, will go straight to decomp phase
common cause: SCI, poisoning
Cardiogenic: inability of heart to pump adequately, compensation mechs dont work= decomp phase.
common cause: AMI, tension pneumo,cardiac tamponade, PE
Septic: Sever widespread infection, cellular necrosis and inlam response interefer with compensatory effects
Anaphylactic: severe allergic rxn, histamine release, relatieve fluid shift:vasodilation and > cap permab, compensation fails due to vasodiln
what are the stages relating to capillary/cellular relationship?: stage 1:vasoconstrn,
velocity of bld passing thru >causing > in cap hydrostatic pressure.
O2/nutrient delivery <, anaerobic metab starts, possible leaky cap sydrome.
BP, HR, normal
Stage 2: capillary and venule opening
blood pools and stagnates
vasular space expands due to hypoxemia and acidosis.
< VR, >acidosis, hypercoagulation.
HR RR cap refill >
BP normal
Stage 3: DIC- coagn of microcric clogs caps. <o2, nut del and waste removal
>lactic acid, cells leak and burst and die
micro infacs occur
BP< Bld transfn req for surv)
Stage 4: MOF
orgnans necrosed and die.
What are the stages of shock?: Compensated
ppting event causes <BP. mild sns response, > catecholamines maintains CO and BP
<perfn and >acidosis, = >RR
S/S of compensated shock?: Mild tachycardia +/- >RR
slighty cool, pale
BP stable, poss slight > in sys
pt may be slightly confused/ lethargic
Next stage?: Decompensated
< BP <perfusion <pulse pressure as compensn fails
2ndry sns response init, hormonal RAA actvtd
pt becomes hypoxic >ischemia & acidosis
Signs and sypmtoms of decompensation stage?: <BP
>RR, > HR
pale cool sweaty
devel ACS
< urine output
last stage?: Decompensation
cellular necrosis leads to cell lysis, ++acidosis
perhip vasodiln, microemboli
cerebral + myocardial hypoxia
Irreversible S/S?: Bradycardia, ++ <BP
abnormal Resps
ACD= unconc
cyanosed skin
DEATH
SPINAL INJURIES what types of spinal injuries can occur?: -Axial loading: vertical
compression
-Hyper- flxn, extn, rotn
-lateral bending
-Distraction(pulling apart)
What is central cord sydrome?: motor impairment of upper extremeties
Brown-Sequard sydrome: herniation of spinal cord
Anterior cord sydrome Posterior cord syndrome: Paralysis < level of inj

motor& sensory fn preserved
what does SCIWRA syndrom stand for?: spinal cord injury without radiological abnormality.
What are some general s/s of SCI?: CARDIAC
bradycardia
skin flushin below inj
hypotension
no shivering!!!
RESP S/S?: <RR
Paradoxical breathing, due to loss of control of phrenic nerve
(deep breath & coughing reflexes
gone)
mucous prdn?
GIT S/S?: flaccid areflexia
urinary distension
Gi atony
incontinence
priapism
What signs would lead you to suspect a SCI?: Pain/ hematoma along spine
unexplained < bp < hr
inapprop vasodlin
flaccid paralysis
any pt w head inj
Management of Spinal injuries?: recognise inj!!
immobilise if meets major trauma criteria
normal mgmt, o2 ventiln, monitor,pain relief etc
head trauma, what types are there?: mandible #, mid face #, nose #
What is the pahtohpys of a pneumothorax?: When the lung integrety is boken
the plueral space gets air inside, and air pushes into the lung tissue, as the pressure increases the inspired air cant enter the lung.
What are signs and symptoms of pnemo?: vena cava is compressed, meaning decreased venous return, < CO
-history of chest trauma
-pain-mediastinal shift
-distended neck veins
What are the most important three signs denoting a tension pnemo is occuring?: Altered concious state
increasing resp distress
inadequate perfusion, inclu <BP
also < breath sounds, subcutaneoud emphysema
What is the treatment for a tension pneumo?: to decompress the chest
test first w 23 g needle and 5ml saline. if +ve, decompress with 14 g cannula
ABDO INJURIES Liver trauma: liver lac common in blunt or penetr trauma. (++ bld loss)
Presnt with upper R quadrant pain.
Splenic trauma: most common in blunt abdo inj
present w <BP
if ribs 7-10 on L damaged, consider spleen damage
can have Kehrs sign: L shoulder tip pain
Renal trauma: Mostly in blunt inj can ++bleed into retrop space. flank bruising late sign
can present w pain on inspriation
COMPARTMENT SYNDROME what is it??: the increase of pressure within a confined space causing microcirculation injury. Muscular fascia doesnt stretch, creating rigid compartments. swellin in them cause ++ pressure
What is the pathophys?: death of large blocks of muscle
sim to rhabdo, but complicated by traumatic inj to bone and tissue
Takes approx 1 hr to devel, but toxins continue to leak into circn 60 hrs post release.
What happens next?: when pressure in compartment is > than capill pressure= ischemia and odema => infarction of compartment contents
ischemia and necrosis can still occur even if pulse still present
how long can muscles and nerves go without O2 before permanent damage occurs?: for 4 hours, after that they are irrepairable.
the increasing pressure leads to what consequences?: odema
microcircn obstruction
<arterial and lymph flow
ischemia to musc, nerve and bv
What happens to prefusion pressure when intracompartmental pressure rises?: it increases to try and overcome it. as it rises to a level, autoregn mechs fail and cascade of injury occurs
What happens to capillaries as venous pressure rises?: venous pressure wil rise and intracompartmental pressure rises. when venous pressure is greater than Cap Perf Pressure, the capills wil collapse: no cell metabolism!
what happens when capillaries dont work?!: no o2/ nutrient del or waste rem
cells relase substs that > vessel permability
capills loose fliud, >tissue pressure,>injury
nevrve condn<, pH<
musc tissue necrosis:myoglobin
What are the best sites for this to occur?: upper arm-2 big comps
forearm
buttocks-3 gluteal comps
thigh-3 large comps
lower leg -4 tight comps:highly suscept:
What can it result from?: Increased compartment contents OR
Decreased compartment size
What are some causes?: Trauma, hemorrhage, odema, coagulopthies, others
Odematous causes?: Post ischemic swelling
prolonged immobilisation
thermal injury
exertion
venous disease
envenomation
Haemorrhagic?: Bleeding disorder
Vessel lac
Anticoag therapy
# of leg/arm bones
Mortality/Morbidity?: May result in loss of limb
can lead to rhabdomyolysis
anticoagn theraphy sig > liklihood of compartment syndr
What are the signs and symptoms of compartment syndrome?: -Pain++ worse w movt/pressure
-Parasthesia; loss of feeling below area
-Severe pain on pasive strech
S/S cont:: -poikilothermic(env temp)
-pressure (palpable on site)
-Pallpr/pulseless, late signs
Management?: DONT: ice, elevation

DO: o2 R+R splint for comfort in approp, IV tkvo, Fentanyl prefferd as no vasodiln
Any further managment that could be of benefit in hosp?: hyperbaric O2
adressed main concern of ishcemia,allows o2 del W < pressures, reduces reperfusion injury.
What is Rhabdomyolysis???: breakdown of skeletal muscle releasing toxins into the circulation.
is irreversible
What is different about the electrolyte distribution across cell membranes?: Na, Ca, Cl, and HCO3 are extracell
Whilst K, Mg and PHo4 usually intracell
What maintains these balances?: Cell membrane
Na-K pumps
Electrolyte balances (homeostasis)
What changes to these can occur? Cell membrane?: Physical barrier that can have injury as a result of crushing, tearing, burns, poisons,or dissolution
= intracell contents escape and extracell enter
Na-K pumps?: preserves electrolyte balances
ATP dependt. if no O2 stops working quickly.
Electrolyte blances?: can have imbalances that will effect Na-K pumps as well as homeostasis
imbalances can result from vomiting, diarrhea, extensive diuresis
Can many things case Rhabdomyolysis?: yes, more than 100 conditions, both traumatic and non traumatic
How can we diagnose Rhabdo?: look for
MOI
Stiffness, wkness, malaise
low fever
musc swelling and tenderness
brown urnie(myoglobin)
-may be asymp-
What is the management?: Reassurance, O2, Monitor
pain relief
IV fluids- up to 1.5l/hr to help kidneys
kidneys are at risk of failure due to nephrotoxin myoglobin from musc breakdown
What is crush syndrome??: reperfusion injury as a result of traumatic rhabdomyolysis
severity is related to magnitude and durn of force, and muscles involved
What factors would lead you to consider crush syndrome?: 1 compramise of large muscle mass
2 Prolonged compression (>1hr)
3 Compramised vascular supply
What is the process?: Go through rhabdo,then pressure released.
causes vol+electrolyte changes
fluid shift, fliud shunting
hyperkalemia
arryth due to >k, <ca
metab acidosis
ARF
Common causes: anything that traps pppl.
Large scale disasters, vehicle accidents.
legs most commonly affected
Mortality/ Morbidity?: Sht term:death from hypoval and arryth
long term:renal failure, comlplics eg ARF, ARDS, infn, sepsis, DIC
How to diagnose crush syndr?: compression >1 hr
large musc mass invovled
absent distal pulse and cap refill
signs of shock
ECG changes: peaked t waves
Management of crush syndrome?: reassure, consider other injs?
o2, monitor, pain relief-morph(ketamine+/-midaz)
IV >bore,2lt bolus + 1.5/hr, (dont use hartmanns as K)
?NaHCO3 max 200ml

Start Studying!

Deck Info

Number of cards 95