Quiz 1 - Modules 1, 2, 3 Flashcards
Canadian Triage Acuity Scale (CTAS)
help assess and determine severity of presenting problems
organize patient care so that most acute cases are prioritized
help determine appropriate treatment
CTAS scores
red evos use less noobs
1 - resuscitation
2 - emergent
3 - urgent
4 - less urgent
5 - non urgent
Level of urgency definition
classification + prioritization of pt health concern, problem, condition
Levels of urgency
stable
unstable
potentially unstable
Stable LOU
normal clinical findings
hx not life or limb threatening
Unstable LOU
abnormal clincial findings
history considered life or limb threatening
Potentially unstable LOU
normal clinical findings
history warrants concern/ongoing observation
potential for deterioration
Emergency assessment framework
Primary assessment
Secondary assessment
Primary assessment components “CABCDEFG”
CAB vs. ABC (need for compressions/control bleeding)
airway/c-spine control
breathing
circulation
disability, doctor, dextrose, discomfor,
expose
full vital signs + family presence
go back and reassess
Secondary assessment components
subjective hx (LOTTAARP - hx of presenting illness)
objective assessment (H2T)
focused system assessment
journey (admission, diagnostics, discharge)
Subjective data
data obtained from individual or witnesses
ex: pt reports feeling SOB
Objective data
data observable to others
ex: pt has demonstrated WOB
Airway interventions
oropharynx suction
jaw thrust/chin lift
oral/nasopharyngeal airway
consider/prepared for advanced airway
spinal motion restriction
Breathing interventions
assisted ventilations (BVM/ventilator)
supplemental o2
pulse oximetry
Circulation interventions
inititiate IV/IO access
fluid resuscitation
cardiac monitor
12 lead ECG
Disability interventions
pain management
anti-emetics
notify emergency physician/specialist
prep for CT
Disability assessments
AVPU
GCS
PERRLA
Cincinnati stroke scale (FAST)
Dextrose –> CBG
barriers to assessment: pain, vomiting
need for emergency physician (LOU)
Expose interventions
gown + blanket
active warming procedures
F interventions
full set of vitals
family presence
History/head-to-toe assessment
allergies
medication
past medical hx
last meal
personal hx
risk behaviors (smoking/ETOH/drugs)
safety at home
Journey assessment
lab work
imaging
OR/IR
tubes/lines
unit admission
intrahospital transfer
discharge
LOTTAARP
used for history of present illness
location
onset
type/time
aggravating/alleviating/associated symptoms
radiating
precipitating events
Pediatric secondary assessment
chief complaint
immunizations
isolation
allergies
medications
past medical hx
caregiver impression
events surrounding illness/injury
diet
diapers (hydration status)
symptoms associated w/ illness or injury
AVPU
assess level of consciousness
alert
verbal
pain
unresponsive
GCS components
eye opening
verbal response
motor response
PERRLA
pupils
equal
round
reactive to light
accommodation
FAST components
facial droop
arm drift
slurred speech (or jumbled)
time (immediate intervention)
Adult subjective history
biographical info
chief concern/presenting problem
history of illness (LOTTAARP)
review of systems (what other S/S are present, what other systems may be involved)
allergies/sensitivities
medications
past health history
last meal –> in case emergent procedures needed
personal history –> risk behaviors/safety at hoem
family health history
Neuro assessment
GCS
PERRLA
ROMS
limb strength/equality
arm drift
Respiratory assessment
look (mental status, WOB, cyanosis, cough/sputum, tracheal deviation, injury, chest symmetry)
palpate (tracheal position, areas of tenderness, crepitus, movement of air)
auscultate (presence, depth, bilateral A/E, adventitious sounds)
Cardiovascular assessment
inspect (CWMS, LOC, position, edema)
palpate (pulses, skin, edema)
auscultate (HR, pulse deficit)
heart sounds (quality, s1/s2, abnormal: s3, s4, murmurs, gallops)
pulse deficit
ankle-brachial index (ABI) –> assess for impaired peripheral perfusion
Abdominal assessment
inspect: position, skin, trauma, pulsating masses, symmetry, abdominal control/hernia
auscultate: bowel sounds, bruits over aortic area, fetal HR
palpate: tenderness, guarding/rigidity, masses/pulsations
MSK assessment
inspect: position of extremities (flexion, textension, shortening, rotation), deformities, color
palpate: pain/tenderness, crepitus, CWMS, movement (ROM)
ABG components
pH (7.35-7.45)
HCO3 (22-26)
PaO2 (80-100)
PaCO2 (35-45
SpO2 (>95)
Partial compensation
adjustment in compensatory system but pH still not WIL
Complete compensation
adjustment in compensatory system and pH WIL
Types of buffer systems
chemical (phosphate, red blood cells, protein, ammonia)
respiratory (ventilation)
renal buffering (excretion of acids/retention of bicarbonate)
Pulmonary shunt
alveoli perfused but not ventilated
Anatomic dead space
air that gets stuck in upper respiratory tract + does not participate in gas exchange
Physiologic dead space
alveoli not perfused, but ventilated
Oxyhemoglobin dissociation curve
graph that depicts the relationship between spo2 and paO2
Left shift
increased oxygen affinity
o2 unloading decreases
caused by:
alkalosis
decreased temp
lower 2,3 DPG concentration
Right shift
decreased oxygen affinity
o2 unloading increases
hemoglobin releases oxygen more readily into peripheral tissue, but less able to pick up oxygen
caused by:
acidosis
increased temp
increased 2,3 DPG concentration
Factors affecting hemoglobin binding to oxygen
partial pressure of oxygen (high in lungs, lower in tissue beds)
Mild hypoxemia
Pao2 60-79
SpO2 >/= to 90%
Moderate hypoxemia
PaO2 40-59
SpO2 >/= 75%
Severe hypoxemia
PaO2 <40
SpO2 <75%
End organ perufsion
body’s ability to supply enough oxygen to meet metabolic demand of vital organs (oxygen and nutrients transported via blood)
brain, heart, lungs, GI tract, liver, kidney
Determinants of oxygen supply
arterial oxygen (ventilation [neuromuscular function, compliance], gas exchange [diffusion distance, surface area, hemoglobin saturation])
cardiac output (stroke volume, heart rate)
Ventilation equation
tidal volume x RR
Determinants of oxygen demand
activity
temperature
emotional stressors
Concentration of oxygen in room air
21%
Nasal cannula paramters
flow: 1-6 L
FiO2: 24-44%
Simple face mask parameters
flow:6= 6-10
FiO2 50-60%
Non-rebreather mask
flow: 12-15 L
FiO2: 60-100
Ventilation
physical exchange of air between body + environment
determined by: tidal volume x RR
Diffusion
exchange of gases across the respiratory membrane (alveolar wall + capillary)
influenced by partial pressure of gases (affects concentration gradient)
Perfusion
gas exchange determined by alveolar perfusion + alveolar ventilation
Causes of V/Q mismatch
physiologic shunt
dead space
pulmonary embolus
RUQ organs
liver
R. kidney
colon
pancreas
gallbladder
LUQ organs
liver
spleen
L. kidney
stomach
colon
pancreas
RLQ organs
colon
small intestine
major artery/vein to right left
ureter
appendix
LLQ organs
small intestine
large intestine
left ureter
sigmoid colon
fallopian tube, ovary, spermatic cord
CAB vs. ABC ax
need for CPR –> start compressions before rescue breaths
uncontrolled bleeding
Airway/C-spine ax
look, listen, feel for air movement (stridor, gurgling, anxiety, pt position, chest symmetry)
clarity of speech –> gasping, full setnences
patency vs. obstruction (stridor, gasping, wheezing, snoring, drooling, gurgling)
AVPU –> LOC to determine ability to maintain airway
C-spine injury trauma
Breathing ax
rate + quality of respirations
WOB
lung auscultation
skin color
Circulation ax
skin –> color, warmth, moisture
cap refill
palpate pulses –> quality, rate, rhythm
chest pain
Disability ax
reassess AVPU –> GCS
PERRLA
Cincinatti stroke scale
Dextrose
Barriers to ax: pain, vomiting
Need for emergency physician - LOU
Expose ax
Skin assessment
bruising
wounds
bleeding
mottling
Full set of VS/Family ax
Vital signs
Notify family
Causes of gross abdominal distension
fluid
flatus
feces
fetus
fat
Causes of localized abdominal distension
loculated fluid
mass
hernia
organomegaly
impacted feces
6 P’s of dyspnea
pulmonary/bronchial constriction
possible foreign body (aspiration)
PE
Pneumonia
Pneumothorax
Pump failure (cardiogenic pulmonary edema)
Types of abdominal pain
tension
inflammatory
ischemic
Tension abdominal pain
d/t increased peristalsis
bowel trying to eject irritating substance
stretching of organ capsule (obstruction, inflammation)
frequently change positions to get comfortable
Inflammatory abdominal pain
inflammation of visceral peritoneum (type C fibers)
eventually involves parietal peritoneum –> sharp, localized pain
pain exacerbated by movement
Ischemic abdominal pain
less common but most serious
sudden onset, intense, continuous, progressive
pain not relieved with analgesia
Characteristics of ischemic pain
sudden onset
intense
continuous
progressive –> gets worse with time
Causes of tension abdominal pain
early-stage obstruction
lactose intolerance
gastroenteritis
GERD
celiac
constipation
peptic ulcer
pyelonephritis
IBS
Causes of inflammatory abdominal pain
appendicitis
meckel’s diverticulum
cholecystitis
cholelithiasis
urolithiasis
pancreatitis
ruptured ectopic pregnancy
pelvic inflammatory dx
perforated ulcer
familial mediterranean fever
mittelschmerz
Causes of ischemic abdominal pain
strangulated bowel
late-stage obstruction
intestinal ischemic syndrome
embolism, thrombosis
mesenteric ischemia
torsional occlusion (volvulus)
sickle cell crsisi
ruptured AAA
Perfusion of intestinal mucosa
receives 20-25% of CO
GI system very sensitive to changes in perfusion –> ischemic pain
necrosis can occur 6 hours after symptom onset
WOB indicators
nasal flaring
accessory muscle use
grunting
head bobbing
Effectiveness of breathing indicators
lung auscultation –> air entry to bases
symmetry/extent of chest expansion (deep vs. shallow respirations)
abnormal lung sounds
Inadequate perfusion indicators
tachycardia
decreased LOC
skin color/warmth (pallor, cool)
SpO2
Peds CIAMPEDS
chief complaint
immunizations
isolation
allergies
medications
past history/parental perception
events around illness
diet/diapers
associated symptoms
Types of pain fibers
type a delta (fast, localized, sharp)
type c (slow, diffuse, dull)
Types of pain
parietal = type a
visceral = type c
Types of visceral pain
inflammatory
ischemic
tension (increased peristalsis)
Tension pain
increased force of peristalsis
1) forcefully eliminating an irritating substance
2) moving around an obstruction
3) stretching of organ capsule
S/S tension pain
moving around to get comfortable
vague, deep, poorly localized
Inflammatory pain
usually, deep, poorly localized, diffuse
begins in visceral then spreads to parietal where it becomes sharp + localized
1) appendicitis
Ischemic pain
less common, but most serious
sudden onset, intense, progressive pain, unresponsive to analgesia
1) strangulated bowel
2) mesenteric artery infarct
Treatment for ischemic pain
usually surgical
Injury patterns
blunt
penetrating
Blunt injury
skin surface intact
hematoma, bruising
Penetrating injury
skin surface disrupted
damage to internal tissues
higher r/o infection
Acceleration/deceleration forces
shearing = parallel force causes organs to pull away/fold around ligaments causing hemorrhage
compression = contact with another object
Cavitation
pressure variations caused by internal disruption
with penetrating injury, the force of the object radiates outward (energy transfer) causing displacement of internal structures
can be difficult to detect externally.
ex: gunshot wounds
Permanent cavitation
hole caused by penetrating injury
Temporary cavitation
damage to surrounding tissue
Types of nociceptive pain
superficial
somatic
visceral
Substances associated with pain
bradykinin
prostaglandin
histamine
cytokinin
serotonin
protons
cytokines
neuropeptides (substance P = sensitizes nerve endings)
COX-1 enzymes
involved in homeostasis
found in most tissues + regulate organ function
ex: prostaglandins in kidneys promote afferent arteriole vasodilation + production of stomach mucus + platelet aggregation
COX-2 enzymes
usually inactive except for inflammatory states
activated by trauma/injury
increase nerve sensitivity + function of other mediators
Which drug inhibits phospholipase A2
steroids
Which drug inhibits production of COX-2 enzymes
NSAID
aspirin
COX-2 selective inhibitors
Which drug inhibits central prostaglandins
Tylenol
NSAIDs + digoxin
can increase digoxin levels
r/o toxicity
NSAIDs + methotrexate
can increase methotrexate levels
NSAIDs + lithium
increase plasma concentration of lithium
r/o toxicity
NSAIDs + bleeding
increased r/o bleeding when combined with
steroids
anticoagulants
NSAIDs + renal impairment
increase risk when combined w/
diuretics
ACE-I/ARB
hypovolemic state
Adverse fx of NSAIDs
GI: r/o ulcers + bleeding (inhibits production of mucus + inhibits platelets)
RENAL: r/o AKI d/t afferent arteriole vasoconstriction
RESP: can upregulate LOX causing bronchospasm
BLEEDING: platelet inhibition increases r/o bleedingL
Local anesthesia MOA
block transmission of nerve impulses + ion channels preventing propagation
alters pain sensation without affecting LOC
affects sensory + autonomic nerves
Local anesthesia + nerve fibers affected
sensory = decreased pain
sympathetic = vasodilation + hypotension
motor = muscular weakness
Types of opioids
agonist
partial agonist
Adverse fx of opioids
RESP: decreased LOC = airway risk, respiratory depression, shallow breathing = decreased tidal volume
GI: nausea/vomiting, ileus, constipation
GU: urinary retention
SKIN: pruritis (release of histamine)
CV: hypotension (block sympathetic outflow + histamine rls)
ADDICTION: not for longterm pain mgmt
Early S/S of resp distress
tachycardia
tachypnea
cyanosis
agitation
altered mental status
Causes of anaerobic metabolism
decreased perfusion (less delivery of O2 to tissues)
decreased arterial oxygen content (resp issue)
PaCO2
r/t to metabolic activity
more metabolism = more PaCO2
regulated by ventilation
high ventilation = low PaCO2
low ventilation = high PaCO2
Maximum pH before cellular function fails
<6.8
>7.8
Anion gap
helps classify metabolic acidosis
determined by phosphate/albumin
High anion gap
low bicarbonate (used up for buffering)
metabolic acidosis
Low anion gap
may be d/t low albumin levels (primary anion)
low albumin = increased retention of other anions like chloride of bicarbonate
this then increases the level of anions compared to cations resulting in low anion gap
Unmeasured anions in anion gap
albumin
phosphorous
proteins
Normal anion gap
4-12T
Types of pnuemonia
typical = bacterial (fever, productive cough, sob, consolidation, pleuritic chest pain)
atypical = viral (dry cough, SOB, rales, myalgia, fatigue)
Pneumonitis
non-infectious cause of pulmonary inflammation
usually resolves on its own
Central chemoreceptors
located in the medulla
detect changes in pH of CSF
when pH drops (high CO2) triggers respiratory center to increase breathing
in chronic conditions like COPD, this mechanism can fail and then the body relies on changes in PaO2 to maintain breathing
Peripheral chemoreceptors
located in aortic/carotid bodies
detect changes in PaO2
strongly stimulated when PaO2 <60 transmits signal to increase breathing
