1
Q
as per BLS IV line maintenance standard- paramedic shall monitor a iv line for TKVO is as follows:
A
- the flow rate to maintain patency for <12 years is 15ml/h
- the flow rate to maintain patency for >12 years is 30-60 ml/h
2
Q
as per BLS IV line maintenance standard- paramedic shall monitor a iv line for fluid replacement is as follows:
A
- max flow rate 2 ml/kg to a max of 200 ml/h
- thiamine, multivitamin preparations
-drugs within his/her certification
-KCL for pt >18 to a max of 10mEq in 250ml bag
3
Q
as per BLS IV line maintenance standard- the use of escorts is required for:
A
- use of blood administration
- administration of KCL to pt <18
- used to administer medications
- requires electric monitoring or uses pressurized IV infuser, pump or central venous line
- for a neonate or ped patient <2 years
4
Q
as per BLS IV line maintenance standard- pre transport procedure
A
- confirm physicians written IV order with facility
- determine IV solution, flow rate, catheter gauge, length and cannulation site
- note condition of IV site prior
-amt of fluid remaining in bag
-amt of fluid required for complete transport time
-document
5
Q
as per BLS IV line maintenance standard- during transport procedure
A
- monitor and maintain iv at prescribed rate
if iv becomes dislodged or interstitial, discontinue iv and remove catheter with aseptic technique - confirm condition of catheter if removed
6
Q
as per BLS IV line maintenance standard- when should iv bag be changed
A
when there is approx 150 mls of solution remaining
7
Q
as per BLS DNR- what are the life saving measures outlined
A
- chest compressions, defibrillation, artificial ventilation, insertion or OPA,NPA or SGA, endotracheal intubation, transcutaneous pacing, resuscitation drugs (antiarrhythmics, vasopressors, and opioid antagonists)
8
Q
as per BLS DNR- what does do not resuscitate mean
A
means that the paramedic will not initiate any of the life saving interventions listed
9
Q
as per BLS DNR- what does treatment mean
A
any action or service that is provided for therapeutic, preventative, palliative, diagnostic, cosmetic or other health related
10
Q
as per BLS DNR- what does a valid DNR need to include
A
-name of pt
-checked box to identify current plan of treatment OR physicians current opinion that doesn’t include CPR
- checked box that identify professional designation who signed the form
- printed name of the health professional that signed
- signature of health care professional
- date form was signed which must be the same or day that precedes the date
- can be original or a copy
11
Q
as per STEMI bypass- what are the conditions
A
- > 18
- chest pain or equivalent w MI or cardiac ischemia
- onset <12 hours
-12 lead that indicates acute MI/STEMI
a) at least 2mm ST elev. in leads V1-V3 and/or
b) at least 1mm ST elev. in at least 2 other contiguous leads OR
c) 12 lead ECG interpretation of STEMI
12
Q
as per STEMI bypass- what are the contraindications
A
-CTAS 1, and unable to secure airway or ventilate
-12 lead consistent w LBBB, vent. paced rhythm or any STEMI imitator
-transport time to PCI >60 mins from pt contact
- pt is experiencing complication req. PCP diversion:
a)mod-severe resp distress
b)hemodynamic instability or symptomatic SBP <90
c)VSA without ROSC
- pt is experiencing complication req ACP diversion:
a)vent. inadequate
b) hemodynamic instability unresponsive to ACP treatment/mgmt
c)VSA without ROSC
13
Q
IV catheter colours & sizes
A
Orange- 14g
Grey- 16g
Green- 18g
Pink- 20g
Blue- 22g
Yellow- 24g
14
Q
normotension in adults
A
> 100mmhg
15
Q
hypotension in adults
A
SBP <90 mmhg
16
Q
bradycardia in adults
A
<50bpm
17
Q
tachycardia in adults
A
> 100bpm
18
Q
tachypnea in adults
A
> 28 breaths
19
Q
0-3 mons hr and rr
A
-90-180 hr
-30-60 rr
20
Q
3-6 mons hr and rr
A
- 80-160 hr
-30-60 rr
20
Q
6-12 mons hr and rr
A
-80-140 hr
-25-45 rr
21
Q
1-3 y hr and rr
A
-75-130 hr
-20-30 rr
22
Q
6y hr and rr
A
-70-110 hr
-16-24 rr
23
Q
10y hr and rr
A
-60-90 hr
- 14-20 rr
24
normotension in peds
>90mmhg + 2xage
25
hypotension in peds
<70 mmhg + 2xage
26
weight calc for peds
2xage + 10
27
hypoglycemia (<2)
<3mmol/L
28
hypoglycamia (>2)
<4mmol/L
29
definition of SPO2
Saturation of Peripheral Capillary oxygenation.
Pulse oximetry measures oxygen saturation levels.
30
definition of ETCO2
measures ventilation status. Is the CO2 in the
airway at the end of exhalation.
31
what is the respiratory cycle in ETCO2
ventilation + circulation + metabolism = gas exchange
32
what is dead air space
ventilated areas that do not participate in gas exchange
33
why capnography?
because respirations, ventilations and oxygenation are very different concepts
34
what is capnography
- Represents the amount of CO2 in exhaled air
-The number- “Capnometry”- partial pressure of
CO2 at the end of exhalation
35
how is ETCO2 measured
- pt who are breathing: nasal prongs
-pt with assisted ventilations: device attached to BVM
36
pt respiratory rate when Co2 is increased
should increase
37
pt respiratory rate when Co2 is decreased
should decrease
38
how do we assess ventilations
-chest rise and fall
-respiratory efforts
-auscultation
-respiratory rate
39
why is capnography important
verification of proper tube placement. no waveform = no tube
40
quantitative waveform
an actual numeric value associated with an electronic device: 35-45mmhg
41
Qualitative waveform
low/medium/high value- give range vs actually number. colorimetric device is an example
42
phase 1
(A-B) inspiratory baseline (low CO2 a its inspired air)
43
what is PaCo2
Partial Pressure of Carbon Dioxide in arterial blood
gases. The PaCO2 is measured by drawing the
ABGs, which also measure the arterial PH
-normal is 35-45 mmhg
44
What is B in waveform
the start of alveolar exhalation
45
phase 2
(B-C) exhalation upstroke (dead space gas mixes with lung gas)
46
phase 3
(C-D) continuation of exhalation (gas is all alveolar now, rich in CO2)
47
what is D in waveform
the end tidal value, peak concentration
48
phase 4
(0)(D-E) start of inspiration
49
sudden loss of waveform
-ET tube disconnected, dislodged kinked, or obstructed
50
decreasing ETCO2
-et tube cuff leak
-ET tube in hypo pharynx
-partial obstruction
51
cpr assessment
attempt to maintain minimum of 10mmhg
52
sudden increase in ETCO2
ROSC
52
bronchospasm
-sharkfin appearance
-asthma or COPD
53
hypoventilation
long flat waveforms
54
hyperventilation
quick small waveforms
54
decreased etco2
apnea or sedation
55
why the slope in etco2 with bronchospasm?
Because the movement of air at the alveoli is
delayed in a person with bronchospasm, the rise
to the plateau is more gradual and the plateau
itself becomes sloped
56
hyperventilation-low co2
they are blowing off large amounts due to the increased RR
57
what causes hyperventilation
anxiety, bronchospasm, pulmonary embolus
57
what causes low etco2
cardiac arrest, hypotension, decreased cardiac output, cold
58
hypoventilation-high co2
they are retaining CO2 due to slowed RR
59
what causes hypoventilation
overdose, sedation, intoxication, postictal states, head trauma, stroke, tiring CHF, fever, sepsis, SOB
60
when cardiac output is normal...
ETCO2 measures ventilation
61
when cardiac output is decreased...
ETCO2 measures cardiac output
62
what does it mean when cardiac output fails
very little metabolism takes place and very little blood flows through the lungs, resulting in little perfusion and gas exchange; ie cardiac arrest
63
ETCO2 in a cardiac arrest
cardiac arrest is the ultimate shock state, there is no metabolism and no CO2 production unless CPR is being done
64
ETCO2 of <10mmhg indicates...
compressions are not deep or fast enough
or
pt will not survive
65
spike in ETCO2 meaning
circulation is restored, even if you can't feel a pulse, circulation must be present
66
why is there a low survival rate with low ETCO2
If a relatively high ETCO2 can be accomplished by
good CPR- it can be assumed that cardiac output
is high enough to support a successful
resuscitation
-If a patient has been VSA for a long time,
vasodilation and sluggish blood flow prevents the
build up of significant cardiac output despite good
CPR
67
why the sudden spike in ETCO2 for a ROSC
- Large amounts of acidic blood are suddenly returned to the lungs and high amounts of CO2 diffuses into the alveoli
- This flood of CO2 causes a remarkable sharp rise in the ETCO2 levels to much higher then normal
68
what are sudden spikes in ETCO2 considered
signs of life, complete a pulse check and reassessment
69
what is the tidal volume?
amount of air that a patient takes in (goes in) during one breath
70
macro drip sets
10/15/20 gets/ml
- most commonly utilized administration
- effective for TKVO and large fluid admins (bolus)
70
what are the indications for IV therapy
- administer fluids TKVO
- administerdrugs
- obtain specimens for laboratory determinations
71
micro drip sets
always 60 gtts/ml
- to deliver meds over long periods of time
- assist in the precise measurements of medications
- to control the amount of fluid
- to control fluid overload in certain patients.
72
adult catheter sizes
14/16/18/20
73
elderly catheter sizes
18/20/22
74
pediatric catheter size
22/24
75
what does catheter size depend on
- working diagnosis
- age/health/ size/ or just TKVO
76
what is a crystalloids
dissolving crystals such as SALT and SUGARS in water. contain NO proteins
- example: NS and LR
77
crystalloid action
remains in the intravascular space for only a short period of time before diffusing across the capillary walls into the tissue
78
colloids description
contain large molecules such as PROTEINS
- example: plasma substitutes, packed RBC and while blood, plasmanate, dextran, hetastarch
79
colloids action
do not pass through the capillary membrane as readily as colloids
80
hypotonic
lower solute in the solution then the cell, causes water to go into the cell
81
hypotonic example
NS,LR
82
hypertonic
higher solute in the solution causes water to leave the cell
83
hypertonic example
mannitol
84
isotonic
equal inside and outside the cell
85
checking the solution
1. Leaks/precipitation – while in the plastic wrap
2. Correct Solution Name
3. Expiration Date
4.Cloudiness/Discoloration
5. Each bag contains enough solution to: Flush the administration set – good for 24 hours, allow for accurate readings of volume even with sterile air in the bag
86
priming an IV bag steps
1. Select the appropriate IV tubing. Inspect the tubing, the roller clamp, the injection
ports & the luer lock connector for cracks, use and sterility.
2. Select the appropriate sized IV bag. Inspect for cloudiness, precipitate and cracks/leakage. Check the expiry date, and ensure the fluid is the proper type (Normal
Saline or 0.9% saline).
3. Close the roller clamp.
4. Remove the cap on the IV tubing closest to the drip chamber. Ensure sterility! Remove
the plastic tab on the IV bag. Connect the two.
5. Squeeze the drip chamber. Fill it ½ full.
6. Open the roller clamp slightly to advance the fluid down the tubing.
7. When the fluid approaches an injection point, invert the port and strike the port, forcing air out and fluid in. Repeat as many times as needed.
8. Close the roller clamp when all the air is expelled from the tubing.
87
primed bags must:
have date, time, and name
- only good for 24-48 hours
88
equipment required for iv
- tourniquet
- 2x2/4x4/ band aids
-IV pole
- opposite
- alcohol wipe
- sharps container
- catheter
administration set/ iv bag or saline lock
89
iv sites are based on
- visibility of veins
- stability of veins
90
IV contraindications
-Presence of an AV Fistula
- Anticipated locations of surgery
- Veins that are firm or sclerosed
- Evidence of phlebitis or
thrombosis
- Mastectomy
- Lymph Node Removal
91
procedure of IV
- communication
- infection control
- site selection
- peripheral vasodilation
- gather equipment
-apply gloves for personal and patient protection
- select puncture site
- Apply tourniquet above antecubital space
- Prepare the puncture site, cleansing the area with alcohol or wipes (per protocol)
- Remove protective cover from catheter – out of
patient’s view. “sharp out"
- stabilize the vein
- pass through the skin into vein
- look for flashback
- slide catheter over needle into vein
- release tourniquet
- secure
- apply pressure on the end of catheter
- withdraw needle
- attach tubing
92
unsuccessful IV causes
- angle of initial entry too steep, cut through vein
-not enough tension- vein rolling
- attempting while in a hurry
- stylet not retracted enough during disconnection phase
- lack of confidence/poor vein location
93
venous pressure
position of pt extremity
94
vein spasm
irritating- or chilled fluids= reflex to occur
95
phlebitis and thrombi
initial decrease in flow rate due to spasm = inflammation to vein/or clot formation
96
local complications
- pain and irritations
- infiltration and extravasation
- phlebitis
- thrombosis and thrombophlebitis
- hematoma formation
- venous spasm
- vessel collapse
- cellulitis
-nerve, tendon, ligament, and limb damage
96
viscosity
thickness of fluid- high concentrations of dextrose tend to flow at slower rates
97
mechanical complications
-changes in the position of needle
- Height of solution
- Amount of solution
- Position of patient- kinked tubes
- Disconnected tubes
- Plugged air vents &/or plugged needles/cannula
98
systemic complications
-Contamination and infection
- Hypersensitivity reactions
- Sepsis
- Emboli (blood clot, air, and catheter)
99
indications for king LT
alternative to bag mask OPA/NPA ventilation when an advanced airway device is required for airway management
99
king LT complications
- Laryngospasm, vomiting, and possible hypoventilation may occur.
- Trauma may also result from improper insertion technique.
- Ventilation may be difficult if the pharyngeal balloon pushes the epiglottis over
the glottic opening
100
confirmation of SGA
- chest auscultation
-chest rise
- non waveform ETCO2
- tube misting
101
contraindications for king LT
- Does not eliminate risk of vomiting and aspiration
- High airway pressures can cause air to leak into stomach or out of mouth.
- Do not use in patients with intact gag reflex, esophageal disease, or who have ingested caustic substance.
- Airway obstruction
102
king LT insertion
elect the appropriate size tube, based on the patient's height:
* Size 3: 4 to 5 ft (122-155 cm)
* Size 4: 5 to 6 ft (155-180 cm)
* Size 5: > than 6 ft (180 cm)
* Apply lubricant to the beveled distal tip and posterior aspect of the tube, taking care to avoid introduction
of lubricant in or near the ventilatory openings.
* Pre-oxygenate via BVM.
* Position the head. The ideal head position for insertion of the KING LTS-D is the “sniffing position”.
However, the angle and shortness of the tube also allows it to be inserted with the head in a neutral
position. For obese patients, elevation of the shoulders and upper back should be considered.
* Hold the KING LTS-D at the connector with dominant hand.With non-dominant hand, perform a tongue-
jaw lift and insert tube into corner of mouth.
* With the KING LTS-D rotated laterally 45-90 degrees, such that the blue orientation line is touching the
corner of the mouth. Introduce tip into mouth and advance behind base of tongue.
* As tube tip passes under tongue, rotate tube back to midline (blue orientation line faces chin).
* Without exerting force, advance tube until base of connector is aligned with teeth or gums.
* Advance the device until the lips are rest between the black bands on the dev
103
pathophysiology of asthma: bronchoconstriction
smooth muscle contraction narrows the airway
103
igel insertion
1. Remove i-get from protective cradle or pack
2. Grasp lubricated I-Gel firmly along the integral bite block. Position device so
the cuff outlet is facing towards patient’s chin.
3. Gently press down on chin to open mouth (no fingers or thumbs in mouth).
4. Introduce leading soft tip into pt’s mouth in a direction towards hard palate.
5. Glide the device downwards and backwards along the hard palate with a
continuous but gentle push until definitive resistance is felt. Sometimes a feel
of ‘give-way’ is felt before end point resistance is met. This is the due to the
passage of the I-Gel bowl through the faucial pillars. Continue to insert device
until definitive resistance is felt.
103
when do we remove a SGA in a rosc
- only if gag reflex is stimulated, or patient begins to vomit
104
complications of IGEL
- trauma to the pharyngo-laryngeal framework
● Down-folding of epiglottis (more common in
children)
● Gastric insufflation, regurgitation and
inhalation of the gastric contents
● Nerve injuries, vocal cord paralysis, lingual or
hypoglossal nerve injuries
● If placed too high in the pharynx, may result
in a poor seal and cause excessive leakage
● Laryngospasm
104
when do we place a SGA
- BLS airway management is ineffective
- prolonged extrication
105
signs and symptoms of asthma
-Dyspnea
-Wheezing (especially expiratory)
-Prolonged expiratory phase
-Cough (may be dry or productive)
-Chest tightness
-Use of accessory muscles
- Decreased oxygen saturation
105
pathophysiology of asthma: excess mucus production
further obstructed airflow
105
pathophysiology of asthma: mucosal edema
inflammatory response causes swelling
106
pathophysiology of asthma: air trapping
causes difficulty with expiration and hyperinflation of the lungs
106
what causes decreased breath sounds (silent chest)
Decreased breath sounds indicate severe airway obstruction, where minimal
or no air is moving in or out. Silent chest is a critical sign of impending
respiratory failure
107
5 respiratory reasons for SOB
- asthma
-COPD
-respiratory infections
-anaphylaxis
-aspiration
107
what is the role of epinephrine in asthma exacerbation
non-selective adrenergic agonist that:
- beta-2 effects: promotes bronchodilation by relaxing smooth muscle in the airway
- alpha effects: reduced mucusal edema by vasoconstriction
- beta-1effects: increases hr and contractility, improving perfusion in severe cases
108
3 cardiac reasons for SOB
- myocardial infarction
-CHF
- pulmonary edema
109
3 other reasons for SOB
-CVA
-toxicology effets
-metabolic acidosis
110
signs and symptoms of emphysema
- Shortness of breath, especially during physical activity.
-Pursed-lip breathing.
- Barrel-shaped chest.
- Use of accessory muscles for breathing.
- Decreased breath sounds and wheezing.
- Peripheral cyanosis in severe cases.
- Chronic cough, often with minimal sputum production
111
common causes of emphysema
- longterm smoking
-chronic exposure to airborne irritants
-genetic factors
-hx of repeated respiratory infections
112
pathophysiology of emphysema: alveolar distraction
long term exposure to irritants damages alveolar walls, leading to loss of elasticity
113
pathophysiology of emphysema: air trapping
damaged alveoli lose the ability to deflate fully, causing air to be trapped
114
pathophysiology of emphysema: hyperinflation
over distended lungs reduce the diaphragms efficiency.
115
pathophysiology of emphysema: impaired gas exchange
reduced alveolar surface area decreases oxygen and carbon dioxide exchange
116
what is the major pathological change associated with emphysema
The destruction of alveolar walls and the resultant loss of elastic recoil, which
causes air trapping and reduced gas exchang
117
potential life limb threats for SOB
- partial a/w obstruction
-asthma
-anaphylaxis
-aspiration
-inhalation of toxic gases or smoke
-pneumothorax
-COPD
-respiratory infections
117
target SPO2 for emphysema
88-92
117
4 signs of a silent MI
- unexplained fatigue or weakness
- mild or absent chest pain
- SOB
-nausea, dizziness, or diaphoresis without classic ischemic symptoms
117
pathophysiology behind cariogenic shock
-decreased myocardial contractility-reduced cardiac output-systemic hypo perfusion.
- tissue hypoxia-lactic acidosis-multi organ dysfunction
118
signs and symptoms of LHF
dyspnea, orthopnea, crackles, fatigue, pink frothy sputum, tachycardia
119
signs and symptoms of RHF
peripheral edema, JVD, ascites, hepatomegaly, weight gain
120
primary issue RHF
blood backs up into systemic circulation
120
primary issue of LHF
blood backs up into the lungs, causing pulmonary congestion
120
patho of heart failure
Heart failure occurs when the heart cannot pump effectively, leading to
inadequate perfusion of tissues and retention of fluid.
120
what is LHF caused by
Often caused by ischemic heart disease, hypertension, or
valvular dysfunction. It increases pulmonary pressures, causing
pulmonary edema
120
what is RHF caused by
Often secondary to LHF (cor pulmonale) or pulmonary
hypertension. Leads to systemic venous congestion and peripheral
edema
121
CHF exacerbations often occur in the early morning due to...
-increased vagal tone and catecholamine surges.
- Recumbent positioning overnight leading to fluid redistribution and
pulmonary congestion.
- Diurnal variation in renal perfusion and sodium/water retentio
121
medical cardiac arrest special considerations (1 analysis).
1. pregnancy presumed to be ≥ 20 weeks gestation (fundus above umbilicus, ensure manual displacement of uterus to left);
2. hypothermia;
3. airway obstruction;
4. non-opioid drug overdose/toxicology, or;
5. other known reversible cause of arrest not addressed.
121
medical tor conditions
- >16
-LOA altered
-arrest not witnessed by paramedic AND
-no ROSC after 20 mins of resuscitation AND
-no defibrillation delivered
121
medical tor contraindications
- known reversible cause of the arrest unable to be addressed
-pregnancy presumed to be >20 weeks
-suspected hypothermia
-airway obstruction
-non opioid drug overdose/toxicology
121
>24 hrs to <8 years joule settings
initial:2j/kg
subsequent:4j/kg
122
epinephrine treatment (MCA)
0.01mg/kg
-max 0.5
-1 time
123
trauma TOR contraindications
- age <16
-defib delivered
-signs of life at any time since fully extricated
-rhythm PEA and closest ED <30 mins away
-patients with penetrating trauma to the head/neck and lead trauma hospital <30 min transport time away
123
trauma tor conditions
- >16
-LOA altered
-SBP N/A
- no palpable pulses AND
- no defibrillation delivered AND
-rhythm systole AND
- no signs of life at any time since fully extricated OR
- signs of life when fully extricated with the closest ED >30mins transport away
-rhythm PEA with the closest ED >30 min transport time away
EMRG 1300 FINAL
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