Unit 6 Flashcards
High pressure system
Begins at cylinder, ends at cylinder regulators Hanger yoke Yoke block with check valves Cylinder pressure gauge Cylinder pressure regulators
Intermediate pressure
Begins at pipeline, ends at flowmeter valves Pipeline inlets Pressure gauges Oxygen pressure failure device Oxygen 2nd stage regulator Oxygen flush valve Ventilator power inlet Flowmeter valves
Low pressure
Begins at flowmeter tubes, ends at common gas outlet Flowmeter tubes (Thorpe tubes) Vaporizers Check valve Common gas outlet
Low pressure leak test
(Negative pressure test)
Assess from flow meter valves to common gas outlet
Atttach bulb to common gas outlet and creat negative pressure
Fail=blurb inflates within 10 seconds
NO FGF and vent off
Vaporizers off first and then repeated with each vaporizer on
Best way to test a vaporizer leak
High pressure leak test
Closing APL valve and pressuring to 30cm/H2O
Pressure should remain constant
No check valve- checks entire breathing circuit and low pressure system
Check valve- checks breathing circuit and low pressure system, NOT between check valve and low pressure system
5 task of oxygen
O2 pressure failure alarm O2 pressure failure device (Failsafe) O2 flowmeter O2 flush valve Ventilator drive gas
Air PISS
1,5
Oxygen PISS
2,5
Nitrous oxide PISS
3,5
Cylinder colors
Standard in US, NOT in WHO
Air= black and white (yellow in US)
Oxygen= white
Nitrous= blue
Air tank
1900 psi
625 L
Oxygen tank
1900 psi
660 L
Nitrous oxide
745 psi 1590 L Wt full 20.7 lb Wt empty 14.1 lb Psi changes when its 3/4 empty, 400 L left (Barish says 250) Change when psi falls below 745
Fire triad
Oxidizer, fuel, igniter
Oiling cylinder valve increases fire risk-only need a heat source
American society for testing and materials
Anesthesia machine components
DOT
Standards for gas cylinders
FDA
Checkout procedures
OSHA
Occupational exposure for volatiles
Oxygen pressure fail safe
Protects against low O2 pressure in machine
Not actually failsafe- crossover can cause hypoxic mixture
Intermediate pressure system
2 components 1. When less than 28-30 psi 2. Reduces and stops nitrous flow when O2 pipeline less than 20 psi
Spring pressure that closes- O2 only thing that goes straight through
Disconnect O2 pipeline with N2O on and watch N2O flowmeter
Hypoxia prevention safety device
Prevents a hypoxic mixture with flow valves
Limits N2O flow to 3 times O2 flow (N2O max is 75%)
Can’t prevent hypoxic mixtures:
O2 pipeline crossover
Leaks distal to flow meter
3rd gas administration
Defective mechanic/pneumatic components
Annular space
Area between float and side wall of flowmeter
Internal diameter
Narrowest at base and widens along ascent
Floats read at top
Skirted, plum bomb, non rotating
Read in the middle
Ball
Reynolds number
(Density x diameter x velocity)/viscosity
Re<2000= laminar flow (dependent on gas viscosity)
Re > 4000= turbulent flow (depending on gas density)
2000-4000= transitional flow
calculating FiO2
(Air flow rate x 21) + (O2 flow rate x 100)/ total flow rate
Vt with fresh gas coupling
Vt set on ventilator + FGF during inspiration - volume lost to compliance
- Convert fresh gas flow from L/min to mL/min
- Multiple by FGF by the percentage of time in inspiration (1:2 IE= 33.33%)
- Divide 2 by RR.
- Add set Vt to 3.
Most new ventilators decouple so this does not apply
Compliance
Change in volume/ change in pressure
Elastic properties of lungs and chest wall
Dynamic- during air movement, measure of resistance and tendency of lungs to collapse
Static- when no airflow, measure of lungs tendency to collapse
Volume lost to circuit
Circuit compliance x peak pressure
Some of Vt used to expand circuit
Splitting ratio
Amount of FGF is directed towards the liquid anesthetic
1 mL of liquid anesthetic
Produces about 200 mL of anesthetic vapor
FGF entering chamber is 100% saturated
Latent heat of vaporization
of calories needed to convert 1g of liquid into vapor without a change in temp
Temp compensating
Heat carried away by vaporized molecues= anesthetic agent cooling
Decreases vapor pressure and vaporizer output
Temp compensating valve adjusts ratio of vaporizing chamber flow to bypass flow and guarantees constant vaporizer output with variable temps
Pumping effect
Gas that has already left vaporizer to go back through
Normally due to PEEP with low FGF, low concentration, low anesthetic in chamber
ML of liquid anesthetic used per hour
Vol% x FGF in L/min x 3
Desflurane vaporizer
Injects des into FGF
Heated to 39 C and 2 atmospheres
Does NOT compensate for changes in elevation
Higher altitude= partial pressure is lower
Lower altitude= partial pressure is higher
Calculating vaporizer output at elevation
Required dial setting= (normal dial setting x 760)/ambient pressure (mmHg)
Higher altitude= higher setting
Lower altitude= lower setting
Fuel cell vs paramagnetic
Fuel cell- calibrated daily, components must be replaced over time
Paramagnetic- self calibration, magnetic attraction
Oxygen analyzer
Monitors O2 concentration
Detects pipeline crossover
Detects leak most common=disconnect, 2nd most common= CO2 canister
Oxygen consumption for average adult
250 mL/min
O2 flush valve
35-75 mL/min
50 psi pressure (pipeline pressure)
Dont press during inspiration- ventilator spill valve is closed
Spill valve
Circuit pressure 2-4 cm H2O sends expired gas to scavenger
Inspiratory pressure limiter
Circuit pressure above certain level= gas ventilated to scavenger
Like APL that impacts ventilators
Piston vent
Uses electric motor to generate positive pressure
Will not consume tank O2 in event of pipeline failure- no O2 as driving gas
Positive pressure relief valve- opens at 75 +/- 5 cm H2O
Negative pressure relief valve- opens at -8 cm H2O, entrains room air leading to O2 and anesthetic agent dilution
Fresh gas decoupling= no Vt change with FGF, RR, or I:E
VCV
Preset vT
Ins pressure varies with compliance changes
Inspiratory flow constant
PCV
Preset insp pressure
VT and inspiratory flow vary
Increased resistance or decreased compliance=Vt problems
Decelerating flow pattern
Ethyl violet
Changes to purple at pH less than 10.3
reaction of CO2 with soda lime
CO2 + H2O = H2CO3 (carbonic acid)
H2CO3 + 2 NaOH = Na2CO3 + 2 H2O + heat
Na2CO3 + Ca(OH)2 = CaCO3 (calcium carbonate) + 2 NaOH (sodium hydroxide)
Best granule size
4-8 mesh
Calcium hydroxide lime (Amsorb)
CO2 + H2O= H2CO3
H2CO3 + Ca(OH)2 = CaCO3 + 2H2O + energy(heat)
No CO and very title compound A
Lower fire risk
Less absorbent capacity
Absorbent capacities
Soda lime 26L of CO2 per 100 g
Calcium hydroxide lime 10.6 L per 100g
OSHA recommendations for anesthetic gas
N2O < 25 ppm
Halogenated agents < 2ppm
Halogenated agents with N2O < 0.5 ppm and 25 ppm
Expiratory valve failing
Beta angle wider during inspiratory phase
Baseline doesn’t return to 0
Mapleson A
Bag after FGF hanging down
Best for spontaneous ventilation
Requires 20 L/min FGF for controlled ventilation
Mapleson D
Reservoir, APL, FGF
Bain= modified version
Mapleson B
Reservoir, FGF, APL (corigated and longer tubing)
Mapleson C
Reservoir, FGF, APL (Short)
Mapleson E
Ayers T piece
No APL or reservoir bag
Mapleson F
Jackson Rees
APL, reservoir, FGF
Mapleson with SV
A > DFE > CB
Mapleson controlled ventilation
DFE> BC> A
FGF to prevent rebreathing
2.5x patients minute ventilation
Bain system
Modified mapleson D
FGF enters inner tubing and exhaled goes through corrugated tubing
Good for spontaneous and controlled
Pethick test- occlude elbow and patient end, close APL, fill circuit with O2 flush, remove occultism at elbow while flushing
Patent inner tubing =collapsing reservoir bag due to Venturi
Resistance
(Airway pressure- alveolar pressure)/ FGF
Peak inspiratory pressure (PIP)
Maximum pressure during inspiration
Dynamic compliance= tidal volume/ (PIP-PEEP)
Plateau pressure (PP)
Pressure in smal airways and alveoli after tital volume is delivered
During inspiratory pause
Barotrauma risk increased with pressure > 35 cm/H2O
Static compliance= tidal volume/ (plateau pressure- PEEP)
normal static compliance
Adult 35-100 mL/cmH2O
Child > 15 mL/cmH2O
PIP and PP changes
Increased PIP and PP= compliance decreased or tidal volume increased
Increased PIP with no change in PP= increased resistance or increased inspiratory flow rate
CO2 waveform
A= start of flat phase
Phase 1= flat phase
Alpha angle- measured at point C, normally 100-110 degrees, increased= expiratory airflow obstruction
Beta angle- measure at point D, should be 90 degrees, increased in some rebreathing scenarios
CO2 analysis methods
Mainstream (in line)- attached to ETT, faster response time, increases dead space
Sidestream (diverting)- outside of airway, slower response time due to pumping air away, need a water trap
Beer lambert law
Intensity of light transmitted through a solution (blood) and a solute (hemoglobin)
Pulse oximetry
Pulse ox wavelengths
2 of them
- Red light (660 nm)- absorbed by deoxyhemoglobin (higher in venous blood)
- Near infrared light (940 nm)- absorbed by oxyhemoglobin (higher in arterial blood)
SpO2
Oxygenated hgb/ (oxygenated hgb + deoxygenated hgb) X 100%
Light changes through pulse ox cycle
Trough- greater amount of venous blood
Peak- greater amount of arterial blood
Pulse ox calculates absorption ratio on continuous basis
SpO2 response time
Fast= ear, nose, tongue, esophagus, forehead Middle= finger Slow= toe
SPO2 and PaO2
SPO2 90%= PaO2 60 mmHg
80%= 50 mmHg
70%= 40 mmHg
Oxyhemoglobin dissociation curve
Left= increase infinity
Decrease temp, 23 DPG, CO2 H+
Increase pH, HgbMet, HgbCO, HgbF
What does pulse pressure monitor
Hemoglobin saturation
Heart rate
Fluid responsiveness (PP variation)
Perfusion- ex: R side for innominate artery in mediastinoscopy
Pulse ox error margin
2-3% between 70 and 100%
3% between 50-70%
Methemoglobin
Absorbs 660 and 940 equally
Absorption ration areas at 85%
Underestimates if > 85%
Overestimates if < 85%
Carbohemoglobin
Absorbs 660- same as O2Hgb
Overestimates SpO2
Factors that impact pulse ox
Dyes Nail polish- blue, black, green Non pulsatile flow Motion artifact Cautery Pulsatile venous flow- tricuspid regurg
Things that dont impact pulse ox
Hemoglobin S Hemoglobin F Jaundice Flouorescein Polycythemia Acrylic nails
Infrared spectrophotometry
Most common exhaled gas analysis method
Each gas absorbs different wavelength of infrared light
Greater conc of gas absorbs more infrared light so light intensity back to sensor is less
Can not measure O2
Mass spectrometry
Puts electrons in gas sample creating ion fragments
Particles become charge and are identified based on mass
May be used for more than one patient at once
Raman scatter spectrometry
Argon laser used to produce photons that collide with gas molecules
Scatter of photons measured to identify gas and concentration
Piezoelectric crystals
Incorporates alipid layer on the crystal
Responds to individual gases as they make contact and get absorbed
Can’t identify more than one gas at once
BP cuff distance change
Every 10 cm= BP change by 7.4 mmHg
Every inch= BP change by 2 mmHg
A line waveform
SBP= peak of waveform DBP= trough of waveform PP= Peak - trough Contractility= upstroke SV= area under curve Closure of aortic valve= dicrotic notch
ABP waveform flush test
Optimally damped- baseline after 1 oscillation
Under damped- baseline after several oscillation= SBP overestimated, DBP underestimated, MAP accurate
Over damped- baseline with no oscillations= SBP underestimated, DBP overestimated, MAP accurate, causes- air bubble/ clot or low bag pressure
Insertion to Vena cava/RA junction
Subclavian 10 cm Right IJ 15 cm Left IJ 20 cm Femoral 40cm R median basilic 40cm L median basilic 50 cm
Vena cava/ RA junction to Cather tip
RA 0-10 cm
RV 10-15 cm
PA 15-30 cm
PAOP 25-35 cm
Central line complications
L IJ= added risk of puncturing thoracic duct (chylothorax)
Dysrhythmias= most common complication
Infection rate increases after 3 days
No PAC with LBB- can cause RBB= complete heart block
A wave CVP
RA contraction
Just after P wave
C wave CVP
RV contraction (bulging tricuspid valve in RA) Just after QRS complex
X descent CVP
RA relaxation
ST segment
V wave CVP
Passive filling of RA
Just after T wave begins (ventricular repol)
Y descent (CVP)
RA empties through open tricuspid valve
After T wave ends
Phlebostatic axis
4th intercostal space mode anteroposterio level
Where should CVP be measured?
End expiration
Not impacted by intrathoracic pressure there
Normal CVP
Adult 1-10 mmHg
Low= low intravascular volume High= hypervolemia, decreased ventricular compliance, increased thoracic pressure
CVP is a function of
Intravascular volume
Venous tone
RV compliance
Assume RV and LV output = and that RAP reflects LVEDP
RVP
Systolic pressure increases
Diastolic= CVP
15-30/0-8
PAP
Systolic= same
Diastolic rises
Dicrotic notch formed
15-30/5-15
PAOP
5-15 Or wedge pressure CVP of left heart A wave= left atrial systole C wave= mitral valve elevation into LA during LV systole V wave= passive left atrial filing
zone of lung for tip of PA cath
Zone III
Most accurate estimation of LVEDP
Dependent region
Clues PA tip isn’t in zone 3
PAOP > PAEDP
Nonphaseic PAOP tracing
Inability to aspirate from distal port when ballon wedged
Thermodilution
Injected through proximal port of PA cath
Stewart Hamilton equation plots temp change vs time
AUC inversely proportional to CO
high CO= small AUC
Low CO= large AUC
Influencing themodilution CO measurements
Underestimates- injecting too much or too cold fluid
Overestimates- injecting too little or too hot fluid, wedge PAC, thrombus on tip
Unable to predict- shunt, tricuspid regurg
Mixed venous oxygen saturation
SvO2= SaO2- (VO2/(Q x 1.34 x Hgb x 10)) Normal= 65-75%
VO2= oxygen consumption SaO2= loading of hemoglobin in arterial blood
Need a PA cath to get blood from SVC, IVC, and coronary sinus together
Filling during insp and expiration
Inspiration- positive pressure augments LV and increases SV
Expiration- LV filling decreases and reduces SV
Hypovolemia= greater SVV
Preload responsiveness
200-250 mL fluid bolus improves SV > 10%
Measurement usually 13-15%
anterior internodal tract
Bachman bundle
Extends into LA
Middle internodal tract
Wenckeback tract
Posterior internodal tract
Thorel tract
Cardiac conduction velocities
SA and AV nodes= 0.02- 0.1 m/sec (slow)
His bundle, bundle branches, and purkinje= 1-4 m/sec (fast)
Myocardial muscle cells= 0.3-1 m/sec (intermediate)
Function of- resting potential, amplitude of AP, rate of change in potential during phase 0
Vector of depolarization
Positive deflection- vector travels towards from + electrode
Negative deflection- vector travels away from + electrode
Biphasic deflection- vector travels perpendicular to + electrode
Bipolar leads
I- lateral, CxA
II- inferior, RCA
III- inferior, RCA
Limb leads
AVR
AVL
Lateral
CxA
aVF
Inferior
RCA
Precocial leads
V1- septum, LAD V2- septum, LAD V3- anterior, LAD V4- anterior, LAD V5- lateral, CxA V6- lateral, CxA
Axis deviation
Use lead 1 and aVF
+ and += normal (between -30 and +90)
- and -= extreme R
Leads are Reaching towards each other(I down and aVF up)= R (greater than 90)
Leads are Leaving each other (I up and aVF down)= L (less than -30)
Vector direction with hypertrophy and MI
Hypertrophy- towards it (more to depolarize)
MI- away from it (has to move around it)
Bainbridge reflex
Causes sinus arrhythmia
increased venous return stretches RA and SA node causing increase HR
Inhalation= increased venous return
Sinus Brady treatment
Atropine- can have paradoxical Brady
Transcutaneous pacing
Glucagon- B blocker of Ca blocker overdose, increases cAMP, 50-70 mcg/kg q 3-5 min, 2-10 mg/hr infusions
Brigade syndrome
Na ion channelopathy in heart
Most common sudden nocturnal death from Vtach or fib
Common in SE Asian males
EKG- RBBB, ST segment elevation in precordial leads
ICD or pad placement in surgery
2nd degree heart block type I
Mobitz I, Wenckebach
PR interval longer with each cycle and last P wave doe snot conduct
Give atropine if symptomatic
2nd degree heart block
Mobitz II
Some P’s conduct, others don’t
Usually 2:1 or 3:1 ratio
High risk of conversation to complete
3rd degree heart block
Atria and ventricles have separate rates
Complete dissociation
Class 1 antiarhythmic
Na+ channel blockers
1A- quinidine, procainamide, disopyramide
Phase 0 dep, prolonged phase 3 repol
1B- lidocaine, phenytoin
Phase 0 dep, shortened phase 3 repol
1C- flea indie, propafenone
Strong phase 0 dep
Class 2 antiarhythmics
Beta blockers
Slows phase 4 depol in SA node
Class 3 antiarhythmics
K+ channel blockers
Amiodarone, bretylium
Prolongs phase 3 repolarization
Increased effective refractory period
Phase 4 antiarhythmics
Ca Channel blockers
Verapamil, dilt
Decreased conduction velocity through AV node
Adenosine
Endogenous nucleoside that slows conduction through AV node
Causes K to move into cell (hyperpolarized) and reduces action potential duration
Rapid plasma metabolism
SVT and WPW, NOT a fib, a flut, or Vtach
Can cause brnochospasm
WPW syndrome
Most common pre excitation syndrome
Direct accessory conduction pathway (Kent’s bundle) that bypasses AV node
EKG- delta wave, short PR interval, wide QRS, possible T wave inversion
A fib- give procainamide
Tachycardia with WPW
AV nodal reentry tachycardia (AVNRT)
Orthodromic AVNRT
More common
Atrium to AV node to ventricle to accessory pathway to atrium
Narrow QRS
Block conduction at the AV node to increase AV node pathway
Antidromic AVNRT
Rare
Atrium to accessory pathway to ventricle to AV node to atrium
Wide ARS
Block accessory pathway- procainamide, amiodarone, cardiversion
Do NOT give agents that increaseAV refractory, favors accessory pathway, can induce V fib
Avoid- adenosine, dig, dilt and verapamil, beta blockers, lidocaine
More dangerous- gatekeeper function of AV node bypassed
Drugs that are safe for all AVNRT
Amiodarone
Cardiversion
Definitive treatment of WPW
Radio frequency ablation
LA pathway
Thermal injury to LA and esophagus
Monitor esophageal temp
Tornadoes de Pointes
Polymorphic v tach causes by delay in ventricular repolarization (phase 3)
Associate with a long QT
Men > .45 sec
Women > 0.47 sec
Can be caused by R on T phenomenon
Treatment- mag, cardiac pacing
Prevention- avoid SNS stim, beta blockers
Tornadoes mnemonic
POINTES Phenothiazines Other meds- methadone, droperidol, haldol, zofran, halogenated agents, amiodarone, quinidine Intracranial bleed No known cause Type I antiarhythmics Electrolyte disturbances- low K, low Ca, low Mg Syndromes- Romano ward, Timothy
Pacemaker designation
1- paced 2- sensed 3- response 4- programmability 5- pacemaker can pass multiple sites
Magnet
Pacemaker- usually converts to asynchronous, best answer is to consult manufacturer
ICD- suspends ICD and prevent shock
Pacemaker and ICD- suspends ICD and prevents shock, NO pacemaker effect
Conditions that make myocardium more resistant to depol
May fail to capture K disturbance Hypocapnia Hypothermia MI Fibrotic tissue around pacing leads Antiarhythmics meds
Cerebral oximetry
Measures venous O2 sat
Detects regional O2
Can’t measure pulsatile flow- detect venous oxyhemoglobin saturation and extraction
> 25% change from baseline suggests reduced oxygenation
EEG waves
Beta- high frequency, low voltage, awake or light anesthesia
Alpha- medium frequency, awake but restful with eyes closed
Theta- general anesthesia and children sleeping
Delta- low frequency, GA, deep sleep, and brain injury
