Flashcards in Final Review Deck (93):
Where is the larynx?
Inside of the thyroid cartilage, between the pharynx and trachea
- in adults: anterior to 3rd-6th cervical vertebrae
- at birth: level C3-4
What is A-O extension normally?
What are the different Mallampatti classes?
- Class 1: full view of uvula and tonsillar pillars, hard and soft palate
- Class 2: partial view of uvula or uvular base, partial view of tonsils, soft palate
- Class 3: soft palate only
- Class 4: hard palate only
(3 and 4 predict difficult intubation)
What structures does the sphenopalatine ganglion (middle division of CN V) innervate?
- nasal mucosa
- superior pharnx
—> to numb: hurricane spray- would only need to numb for fiberoptic intubation
What structures does the glossopharyngeal nerve (CN IX) innervate ?
(Lingual back 1/3, pharyngeal, tonsillar nerves)
- oral pharynx
- supraglottic region
—> to numb: gargle with lidocaine
What structures does the internal branch of the superior laryngeal nerve (CNX) innervate?
- mucus membrane above the vocal cords
—> to numb: garble with lido or use nebulized lidocaine
What structures does the recurrent laryngeal nerve (CNX) innervate?
**below the vocal cords
—> to numb- needle through cricothyroid membrane and splash lidocaine-numbs vocal cords
What is true regarding the Superior Laryngeal Nerve (SLN)?
Comes from vagus nerve and divides into 2 branches:
1.) Internal SLN: provides sensation to supraglottic and ventricle compartments
** STIMULATION CAUSES LARYNGOSPASM ***
2.) External SLN:provides MOTOR international of CRICOTHYROID MUSCLE
What is true regarding the Recurrent Laryngeal Nerve (RLN)?
- passes under aortic arch
- provides SENSORY innervation to infraglottis
-*** motor innervation to all larynx EXCEPT cricothyroid muscle
What happens when the RLN is stimulated?
Stimulation causes Abduction of VC (stim. Below the cords causes them to open up so you can cough it out)
—> damage to RLN causes VC adduction
How do you know if the RLN has been damaged?
- will be unable to phonate properly
- persistent hoarseness
What is the smallest part of the airway in adults vs children?
Adults: vocal cords
How many cartilages are in the trachea and what vertebra is it located between?
- 25 C shaped cartilages
- extends from C6-T5
Where is the carina?
25cm from the teeth
What happens if you tickle the carina with the ETT?
Where does gas exchange start?
Which nerves innervate the diaphragm?
Phrenic nerve (C 3,4,5 keep the man alive)
Which nerves innervate the external intercostal muscles?
Intercostal nerves T1-T11
Why is the right hemidiaphrgm higher than the left?
Because of the liver
Are pleural pressures negative or positive?
If positive lung will collapse
What is the total lung capacity?
TLC= IRV + TV + ERV + RV
What is the vital capacity?
VC= IRV + TV + ERV
What is the functional reserve capacity?
FRC= ERV + RV
What is the inspiratory capacity?
IC= IRV + TV
What is residual volume and what cannot measure it?
Residual volume= volume always in the lungs that cannot be exhaled
- cannot be measured by spirometry alone,thus FRC and TLC cannot be determined using spirometry alone
How can FRC and TLC be determined?
What does an extra thoracic obstruction mean?
Inspiratory problem—> floppy tumor above the vocal cords, obstructing during inspiration and then moving to clear airway during expiration
What does an intra thoracic obstruction mean?
Expiratory problem —> obstruction below the vocal cords, floppy tumor that allows air to be inspired and obstructs during expiration
What does surfactant do?
- Lowers surface tension of alveoli and lung
- increases compliance of lung
- reduces work of breathing
- promotes stability of alveoli
- alveoli have a tendency to collapse d/t strong surface tension of water
- Prevents transduction of fluid into alveoli
- reduces surface hydrostatic pressure effects
- prevents surface tension from drawing fluid into alveoli from capillary
* the more surfactant, the better it works
What is Poiseulle’s Law?
L= length of tube
N= viscosity of fluid
*** reducing r by 16% will double the Resistance
** reducing r by 50% will increase R 16 fold
When BP increases in the pulmonary system what will happen to resistance and why?
Resistance will decrease because of recruitment and distension—-> increased flow (different than systemic circulation)
Define recruitment and distension?
Recruitment= opening of previously closed vessels
Distension= increasing the caliber of the vessels
What percentage of alveolar surface is covered by capillary bed?
Total capillary surface area almost equals _________ _______ _______.
Alveolar surface area
—> with each heart beat you replace capillary blood volume
How much blood volume is in the pulmonary capillaries?
70mL (1mL/kg body weight) at rest
200 mL maximum anatomical volume
What do pulmonary edema and fibrosis do?
Increase space between alveoli and capillary —> slows down diffusion
What is true regarding the different lung zones?
- Zone 1: no flow, no gas exchange occurring, happens with positive pressure ventilation —> can actually worsen ventilation
- Zone 2: intermittent flow and ventilation
- Zone 3: ideal
- during exercise entire lung is converted to zone 3
What are endogenous vasoconstrictors?
- reduced PaO2
- increase PaCO2
- thromboxane A2
- a-adrenergic catecholamines
What are endogenous vasodilators?
** increased PaO2**
- NITRIC OXIDE—> when O2 present, NO released—> vasodilates
When O2 absent, no NO released (vasoconstriction to shunt blood away from hypoxic lung area)
- ß- adrenergic catecholamines
What causes hypoxic pulmonary vasoconstriction?
Alveolar Hypoxia, enhanced by hypercapnia and acidosis
- localized response of pulmonary arteries
- shifts flow away from hypoxic areas toward better ventilated regions
- results from decreased formation and release of nitric oxide by pulmonary endothelium in hypoxic region
On RA what is alveolar PaO2?
What is the minimum alveolar O2 ventilation?
What is the normal alveolar PCO2?
What is normal CO2 production?
What is Fick’s law?
Diffusion= (A x ∆pp x D)/T
A= cross sectional area of membrane
D= gas coefficient
T= thickness of membrane
* the thicker the membrane, the less the diffusion
What are normal PVO2 and CVO2 levels in the blood?
What is the difference between a shunt and dead space?
Shunt= perfusion but no ventilation
- shunted blood is not oxygenated
- the greater the shunt, the greater the amount of blood that fails to be oxygenated in lungs
Dead space= ventilation but no perfusion
- includes wasted ventilation and anatomical dead space
* when physiologic dead space is great much of work of breathing is wasted effort because ventilated air does not reach blood
What is the Hgb P50 point?
The point where the sat is 50% and PaO2 is 27mmHg
What is the 40, 50, 60 rule?
When PaO2 is 40, 50, 60
O2 sat is 70, 80, 90
What causes a right shift on the Hg-O2 dissociated curve?
Hb has less affinity for O2, release O2, sat will be less for a given PO2
- increased CO2- cellular metabolism
- increased temp- increased metabolism, increased H+, lactic acid production, Bohr effect, increased 2,3 DPG production
What is the CaO2 and how can it be determined?
The sum of O2 carried on Hb and dissolved in plasma
CaO2= (SO2 x [Hb]x 1.31) + (PAO2 x 0.003)
1.31= O2 binding to Hb (ml/gm)
What is DO2?
DO2= CaO2 x CO
How is CO2 transported?
Mostly as HCO3 (bicarbonate)
What does the dorsal respiratory group (DRG) do?
- control inspiration ad respiratory rhythm during restful breathing
- located in the medulla
- vagal (X) and glossopharyngeal (IX) nerves deliver sensory info to DRG
The DRG receives signals from which 3 sources?
1.) peripheral chemoreceptors
3.) lung receptors
What does the chemo-sensitive area of the brain stem do?
- highly sensitive area on the ventral medulla surface —> central chemoreceptors
- respond to changes in blood H+ concentration
- stimulate other portions of the respiratory center
Are concentrations of CO2 equal in the blood and brain?
Yes, because CO2 is so highly permeable to the BBB
—> CO2 is very permeable to the BBB
- CO2 reacts with H2O to form carbonic acid, which dissociates to HCO3 and H+
—> H+ stimulates chemo sensitive area
What is the primary respiratory drive?
Increase in CO2 (>35mmHg) drastically increases ventilation
Where are the peripheral chemoreceptors located and what do they do?
Carotid bodies: act on DRG via CN IX
Aortic bodies: in aortic arch, act on DRG via CN X
Stimulate breathing changes when hypoxia is present
At what O2 level will hypoxia stimulate changes in breathing?
(This range is when Hg-O2 sat decreases rapidly)
What are high risk PFT results?
- FEV1 <2L
- FEV1/FVC <0.5
- VC < 15mL/kg in adults, <10mL/kg in children
- VC <40-50% of predicted (normal is 80%)
What are the intubation criteria in acute respiratory failure?
- MIF more negative than -20cmH2O
- oxygenation: hypoxic on supplemental O2
- PaO2<70mmHg on FiO2 of 40%
- A-a gradient >350 mmHg on 100% FiO2
- PaCO2 >55 (except in chronic hypercarbia)
- Vd/Vt >0.6 (normal dead space is 30%)
- airway burn, chemical burn, epiglottitis, mental status changes, rapidly deteriorating pulmonary status, fatigue
Explain post op extubation criteria?
- VSS, awake and alert, RR <30
- ABG on FiO2 of 40%—> PaO2 70 and PaCO2 <55
- MIF is more negative than -20 cm H2O
- VC >15mmHg
- life head, squeeze hands, follow commands
What are ABG norms?
BE: -3 to +3
Numerically, how does PCO2 affect pH?
An increase in PCO2 by 10mmHg causes a decrease in pH by 0.08 (and vice versa)
* helps decide if pt is in a true respiratory acidosis
What is the difference between hypoxemia and hypoxia?
Hypoxemia= decreased PO2 in blood <75mmHg
Hypoxia= a low O2 state
What is an A-a gradient, and what is normal?
A measure of efficiency of lung
Normal A-a= approximately (age/3)
A-a gradient can still be normal with hypoventilation or low FiO2
What is the treatment for an abnormal A-a gradient?
Treat underlying cause
What is the rule regarding bicarbonate and pH?
A decrease in bicarbonate by 10 mmoles decreases the pH by 0.15 (and vice versa)
What is true regarding pulse oximetry?
* MANDATORY INTRA-OPERTIVE MONITOR **
- pulse must be present to detect
- depends upon observation that oxygenated and deoxygenated Hgb differ in their absorption of red and infrared light
What 2 wavelengths are used in pulse oximetery and what do they detect?
940 nm—> infrared light, oxyhemoglobin absorbs more of this light, corresponds to 100% saturation
660nm—> red light, deoxyhemoglobin absorbs more of this light, corresponds to 50% saturation
What are limitations of pulse oximetry?
- carboxyhemoglobin (COHb): shows 100% on pulse ox
- need co-oximeter to distinguish
- methemoglobin (MetHg): Fe in Hb is oxidized to +3 form and cannot transport O2
- cyanosis when 15%
- absorbs equally at both wavelengts—> will see O2 sat of 85%
What causes methemoglobin?
- benzocaine (hurricane spray)
What will not effect pulse ox?
Fetal hemoglobin and billirubin
What is true of capnography? (And VERY important)
Rapidly and reliably indicates esophageal intubation, but does not reliable detect endobronchial intubation
—-> ETCO2 is he gold standard for tracheal intubation
In the awake and lateral position what is true regarding the dependent lung?
Is better perfused and ventilated than non-dependent lung d/t gravity
With induction of anesthesia, what is true regarding the dependent and non-dependent lung?
The non-dependent lung ventilates more while the dependent lung is more perfused—> creates a V/Q mismatch
- following path of least resistance, most conditions favor the non-dependent lung
What are factors that inhibit hypoxic pulmonary vasoconstriction?
- very high or very low pulmonary artery pressures
* HYPOCAPNIA: don’t hyperventilate!!!
- high or very low mixed venous PO2
* VASODILATORS: nitroglycerin, nitroprusside, ß-adrenergic agonists (dobutamine), calcium channel blockers
- pulmonary infections
* INHALATION AGENTS
During one lung ventilation, where do you want your FiO2, ETCO2 and Vt?
FiO2–> 0.8 to 1.0
If hypoxia occurs during one lung ventilation what can you do?
Add 5 cmH2O CPAP to non-dependent lung (warn surgeon)
- add 5 cmH2O PEEP to dependent lung
- increase both CPAP and PEEP slowly
- use suction cath to bleed a low flow of O2 to non-dependent lung
- ask surgeon to clamp ligate non-dependent PA
What causes malignant hyperthermia?
The ryanodine receptor fails in the sarcoplasmic reticulum, leading to decreased re-uptake of calcium from within the cell—>causing a 500 fold increase in intracellular calcium
- this leads to sustained muscle contraction, glycolysis and heat production
- abnormal excitation-contraction coupling results in prolonged and irreversible muscle contracture
What are clinical signs of MH?
***** SPIKE IN ETCO2–> 2-3 times, most specific sign
- decrease in SaO2, SPO2 and mixed venous O2
- rigidity despite muscle relaxant onboard
- unstable BP
- trismus(masseter spasm) after succinylcholine
- darkening of blood in surgical field
- cola-colored urine
- heating and exhaustion of CO2 absorbent
What lab values will be seen with MH?
- initial metabolic acidosis, followed by combined metabolic and respiratory acidosis
- hyper- K, Ca, Phos
- CK > 1000 IU
What factors will increase MAC?
- age: term infants to 6 mos has highest MAC requirement ***.
* CHRONIC ETOH ABUSE
- drugs that increase CNS catecholamines—> cocaine, acute meth intox
What factors decrease MAC?
- hypothermia: for every 1˚C drop in body temp, MAC decreases 2-5%
- prep meds, IV anesthetics, opioids
- neonate/premature infants
- acute ETOH intoxication
- alpha 2 agonists
- calcium channel blockers
- severe hypoxemia - PaO2< 38mmHg
What are factors that have no effect on MAC?
- thyroid gland dysfunction
- duration of anesthesia
- high or low K
- high or low CO2
What is the second gas effect?
The ability of large volume uptake of first gas (N2O) to accelerate the rate of rise of alveolar partial pressure of a concurrently administered companion gas, thus speeding induction
What is diffusion hypoxia?
Dilution of alveolar O2 concentration by a large amount of N2O “outgasing” or leaving pulmonary blood after stopping N2O administration
—> especially with decreased FRC (pregnancy, obesity, children)
* don’t extubate while on 70% N2O
—> treat with 100% FiO2 following N2O use
What does smoking do to the body?
- doubles CAD risk
- 6 xs increase of post-op complications
- COHb can be up to 15%
- 25 pack year increases physiologic age by 8 years
* nicotine stimulates the sympathetic ganglia—> increase in Hr, BP and SVR-persists for 30minutes after last cigarette
- irritant to airway:
- increases mucus production, inflammatory response, protein enzyme release
- reduces ciliary activity, pulmonary macrophage activity, surfactant integrity
What must you make sure to do for a smoker prior to induction?
Pre-oxygenate well (Et O2 80-90)
Avoid instrumentation of airway until deep level of anesthesia
What is true regarding smoking cessation?
Advise to stop smoking at least 12 hours prior to surgery
- 12-24 hours without smoking will reduce COHb and nicotine levels to that of a non-smoker
- after 2 days: airway reactivity decreases
* CESSATION OF >8 WEEKS WILL REDUCE POST OP PULMONARY COMPLICATIONS
- >2 years will reduce risk of MI to that of nonsmoking population
What ventilator adjustments should be made in a COPD patient intraoperatively?
- Longer e time 1:3
- closely monitor peak pressures-avoid rupturing bullae, PTX
- CO2 retainers: keep ETCO2 near baseline to avoid alkalosis
(Keep in mind there is a large gradient between ETCO2 and PaO2 d/t air trapping)