Respiratory Flashcards
Alveolar gas equation
PAO2 = FiO2 x (Pb - PH20) - (PaCO2/RQ)
Pb = barometric pressure (760mmHg unless given other) PH20 = humidity inspired gas (47mmHg) RQ = 0.8
3 → of anatomic shunt
Thebesian veins (drain left heart) Bronchiolar veins (drains bronchial circulation) Pleural veins (drains bronchial circulation)
R—>L shunt d/t intracardiac lesion
AV malformations that develop from liver disease
V02 (oxygen consumption)
V02 = CO x (Ca02 - Cv02)
V02 is the difference between the amount of 02 that leaves the lungs and the amount of 02 that returns to the R heart. Based on Fick principle
- for 70kg adult, 250mL/min
- 3.5mL/kg/min
We can say whole body V02 is about 25%
Treatment for methemoglobinemia
IV methylene blue 1-2mg/kg
Only muscle that tenses (elongates) vocal cords
Cricothyroid
What does the internal branch of the SLN innervate?
Posterior epiglottis, laryngeal mucosa to the level of the cords
SLN block
3mL bilaterally at the inferior aspect of the greater cornu of hyoid bone
Is right or left RLN more prone to injury? Why? Structures?
L RLN loops under aorta, so more susceptible (MS, PDA ligation, aortic arch aneurysm, thoracic tumor)
R RLN loops under right subclavian artery (thyroid/parathyroid surgery, LMA or ETT, neck tumor, neck extension)
Location of adult and pediatric larynx
adult: C3-C6
Peds: C2-C4
2 → of angioedema, and their treatments?
1) ACEIs: epi, antihistamines, steroids (just like anaphylaxis)
2) Hereditary angioedema, or C1 esterase deficiency: (C1 esterase concentrate or FFP)
Congenital syndromes associated with large tongue
- beckwith syndrome
- trisomy 21/downs
Congenital syndromes associated with small/underdeveloped mandible
- Pierre robin
- Goldenhar
- Treacher Collins
- Cri du Chat
(“Please get that chin”)
Congenital syndromes associated w cervical spine abnormality
- Klippel-Feil
- Trisomy 21
- Goldenhar
Choanal atresia
Blockage of nasal airway by tissue
Micrognathia or mandibular hypoplasia
Small, underdeveloped mandible
3 Key processes of aerobic metabolism
- ) Glycolysis: 1 glucose → 2 pyruvic acid (2 ATP)
- ) Kreb’s Cycle: happens in mitochondria. Makes H+ ions (in form of NADH) to use for electron transport (2 ATP)
- ) Electron transport/oxidative phosphorylation: Yields 34 ATP, C02, and H20.
Criteria for pulmonary artery hypertension
- Mean PAP at least 25mmHg
- PAOP no more than 15mmHg
Where does the tip of an LMA sit?
Cricopharyngeus muscle (UES)
Solubility coefficients of 02 and C02
02: 0.003mL/dL/mmHg
C02: 0.067mL/dL/mmHg
So…. C02 is 20X more soluble than 02.
Sp02% and corresponding Pa02 values
Sp02 90% = Pa02 60mmHg
Sp02 80% = Pa02 50mmHg
Sp02 70% = Pa02 40mmHg
Bohr effect
C02 and H+ ions → conformational change in Hgb molecule; which facilitates release of 02. (→ R shift on dissociation curve)
Basically, it means that C02 and H+ (acidity) → Hgb to release more 02. Makes sense if you think about it.
Difference between static and dynamic compliance
STATIC: plateau pressure, function of lung/chest wall compliance only.
DYNAMIC: peak pressure, function of airway resistance + lung/chest wall compliance and their interaction. Dynamic compliance is what changes with resistance changes.
02 content
Ca02 = (1.34 x Hgb x Sa02) + (Pa02 x 0.003)
Normal is 20mL 02/dL blood
Laryngospasm reflex arc
AFFERENT: SLN, internal branch
EFFERENT: SLN, external branch, + RLN
Estimation of shunt %
Shunt ↑ 1% for every 20mmHg ↑ in A-a gradient.
Things that increase PVR
Hypoxia, low Fi02, Hypercarbia, Acidosis PEEP, High airway pressure Polycythemia Hypothermia SNS stim/Vasoconstrictors Surgical stress
N20, ketamine, desflurane
General rule about changes in PA02/Pa02 gradient versus changes in PAC02/PaC02 gradient
This is a generalization BUT….
- ↑ Vd affects PaC02 (can’t get blown off)
- ↑ shunt affects Pa02 (02 can’t get dropped off)
Short term benefits of smoking cessation
SNS stim ↓ after 20-30 min
P50 returns to normal in about 12 hours (Ca02 improves)
Intermediate term benefits smoking cessation
About 6 weeks
- Mucociliary clearance improves
- Sputum production ↓
- Pulmonary immune function improves
- Airway function improves
- Hepatic enzyme induction begins to subside
LMA sizes
1 = <5kg | 4mL air 1.5= 5-10kg | 7mL air 2= 10-20kg | 10mL air 2.5= 20-30kg | 14mL air 3=30-50kg | 20mL 4=50-70kg | 30mL 5=70-100kg | 40mL
When bronchial blockers are useful
Patients who need OLV who….
- <12 year old
- trached
- Have a single lumen ETT already
- Need to stay tubed after surgery and you’re too lazy to use a cook catheter to change it out at the end of the case
Small lumen permits air suctioning, but thicker stuff can clog it
Common CXR findings of COPD
↑ AP diameter
Flattened diaphragm
↑ WOB (airway destruction)
Pulmonary bullae
Don’t use n20.
How does PaC02 affect MV
Every 1mmHg increase in PaC02 above baseline will ↑ MV by 3L/min
Tightly controlled by central chemoreceptor in the medulla
→ of L shift of oxyHgb curve
↑ affinity for 02 (doesn’t offload into tissues as well)
[hypothermia, alkalosis]
-↓ temp
-↓ 2,3DPG
-↓ C02
-↓ H+
HgbMet, HgbCO, HgbF
→ of R shift of 02hgb curve
R → release → offloads into tissues more easily
[hyperthermia, acidosis, think sepsis]
- ↑ temp
- ↑ 2,3DPG
- ↑ C02, H+, ↓ pH
Some things that you would think would mess with Sp02 but don’t
Fluorescin, HgbF, HgbS, jaundice, polycythemia, acrylic nails
Most common method of measuring exhaled gases in OR
Infrared absorption spectrophotometry
BP cuff sizing
Ideal bladder length is 80% of extremity circumference, ideal width is 40% circumference
Cuff that is too small overestimates SBP
Cuff that is too large underestimates SBP
How does arterial pH change with PaC02 change
Acute resp acidosis.
→ pH ↓ 0.08 q 10mmHg ↑ C02
Chronic resp acidosis:
→ pH ↓ 0.03 q 10mmHg ↑ C02
Pressure needed to ventilate through cric, with jet ventilation
50ish psi
- jet ventilator attached to machine
- 02 tank with pressure regulator set to 50psi
- 02 flush valve on machine
Low pressure sources won’t work
Which drugs INHIBIT HPV
Volatile anesthetics at 1.5MAC Vasodilators (NTG, SNP, PDE inhibitors, some CCBs) Vasoconstrictors Hypervolemia Hemodilution PEEP Large TV Alkalosis (hypocapnia) Hypothermia
MRI safe LMA
Classic
Conditions that may benefit from permissive hypercapnia
ARDS -
- trades off strict c02 control for better control of minimizing mean airway pressures
Most important predictor of pulmonary postop complications
Site of surgery
How to estimate Fi02 when using nasal cannula
1L = 24% 2L = 28% 3L = 32% 4L = 36% 5L = 40% 6L = 44% (this is the maximum)
Absorption atelectasis
Excessive oxygen administration
Can cause shunt,
VC, FRC normal values
VC: 60-70mL/kg
FRC: 35mL/kg
Things spirometry can’t measure
-Residual volume, TLC, FRC
Components of FRC
RV + ERV
Things that INCREASE FRC
Old age, prone, sitting, maybe lateral, COPD, PEEP, Sigh breaths/recruitment maneuvers
Things that ↑ closing volume
COPD LV failure Obesity Smoking Extreme age Pregnancy
CLOSE-P
D02
D02 = Ca02 x CO x 10
Normal is 1000mL/min
Mechanisms of C02 transport out
Bicarbonate 70%
→ dependent on carbonic acid RXN
→ HC03 is transported back out of erythrocytes after this RXN happens and Cl- shifts into the cell to maintain electro neutrality - this is the hamburger shift
Bound to Hgb 23%
→ C02 binds with amino groups on Hgb as well as other plasma proteins
Dissolved in plasma 7%
→ solubility coefficient of 0.067mL/dL/mmHg
Haldane effects
Describes C02 carriage/curve
(Don’t confuse with Bohr effect - that describes 02 carriage/curve)
O2 → erythrocytes to release C02
Basically, deoxygenated Hgb is able to carry more C02.
Lower P02 → more C02 carried
Higher P02 → less C02 carried
Consequences of hypercapnia
Hypoxemia, SNS stim, cardiac/smooth muscle depression, ↑ MV, hyperkalemia, hypercalcemia, ↑ ICP, ↓ LOC
Neural respiratory center
Located in RAS in medulla and pons.
- Dorsal resp: → inspiration, in medulla. Pacemaker for inspiration.
- Ventral resp: → expiration, in medulla. Primarily active during expiration.
-Pneumotaxic: → Upper pons. inhibition of DRC. Triggers end of inspiration.
→ strong stimulus = rapid shallow breathing
→ weak stimulus = slow deep breathing
-Apneustic: → Lower pons. stimulation DRC. Antagonizes pneumotaxic.
Most important stimulus for central respiratory chemoreceptor
↑ in H+ ion concentration in CSF
Hypoxic ventilatory response
Via peripheral chemoreceptors located in carotid body, also aortic arch
Pa02 <60mmHg triggers Glomus cells → action potential via HERING’s nerve → Glossopharyngeal → afferent pathway terminates in inspiratory center in medulla
→ ↑ MV to restore Pa02
Peripheral chemoreceptors respond to Pa02
Central chemoreceptors respond to PaC02
Conditions that impair the hypoxic ventilatory response
CEA severs afferent limb of HVR, why you can’t do BLL CEA simultaneously or very close together. Takes time for body to recalibrate.
Sub-anesthetic doses of inhalation and IV anesthetics (0.1MAC) depress hypoxic ventilatory drive, so postoperative hypoxia isn’t always countered by a reflexive ↑ in MV
HPV
Local RXN that occurs in response to ↓ ALVEOLAR 02 (not arterial)
Minimizes shunt flow by ↑ PVR in poorly ventilated areas
Inhibited by IAs, vasodilators, PDEIs, dobutamine (therefore these things can worsen shunt)
Vasoconstricting drugs may constrict well oxygenated areas and also contribute to shunt
IV anesthetics PRESERVE HPV
Best test of airflow in medium sized airways
FEV25-75%
Patient specific risks for postop pulmonary complications
Age >60 Asa >III CHF COPD Smoker
Surgery specific risk factors for post op pulmonary complications
Aorta > thoracic > upper ABD = neuro = PVD > emergency
Duration of anesthesia > 2.5hrs
GA
Lab specific factors of post op pulmonary complications
Albumin <3.5g/dL (indicates poor nutritional status)
ABGs and PFTs are only useful in patients undergoing lung resection
Examples of acute intrinsic restrictive ventilatory defects
Upper a/w obstruction (neg pressure pulmonary edema) Aspiration Naloxone Cocaine OD Reexpansion of collapsed lung Neurogenic
Examples of chronic intrinsic restrictive ventilatory defects
Sarcoidosis
Drug induced pulmonary fibrosis (amiodarone)
Most sensitive indicators of VAE
TEE Doppler EtC02 CO, CVP Stethoscope, BP, EKG
TX VAE
100% Fi02 Flood field with NS If insufflated, desufflate Durant maneuver: place pt in L lateral position Aspirate air from CVL if present Hemodynamic support
Key anesthetic consideration for patients with pulmonary HTN
They are relatively preload dependent, treat hypotension aggressively
Drugs you can give via ETT
NAVEL
Narcan, atropine, vasopressin, epi, Lidocaine
Normal inspiratory force
75-100cm H20
<25 is a strong indication for mechanical ventilation
Best predictors of pulmonary complications postop for thoracic surg patients
FEV1< 40% predicted
DLCO <40% predicted
V02 max <15ml/kg (normal is 27-40)
Split lung VQ testing is indicated when preop assessment indicates ↑ risk of postop complication (anything less than the above values).
→ If V02max max isn’t available, ask patient if they can climb 2 flights of stairs. If not, patient is at risk.
Absolute indications for OLV
Infection, massive hemorrhage (isolation to avoid contamination)
Bronchopleural fistula, surgical opening major airway, large unilateral lung cyst or bullae, life threatening hypoxemia r/t lung disease
UNILATERAL BRONCHOPULMONARY LAVAGE for pulmonary alveolar proteinosis
DLT size and depths
Men: 39-41 French, 29cm depth
Women: 37-39 French, 27cm depth
Bronchial cuff: 1-2mL air
Tracheal cuff: 5-10mL air
How does PEEP help during OLV?
Non-dependent lung: ↑ FRC by pushing the lung up on the compliance curve and prevents excess shearing stress of repeated alveolar opening and closing.
Dependent lung: may improve FRC or may worsen shunt by directing more blood flow towards non ventilated lung. Pay close attention
Thyromental distance
<6cm or >9cm might predict difficult laryngoscopy
Complications of cricoid pressure
Can ↓ LES
Can make laryngoscopy more difficult
SNS signs of hypercarbia
DIRECT effects of hypercarbia are myocardial depression and local vasodilation HOWEVER the hypercarbic patient will respond with ↑ SNS activity
- vasoconstriction
- ↑ contractility
- QT prolongation
- ↑ serum K+
