Flashcards in Respiratory Physiology Deck (72)
How does oxygen consumption and CO2 production change with GA?
Decreases both by ~15%
What is the RQ for carbohydrates? Proteins? Lipids?
How would a hemi-diaphragmatic paralysis decrease pulmonary function?
~25% (diaphragm accounts for 75% of chest volume change)
What is the end-expiration intrapleural pressure in a healthy patient?
-5 cm H2O (while alveolar pressure is 0 since there is no air flow): this keeps the alveoli open
What is Laplace's law?
Alveolar pressure = 2 * (surface tension / radius)
How does surfactant affect smaller alveoli compared to larger ones?
Surfactant is more concentrated in smaller alveoli so it decreases surface tension to a greater extent than in large radii alveoli
What makes up FRC?
Expiratory reserve volume + residual volume
Factors that decrease FRC?
Restrictive lung disease, obesity, pregnancy, posture (standing>sitting>supine>prone), height (taller people have more FRC), gender (men have more FRC than women)
What patient postures have the most reduced FRC?
Supine > prone > sitting > standing (least reduction in FRC)
What is closing capacity?
Volume at which small airways begin to close; Residual volume + closing volume
How does closing capacity change with obesity?
It does not change; however, ERV decreases and so FRC decreases causing tidal volumes to shift towards residual volume; since closing volume has not changed, the tidal volumes are not less than closing capacity
How does closing capacity change with age?
Increases with age (or any disease states within the lungh like COPD, etc that increase airway obstruction)
How does closing capacity change with GA?
Decreases under general anesthesia (bronchodilation of volatile anesthetics so you decrease airway obstruction leading to decreased closing capacity)
What is the formula for airway resistance for laminar flow?
Resistance = (8 * length * viscosity) / (pi * radius^4)
What is the major determinant for turbulent flow?
Formula for Reynold's number
R = (velocity * diameter * density) / viscosity
What Reynold's number indicates turbulent flow?
What happens to FRC under GA?
Decreases (ribcage moves inward in supine position + abdominal contents fall into thorax)
Would positive-pressure ventilation increase or decrease dead-space?
Increase by ~50%; higher alveolar pressure = West zones moved downward: alveoli at apex that were barely being perfused due to low arteriolar pressures will be totally occluded = ventilation without perfusion (dead space)
In a normal, sitting patient, where is ventilation and perfusion at its maximum?
Both are maximal near the base
Non-cardiac causes of acute pulmonary HTN?
Hypoxia, hypercarbia, acidosis, autonomic system
What does hypocarbia do to pulmonary vasculature?
Pulmonary vasodilator and causes bronchoconstriction
How does the effects of hypoxia, acidosis, and hypercarbia differ between pulmonary and systemic vasculature?
What anesthetic inhibits hypoxic pulmonary vasoconstriction?
N2O and volatile agents (2 MAC), inhaled nitric oxide, nitrates
What is the alveolar gas equation?
PAO2 = FiO2 ( Pbarometric - PH2O) - PaCO2/RQ
How does an increase in cardiac output change the A-a gradient?
1. increased CO = increased mixed venous PO2, and more left over oxygen
2. Intrapulmonary shunting decreases
You get a decrease in the A-a gradient
What is responsible for the ventilatory response to hypercarbia?
Chemoreceptors in contact with the 4th ventricular CSF on the anterolateral surface of the medulla; BBB permeable to CO2 which reacts with H20 forming H+ ions = lowering pH = stimulates chemoreceptor
What region of the brain coordinates inspiration?
Dorsal & ventral medullary center
What region of the brain coordinates expiration?
Ventral medullary center
What does the carotid and aortic bodies respond to?
Primary responsible for increasing ventilation in response to HYPOXIA
Why do you not give severe COPDer's too much supplemental oxygen?
High O2 levels interrupt needed hypoxic pulmonary vasoconstriction (since these patients have severe V/Q mismatch)
After a carotid endarterectomy, how long does it take for the carotid bodies to become functional again?
Up to a year
Why wait to do a contralateral carotid endarterectomy if one side was recently done?
The patient will not be able to respond with their peripheral O2 chemoreceptors (takes up to a year)
What would blood in the ventricles due to respirations?
H+ ions in blood will decrease pH, stimulating the chemoreceptors on the anterolateral surface of the medulla exposed to the 4th ventricle = increased minute ventilation
If an asthmatic becomes bronchospastic after intubation, what is the underlying cause?
Activation of vagal stimulation
Treatment for profound bronchospasm after intubation?
Epinephrine IV 20 mcg (albuterol can only be used if there is air movement)
Chronic bronchitis or emphysema: risk of right heart failure?
What is bronchiectasis?
Permanent dilation of bronchi from destructive inflammatory changes usually secondary to recurrent infections
What do you suspect with an increased end tidal nitrogen?
Venous air embolism
What would the flow volume loop look like for a variable intrathoracic lesion?
Obstruction on expiration
What would the flow volume loop look like for a variable extrathoracic lesion?
Obstruction on inspiration
What portion of the brain controls rate and pattern of breathing?
What is the role of the apneustic center?
Antagonizes the effects of the pneumotaxic center
What is the Hering-Breuer Reflex?
Overinflation of lung -> stimulation of lung stretch receptors -> activates apneustic center -> inhibits inspiratory center -> inspiration stops
Where are the peripheral chemoreceptors located and what cranial nerves are they associated with?
Carotid bodies (CN IX), aortic bodies (CN X)
At what PaO2 do the peripheral chemoreceptors activate?
How are peripheral chemoreceptors affected by volatile anesthetics?
Response to hypoxia is eliminated by as little as 0.1 MAC
How is CO2 transported in the vasculature?
85% in bicarbonate, 10% bound to amino acids, 5% dissolved
How does an increase in PaCO2 affect cerebral blood flow?
Increased CO2 increases CBF through NO and PGI2-mediated vasodilation
How does hypercarbia affect the cardiovascular system?
CO2 is a direct cardiac depressant balanced by increases in SNS activity (causing elevated MAP and CO)
What should you worry about with Halothane and hypercarbia?
Halothane sensitizes the myocardium to epinephrine so you increase the risk of arrhythmias from the SNS activation of hypercarbia
How does hypocarbia affect the CV system?
Decreases cardiac output
What does hypercarbia do to the GI system?
Increases hepatic and portal venous blood flow (while the SNS activation will cause constriction)
What lung cells make surfactant?
Type II pneumocytes
What increases the P50 (PO2 at which Hgb is 50% saturated)?
Right shift in the oxyhemoglobin dissociation curve (hyperthermia, acidosis, pregnancy, increased 2,3 DPG, volatile anesthetics, sickled hemoglobin)
What decreases the P50 (Po2 at which Hgb is 50% saturated)?
Left shift in oxyhemoglobin dissociation curve (hypothermia, alkalosis, fetal hemoglobin, hethemoglobin, carboxyhemoglobin, decreased 2,3 DPG)
What muscles are involved in inspiration? Expiration?
Inspiration: diaphragm, scalenes, SCM, external intercostals, large back muscles (big breathe)
Expiration: passive process, internal intercostals (forced), abdominal muscles
What makes up the majority of airway resistance: conducting airways, transitional airways, respiratory airways?
Conducting airways (90%) which include larger airway to the terminal bronchioles
What kind of flow (laminar or turbulent) is seen in the conducting (larger) airways? In the terminal bronchioles?
Larger: turbulent flow
Terminal bronchioles: laminar flow
How does PaO2, PaCO2 and CSF fluid change with increased elevation?
PaO2 decreases (since atmospheric pressure decreases), this causes increased ventilation which leads to a decreased PaCO2 -> alkalosis -> H+ moves out of CSF to the plasma to correct the alkalosis -> increased CSF pH
How do volatile anesthetics affect CO2 responsiveness?
1. Increases PaCO2 before normal ventilation
2. Decreased responsiveness in ventilation per PaCO2
What is dead space ventilation? What is a shunt?
Dead space: ventilation without perfusion
Shunt: Perfusion without ventilation
What is the P/F ratio and what is a normal ratio?
PaO2/FiO2, normal is greater than 300
What does the flow loop look like for a patient with obstructive lung disease?
Near normal inspiratory loop (lower) with a scooped expiratory curve (overcoming the lesion)
What is FEF25-75?
Forced expiratory flow between 25% of FVC and 75% of FVC
Generally effort independent (unlike FVC or FEV1) and an early indicator of obstructive disease
When is FRC the lowest in the post-operative period?
12 hour post op
Following cessation of smoking, how long does it take for ciliary function to return to normal? Normal carboxyhemoglobin levels? Maximal benefits?
Ciliary function: 2-4 weeks
Carboxyhemoglobin levels: 24 hours
Maximal benefits: 8+ weeks
What ECG findings do you expect to see in a patient with COPD?
Right-heart strain (i.e. poor R-wave progression, enlarged P-waves, R>S in V1, RBBB, RAD)
How would an upper abdominal surgery affect PFTs?
Decreases FRC (decreased lung compliance and increases shunting and hypoxia) secondary to a ~25% decrease in ERV and increase in RV by ~10%
Which is the best anatomic estimate for the level of the carina: 3rd thoracic vertebrae, sternal angle, nipple line, one finger breadth below the sternal notch
What pressure is the best marker for dynamic compliance? Static compliance?
Dynamic: Peak pressure
Static: Plateau pressure