HY Respiratory Phys + Karius review Flashcards
Ratio of what molecules produced by the lungs is a marker for lung maturity?
Lecithin:sphingomyelin ratio. Usually greater than 2
Diameter of airways depends upon the balance between what two molecules produced in the lung
prostaglandins (bronchodilation) and Histamine (bronchoconstriction)
Which molecule is produced by the lung such that when inhibited produces a build up product that causes a dry cough
Angiotensin Converting enzyme
What important coagulation cascade cofactor is produced in the lung?
Kallikrein
What is residual volume (RV)?
volume that remains in lungs after a maximal expiration
What is tidal volume (TV)?
Volume inspired with each normal breath
What is inspiratory reserve volume (IRV)?
volume that can be inspired over and above the tidal volume. Used during exercise
What is expiratory reserve volume (ERV)?
Air that can still be breathed out after normal expiration
What is inspiratory capacity?
IRV + TV
What is functional residual capacity
RV + ERV. Volume of gas in lungs after normal expiration; includes RV, cannot be measured on spirometry
What is vital capacity?
TV + IRV + ERV = max volume of gas that can be expired after a maximal inspiration
What is total lung capacity?
IRV + TV + ERV + RV = volume of gas present in lungs after a maximal inspiration. (notice it includes RV which cannot be measured by spirometry)
Differentiate between anatomic vs physiologic dead space and alveolar dead space.
Dead space is area of the respiratory system that do not participate in gas exchange. Anatomic dead space = conducting zones of respiratory system. Physiologic dead space = anatomic dead space in a non diseased state; in a disease state physiologic dead space = anatomic dead space + functional (alveolar) dead space. Alveolar dead space = alveoli which receive ventilation but are poorly perfused (apex of lung biggest contributor to alveolar dead space)
How is physiologic dead space calculated?
Vd/Vt = (PaCO2 - PeCO2) / PaCO2
Vd = phys dead space+anatomic dead space + alveolar dead Vt = Tidal volume PaCO2 = arterial PCO2 PeCO2 = expired air PCO2
Taco, Paco, Peco, Paco (refers to orer of variable )
What is minute ventilation and how is it calculated?
Total volume of gas entering lungs per minute
Ve = VT x RR
What is alveolar ventilation and how is it calculated?
volume of gas per unit time that reaches alveoli.
Va = (Vt-Vd) x RR
Normal values: Vt = 500/breath; Vd = 150 mL/breath; RR = 12-20
Elastic recoil is the tendency of lungs to collapse inward and chest wall to spring outward. These two recoils equals to zero at what point?
FRC (functional residual capacity)
At FRC, indicate at what level of each of these factors are in:
A. Airway and alveolar pressure
B. Intrapelural pressure
C. PVR (pulmonary vascular resistance)
A. 0
B. Negative value
C. At minimum resistance
What is lung compliance defined as?
Change in lung volume for a change in pressure; expressed as deltaV/deltaP and is inversely proportional = lung easier to full at high compliance; lung harder to fill at low compliance
What are some diseased states in which lung compliance:
A. decreased
B. Increased
A. pulmonary fibrosis, pneumonia, pulmonary edema
B. emphysema, normal aging
What is hysteresis?
The combo of inhalation and deflation curve of pressure volume curve). The transpulmonary pressure vs Volume curve of inhalation is different from the Pressure vs Volume curve of exhalation, the difference being described as hysteresis. Lung volume at any given pressure during inhalation is less than the lung volume at any given pressure during exhalation.
with decreased O2 explain the difference between pulmonary blood flow and systemic blood flow
Decreased O2 levels leads to vasodilation of peripheral arteries thus increased blood flow and the opposite is true for pulmonary circulation: with decrease O2 –> vasoconstriction –> decreased flow –> shunting of blood from poorly ventilated areas to more to well ventilated areas. In sum: increase PaO2 blood flow increase in the lungs, but decrease blood flow systemically
Differentiate difference pulmonary circulation and systemic circulation
Pulmonary = low pressure system 24/12 mmHg Systemic = high pressure system 120/80 mmHg
Gases must diffuse from air to blood. The rate of diffusion depends on what factors?
- Pressure difference (air - blood)
- area of alveoli for diffusion
- Thickness of alveolar tissue
What is the Fick’s Law of diffusion?
V(gas) = (A/T) x D x (P1-P2) aka Vgas = Area x D x pressure difference / thickness
Vgas = rate of gas diffusion
A= surface area for exchange
T = thickness of membrane between alveolar gas and capillary blood
- (p1-P2) = gas partial pressure difference alvolar gas and capillary blood
D = diffusion constant
Diffusion is impacted by diseased states. State what variable in Fick’s Law of diffusion is altered due to the following diseased states:
A. Emphysema
B. Pulmonary fibrosis
A. decreased Area
B. Increased thickness
How long does RBC remain in pulmonary capillary, and how long does it take for equilibrium for the exchange of CO and O2 to take place?
RBC remains in caps for 0.75 sec and equilibrium is reached in .25s in normal lung at resting state. Exercise reduces equilibrium time, but there is still enough reserve for full equilibrium of oxygen in a healthy individual
Diffusion and perfusion are factors for a gas to reach max level in circulation. For the each of the following gases indicate and explain the their limitations in reaching max in circulation:
A. CO
B. N20
C. O2
A. Diffusion limited. The barrier from alveoli to capillary (diffusion thickness) retards their diffusion
B. N20 is perfusion limited. They are able to easily diffuse across the diffusion barrier, thus their max level in circulation will be depended on blood flow (perfusion)
C. O2 is perfusion limited. Similar idea as N20
How is pulmonary vascular resistance calculated?
PVR = P (pulm artery) - P (left atrium) / CO
At what point is pulmonary vascular resistance the lowest?
At FRC.
What happens to pulmonary vascular resistance during inspiration? during expiration?
Resistance during both
Hemoglobin is a 4 polypeptide subunits with 2alpha and 2 beta and usually exists in what two forms?
- Taut: deoxygenated = low affinity for O2, promotes release/unloading of O2
- Relaxed: oxygenated = high affinity for O2 and exhibits positive cooperativity and negative allosteric ;
what factors favors the taut form of hemoglobin and thus shifts the oxygen-hemoglobin dissociation curve tot he right.
remember by: right shift —> ACE BAT’s right handed
- Acid (increased H+)
- CO2
- Exercise
- 2,3 BPG
- Altitude
- Temp
Is hemoglobin in the taut form or relaxed form in peripheral tissues?
Taut form in tissues and relaxed form in lung.
Taut in Tissues; Relaxed in Respiratory area
Carboxyhemoglobin is Hb bound to CO instead of O2 and shifts the curve to _
left. Decrease O2 unloading in tissues. CO binds Hb 200x with greater affinity than O2. Treat with 100% O2 in hyperbaric chamber
How is O2 content in blood calculated?
O2 content = (O2 binding capacity) x (% sat) + Dissolved O2
O2 content = 1.34 x Hb x OaO2 + 0.003
- O2 binding capacity is determined by Hb = 20.1 mL O2/dL
- % saturation is determined by measuring via pulse oximetry
- Dissolved O2 is 0.003 ( negligible since number is so small)
What is A-a gradient?
The difference in pressure in alveoli and in blood
PAO2 - PaO2 = 10-15mmHg
How is alveolar gas pressure calculated?
PAO2 = PIO2 - (PaCO2/R)
aka
150mmHg^a - (paCO2/.8)
PAO2 = alvolar PO2 PIO2 = PO2 in inspired air PaCO2 = PCO2 in arteries R = respiratory quotient: CO2 produced/O2 consumed. normallly it's 0.8
Increased A-a gradient can be seen in what clinical situations?
Hypoxemia as due to shunting, V/Q mismatch, fibrosis
What does it mean when A-a gradient is normal, but pt is hypoxemic?
Since A-a gradient is normal that means alveoli and pulmonary vasculature are working properly but pt is not inhaling enough O2 which can be due to hypoventilation as seen in narcotics, neuromuscular weakness, obesity, high altitude. Can be treated with giving O2.
What is the implication of high A-a gradient hypoxemia?
High A-a gradient means alveoli can’t get O2 to blood, in other words blood is not going to working alveoli. Most lung diseases usually has high A-a gradient.
What are the three main mechanism that which produces a high A-a gradient?
- Fibrosis: loss of alveoli for diffusion, increased A-a gradient and hypoxemia
- Shunt: blood not flowing past alveoli with O2 (anatomic and physiologic shunting)
- Altered VQ mismatch
Ideally V/Q ratio should be 1, but due to anatomy and physics, what is “normal” V/Q ratio?
0.8 and depends on normal RR, TV, and CO.
It reaches 1 during exercise cuz CO is increased.
What is the V/Q ratio at the apex of the lung vs base of the lung?
Apex V/Q = 3 (wasted ventilation) high ventilation with high O2, low CO2
Base: 0.6 (wasted perfusion) low ventilation with low O2, high CO2.
What makes up the conducting zone and respiratory zones?
Conducting zone: trachea; bronchi; bronchioles; terminal bronchoioles
Respiratory zone: Respiratory bronchioles; alveolar ducts; alveolar sacs
which type of alveoli are responsible for surfactant production
Type II alveolar cells (aka type II pneumocytes)
What is approximate pressure inside the alveoli during inspiration and expiration?
Inspiration: about -1mmHg
Expiration: about +1mmHg
When is the intrapleural pressure the lowest?
Right after inspiration and beginning of expiration. It’s -6mmHg. Normally it’s -2.5mmHg at the start of inspiration.
Which lung volume cannot be exhaled out?
RV
Which lung volume cannot be measured via spirometry
Residual volume and any capacity that includes it
What is forced vital capacity (FVC)?
Largest amount of air that can be expired after a maximal inspiratory effort. It’s frequently measured clinically as an index of pulmonary function
What is FVC1?
The fraction of the vital capacity expired during first second of a forced expiration
In a normal lung, what is the FEV1, FVC, and FEV1/FVC ratio?
FEV=Forced expiratory volume
FVC = Forced vital capacity
FEV1 = 3.3L FVC = 4.0L FEV1/FVC = 83%
In normal lung, most of FVC can be expired within 2sec.
In obstructive lung diseases, describe how FEV1, FVC, and FEV1/FVC ratio changes
FEV1 = 1 L (significantly lower than normal) FVC = 2 L (half of normal) FEV1/FVC = 50% (about 30% less than that normal)
Notice both FEV1 and FVC is significantly reduced. Further more, even in that reduced FVC, it takes almost twice as much time (about 4 sec) to expire the FVC
In a restrictive lung disease, explain what changes are seen in FEV1, FVC and FEV/FVC ratio.
FEV1 = 1.8 FVC = 2.0 FEV1/FVC = 90%
The pressure volume curve takes different paths in inspiration and expiration (they do not follow the same path). Why?
The surface tension (between the air inhaled and the tissue (which is essentially water) is what makes the curve to be different
What is the role of surfactant and how does it prevent the alveoli from collapsing during expiration?
The low surface tension when alveoli are small are due to surfactant in the fluid lining the alveoli. If the surface tension is not kept low when the alveoli become smaller during expiration, they collapse in accordance with law of Laplace. In spherical structures like the alveolus, the distending pressure (P) equals two times the tension (T) divided by the radius. (P=2T/r); if T is not reduced as r is reduced, the tension overcomes the distending pressure. Surfactant
what drives net flow of O2 into the blood and CO2 out of the blood in the pulmonary system?
partial pressure difference between air and blood for O2 and CO2.
what are the major ways O2 is carried in blood?
Most are bound to Hb, and small amounts are dissolved.
How is CO2 carried in blood?
CO2 in blood is rapidly converted into H2CO3 due to activity of carbonic anhydrase. CO2 also readily forms carbamino compounds with blood proteins (including HB0. the rapid net loss of CO2 allows more CO2 to dissolve in blood
what is the role of Pre botzinger complex in respiratory control?
Located on either side of medulla, contains synaptically coupled pacemaker cells that allow for rhythmic generation of breathing. the spontaneous activity of these neurons can be altered by neurons in pneumotaxic center
Peripheral chemorecetpros are located on _ and are sensitive to changes in _
Aortic an carotid bodies.
PaO2, PaCO2, and pHa
What kind of breathing patterns is seen in patient with diabetic acidosis?
Kussmaul
Where are central chemoreceptors located and what are they sensitive to?
Located on ventral surface of medulla and sensitive to CO2.
Rapidly-adapting pulmonary stretch receptors trigger _ in response to various irritants.
Cough
Slowly adapting pulmonary stretch receptors are important for _
telling the brain how much air is in the lungs which then would trigger expiration/ decrease inspiration.
Which pulmonary stretch receptors are important in babies to control respiratory rate.
slowly adapting pulmonary stretch receptors.
In adults, during exercise which receptors allows to increase tidal volume?
slowly adapting pulmonary stretch receptors.
J receptors are located _ and are important in detecting _ which produces _ breathing pattern.
Located on juxtaalveolar wall and detects fluid flow. Important in detecting edema, and produces rapid shallow breathing as seen in pts with restrictive disease
Pt takes a breathe in as deeply as possible and exhales forcefully into a spirometer until all possible air has been expelled. What volume/capacity was measured?
Vital capacity
An increase in what will decrease the amount of oxygen that crosses the alveolar barrier in one minute?
The diffusion distance across the alveolar barrier