Respi 1 Flashcards
How is Polycythemia determined and what are the two types?
Polycythemia is based on hematocrit levels (Men hct > 52%, Women hct > 48%).
>Relative polycythemia (normal RBC mass) - dehydration, excess diuresis.
>Absolute polycythemia (inc. RBC mass) - Primary (polycythemia vera), Secondary (hypoxia, EPO-producing tumors)
Where do you insert a chest tube to drain pleural effusion? What structures does the tube penetrate?
Insert tube into 4th or 5th ICS at anterior axillary or midaxillary line.
Tube traverses Serratus anterior, intercostal muscles, and parietal pleura.
At what points should a needle be inserted for thoracentesis?
Above 8th rib MCL, 10th rib MAL, or 12th rib paravertebral line.
Inserting lower than these points increases risk of penetrating abdominal structures (liver). Inserting on inferior margin of rib risks damaging neurovascular bundle.
What is the normal A-a gradient and what does it represent?
Normal A-a gradient is 5-15 mmHg. Alveolar PO2 is normally at 105 mmHg, but it later becomes 100 mmHg as arterial PO2 in the systemic circulation. This is because deO2 blood from the bronchial veins and Thebesian veins are added by the time blood in the pulmo vessels reaches the LA. The A-a gradient is a little higher in older individuals.
What are the causes of hypoxemia w/ Normal A-a gradient and hypoxemia w/ increased A-a gradient?
> Normal A-a gradient (low PaO2 is directly due to low PAO2): alveolar hypoventilation, high altitude.
Increased A-a gradient: V/Q mismatch (PE, COPD), O2 diffusion impairment (ILD), R-L shunting (septal defect, pulmo edema)
Why are patients w/ cerebral edema hyperventilated?
CO2 is a potent cerebral vasodilator. If PCO2 inc. from 25 to 100 mmHg, there is inc. cerebral blood flow. Dec. PCO2 causes dec. cerebral blood flow and thus dec. cerebral perfusion. Hyperventilating a patient w/ cerebral edema induces hypocapnea – dec. cerebral blood flow, dec. ICP.
(On the other hand, panic attacks can also induce hyperventilation and hypocapnea, and this may induce neuro sx like dizziness)
Perfusion-limited vs. Diffusion-limited gas exchange
> Perfusion-limited: gas exchange limited by RATE OF BLOOD FLOW thru pulmo capillaries; if gas can rapidly diffuse across alveolar membrane, then equilibrium point of gases can be reached w/in the first 1/3 of capillary (O2, CO).
Diffusion-limited: gas exchange depends on DIFFUSION RATE across alveolar membrane; incomplete equilibration by the time a certain amount of blood reaches the end of the pulmo capillary (ex. CO due to it’s strong binding capacity to Hgb)
If a patient were to have high altitude exposure for about 2 days, what would their arterial blood gas values look like?
High altitude induces hypoxemia and tissue hypoxia –> peripheral chemoreceptors triggered –> hyperventilation, fall in PaCO2 –> Compensatory Respiratory Alkalosis (by 24-48 hrs, delayed renal compensation by HCO3 loss)
Surfactant decreases surface tension as alveoli decrease in size during expiration. How is this applicable to Laplace’s law and its effect on alveoli of varying sizes?
P = 2T/r
W/ constant surface tension, a sphere w/ a smaller radius will have higher distending pressure than a larger sphere, causing the smaller to collapse while the larger one gets bigger. In alveoli, surfactant reduces the difference in distending pressures b/w alveoli of varying sizes, preventing the collapse of the smaller alveolus and the unchecked expansion of the larger one. Surfactant is more concentrated as alveolar size decreases, and it spreads out as size increases.
At what point on a spirometry tracing is Pulmonary vascular resistance (PVR) lowest? Why?
PVR is increased both at high and low lung volumes. Inspiration causes stretch of alveolar vessels by the expanding alveoli. Expiration causes dec. radial traction on extra-alveolar vessels and also compression of extra-alveolar vessels by the (+) intrathoracic pleural pressure. Therefore, total PVR is lowest at Functional Residual Capacity, where the resistances of alveolar and extra-alveolar vessels are equal.
