;;1. A comatose patient with no spontaneous respiration is placed on mechanical ventilation with the following settings:
Tidal Volume (VT)= 1000 ml
Respiratory frequency (f) = 10 breaths/min
Inspired O2 concentration = 40% (FIO2 = .4)
The following measurements are made:
Arterial PCO2 = 40 mmHg
Mixed expired PCO2 = 30 mmHg
Arterial PO2 = 95 mmHg
a. Calculate minute ventilation (VE)
VE = VTx FR = 1000 x 10 = 10 L/min
b. Calculate dead space to tidal volume ratio (VD/VT)
VD/VT = (PaCO2 - PECO2)/PaCO2 = (40=30)/40 = 0.25
c. Calculate alveolar volume (VA)
VA = VT - VD = VT - (VTx0.25) = 1000 - 250 = 750 ml
d. Calculate alveolar ventilation (VA)
VA = VE - VDxFR = 10000 ml/min - (250 x 10) = 7500 ml/min
e. If extra tubing with a volume of 250 ml were added to the system in a position such that it provided additional dead space, what would be the new VD/VT? What would be the new PaCO2?
VD/VT = (250=250)/1000 = 0.5
Pa = PECO2/(1-VD/VT) = 30/(1-0.5) = 6.0
f. Using the original ventilator setting and arterial blood gases calculate the alveolar-arterial O2 difference.
P(A-a)O2 = PAO2 - PaO2 = PAO2 - PaO2 =
FIO2(Patm - PH2O) - PaCO2/R - PaO2 =
(0.4) (760 - 47) - 40/0.8 - 95 = 140.2
2. Consider the following situations and very briefly explain in each case the reason for hypoxemia.
Exercise induced increase in cardiac output
Decreased pulmonary capillary transit time diffusion impairment hypoxemia
Filling of alveoli with proteinaceous material
Increased diffusion path length diffusion impairment hypoxemia
Pulmonary edema
Increased diffusion path length diffusion impairment hypoxemia
Thickening of alveolar capillary membrane
Increased diffusion path length diffusion impairment hypoxemia
Pulmonary embolism
Blockade of pulmonary vessels with emboli mean pulmonary-capillary transit time shorter because unchanged cardiac output must traverse a smaller capillary volume in less time diffusion impairment due to reduction of functioning pulmonary capillary bed hypoxemia
Ascend to high altitude (I'm not talking about dying and going to heaven!)
This will cause reduced driving pressure for O2 diffusion, and will therefore slow the rise time of pulmonary capillary PO2
Is CO2 diffusion a problem in mild cases of diffusion impairment? No because moderate diffusion impairment is accompanied by a decreased PaO2, a widened PA-a O2 and a relatively normal PaCO2
3. You are the chief resident in emergency medicine one night when a 35 year old female comes in markedly flushed, afebrile, tachypneic but comatose after a week of “speed-balling” (repeated dosing of cocaine without food etc), you quickly intubate her and get an SaO2 while your waiting for the blood gases to come back. Initial labs reveal a hemoglobin of 16 mg/dl and a hematocrit of 43.
a). Her SaO2 reads 63%, what is the quantitative saturation of her hemoglobin?
With a hemoglobin of 16 mg/dl and a O2 concentration of 1.34 mlO2/mg Hb = 21.4 mlO2 / dl = maximal O2 concentration is 214 mlO2 / L. 63% of which is saturated with O2 therefore there is 128.6 mlO2 /L blood.
b) Getting a thorough history from her mildly intoxicated boyfriend, you reveal that she was found in a garage with the car running. Immediately, you get a blood PCO which reveals a reading of 0.5mmHg. Realizing the danger of the situation, you quickly cross match her blood type and transfuse 4 units of packed RBCs and place her on a ventilator with 100% O2… why?
With a PCO of 0.5 mmHg 50% of the blood is saturated with CO; which means that 50% of blood is unable to bind O2, only way to treat is to increase O2 concentration and infuse blood.
c) Blood gases come back with the following values: pH 7.32; PCO2 = 60; PO2 = 47mmHg on room air.
What mechanisms help the patient unload O2 under a very high O2 demand situation?
Haldane effect; Bohr effect (since its been a week, can be questionable whether she is having 2,3 BPG to increase O2unloading as well.
4. Quickie question: Why can it be said that the total CO2 concentration approximates the HCO3- concentration?
Since 90% of CO2 is stored as bicarbonate, it is a good approximation.
b) In what ways is CO2 transported in the blood?
Carbamino Hb, HCO3-, CO2; H2CO3.
5) You are a fourth year medical student at CHS when you see your old pal Dr. Ignarro walking down the corridor as you are walking to clinic, realizing his infatuation with NO, you worry that he will “pimp” you on NO. Which he does: He asks “Knowing that you did learn something from my class, Dr ____, I hope you can tell me how the respiratory system avails itself to clear the bodily secretion of NO.
When O2 is not bound to Hb, it can be used to transport NO to the lung where it is released with CO2.
6) It is 2010; the dawning of a new era, and you are the chief resident in the department of surgery, as you smirk at all the medical students rushing behind you and the other medical students cringing as you walk by; you see an old crotchety but tall man in the distance down the corridor, he is now stooped over, but you can make out that it is your old buddy Dr. Cooper the respiratory physiologist on his rounds; you quickly tell your medical students and team that they should prepare to be pimped by Dr. Cooper, who asks in a lofty English accent:
a)Tell me about the perfusion zones of the lung, and why we place the swan ganz catheter in zone 2 of the lung?
Zone 1: high ventilation; low perfusion above level of heart
Zone 2: at level of heart; good matching
Zone 3: gravity compression; poor perfusion; poor ventilation
Place the swan ganz at Zone 2 to measure best V/Q because blood is preferentially shunted here.
b)What mechanism does the lung use to modulate blood flow to different parts of the lung to insure proper oxygenation?
V/Q matching and hypoxic VASOCONSTRICTION; this way poorly oxygenated areas shunt blood to better oxygenated areas.
c)How is a non-cardiac right-to-left shunt possible in the lung?
A poorly ventilated, highly perfused region is a physiological right to left shunt.
7). You are the cardiac catheterization attending at Cedars Sinai medical center, and are “cathing” a patient who seems to have some sort of physiological shunting going on:
You initially get a hemoglobin of 14.5 mg/dl with a hematocrit of 34. SaO2 readings reveal a saturation of 80% on the arterial side and 40% on the venous side; calculate the shunt.
Qs/Qt = (CcO2 - Ca O2) / (Cc O2 – Cv O2) =
14.5 x 1.34 = 19.4 ml O2 / dl blood = 194 ml O2 / L blood
80% saturated = 155.2 ml O2 / L Blood
40% saturated = 77.6 ml O2 / L Blood
shunt = (194 – 155.2) / (194 – 77.6) = 38.8 / 116.4 = 33.3%
V/Q inequality:
Fill in the table with either , , or N (normal)
PaO2 / PAO2 / PaCO2 / V/QHealthy tachypneic person / N / N / / N/ (more volume in dead space- see pg 28 in notes)
Person who inhaled a marble (bronchial plug) / / / /N / (shunt)
Person with a pulmonary embolus / N/ / / (reflex vent) / (dead space)
Tachycardia / ( transit time) / N / N / N
Pulmonary edema:
Fill in the chart with either , , N (normal)
Disorder / Hydrostatic pressure gradient / Oncotic pressure gradientCongestive Heart Failure / / N
Liver disease / N /
Rt heart failure / N / N
Left heart failure / / N
Nephrotic syndrome / N /