Intermediate: ICU Principles Flashcards
What is the oxygen content of arterial blood (CaO2):
Hb X Sata X 1.34
Sata: arterial hgb oxygen saturation
Why is PaO2 so important?
The PaO2 evaluates the efficacy of gas exchange. As mentioned above (question 1), the amount of dissolved oxygen in blood is very little compared to that bound to Hb. Therefore Hb is the principle determinant of the ‘level’ or content of oxygen. Hb saturation curve is plotted against PaO2, because the PaO2 at various levels determines the % saturation of Hb.
Normal VO2 and VCO2:
Note that when VO2 is 250 and VCO2 of 200 the RQ is 0.8.
What is dysoxia?
Normal Satmv?
The point where VO2 decreases due to the DO2 decreasing (no more oxygen can be extracted) is called dysoxia.
Basically, when VO2 starts outpacing DO2, the mixed venous sat will start dipping below 70% (70-75% is around normal)
So what do you do when your patient has a Satmv?
Consider if DO2 is ok: arterial saturation low (increase FiO2, PEEP), Hb low (transfusion), cardiac output low (inotrope, fluid bolus, etc). If you have no further optimization options for DO2, start thinking about decreasing VO2 (decrease temperature, decrease nutrition (generally bad idea), paralyze (generally bad idea), etc).
patient in the ICU with severe hypoxia and inadequate delivery of oxygen to tissues is found to have an increasing level of lactic acid and a decreasing pH. Which of the following are true regarding this patient:
A. Glycolysis has stopped occurring
B. Anaerobic metabolism is associated with lactic acid production, but does not explain the low pH
C. The pH is low because there is insufficient oxygen in the final step in the electron transport chain
D. This is a result of overfeeding with TPN
C: The pH is low because there is insufficient oxygen in the final step in the electron transport chain
When oxygen is not present, the ETC comes to a halt (O2 accepts the electrons donated by the citric acid cycle). In this situation cellular respiration is anaerobic and far fewer ATP molecules are produced. Additionally, lactic acid accumulates causing an anion gap metabolic acidosis.
True or False? NTG primarily decreases preload, not afterload.
TRUE
A patient has an elevated Satmv, which of the following is most likely:
A. Cirrhosis, CI 5.2, arterial Sat 92%
B. Septic, Hb 6.5, PaO2 62
C. Severe COPD with erythrocytosis, EF 35%, sat 90%, Hb 18
D. Healthy 25 year old in hyperbaric chamber at 2 atmospheres, FiO2 100%
Go through these
A: Cirrhosis, CI 5.2, arterial Sat 92%
This is a tough one, lets go through each in turn. A cirrhotic patient tends to have high cardiac index (CI) as well as a propensity for peripheral AV shunting both of which cause an increased mixed venous sat (SVO2), since a lot of oxygen is delivered and with AV fistulas, less O2 will be consumed. Low arterial saturations are common in ESLD patients due to an increased shunt fraction due to atalectasis and pulmonary AV fistulas which . This does limit DO2 (oxygen delivery), but the very high CO compensats for the low arterial saturation.
The septic patient tends to have an elevated Satmv (on exams!) because of high CO and decreased utilization of oxygen (sick mitochondria), but given the very low Hb and a PaO2 which correlates to a saturation in the low 90s, the oxygen delivery is still likely lower than the patient in choice A.
The patient in choice C has a lot of Hb, but a low CO in all likelihood. Even though each cc of blood can carry more oxygen than the other patients, he is unable to substantially increase the DO2 due to the poor heart function.
A hyperbaric chamber can increase PaO2, but cannot make a Hb molecule more than 100% saturated which accounts for the great majority of oxygen content. This patient would likely have a high-normal Satmv, not an elevated one.
Why is the SatMV higher in sepsis?
It should be noted the reason for this is not entirely clear. Mitochondrial oxygen utilization is impaired, which would in that sense decrease the consumption of oxygen. However, there is a wide spread activation of the immune system, referred to as the ‘respiratory burst,’ where overall oxygen consumption is in fact increased. The increase in Satmv is most likely due to increased oxygen delivery primarily through increased CO.
A leftward shift of the oxygen Hb saturation curve secondary to hypocarbia is called:
A. Fick principle
B. Bohr effect
C. Haldane effect
D. Law of LaPlace
Explain them all
This is a backwards stated question because Bohr effect essentially means that increasing CO2 binding to Hb (by increasing PaCO2) will cause an increased release of oxygen (in other words right shift). Therefore, the opposite must be true, that hypocarbia causes a left shift. Haldane effect is similar. This states that when deoxygenated, Hb can bind more CO2 (and therefore work as a buffer). Fick principle is what we’ve been talking about all along, relating oxygen delivery to consumption. LaPlace’s law relates pressure to wall tension [Pressure = (2 X Tension X Wall Thickness)/ Radius].
patient’s respiratory quotient increases from 0.8 to 0.85, what is the most likely reason:
D: Increase in carbohydrate proportion in TPN
The RQ is the balance between the production of CO2 and consumption of O2, or VCO2/ VO2. Nutrition can effect CO2 production in that carbohydrates, protein, and fat produce 1.0, 0.8, and 0.7 units of CO2 for every unit of O2 consumed. In patient’s nearing respiratory failure, decreasing carbohydrates and increasing lipids can decrease the overall RQ meaning the patient needs to expel LESS CO2 per O2 consumed. The other answers will not change the RQ.
Does Respiratory quotient change in preggo?
No
The majority of blood CO2 is held as _____ in ______
bicarbonate in the plasma and RBCs
A patient’s PaCO2 is 40 mm Hg, what is the likely mixed venous PCO2 (PmvCO2) (in mm Hg):
C: 46
The PmvCO2 is normally about 46 as it enters the lungs and is 40 as it exits (PaCO2).
Wedge pressures in ARDS:
Classically, the definition has included a wedge pressure < 18 to essentially rule out a cardiogenic cause of the pulmonary oedema.