Partial pressure of gases in Aveoli: 1) PO2 in alveoli is 100 mm hg and thats because a) the fresh air entering the

alveoli that has PO2 160 mm hg will mix with the air in alveoli already present from previous expiration which has low PO2, and b) when air enter to lungs through air ways it will be humidified by adding water vapor to it and by this reducing O2 percentage in the inspired air and resulting reduced PO2 2) We can consider that PO2 in the inspired air is constant 100 mm hg with little variation between inspiration and expiration (thats because there is always some volume of air remain in alveoli even after forceful expiration called residual volume) 3) Air entering alveoli has very little PCO2 and when mixes with air present in alveoli from previous expiration, which has high PCO2, the resultant PCO2 is 40 mm hg constantly Partial pressures of gases in pulmonary capillaries: 1) Blood coming through venous system from body tissues will be pumped to lungs and pass through pulmonary capillaries. 2) This venous blood has low PO2 because the tissues used the O2 for energy production. So the PO2 in pulmonary blood is low (40 mm hg), and PCO2 is high (46 mm hg) 3) The capillaries come surrounding alveoli, gas exchange will occur from high to low partial pressure and trying to equilibrate 4) Blood leaving pulmonary capillaries has the same PO2 values for alveoli like PO2 is 100 mm hg and PCO 2 is 40 mm hg and this blood will return to heart to be pumped to body tissues 5) Blood coming to capillaries at tissue level will equilibrate with tissue gases which have PO2 40 mm hg and PCO2 46 mm hg, and thus it will deliver O2 to tissues and take CO2 from them and the blood leaving tissues will have PO2 40 mm hg and PCO2 46 mm hg

Mixed venous blood

By the time the blood reaches the pulmonary artery in the right side of the heart, all venous blood has "mixed" with venous systemic system and venous blood of the heart from coronary sinus drainage into the right atrium. Mixed venous oxygen saturation (SvO2) is the percentage of oxygen bound to hemoglobin in blood returning to the right side of the heart. It is the amount of oxygen "left over" after the tissues extracted oxygen. It is used to help us to recognize when a patient's body is extracting more oxygen than normally. An increase in extraction is the bodies way to meet tissue oxygen needs when the amount of oxygen reaching the tissues is less than needed. Caution :There is often little to no correlation between SvO2 and SaO2, PaO2, CO or Hgb, esp. in critically ill patients. The only consistent clinical correlation is the one between SvO2 and O2 ER. Therefore, SvO2 reflects the amount of O2 consumed (demand) by the body tissues
Normal SvO2 ranges from 60-80%. Low SvO2 is an indication of increased oxygen consumption or extraction by tissues. It can also indicate impaired oxygen delivery such as cardiogenic shock. In septic states, the SvO2 may actually be elevated, because tissues cannot effectively extract oxygen from hemoglobin.

What does it tell us? Mixed venous oxygen saturation (SvO2) can help to determine whether the cardiac output and oxygen delivery is high enough to meet a patient's needs.

There are 4 fundamental causes for a drop in SvO2: 1. The cardiac output is not high enough to meet tissue oxygen needs 2. The Hb is too low 3. The SaO2 is too low 4. The oxygen consumption has increased without an increase in oxgyen delivery

Compensation :

ATP (energy) is needed for all cell function and survival. Tissues require oxygen in order to make ATP ( amount of oxygen being received by the tissues falls below the amount of oxygen required (because of need, or decreased supply), the body attempts to compensate as follows: First Compensation: Cardiac Output increases

The cardiac output is increased in an effort to increase the amount of oxygen being delivered to the tissu below.

Oxygen Delivery is the amount of oxygen being sent to the tissues, and is determined by the foll

ATP (energy) is needed for all cell function and survival. Tissues require oxygen in order to make ATP (energy). If the amount of oxygen being received by the tissues falls below the amount of oxygen required (because of an increased need, or decreased supply), the body attempts to compensate as follows: First Compensation: Cardiac Output increases The cardiac output is increased in an effort to increase the amount of oxygen being delivered to the tissues as shown below. Oxygen Delivery is the amount of oxygen being sent to the tissues, and is determined by the following: Oxygen Delivery (DO2) = Cardiac Output (HR X Stroke Volume) X Oxygen Content (Hb X SaO2) If this is not sufficient to meet tissue energy needs, we move to our second compensation. Second Compensation: Tissue oxygen extraction increases. Tissues begin to remove or extract a higher percentage of oxygen from the arterial blood. This results in a reduced amount of oxygen remaining in the blood as it returns to the right side of the heart (decreased SvO2).

If this is not sufficient to meet tissue energy needs, we move to our second compensation.

Third Compensation: Anaerobic Metabolism iIncreases If the tissues fail to receive an adequate supply of oxygen, anaerobic metabolism becomes the only mechanism to produce tissue ATP. Anaerobic metabolism is inefficient, producing a large amount of metabolic waste (e.g. lactic acid) that is difficult for the body to eliminate quickly. It also produces a relatively poor supply of ATP. Prolonged anaerobic metabolism leads to energy depletion and metabolic acidosis. In hypovolemic shock, cardiac output will decrease, and become unable to keep up with the rate of oxygen uptake by the tissue, which further increase the "oxygen consumption/cariac output" figure, increaseing venous oxygen content. While in septic shock oxygen cosumption (tissue extraction) is impaired, and cardiac output is initially high, making the venous oxygen content high, much like the Artervenous shunts you have talked about.. that's why I saw it frequently in questions about septic shock.