<\/p>\n
<\/p>\n
Interactions Article (Part I<\/a>, Part II<\/a>)<\/p>\n <\/p>\n the effects of deadspace on CO2 are ameliorated by an increase in minute volume, unless pt can’t spont breathe<\/p>\n ~35-40% fiO2 will eliminate deadspace effects on O2<\/p>\n Alveolar deadspace in our patients is often caused by decreased lung perfusion<\/p>\n at decreased temperatures, CO2 becomes more soluble<\/p>\n <\/p>\n (Inten Care Med 2011;37:735)<\/p>\n <\/p>\n Figure 17-24 For any given O2 concentration in inspired gas, the relationship between alveolar ventilation and Pao2 is hyperbolic. As the inspired O 2 concentration is increased, the amount that alveolar ventilation must decrease to produce hypoxemia is greatly increased. BTPS, body temperature, ambient pressure, saturated. (Redrawn from Lumb AB: Respiratory system resistance: Measurement of closing capacity. In Lumb AB [ed]: Nunn’s Applied Respiratory Physiology, 5th ed. London, Butterworths, 2000, p 79.) (From Miller’s Anesthesia)<\/p>\n Andrew Farmery writes:\u00a0 It’s just the alveolar gas equation plotted out.\u00a0i.e. it’s simply PA=FI x (PB-PH2O) – (PB x vO2\/VA).<\/p>\n Apneic Oxygenation<\/a> (Anesthesiology 1959;Nov\/Dec:789)<\/p>\n <\/p>\n Desaturation Time with Preox and Occluded Airway<\/p>\n <\/p>\n Simulator of the effect of supp. oxygen on detecting hypoventilation<\/a><\/p>\n <\/p>\n David Story finally put into the literature<\/a>\u00a0something I have been wrestling with forever. The PaCO2 in the Alveolar Gas Equation is simply there to represent alveolar ventilation, it doesn’t imply PaCO2 affects PaO2\/PAO2.<\/p>\n <\/p>\n Mask adds 82 cc of deadspace compared to tube, even though it is actually 125 cc more space (BR J Anesth 1969;41:94)<\/p>\n J Clin Anesth. 1989;1(5):328-32. Links Comment in: J Clin Anesth. 1989;1(5):323-7. J Clin Anesth. 1991 Jan-Feb;3(1):82-4. The PaCO2 rate of rise in anesthetized patients with airway obstruction. Stock MC, Schisler JQ, McSweeney TD. Department of Anesthesiology, Emory University School of Medicine, Atlanta, GA. Apneic, anesthetized patients frequently develop airway obstruction or may be disconnected from ventilatory support. The rate of PaCO2 rise is usually assumed to be equal to that of anesthetized humans who are receiving apneic oxygenation. Apneic oxygenation may eliminate CO2 because it requires a continuous O2 flow. The CO2 rate of rise in anesthetized humans with airway obstruction was measured. Fourteen consenting healthy adults were monitored continuously with pulse oximetry and EKG. Enflurane–O2 anesthesia was established for at least 10 minutes with normal PaCO2 without neuromuscular blockade so that anesthesia was deep enough to prevent spontaneous ventilation. Then, patients’ tracheal tubes were clamped. Arterial blood samples were obtained before and after 0, 20, 40, 60, 120, 180, 240, and 300 seconds after clamping, provided that oxyhemoglobin saturation exceeded 0.92. The equation that best described the PaCO2 rise was a logarithmic function. Piecewise linear approximation yielded a PaCO2 increase of 12 mmHg during the first minute of apnea, and 3.4 mmHg\/minute thereafter. These values should be employed when estimating the duration of apnea from PaCO2 change for anesthetized patients who lack ventilatory support. In addition, it appears that the flows of O2 that most earlier investigators used when delivering apneic oxygenation probably did not eliminate significant CO2 quantities.<\/p>\n <\/p>\n <\/p>\n PaCO2=VCO2 (production) \/ (VE x (1- Vd\/Vt)<\/p>\n VE=minute ventilation Vd=deadspace Vt=tidal volume<\/p>\n <\/p>\n Bohr Equation Vd\/Vt=(PaCO2-PetCO2)\/PaCO2<\/p>\n Normal=0.2-0.4<\/p>\n <\/p>\n <\/p>\n Spontaneous breathing patients will breathe at a PaCO2 of 50; with preoxygenation, it is a PaCO2 of 60<\/p>\n <\/p>\n In an apneic anesthetized patient the rate of CO2 rise<\/p>\n 12 mmHg in the 1st minute<\/p>\n 3.5 mmHg per minute thereafter<\/p>\n (Anesthesiology 1961;22:419, J Clin Anesth 1989;1:328)<\/p>\n <\/p>\n Hypercapnea<\/p>\n VT=VA+VD (Alveolar\/Deadspace)<\/p>\n PaCO2=PACO2 in normal lungs<\/p>\n <\/p>\n Increased CO2 production (hypermetabolic states)<\/p>\n Decreased Alveolar ventilation\/Increased deadspace ventilation<\/p>\n Decreased Tidal Volume<\/p>\n <\/p>\n <\/p>\n 8+Age\/5 is normal<\/p>\n <\/p>\n Best article<\/a><\/p>\n Justification for abbrev.<\/a><\/p>\n How mixed venous changes screws this stuff up<\/a><\/p>\n Type I-hypoxemic, PaO2<60<\/p>\n Type II-hypercapneic w\/wo hypoxemia, PaCO2>50<\/p>\n <\/p>\n Mechanisms of Hypoxemia<\/p>\n PAO2=FiO2(PB-PH2O) – PaCO2\/R<\/p>\n R=.8<\/p>\n <\/p>\n <\/p>\n Reabsorbtion atelectasis and loss of hypoxic pulmonary vasoconstriction may actually cause hypoxemia to get worse in the presence of high fiO2 and shunt.<\/p>\n <\/p>\n article on the mechanisms of hypoxemia (intensive care medicine 2005;31:1017-1019)<\/p>\n <\/p>\n <\/p>\n <\/p>\n Decreased PaO2 can actually lower respiratory drive in the critically ill, studies done in patients with cardiogenic shock.<\/p>\n Primary neurologic problems can result in decreased respiratory drive.\u00a0 these include AML, spinal cord injuries, guillain-barre, and muscular disorders.<\/p>\n Respiratory muscle fatigue from COPD\/Asthma, ARDS, etc.<\/p>\n <\/p>\n Increased production in sepsis, hypothermia, salicilates,<\/p>\n Increased deadspace ventilation<\/p>\n Hypercapnia can decrease respiratory drive.<\/p>\n <\/p>\n <\/p>\n shift to the right is right (good) i.e. more O2 released to cells<\/p>\n <\/p>\n <\/p>\n the first equation you need is the<\/p>\n CaO2=(Hb) x 1.38 x SaO2 + (0.003 x PaO2)<\/p>\n 1.38 is the carrying capacity of a gram of Hb<\/p>\n <\/p>\n normally 17-20 cc\/dL<\/p>\n <\/p>\n Note that >99% of the capacity is from Hb binding<\/p>\n <\/p>\n DO2=CaO2 cc\/dL x (CO L\/min) x 10<\/p>\n <\/p>\n 10 is the conversion factor to convert L to dL<\/p>\n normally 950-1150 cc\/min<\/p>\n <\/p>\n DO2I=CaO2 x CI x 10<\/p>\n normally 550-650 cc\/min\/m2<\/p>\n <\/p>\n Fick Equation<\/p>\n VO2=(CaO2-CvO2) x CO x 10\u00a0\u00a0\u00a0 or<\/p>\n VO2=1.38 (Hb)(CO)(SaO2-SvO2)\/10<\/p>\n normally 240-290 cc\/min<\/p>\n <\/p>\n <\/p>\n VO2=oxygen consumed<\/p>\n DO2=Oxygen delivered<\/p>\n <\/p>\n VO2\/DO2 is normally 0.22-0.27 (0.25)<\/p>\n Rising VO2\/DO2 ratio is a sign of inadequate tissue oxygenation<\/p>\n <\/p>\n <\/p>\n CvO2=(Hb) x 1.34 x SvO2 + 0.003 x PvO2<\/p>\n Normally 15 cc\/dl<\/p>\n <\/p>\n <\/p>\n VO2I=(CaO2-CvO2) x CI x 10<\/p>\n Normally 115-165 cc\/min\/m2<\/p>\n <\/p>\n PvO2 of 28 is required to cause oxygen to diffuse into cells, below this point anaerobic metabolism occurs. This is equivalent to an SvO2 of 50% unless the oxyhemoglobin curve is shifted.<\/p>\n <\/p>\n vasoregulation is an important factor that can not be measured.<\/p>\n <\/p>\n Cirrhosis and sepsis look hemodynamically identical<\/p>\n <\/p>\n capillary shunt<\/p>\n blood flowing past unventilated alveoli<\/p>\n atelectasis<\/p>\n pneumonia<\/p>\n ards<\/p>\n pulmonary edema<\/p>\n <\/p>\n anatomic shunt<\/p>\n positive pressure may worsen<\/p>\n <\/p>\n <\/p>\n overventilation compresses blood vessels leading to increasing shunt and increasing deadspace<\/p>\n <\/p>\n <\/p>\n <\/p>\n Ve=minute volume<\/p>\n Ve=Vd + Va<\/p>\n <\/p>\n <\/p>\n we compensate by increasing CO and increasing oxygen extraction<\/p>\n we can decrease extraction ratio to get venous sat of 40%<\/p>\n we can easily triple CO or up to 20 L\/min<\/p>\n <\/p>\n <\/p>\n <\/p>\n <\/p>\n <\/p>\n PaO2<\/p>\n PaCO2<\/p>\n SaO2 or SpO2<\/p>\n SvO2 (Mixed Venous)<\/p>\n Venous Oxygen Tension PvO2<\/p>\n Hb<\/p>\n CO<\/p>\n <\/p>\n Pulmonary Capillary O2 Content (CcO2)<\/p>\n Arterial Oxygen Content (CaO2)<\/p>\n Venous Oxygen Conent (CvO2)<\/p>\n Arterial-venous oxygen content difference (Ca-vO2)<\/p>\n Oxygen utilization coefficient (OUC)<\/p>\n Oxygen Delivery Index (DO2I)<\/p>\n Oxygen Consumption Index (VO2I)<\/p>\n Intrapulmonary Shunt (Qsp\/Qt)<\/p>\n Cardiac Index (CI)<\/p>\n <\/p>\n Oxygen content=oxygen bound to Hb + oxygen dissolved in plasma<\/p>\n Oxygen bound=Hgb concentration x (1.34 cc oxygen per g Hb) x saturation of Hb<\/p>\n Oxygen dissolved=blood oxygen tension x (0.0031 solubility coefficient of oxygen in blood)<\/p>\n <\/p>\n <\/p>\n CcO2 = pulmonary end-capillary oxygen content<\/p>\n = oxygen bound to Hgb as it leaves the alveolus<\/p>\n = (1.34 x Hgb x 1.0) + (PAO2 x 0.0031)<\/p>\n The saturation of oxygen in the pulmonary end-capillary should be 1.0 if FiO2 > 0.21 PAO2 = alveolar oxygen tension = FiO2 x [(PB-PH20)-(PaCO2\/RQ)] PB = barometric pressure, PH2O = water vapor pressure, RQ = respiratory quotient = 0.40 x [(760 torr – 47 torr) – (40 torr\/0.8) (assuming normal values) = 0.40 x 663 torr = 265 torr PAO2 can also be approximated rapidly at the bedside as 700 torr x FiO2 – 50 torr = 20.1 ml O2\/dl blood + 0.8 ml O2\/dl blood (assuming normal values) = 20.9 ml O2\/dl blood<\/p>\n <\/p>\n CaO2 = arterial oxygen content = arterial oxygen content as blood leaves the heart = oxygen bound to Hgb in arterial blood (98 %) + oxygen dissolved in arterial plasma (2%) = (1.34 x Hgb x SaO2) + (PaO2 x 0.0031) 1.34 mL of oxygen can be carried on each gram of human hemoglobin; this number varies from species to species = (1.34 x 15 g x 1.0) + (100 torr x 0.0031) (assuming normal values) = 20.1 ml O2\/dl blood + 0.31 ml O2\/dl blood = 20.4 ml O2\/dl blood<\/p>\n <\/p>\n CvO2 = venous oxygen content = venous oxygen content as blood returns to the heart = oxygen bound to Hgb in venous blood (>99%) + oxygen dissolved in venous plasma (<1%) = (1.34 x Hgb x SvO2) + (PvO2 x 0.0031) PvO2 can be measured with a venous blood gas, or estimated as 35 torr with high accuracy = (1.34 x 15 g x 0.75) + (35 torr x 0.0031) (assuming normal mixed venous oxygen saturations) = 15.1 ml O2\/dl blood + 0.11 ml O2\/dl blood = 15.2 ml O2\/dl blood<\/p>\n <\/p>\n Ca-vO2 = arterial-venous oxygen content difference = CaO2 – CvO2 = 20.4 ml O2\/dl blood – 15.2 ml O2\/dl blood = 5.2 ml O2\/dl blood<\/p>\n <\/p>\n Once the oxygen contents throughout the vascular circuit have been calculated, the amount of oxygen delivered to the tissues (oxygen delivery index or DO2I) and the amount of oxygen consumed by the tissues (oxygen consumption index or VO2I) can be calculated. DO2I = oxygen delivery index = volume of gaseous O2 pumped from the left ventricle per minute per meter squared BSA = CI x CaO2 x 10 dL\/L (the 10 dL\/L corrects for the fact that CI is measured in L\/min\/m2 and oxygen content is measured in ml\/dl) = ~600 ml O2\/min.m2 VO2I = oxygen consumption index = volume of gaseous O2 consumed by the body per minute per meter squared BSA = volume of oxygen leaving the heart – volume of oxygen returning to the heart = [(CI x CaO2) – (CI x CvO2)] x 10dL\/L = CI x Ca-vO2 x 10 dL\/L = ~150 ml O2\/min.m2 Two oxygenation parameters characterize the relative balance between oxygen delivery and oxygen consumption (\u0093supply versus demand\u0094): the oxygen utilization coefficient (OUC) and the mixed venous oxygen saturation (SvO2). The OUC, also known as the oxygen extraction ratio or O2ER, is the percentage of delivered oxygen which is consumed by the body and is calculated as follows: OUC = Oxygen utilization coefficient = VO2I \/ DO2I = ~0.25 If the SaO2 is maintained at a relatively high level (> 0.92), the OUC can be approximated as: = 1- SvO2<\/p>\n <\/p>\nNunn Resp Physiology<\/h4>\n
<\/span>Deadspace Review<\/span><\/h2>\n
<\/span>Alveolar Ventilation for Oxygenation<\/span><\/h2>\n
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<\/a><\/p>\n<\/span>Deadspace<\/span><\/h2>\n
<\/span>What determines Venous Saturation<\/span><\/h2>\n
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<\/a><\/p>\n<\/span>Alveolar Ventilation for CO2<\/span><\/h2>\n
<\/span>Aa Gradient<\/span><\/h2>\n
<\/span>Hypoxemia<\/span><\/h2>\n
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<\/span>West Zones<\/span><\/h2>\n
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<\/a><\/p>\n<\/span>Hemoglobin Saturation Curve<\/span><\/h2>\n
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<\/a><\/p>\n<\/span>Oxygen Transport<\/span><\/h2>\n
<\/span>Oxygen carrying capacity of blood<\/span><\/h3>\n
<\/span>Oxygen Delivery to Tissues<\/span><\/h3>\n
<\/span>Oxygen Consumption by Tissues<\/span><\/h3>\n
<\/span>Is oxygen delivery adequate for the patient’s needs?<\/span><\/h2>\n
Measured<\/h4>\n
Calculated<\/h4>\n
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