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Interactions Article (Part I, Part II)
the effects of deadspace on CO2 are ameliorated by an increase in minute volume, unless pt can't spont breathe
~35-40% fiO2 will eliminate deadspace effects on O2
Alveolar deadspace in our patients is often caused by decreased lung perfusion
at decreased temperatures, CO2 becomes more soluble
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)
Apneic Oxygenation (Anesthesiology 1959;Nov/Dec:789)
Desaturation Time with Preox and Occluded Airway
Simulator of the effect of supp. oxygen on detecting hypoventilation
Mask adds 82 cc of deadspace compared to tube, even though it is actually 125 cc more space (BR J Anesth 1969;41:94)
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.
PaCO2=VCO2 (production) / (VE x (1- Vd/Vt)
VE=minute ventilation Vd=deadspace Vt=tidal volume
Bohr Equation Vd/Vt=(PaCO2-PetCO2)/PaCO2
Normal=0.2-0.4
Spontaneous breathing patients will breathe at a PaCO2 of 50; with preoxygenation, it is a PaCO2 of 60
In an apneic anesthetized patient the rate of CO2 rise
12 mmHg in the 1st minute
3.5 mmHg per minute thereafter
(Anesthesiology 1961;22:419, J Clin Anesth 1989;1:328)
Hypercapnea
VT=VA+VD (Alveolar/Deadspace)
PaCO2=PACO2 in normal lungs
Increased CO2 production (hypermetabolic states)
Decreased Alveolar ventilation/Increased deadspace ventilation
Decreased Tidal Volume
8+Age/5 is normal
Type I-hypoxemic, PaO2<60
Type II-hypercapneic w/wo hypoxemia, PaCO2>50
Mechanisms of Hypoxemia
Inadequate PAO2
Alveolar Hypoventilation
Decreased FiO2/Increased Altitude
V/Q Mismatch
Shunt (Will not improve with O2)
Intrapulmonary (Pneumonia, ARDS)
Intracardiac
Intravascular
Diffusion Abnormality
Low SvO2
PAO2=FiO2(PB-PH2O) - PaCO2/R
R=.8
Reabsorbtion atelectasis and loss of hypoxic pulmonary vasoconstriction may actually cause hypoxemia to get worse in the presence of high fiO2 and shunt.
article on the mechanisms of hypoxemia (intensive care medicine 2005;31:1017-1019)
Decreased PaO2 can actually lower respiratory drive in the critically ill, studies done in patients with cardiogenic shock.
Primary neurologic problems can result in decreased respiratory drive. these include AML, spinal cord injuries, guillain-barre, and muscular disorders.
Respiratory muscle fatigue from COPD/Asthma, ARDS, etc.
Increased production in sepsis, hypothermia, salicilates,
Increased deadspace ventilation
Hypercapnia can decrease respiratory drive.
shift to the right is right (good) i.e. more O2 released to cells
the first equation you need is the
CaO2=(Hb) x 1.38 x SaO2 + (0.003 x PaO2)
1.38 is the carrying capacity of a gram of Hb
normally 17-20 cc/dL
Note that >99% of the capacity is from Hb binding
DO2=CaO2 cc/dL x (CO L/min) x 10
10 is the conversion factor to convert L to dL
normally 950-1150 cc/min
DO2I=CaO2 x CI x 10
normally 550-650 cc/min/m2
Fick Equation
VO2=(CaO2-CvO2) x CO x 10 or
VO2=1.38 (Hb)(CO)(SaO2-SvO2)/10
normally 240-290 cc/min
VO2=oxygen consumed
DO2=Oxygen delivered
VO2/DO2 is normally 0.22-0.27 (0.25)
Rising VO2/DO2 ratio is a sign of inadequate tissue oxygenation
CvO2=(Hb) x 1.34 x SvO2 + 0.003 x PvO2
Normally 15 cc/dl
VO2I=(CaO2-CvO2) x CI x 10
Normally 115-165 cc/min/m2
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.
vasoregulation is an important factor that can not be measured.
Cirrhosis and sepsis look hemodynamically identical
capillary shunt
blood flowing past unventilated alveoli
atelectasis
pneumonia
ards
pulmonary edema
anatomic shunt
positive pressure may worsen
overventilation compresses blood vessels leading to increasing shunt and increasing deadspace
Ve=minute volume
Ve=Vd + Va
we compensate by increasing CO and increasing oxygen extraction
we can decrease extraction ratio to get venous sat of 40%
we can easily triple CO or up to 20 L/min
PaO2
PaCO2
SaO2 or SpO2
SvO2 (Mixed Venous)
Venous Oxygen Tension PvO2
Hb
CO
Pulmonary Capillary O2 Content (CcO2)
Arterial Oxygen Content (CaO2)
Venous Oxygen Conent (CvO2)
Arterial-venous oxygen content difference (Ca-vO2)
Oxygen utilization coefficient (OUC)
Oxygen Delivery Index (DO2I)
Oxygen Consumption Index (VO2I)
Intrapulmonary Shunt (Qsp/Qt)
Cardiac Index (CI)
Oxygen content=oxygen bound to Hb + oxygen dissolved in plasma
Oxygen bound=Hgb concentration x (1.34 cc oxygen per g Hb) x saturation of Hb
Oxygen dissolved=blood oxygen tension x (0.0031 solubility coefficient of oxygen in blood)
CcO2 = pulmonary end-capillary oxygen content
= oxygen bound to Hgb as it leaves the alveolus
= (1.34 x Hgb x 1.0) + (PAO2 x 0.0031)
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
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
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
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
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 (“supply versus demand”):
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
MIXED VENOUS OXIMETRY The SvO2, by providing a continuous “online” indication of the relative balance between VO2I and DO2I, can be used:
1) as an "early warning signal" to detect the onset of oxygen transport imbalance before clinical deterioration occurs
2) to evaluate the efficacy of therapeutic interventions such that physiologic end-points are reached more quickly
3) to identify potentially detrimental consequences of “patient care” (suctioning, positioning, etc.) that might otherwise go unnoticed It is essential to remember that the SvO2 is a "flow-weighted average" of the venous saturations from all perfused vascular beds. Thus, the SvO2 does not reflect the oxygen transport adequacy of non-perfused vascular beds nor does a “normal” SvO2 mean that all tissues are adequately oxygenated. It is only an average estimate of venous saturation for the whole body. It provides an impression of the overall balance between VO2I and DO2I, but does not yield information about the adequacy of perfusion of any individual vascular bed. If the SvO2 falls, VO2I is increasing (and may lead to anaerobic metabolism if DO2I is not sufficient) or DO2I is decreasing. If the SvO2 increases, VO2I is decreasing, DO2I is increasing, blood is being shunted pass vascular beds without releasing its oxygen (such as in sepsis or cirrhosis), or oxygen uptake by the tissues is decreased. There are four determinants of SvO2: Hgb, cardiac output, SaO2, and VO2I.
There are thus four main causes of low SvO2:
1) anemia,
2) low cardiac output,
3) arterial desaturation
4) increased VO2I.
In the presence of low SvO2, changes in these four parameters should be investigated. There are two common sources of error in venous oximetry measurements. The use of continuous venous oximetry relies on reflectance spectrophotometry technology. If the catheter is not properly calibrated via either an in vitro calibration prior to catheter insertion or an in vivo calibration via a mixed venous blood gas, the SvO2 values obtained may not accurately reflect the true oxygen transport balance. Careful attention should be given to catheter calibration to prevent such errors. The second source of error is catheter malposition. If the catheter tip is against the wall of the pulmonary artery, the light reflected back to the catheter will be amplified artificially increasing the SvO2 measurement. Proper catheter positioning is essential to obtaining reliable SvO2 values. Thus, SvO2, although not a specific indicator of the cause of hemodynamic and oxygen transport compromise, is a sensitive “online” monitor of the adequacy of balance between oxygen delivery and oxygen consumption accurately predicting potentially detrimental changes in patient status before they become clinically apparent. This allows appropriate therapeutic interventions to be initiated prior to the development of severe changes in a patient’s cardiorespiratory status.
FUNDAMENTAL QUESTIONS TO BE ANSWERED IN EVALUATING OXYGEN TRANSPORT
1) Is DO2I adequate for the patient's needs?
• DO2I should be at least 10mL/kg/min
• If inadequate, check the OUC; it should not exceed 0.35 as this suggests that oxygen supply is barely meeting oxygen demand
• Remember that SvO2 ≅ 1-OUC (for SaO2 > 0.92); this can be used as a rough approximation in assessing the adequacy of oxygen transport balance
• Ensure that the patient’s hemoglobin is appropriate for their degree of shock; consider transfusion of packed red blood cells if DO2I is inadequate When oxygen delivery (DO2I) exceeds oxygen demand, oxygen consumption will “plateau” and will no longer rise as oxygen delivery increases (Figure 3). This balance where DO2I meets the cellular needs of the body should be the goal in critical care. At the point where DO2I no longer meets oxygen demand (the so called “critical DO2”), oxygen consumption becomes “supply dependent”.
In this region of supply dependency, increases in DO2I result in increases in VO2I indicating that the body’s oxygen demands were not previously being met. DO2IVO2I"Supply Dependency""Critical DO2" Figure 3:
Oxygen Supply Dependency One of the most important determinants of tissue oxygen delivery is the arterial hemoglobin concentration. While oxygen delivery from the left ventricle is linearly related to the hemoglobin concentration, capillary flow may be impaired at extremely high hematocrits. The optimal hemoglobin concentration to maximize tissue oxygen delivery seems to be in the range of between 10 and 13 grams per deciliter. Whether or not transfusion to achieve these high hemoglobin levels improves outcome remains to be proven. Since loading oxygen on to the hemoglobin molecules is rarely a significant problem, attention must be turned to factors which will help unload oxygen from the hemoglobin at the tissue level. Judicious amounts of acidemia, hypercarbia, and fever all produce a right shift in the oxyhemoglobin association curve and may improve tissue unloading of oxygen (Figure 4). Figure 4: Oxyhemoglobin Dissociation Curve
2) Is cardiac output adequate for oxygen consumption?
• Check the Ca-vO2 If < 5 ml O2/dl blood, then cardiac output is sufficient to meet the body's demands for oxygen. If > 5 ml O2/dl blood, the body is extracting an abnormally high percentage of oxygen from the blood as it passes through the tissues and attempts to increase cardiac output (and therefore DO2I) should be undertaken.
• Check the heart rate and stroke volume Cardiac output is equal to the sum of all of the stroke volumes produced each minute. Very high heart rates may reduce diastolic time and ventricular filling, thereby impairing stroke volume. While the optimal heart rate is unknown, heart rates < 80 or > 120 beats per minute are probably not optimal in critically ill adult patients. Patients with such high heart rates may benefit from fluid resuscitation, beta-blockade, or correction of abnormal cardiac rhythms (such as atrial fibrillation) that can reduce diastolic filling time. Stroke volume should also be optimized through fluid resuscitation.
3) Is oxygen consumption adequate for demand?
• Check a lactic acid level If > 2.5 mmol/L, lactic acid
is being produced secondary to anaerobic metabolism (an imbalance between oxygen
supply and demand) and attempts to increase cardiac output and DO2I should be
undertaken. If the lactic acid level is high and SvO2 is normal, the
elevation in lactic acid is probably due to a previous episode of anaerobic
metabolism and oxygen debt.
6 Revised 7/9/02
If the lactic acid level is high and SvO2 is low, anaerobic metabolism is
likely still occurring and must be treated aggressively.
4) Is the patient's hypoxemia due to a pulmonary problem (i.e., increased intrapulmonary shunt) OR to a low flow state (i.e., low Ca-vO2)?
• Calculate the patient's intrapulmonary shunt (Qsp/Qt) INTRAPULMONARY SHUNT “Intrapulmonary shunt" (or "venous admixture") refers to blood which does not pass through ventilated portions of the lung and leaves the lungs desaturated resulting in a depressed PaO2.
In the normal lung, there are three potential sources of shunt:
1) bronchial artery blood which enters the pulmonary veins after giving up some of its oxygen to the bronchi
2) desaturated blood which enters the left ventricle via the Thebesian veins after perfusing the myocardium
3) normal alveolar collapse in the apices of the lungs (West’s Zone I lung)
Normal intrapulmonary shunt is 2-5%. It may exceed 50% in patients with severe acute respiratory distress syndrome (ARDS).
Intrapulmonary shunt is an example of an "oxygen refractory" hypoxia: the shunted blood is not exposed to ventilated alveoli and cannot be saturated with oxygen regardless of the oxygen fraction administered.
It is calculated automatically by the bedside monitors. The ventilation-perfusion index or “VQI” on the Edwards Explorer and Vigilance monitors is an “online” approximation of Qsp/Qt which provides a minute-to-minute estimate of the degree of intrapulmonary shunt. The derivation of the shunt equation is included below.
Qt = total cardiac output Qs = shunted portion of cardiac output Qns = normal pulmonary end-capillary blood flow that is not shunted past abnormal alveoli
Qt = Qs + Qns or Qns = Qt - Qs Qt (CaO2) = total oxygen delivered to the body (DO2) Qs (CvO2) = oxygen content of shunted blood Qns (CcO2) = oxygen content of end-capillary blood Therefore, [Total oxygen delivered equals the sum of oxygen in both shunted and non-shunted blood] Qt (CaO2) = Qs (CvO2) + Qns (CcO2) Qt (CaO2) = Qs (CvO2) + (Qt - Qs)(CcO2) [Substituting (Qt - Qs) for Qns] Qt (CaO2) = Qs (CvO2) + Qt (CcO2) - Qs (CcO2) Qs (CcO2 - CvO2) = Qt (CcO2 - CaO2) Qs/Qt = CcO2 - CaO2 [The intrapulmonary shunt equation] CcO2 - CvO2
Microcirculation
(Curr Opin Crit Care 2005;11:240)
Vasodilators in Septic Shock (Inten Care Med 2002;28:1208)
vessels <300 um
Central Venous-Arterial CO2 difference can be used to calculate cardiac index (Inten Care Med 2005;31:818)
CO can also be calculated with glucose clearance (inten care med 2004;30:2067)
Occult hypoperfusion, as evidenced by increased lactate, is associated with increased mortality in hemodynamically stable surg patients (Crit Care 2004;8(2):R60)
arteries and veins are compliant with downstream resistive elements
veins are collapsible when right atrial pressure is less than zero
venous return regulates cardiac output
Compensation for Anemia
shunt causes hypercapnea and by measurement, an increase in physiological deadspace
you don't really see an increase in co2 until shunt % greater than 30
IPAP causes benefits of NIV in asthma, EPAP is the worst (Crit Care 2004;8(2):R72)
CPAP is better for dynamics than EPAP (Anesth 1981;55:416)
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