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Getting more out of blood gas


Evolution of Blood Gas Analysis -
Focusing on the Source of Impaired O2
Supply to the Tissue
Ellis Jacobs, Ph.D, DABCC, FACB Associate Professor of Pathology, NYU School of Medicine Director of Pathology, Coler-Goldwater Hospital and Nursing  Why measure blood gases  Overview of acid-base disturbances  Use of the Acid- Base Chart  Full value of the pO2 assessment via  Oxygen uptake, Oxygen transport, Oxygen release  Why a measured saturation is the best  Assessment of tissue perfusion - Lactate The traditional picture  Traditionally, pO been the sole parameter used for evaluation of patient transport
oxygenation
The traditional picture  Traditionally, pO been the sole parameter used for evaluation of patient transport
 For a complete evaluation of the oxygen status, it is necessary to consider lactate and all parameters involved in oxygen uptake, transport, oxygenation




Example of a flowchart [Adapted from different textbooks and Siggaard-Andersen, O et al. Oxygen status of arterial and mixed venous blood. Crit Care Med. 1995 Jul;23(7):1284-93.


Phase one: Oxygen uptake


pO2(a) – the key parameter  pO2(a) is the key parameter for evaluation of oxygen uptake in the lung  When the pO2(a) is low, the supply of oxygen to cells might be compromised Conditions affecting pO2(a)  The amount of oxygen FO2(I) available
 The degree of intra- and extrapulmonary shunting FShunt
 Hypercapnia, high blood pCO2
 The ambient pressure p(amp)


FO2(I) – fraction of inspired oxygen  Oxygen diffuses from the alveoli into the blood  The higher the oxygen content of the air, the higher pO2(a)  Breathing room air equals an FO2(I) of 21 %  A patient breathing supplemental oxygen may have a pO2(a) as high as 400 mmHg (and the oxygen saturation is normal) Evaluation of PO2 in Adult, Neonatal, and Geriatric Patients Breathing Room Air Arterial PO2 (mmHg) Condition above 80 Normal for adult (< 60 y) above 70 Adequate for age > 70 y above 60 Adequate for age > 80 y Normal neonatal at 5 min Normal neonatal at 1-5 40 to 60/70/80 Moderate to mild hypoxemia Severe hypoxemia Evaluating Arterial Oxygenation in Patients Breathing Lowest FI-O2 (%) Acceptable PO2 (mmHg) 30 150 40 200 50 250 80 400 100 500 Patients with a lower PO may be assumed to be hypoxic on room
Estimated FI-O2 of Air When Breathing 100% Oxygen from Nasal Cannula For each L/min of oxygen flow, add 4% to the estimated FI-O of air in the room, usually 21%. Example: What is the estimated FIO of the air being inhaled by a person receiving 2 L/min oxygen from a nasal cannula? Goals of Oxygen Therapy Treat hypoxemia Decrease work of breathing  Hyperventilation typical response to Decrease myocardial work  Increased cardiac output is a mechanism to compensate for hypoxemia. FShunt is the fraction of venous blood not oxygenated when passing the pulmonary capillaries Examples of different types of shunt Intrapulmonary respiratory Intrapulmonary circulatory • By some called true shunt • Also called ventilation- • Incomplete oxygenation in • Heart defects allowing perfusion disturbance venous blood from left • Incomplete oxygenation in • Insufficient blood perfusion chamber of heart to enter • Lung diseases with inflammation or edema that causes the membranes to


FShunt – measured vs calculated  Shunt is calculated with values from simultaneously drawn arterial and mixed venous  The mixed venous sample must be drawn from the pulmonary artery, as indicated in the  A simpler and faster way to estimate FShunt is from a single  Assuming that the arterio-venous difference is normal, i.e. extraction of 5.1 mL O2 per dL Hypercapnia, high pCO2  Strong hypercapnia significantly decreases alveolar pO2, a condition known as hypoventilatory hypoxemia  The hypoxemia develops because the alveolar gas equation dictates a fall in pO2(a); pO2(A) = pO2(air) – pCO2(A)/RQ  At any given barometric pressure, any increase in alveolar pCO2 (caused by hypoventilation) leads to a fall in alveolar pO2 and therefore also in arterial pO2 Oxygen uptake – a recap  The amount of oxygen FO2(I) available
 The degree of intra- and extrapulmonary shunting FShunt
 Hypercapnia, high blood pCO2
 The ambient pressure p(amp)

Phase two: Oxygen transport ctO2 – the key parameter  Oxygen content, ctO2 is the key parameter for evaluating the capacity for oxygen  When ctO2 is low, the oxygen delivery to the tissue cells may be compromised Does ctO2/pO2 correlate?  A multicenter study on 10079 blood samples [1]  ctO2/pO2 correlation  ctO2 is almost independent of pO2, so full information is needed  E.g. pO2 of 60 mmHg (8 kPa ) corresponds to a ctO2 of 4.8 – 24.2 mL/dL [1] Gøthgen IH et al. Variations in the hemoglobin-oxygen dissociation curve in 10079 arterial blood samples. Scand J Clin Lab Invest 1990; 50, Suppl. 203:87-90  The blood's oxygen content, ctO2, is the sum of  Oxygen bound to hemoglobin and  Physically dissolved oxygen  98% of oxygen is carried by hemoglobin  The remaining 2% is dissolved in a gas form  ctO normal range 18.8-22.3 mL/dL ctO = sO × ctHb × (1 – FCOHb – FMetHb) + αO × pO α is the solubility coefficient of oxygen in blood Conditions affecting ctO2  The concentration of hemoglobin ctHb
 The fraction of oxygenated hemoglobin FO2Hb
 The arterial oxygen saturation sO2
 The presence of dyshemoglobins FCOHb and FMetHb
Improving ctO2  The oxygen content can be improved by the variable factors in the equation ctO = sO × ctHb × (1 – FCOHb – FMetHb) + αO × pO Types of hemoglobin Total hemoglobin Reduced hemoglobin Carboxyhemoglobin  tHb is defined as the sum of HHb+O2Hb+COHb+MetHb  COHb and MetHb are called dyshemoglobins because they are incapable of oxygen  Hemoglobin consists of 4 identical subunits  Each subunit contains an  Each iron can bind to one oxygen molecule, O2  Oxygen binding is  Typical reference range is Carboxyhemoglobin  Causes of raised COHb:  Increased endogeneous production of CO  Breathing air polluted with CO (carbon-monooixde  CO's affinity to Hb is 210 times higher than that of O2  The blood turns cherry-red, but is not always evident  COHb is normally less than 1-2 % but in heavy smokers up to 10 % Endogeneous increase in COHb  Hemolytic condition leads to heme catabolism and thus increased production of CO [1]  Hemolysis induced increase in COHb can be up to 4 % but 8.3 % is also reported [2]  Slight increase in COHb is also a feature of a inflammatory disease, and is thus also seen in critically ill [1] Higgins C. Causes and clinical significance of increased carboxyheomoglobin. www.acutecaretesting.org . Oct 2005. [2] Necheles T, Rai U, Valaes T. The role of hemolysis in neonatal hyperbilirubinemia as reflected in carboxyhemoglobin values. Acta Paediatr Scand. 1976; 65: 361-67 [3] Morimatsu H, Takahashi T, Maeshima K et al. Increased heme catabolism in critically ill patients: Correlation among exhaled carbon monoxide, arterial carboxyhemoglobin and serum bilirubin IX {alpha} concentrations. Am J Physiol Lung Cell Mol Physiol. (EPub) 2005 Aug 12th doi:/0.1152/ajplung.00031.2005 COHb intoxication  COHb intoxication may be deliberate or accidential  In the US is accounts for 40,000 ED visits and between 5 and 6,000 death a year (2004) [1]  Sources of CO – common [2]  Fire, motor-vehicle exhaust and faulty domestic heating  Less commonly, gas ovens, paraffin (kerosene) heaters and even charcoal briquettes [1] Kao L. Nanagas K. Carbon monoxide poisoning. Emerg Clin N Amer 2004; 22: 985-1018 [2] Higgins C. Causes and clinical significance of increased carboxyheomoglobin. www.acutecaretesting.org . Oct 2005. Relationship COHb CO conc. in
inspired air
in blood %
Examples of typical symptoms
No appreciable effect except shortness of breath on vigorous exertion, possible tightness across forehead Shortness of breath on moderate exertion, occasional headache Headache, easily fatigued, judgement disturbed, dizziness, dimness of vision Headache, confusion, fainting, collapse Unconsciousness, convulsions, respiratory failure, death if exposure continues Immediately fatal [1] Higgins C. Causes and clinical significance of increased carboxyheomoglobin. www.acutecaretesting.org . Oct 2005. Clinical cases - Carboxyhemoglobin Read three interesting case stories in "Causes and clinical significance of increased carboxyheomoglobin" by Chris Higgins on www.acutecaretesting.org  Methemoglobin is formed when blood is exposed to oxidizing agents, oxidizing the iron atom: Fe2+ ⇒ Fe3+  MetHb has a very low  The blood typically turns Causes for increased methemoglobin  Inherited – very seldom  Acquired – more frequent  Acquired methemoglobinemia occurs when hemoglobin is oxidized in a rate faster by which methemopglobin is  Drugs or toxins that may cause methemoglobinemia  Acetanilide, p-aminosalicylic acid, amyl nitrate, aniline, benzocaine, cetacaine, chloroquinone, clorfazimine, dapsone, hydroxylamine, isobutyl nitrite, lidocaine, mafenide acetate, menadione, metoclopramide, naphthoquinone, nitric oxide, nitrobezene, nitroethane, nitrofurane, nitroglycerin, nitroprusside, paraquat, phenacitin, phenazopyridine, prilocaine, primaquine, resorcinol, silver nitrate, sodium nitrate, sodium nitrite, sodium valproate, sulphonamide anitibiotics, trinitrotoluene [1] Higgins C. Methemoglobin. www.acutecaretesting.org . Oct 2006. in blood %
Examples of typical symptoms
Is typically well tolerated and, in an otherwise healthy individual, is asymptomatic Typically first sign of tissue hypoxia is cyanosis with skin taking on a classically blue/slate gray appearance. Symptoms: more profound hypoxia, including increased heart rate, headache, dizziness and anxiety, accompany deepening cyanosis as methemoglobin rises above 20 %. May be associated with increasing breathlessness and fatigue. Confusion, drowsiness and coma Methemoglobin Symptoms of methemoglobinemia are generally more severe in a patient who has some pre-existing condition (e.g. anemia, respiratory or cardiovascular disease) that compromises oxygenation of tissues. [1] Higgins C. Methemoglobin. www.acutecaretesting.org . Oct 2006. Clinical cases - Methemoglobin Read three interesting case stories in "Methemoglobin" by Chris Higgins on www.acutecaretesting.org  A 84-year-old man had undergone a left hemicolectomy for bowel torsion. After 10 days he became hypotensive, tachypneic, oliguric, progressively acidotic, and anemic. Also, the patient had passed bloody stools  ctO normal range: 18.8-22.3 mL/dL 1) With a FO (I) of 0.6 a blood 2) After bicarbonate and blood had been administered i.v. – pH = 7.25 pCO = 29 mmHg – pCO2 = 24 mmHg – pO = 169 mmHg – pO2 = 169 mmHg – ctHb = 4.2 g/dL
ctHb = 7.8 g/dL
sO = 98 % – sO2 = 98 % – ctO = 6.08 mL/dL
ctO2 = 10.8 mL/dL
This case is not a real life case – it is made for illustration purposes only Oxygen transport – a recap  The concentration of hemoglobin ctHb
 The fraction of oxygenated hemoglobin FO2Hb
 The arterial oxygen saturation sO2
 The presence of dyshemoglobins FCOHb and FMetHb
Phase three: Oxygen release Conditions affecting release  Oxygen release depends  The arterial and end- capillary oxygen tensions  The hemoglobin-oxygen affinity expressed by the p50 value  p50 is the key parameter for evaluation of oxygen release from hemoglobin Conditions affecting p50  The hemoglobin-oxygen affinity is expressed by the oxygen dissociation curve (ODC), the position of which is expressed by the p50 value
 As illustrated in the flowchart, several conditions can affect the p50 value p50 and the ODC curve The p50 is the oxygen tension at half saturation (sO2 = 50 %) and reflects the affinity of hemoglobin for oxygen Different factors affect the position of the ODC, and p50 express the position of the Typical reference range: 25-29 mmHg Conditions affecting position of ODC Can p50 be read from the ODC curve? [1] If sO2 = 90 % then pO2 = 29-137 mmHg (4–18 kPa) If pO2 = 60 mmHg (8 kPa) then sO2 Conclusion: Need information about p50 via measurement of the factors affecting ODC (MetHb, COHb etc) [1] Gøthgen IH et al. Variations in the hemoglobin-oxygen dissociation curve in 10079 arterial blood samples. Scand J Clin Lab Invest 1990; 50, Suppl. 203:87-90 Oxygen release – a recap  The hemoglobin-oxygen affinity is expressed by the oxygen dissociation curve (ODC), the position of which is expressed by the p50 value
 As illustrated in the flowchart, several conditions can affect the p50 value Some cases using the Flowchart  75-year-old woman  Suffering from anemia, probably due to an ulcer  What to do?  Some of the results from the lab showed pH = 7.40 (7.35-7.45) sO = 97 % (95-99) pCO = 40 mmHg (35-48) FMetHb =0.005 (.002-.008) pO = 98 mmHg (83-108) FCOHb =0.005 (0.0 – 0.008) FO (I) = 0.21 ctHb = 9.0 g/dL (12.0-17.5) p50 = 25.5 mmHg (24-28) ctO = 8.8 mg/dL (18.8-22.3) This case is not a real life case – it is made for illustration purposes only pO 98 mmHg
ctO 8.8 mg/dL
p50 25.5 mmHg
ctHb 9.0 g/dL
No DysHb

True anemia
This case is not a real life case – it is made for illustration purposes only  40-year-old man  Exposed to smoke from a fire  Some of the test results showed pH = 7.400 (7.35-7.45) sO = 97 % (95-99) pCO = 40 mmHg (35-48) FMetHb =0.005 (0.002-0.008) pO = 98 mmHg (83-108) FCOHb =0.300 (0.0-0.008) FO (I) = 0.21 ctHb = 14.5 g/dL (12.0-17.5) p50 = 26.3 mmHg (24-28) ctO = 16.6 mL/dL (18.8-22.2) This case is not a real life case – it is made for illustration purposes only pO 98 mmHg
ctO 16.6 mg/dL
p50 26.3 mmHg
ctHb 14.5 g/dL
COHb 30%

CO poisoning
This case is not a real life case – it is made for illustration purposes only  15-year-old boy  Severe asthmatic attack  Some of the test results showed pH = 7.350 (7.35-7.45) sO = 80 % (95-99) pCO = 35 mmHg (35-48) FMetHb =0.005 (0.002-0.008) pO = 60 mmHg (83-108) FCOHb =0.005 (0.0-0.008) FO (I) = 0.21 ctHb = 14.5 g/dL (12.0-17.5) p50 = 37 mmHg (24-28) ctO = 15.8 mL/dL (18.8-22.3) This case is not a real life case – it is made for illustration purposes only pO 60 mmHg
ctO 15.8 mg/dL
p50 37 mmHg
pCO 35 mmHg
This case is not a real life case – it is made for illustration purposes only Oxygen saturation, sO2 cO Hb + cHHb  sO2 is defined as  The percentage of oxygenated hemoglobin in relation to the amount of hemoglobin capable of carrying oxygen  Typical reference interval 95-99 %  High sO2:  Indicates that there is sufficient utilization of actual oxygen transport capacity  Low sO2:  Indicates that the patient can likely benefit from supplemental  No information about tHb, COHb, MetHb, ventilation or O2-release to tissue 3 different ways to get sO2 1. BG analyzer with CO-OX:
 Measured by the CO-oximeter  Golden standard 2. BG analyzer without CO-OX:
cO Hb + cHHb  Calculated from a pO2(a) via the ODC curve 3. Pulse oximeters BGA without CO-OX  CALCULATED sO2 dependents on  Available information (parameters)  Algorithm applied by manufacturer Correlation of pO2 and sO2 in real life [1]  If sO2 = 90% then pO2 = 29-137 mmHg (4 – 18 kPa)  If pO2 = 60 mmHg (8 kPa) then sO2 = 70-99%  At pO2 = 45 mmHg (6 kPa) and  pH = 7.25, then sO2 = 80 %  pH = 7.40, then sO2 = 88 % [1] Gøthgen IH, Siggaard-Andersen O, Kokholm G. "Variations in the hemoglobin-oxygen dissociation curve in 10079 arterial blood samples" By. Scand J Clin Lab Invest 1990; 50, Suppl. 203:87-90 Why measured over calculated sO2  Several studies are supporting the importance of using a measured sO2 and not calculated  CLSI [1]: "Clinically significant errors can result from incorporation of such an estimated value for sO2 in further calculations such as shunt fraction"  Breuer [2]: "No calculation mode can be performed with constant accuracy and reliability when covering a wide range of acid-base values. If sO2 values are used for further calculations, e.g. for determination of cardiac output, measured values are preferred" [1] Blood gas and pH analysis and related measurements: Approved Guidelines, National Committee for Clinical Laboratory Standards C46-A2, 29; 2009 [2] Breuer HWM et al. Oxygen saturation calculation procedures: a critical analysis os six equations or the determination of oxygen saturation. Intensive Care Med 1989; 15: 385-89 A reliable sO2 (and pO2) matters Hypoxemia - severe
Hypoxemia –moderate
Hypoxemia - mild
Normoxemia
10.6 kPa/80 mmHg Normoxemia
13.3 kPa/100 mmHg Hyperoxemia
16.0 kPa/120 mmHg Hyperoxemia - marked
20.0kPa/150 mmHg  SpO2  Reflects the utilization of the current oxygen transport  Continuous monitoring  Noninvasive method  Easy and convenient  37 out of 42 pulse oximeters companies reported best analytical performance as 1SD of +/- 2 % [1, 2] [1] From as accessed September 2010, [2 as accessed in 2007 Pulse oximeters in the ICU  Reputation: 90'ies studies conclude like these:  "We conclude that the accuracy of the tested nine pulse oximeters does not enable precise absolute measurements, specially at lower oxygen saturation ranges" [1] "Infants with acute cardiorespiratory problems, pulse oximetry unreliably reflects pO2(a), but may be useful in detecting clinical deterioration [2]  A 2010 publication [3]  "The accuracy of pulse oximetry to estimate arterial oxygen saturation in critically ill patients has yielded mixed results. Both the degree of inaccuracy, or bias, and its direction has been inconsistent"…"analysis demonstrated that hypoxemia (sO2(a) < 90) significantly affected pulse oximeter accuracy. The mean difference was 4.9 % in hypoxemic patients and 1.89 % in non-hypoxemic patients (p < 0.004). In 50 % (11/22) of cases in which SpO2 was in the 90-93 % range the sO2(a) was <90 % ".  A 2012 publication [4]  "Despite its accepted utility, it is not a substitute for arterial blood gas monitoring as it provides no information about the ventilatory status and has several other limitations". [1] Würtembe rger G. Accuracy of nine commercially available pulse oximeters in monitoring patients with chronic respiratory insifficiency. Monaldi Arch Chest Dis 1994; 49: 348-353 [2] Walsh, M. Relationship of pulse oximetry to arterial oxygen tension in infants. Crit Care Med 15; 12: 1102-05. [3] Wilson et al. The accuracy of pulse oximetry in emergency department patients with severe sepsis and septic shock: a retrospective cohort study. BMC Emergency Medicine 2010; 10:9 [4] Kipnis, E et al. Monitoring in the Intensive Care . Critical Care Research and Practice, Volume 2012, Article ID 473507, doi:10.1155/2012/473507 Oxygen saturation - Summary  GOLDEN STANDARD is the oxygen saturation measured by the CO-oximeter analysis  Other oxygen saturation methods have various  Oxygen saturation does not give information on oxygen delivery, ventilation, etc. Does the oxygen get to the tissue?  Lactate is a waste product from anaerobic metabolism  Takes place when there is insufficient oxygen delivery to  Thus lactate is an early sensitive indicator imbalance between tissue oxygen demand and oxygen supply Aerobic metabolism Anaerobic metabolism Lactate is used….  ……as a tool for  Diagnostically, admitting and triaging patients  As a marker of tissue hypoperfusion in patients with circulatory shock  As an index of adequacy of resuscitation after shock  As a marker for monitoring resuscitation therapies  Prognostically, as a prognostic indicator for patient From: Bakker J. Increased blood lactate levels: a marker of.? When to measure lactate?  When there are signs and symptoms such as  Rapid breathing, nausea, hypotension, hypovolemia and sweating that suggest the possibility of reduced tissue oxygenation or an acid/base imbalance  Suspicion of inherited metabolic or mitochondrial disorder. Data shows that….  Lactic acidosis  Occurs in approximately 1% of hospital admissions[1].  Has a mortality rate greater than 60% and approaches 100% if hypotension also is present [1].  Elevated lactate  Have been demonstrated to be associated with mortality in both emergency departments and hospitalized patients [2, [1] Burtis CA, Ashwood ER, Bruns DE. In: Tietz textbook of Clinical Chemistry and molecular diagnostics, 5th edition. St. Louis: Saunders [2] Dellinger RP, Levy MM, Rhodes A et al. Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2012. Crit Care Med, 2012; 41: 580-637 [3] Shapiro NI, Howell MD, Talmor D et al. Serum lactate as a predictor of mortality in emergency department patients with infection. Ann Emerg Med, 2005; 45; 524-528. [4] Trzeciak S, Dellinger RP, Chansky ME et al. Serum lactate as a predictor of mortality in patients with infection. Intensive Care Med, 2007; 33; 970-977. [5] Mikkelsen ME, Miltiades AN, Gaieski DF et al. Serum lactate is associated with mortality in severe sepsis independent of organ failure and stock. Crit Care Med. 2009; 37; 1670-1677 Surviving sepsis  The surviving sepsis campaign care bundle recommends, among others, to measure lactate within 3 hours of  If lactate is elevated a second lactate measure could be completed within 6 hours [1]. www.survivingsepsis.org [1] Dellinger RP, Levy MM, Rhodes A et al. Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2012. Crit Care Med, 2012; 41: 580-637 Hyperlactatemia and lactic acidosis  Hyperlactatemia:  Is typically defined as a lactate >2.0 mmol/L  Occurs when the rate of lactate release from peripheral tissue exceeds the rate of lactate removal by liver and  Lactic acidosis  If lactate is > 3-4mmol/L there is increasing risk of associated acidosis  The combination of hyperlactatemia and acidosis is called lactic acidosis, which is a disruption of acid/base balance. Lactic acidosis A and B  Type A (hypoxic)  Inadequate oxygen uptake in the lungs and/or to reduced blood flow resulting in decreased transport of oxygen  E.g.: Shock from blood loss/sepsis, myocardial, infarction/cardiac arrest, congestive heart failure, pulmonary edema, severe anemia, severe hypoxemia , carbon monoxide poisoning  Type B (metabolic)  Conditions that increase the amount of lactate in the blood but are not related to a decreased availability of oxygen  E.g.: Liver disease, Kidney disease, Diabetic ketoacidosis (DKA), Leukemia, HIV, glycogen storage diseases ( like glucose-6- phosphatase deficiency), server infections – both systemic sepsis and meningitis, strenuous exercise  Drugs and toxins typically represent the most common cause of type B lactic acidosis Lactic acidosis and pH  No universal agreement for definition of lactic acidosis [1]  Lactic acidosis is the most common cause of metabolic  Lactic acidosis may not necessarily produce acidemia in a patient as it depends on [1]  Magnitude of hyperlactatemia  Buffering capacity of the body  Coexistence of other conditions that produce tachypnea and alkalosis (eg, liver disease, sepsis).  Thus, hyperlactatemia or lactic acidosis may be associated with acidemia, a normal pH, or alkalemia [1] [1] Acutecaretesting Handbook 2013 – Radiometer Medical - in press [2] Cassaletto J. Differential diagnosis of metabolic acidosis. Emerg Med Clin N Amer, 2005; 23: 771-87. Lactate and oxygen uptake, transport and release [1] [1] Adapted from different textbooks and Siggaard-Andersen, O et al. Oxygen status of arterial and mixed venous blood. Crit Care Med. 1995 Jul;23(7):1284-93. Examples of reference
interval
Short summary
Indicates the acidity or alkalinity of blood. pH is the indispensable measure of acidemia or alkalemia. M 35–48 (4.7-6.4) pCO2 is the carbon dioxide partial pressure in blood. pCO2(a) is a reflection of the F 32–45 (4.3–6.0) adequacy of alveolar ventilation in relation to the metabolic state. 3 is standardized with the aim to eliminate effects of the respiratory component on the HCO3 . HCO3 is classified as the metabolic component of acid- BE predicts the quantity of acid or alkali to return the plasma in vivo to a normal pH under standard conditions. BE may help determine whether an acid/base disturbance is a respiratory, metabolic for mixed metabolic/respiratory problem Base(Ecf) is independent from changes on pCO2 and is also called "in-vivo base excess" or "standard base excess" (SBE). pO2 is the oxygen partial pressure in blood. The pO2(a) is an indicator of the oxygen uptake in the lungs. sO2(a) is the percentage of oxygenated hemoglobin in relation to the amount of hemoglobin capable of carrying oxygen and indicates if there is sufficient utilization of actual oxygen transport capacity. M 13.5-17.5 (8.4–10.9) tHb is defined as the sum of HHb+O2Hb+COHb+MetHb. tHb is a measure of the F 12.0-16.0 (7.4–9.9) potential oxygen-carrying capacity. ctO2 is the blood's oxygen content and is the sum of oxygen bound to hemoglobin and physically dissolved oxygen. ctO2 reflects the integrated effects of changes in the arterial pO2, the effective hemoglobin concentration and the hemoglobin 24–29 (3.2-3.9) p50 is the oxygen tension at half saturation and reflects the affinity of hemoglobin MetHb is formed when blood is exposed to certain oxidizing agents. MetHb has a very low affinity to O2 resulting in decreased oxygen-carrying capacity. COHb is primarily formed when breathing air polluted with CO. COHb is not capable of transporting oxygen. 4.5–14.4 (0.5-1.6) Lactate is a waste product from anaerobic metabolism. Lactate is an early sensitive indicator imbalance between tissue oxygen demand and oxygen supply.  Sources for Scientific knowledge about acute care testing Avoid preanalytical errors app - for smartphones and tablets - for smartphones

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LIVING WELL WITH DEMENTIA IN LEEDS Our local strategy First published draft, June 25th 2012 Open for comment to 30th September 2012 Our vision, values and approach The Dementia Journey - diagram The views of people with dementia, families and carers Dementia-friendly Leeds Prevention and research Early detection and diagnosis

Microsoft word - arztinfo.doc

Der transjuguläre intrahepatische portosystemische Shunt Informationen für den Arzt Stand: Juni 2005 Die pathophysiologisch bedeutsamste Folge der Leberzirrhose ist die Erhöhung des beim Gesunden 3-6 mm Hg messenden Pfortaderdruckes. Steigt dieser auf über 12-15 mmHg an, können Komplikationen der portalen Hypertension auftreten, zu denen die Varizenblutung