PEPconnect

General Laboratory: Blood Gas: Clinical Significance Online Training

Key components of emergency diagnostic procedures include tests that allow physicians to evaluate a patient’s acid-base metabolism, oxygen status, electrolyte and metabolic functions.

Describe acid-base and oxygen status disorders Identify and describe blood gas analysis tests that assess acid-base metabolism and oxygen status Identify and describe cardiac marker tests Identify and describe rapid analysis tests that assess electrolyte and metabolic functions Welcome to the Blood Gas and Rapid Analysis Tests: Clinical Significance online training course. After completing this course, you’ll be able to: Select Next to continue. Tests that help physicians assess acid-base metabolism include the following measured parameters: pH pCO2 Most blood gas analytical systems also calculate certain parameters directly without any "other requirements." These include: HCO3- Total CO2 (tCO2 or ctCO2) Base Excess (BE) or Base Deviation (BA) CO2 - Bonding Capacity   Acid-Base Metabolism Tests Learn the purpose and clinical significance of these tests. Select the tabs below to learn the purpose and clinical significance of Acid-Base Metabolism tests.TitleTextpHTab TitleTextPurpose The term pH describes the hydrogen ion activity of a solution as a negative decadic logarithm of the hydrogen ion concentration (pH = - log H+). Cellular metabolism requires an environment in which the hydrogen ion concentration is within narrow limits. The lungs and kidneys are responsible for regulating the balance. The kidneys regulate the bicarbonate buffer and as a result, 75% of the total buffer capacity. One bicarbonate ion remains in the body for each H+ ion eliminated by the kidneys. This mechanism is not earmarked for rapid reactions. Respiration affects the CO2 concentration. If the pH drops, the CO2 concentration increases. If the pH increases, the CO2 concentration drops. The respiration reacts to changes in the H+ ion concentration within several minutes.    Clinical Significance Extracellular pH closely correlates with intracellular. Therefore, it is particularly important with respect to the intracellular acid-base status. It is used to record acid-base disorders as a result of serious pathological causes such as: Impaired respiratory function Renal or gastrointestinal insufficiency    Reference Range Normal: 7.37 to 7.45 Abnormal: below 7.1 life-threatening acidosis 7.1 – 7.3 serious decompensated acidosis 7.3 – 7.36 and 7.46 – 7.5 minor deviations which require further evaluation 7.5 – 7.6 serious decompensated alkalosis above 7.6 life-threatening alkalosis    Interpreting Results Elevated values: Respiratory alkalosis Alveolar hyperventilation Metabolic alkalosis         •  Gastrointestinal acid loss         •  Often with concomitant hypokalemia  Decreased values: Respiratory acidosis         •  Alveolar hypoventilation         •  Elevated metabolism Metabolic acidosis         •  Often with concomitant hyperkalemia         •  Renal failure         •  Diabetes or alcohol-induced acidosis pancreatic or biliary fistula, diarrhea   pCO2Tab TitleTextPurpose Partial carbon dioxide pressure (pCO2) mainly depends on the pulmonary function and the associated elimination of CO2. Carbon dioxide (CO2) is a metabolic product and is absorbed into the blood to be transported to the kidneys and lungs. CO2 is transported in the blood as: Bicarbonate (HCO3 -) Dissolved CO2 Carbonic acid (H2CO3 -) CO2 is present in the blood in a dynamic state.  Clinical Significance Changes in pCO2 indicate a change in respiratory status. Combining the pCO2 measurement with the pH measurement allows you to determine the bicarbonate (HCO3 -) value by means of the Henderson-Hasselbalch equation. Because the pCO2 value is proportional to the content of dissolved CO2/HCO3 - (the proportionality constant is 0.03), the pCO2 value in combination with the pH can also be useful for the differentiation of acid-base disorders.    Reference Range Normal: 35 – 46 mmHg (4.7 – 6.1 kPa)  Abnormal: 30 – 50 mmHg (4.0 – 6.7 kPa). Primarily caused deviations within this range are deemed minor, but require further evaluation. <25 mmHg/above 60 mmHg (< 3.3/> 8.0 kPa). Acute and therefore not yet renally compensated pCO2 deviations extending into these ranges are life-threatening. Note: The conventional unit mmHg is generally used instead of the S.I. unit Pascal in medicine. The conversion factors are as follows: 1 mmHg = 133.3 Pa.  1 Pascal = 7.5 x 103 mmHg.  Normal pCO2 levels are 35 - 45mmHg. Below 35 is alkalotic, above 45 is acidic.    Interpreting Results Elevated values: Sign of poor gas exchange in the lungs Decreased values: Sign for overly fast or deep respiration Compensated metabolic acidosis   HCO3Tab TitleTextPurpose Bicarbonate ion (HCO3 -) is the main buffer substance in the body and plays a key role in maintaining the pH value in blood. Due to the dynamic CO2 balance, it is available in the blood in large quantities. CO2 is transported in the blood as bicarbonate (HCO3 -), dissolved CO2 and carbonic acid (H2CO3).   The equation emphasizes the relationship between HCO3 - and pH: If HCO3 - increases, the pH value increases If HCO3 - decreases, the pH decreases    Clinical Significance The kidneys are the main organs that control the bicarbonate ion. HCO3 - concentration is clinically significant for the determination of the non-respiratory, renal and metabolic component in acid-base disorders. For example, changes of the HCO3 - concentration in connection with pH values are used for the determination of whether an acidosis or alkalosis of metabolic origin is present. Two bicarbonate versions exist: HCO3 - act (actual bicarbonate): The actual bicarbonate defines the bicarbonate concentration that is actually present with known pH and pCO2 values. The actual bicarbonate calculation is based on the Henderson-Hasselbalch equation. HCO3 - std (standard bicarbonate): This refers to the bicarbonate content of plasma which would be present in blood equilibrated to a pCO2 of 40 mmHg. The standardization makes this parameter independent of the pCO2. However, it depends on the hemoglobin content (cHb) of the blood sample. The standard bicarbonate equation described by VanSlyke and Cullin is used to calculate the standard bicarbonate.  Reference Range Actual bicarbonate: 21 – 26 mmol  Standard bicarbonate: 23 – 27 mmol    Interpreting Results The degree of risk caused by a deviating bicarbonate concentration is measured based on the resulting pH shift.    tCO2Tab TitleTextPurpose Total CO2 quantity or total CO2 is a classic parameter of the acid-base metabolism. In some regions, it is hardly used anymore, because its informational value is only relevant in connection with the HCO3 - std parameter. The total CO2 content is the sum of all respiratory and metabolic buffer factors.    Clinical Significance Combined with pH and pCO2 values, tCO2 is used to evaluate the correlation between respiratory and metabolic factors. Generally, this value is not helpful because the individual itemization of the metabolic and respiratory components is desired. The informational value is greater in connection with HCO3 - std, because HCO3 - std only takes into account the metabolic component.    Reference Range 23 – 28 mmol    Interpreting Results N/A    Base ExcessTab TitleTextPurpose In the term base excess (BE), “excess” is not doing justice to the fact that the base deviation can be positive or negative; it may therefore be misleading. The base deviation is always connected to the “regular range” of the buffer base. The buffer base is defined as the sum of all anionic buffer factors in the blood (HCO3 -, Hb, protein, phosphate), capable of taking up H+ ions. The "regular value" is 48 mmol/L; about half of which is allotted to the bicarbonate in the plasma.    Clinical Significance Base deviation is suitable for evaluating the respective non-respiratory (metabolic, renal, etc.) share of acid-base balance. The causes for the base deviation include: Metabolic causes (metabolic disorder, e.g. diabetes mellitus) Renal causes (renal function impairment, e.g. anuria) Intestinal causes (loss of gastric juice [H+] or duodenal secretion [HCO3 -]) Hepatic causes (impaired hepatic function) Iatrogenic causes (use of infusions with metabolizeable anions such as lactate) Similar to bicarbonate, two versions are available here: Base excess of the extracellular fluid, [BE(ecf) or BE(vv)] for in vivo base excess in older blood gas analytical systems. The base excess of extracellular fluid is calculated via HCO3 - and pH value. Base excess of the blood [BE(B) or BE(vt)] for in vitro base excess in older blood gas analytical systems. In addition to the parameters HCO3 - and pH value, the base excess of the blood takes into account the buffer effect of the blood.      Reference Range -2 to +3 mmol/L  Thus, BA or BE always indicate the deviation of the buffer base with respect to the “regular value” and determine the acid or base quantity in mmol/L required to bring the metabolic part to a pH of 7.4. For example, if the BA was calculated to be +4.5 mmol/L, 4.5 mmol/L of acid are required to titrate the sample back to "0" and to a pH of 7.4 at a pCO2 of 40 mmHg. The quantity of acid or base in mmol/L given to the patient can be calculated using the correction formula BA x 0.3 x body weight [kg].    Interpreting Results As an expression of a lack or excess of base, the significance of the base deviation is therapeutic rather than diagnostic.     CO2Tab TitleTextPurpose CO2 binding capacity or CO2 combining power differs from the tCO2 in that a pCO2 of 40 mmHg is assumed here. The patient’s actual pCO2 is not taken into account, meaning that the acid product H2CO- in the formula remains constant and that changes in the CO2 binding capacity only change the bicarbonate concentration as a result. All measurements and calculations are based on the standard patient temperature of 37°C. When analyzing the samples, the current patient temperature can also be entered. The system then displays all pH and pCO2 values based on both temperatures.    Clinical Significance This parameter is rarely used in the diagnosis of the acid-base metabolism.    Reference Range N/A     Interpreting Results N/A When complete, select the X in the upper-right corner to close the window and continue.     Depending on the change in pH, disorders of acid-base metabolism can be divided into acidosis (pH < 7.37) and alkalosis (pH > 7.45) They indicate the extent to which the buffer and regulation systems (buffering in the blood, respiratory function and renal function) are no longer capable to maintain the pH value of the blood at a constant level. If the cause is a primary change of the pCO2 in the blood, it is referred to as a respiratory disorder, while changes in HCO3- and buffer base concentrations cause metabolic disorders. The laboratory value constellations for disorders involving acid-base metabolism are summarized in the diagram: the primarily altered parameters are characterized by bold arrows. The resulting pH changes and compensatory measures are represented by thin arrows, while the dotted arches mark the direction of the pH value tendency or the compensation events toward the regular value (horizontal line). Respiratory vs. Metabolic Disorders Learn more about respiratory disorders versus metabolic disorders. Respiratory disorders are always due to changes in respiratory behavior: a primary change in CO2 partial pressure (pCO2↓ in case of hypoventilation, and pCO2­↑ in case of hyperventilation) primarily unchanged base deviations (BA or BE = 0). In contrast, metabolic disorders of acid-base metabolism indicate: an increase/decrease of non-volatile acids in the blood (HCO3- or HCO3- and a correspondingly changed base deviation (BA or BE positive or negative) Generally regular CO2 partial pressure, a blood gas analysis and the evaluation of the parameters pH, pCO2, bicarbonate and base deviation are required to determine whether a respiratory or metabolic disorder is present. Altered values of the energy metabolism (metabolites) and the electrolyte metabolism are closely related to these changes. When complete, select the X in the upper-right corner to close the window and continue. Non-respiratory Disorders Learn more about “non-respiratory” disorders. IMPORTANT: Renal function impairment (e.g. anuria) can also lead to changes in pH value. Therefore, renal and metabolic disorders are frequently summarized under "non-respiratory" disorders. These disorders can be partially or completely compensated as a result of the interaction between the buffer pair, i.e. metabolic disorders can be subject to respiratory compensation and vice versa. Compensation refers to an active organ function. Based on the term, it is separate from the buffering as physiochemical process. While the maximum metabolic compensation of respiratory compensation can take several days, the maximum of the respiratory compensation of metabolic disorders (e.g. hyperventilation due to ketoacidosis) is achieved within several hours. When complete, select the X in the upper-right corner to close the window and continue. The Sysmex® CA-600 series coagulation analyzer can use several vial types. Remember to consider the required dead volume when you are selecting a vial. Select each tab below to learn about each of the different types. Metabolic acidosis is defined by a lack of bicarbonate and the associated negative base deviation. In the Henderson-Hasselbalch equation, the ratio is reduced by the decrease in HCO3- and the pH value is decreased as a result.   The decrease in pH stimulates respiration (hyperventilation) and results in respiratory elimination of CO2, used by the organism in an attempt to restore the balance and to compensate the change in pH. Possible causes: renal failure (→ missing or reduced renal acid elimination) ketoacidosis due to decompensated type I diabetes hunger (→ increase in ketonic acids in the blood) alcohol poisoning (→ elevated concentration of non-volatile acids, here acetic acid) diarrhea, pancreatic or biliary fistula (→ loss of bicarbonate-rich secretion) The exact determination of the extent of metabolic acidosis and the timely therapy are required to prevent serious effects on endocrine and immune functions, bone metabolism, cellular activities and on the amino acid protein metabolism. Select Next to continue.   Metabolic alkalosis is defined by an excess of bicarbonate or a loss of H+ ions and the associated positive base deviation. The resulting pH increase causes respiratory dullness, thus leading to an increase in pCO2, which is however limited due to the resulting lack of oxygen. If the alkalosis is not of renal origin, it can be compensated by an increased HCO3- output.   Metabolic alkalosis is always associated with hypokalemia, i.e. a decrease in the potassium value because the H+ ions are substituted by K+ ions. Metabolic alkalosis is far less common than metabolic acidosis. Possible causes: vomiting (loss of gastric juice) stomach probe hypokalemia (laxative abuse, malabsorption) therapy of metabolic acidosis (e.g. intake of bicarbonate) Select Next to continue.   Respiratory acidosis is defined by an elevated pCO2 due to reduced CO2 output of the lungs (hypoventilation). In the Henderson-Hasselbalch equation,   the ratio is reduced due to the CO2 increase, and the pH is decreased as a result. After a start-up time of one to two days, this degradation causes increased renal-back resorption of bicarbonate and an increased acid secretion (output of H+ ions). Possible causes:   blocked respiratory system (foreign body aspiration, bronchial asthma) cardiovascular insufficiency lung disease (extended pneumonia, pulmonary edema, pulmonary emphysema) incorrectly adjusted respiration CNS (skull-brain trauma, encephalitis, Pickwick syndrome, narcotics) thorax (rib fracture). Respiratory acidosis is a life-threatening condition, because: delayed renal compensation causes severely decreased pH values underlying hypoventilation is always associated with an acute lack of oxygen carbon dioxide is immediately diffused into the cells due to hypercapnia. Select Next to continue.   Respiratory alkalosis is defined by a decreased pCO2 due to increased CO2 output by the lungs (hyperventilation).   According to the equation, an elevation of pH occurs which is compensated by the kidneys through increased bicarbonate output. As mentioned above, a start-up time of one to two days is required for renal compensation. The acid to base ratio normalizes again. Respiratory alkalosis is always associated with hypokalemia, i.e. a decrease in the potassium level. Possible causes: psychological reasons such as excitement, fear (stimulated respiration) mechanically-induced hyperventilation/incorrectly adjusted respiration pulmonary fibrosis (gasping) stay at elevated altitudes Select Next to continue.   The evaluation becomes difficult if more than one cause for the disorder or if a concomitant disease involving the compensating organs lungs, kidneys or liver, are present simultaneously. This may be the case in a patient with chronic lung disease (respiratory acidosis) who is experiencing vomiting (metabolic alkalosis) at the same time. Here the disorders partially compensate one another with respect to pH, thus making it more difficult to establish a diagnosis.This emphasizes the necessity to take into account the patient’s overall status as well as other parameters when interpreting the acid-base metabolism: clinical pattern and anamnesis, state of awareness, state of hydration, medication electrolytes (in particular K+, Cl- and anion gap) parameters pO2 and sO2 pH value in urine, ketone bodies, blood glucose, serum creatinine, lactate in the blood, etc. The nomogram developed by Müller-Plathe is useful for the classification of a potential combined disorder.   Acid Base Diagnostic Nomogram Learn about the Acid Base Diagnostic Nomogram. The point of intersection of the respective values for pCO2 (X-axis) and cHCO3- (Y-axis) allows the allocation as pure or combined disorder. When complete, select the X in the upper-right corner to close the window and continue. Key parameters—both measured and calculated—included in blood gas analysis that help physicians assess a patient’s oxygen status include: pO2 (oxygen partial pressure, indicator for the oxygen uptake in the lungs) sO2 (oxygen saturation, oxygen transport indicator) ctO2 (oxygen concentration, oxygen supply indicator) total hemoglobin (cHb) and hemoglobin derivatives (indicators for the hemoglobin/oxygen affinity of the tissue): oxyHb, deoxyHb, COHb, and MetHb. Download and print a copy of the common tests that help assess oxygen status. pO2, O2, ctCO2 Learn more about purpose of O2, sO2, and ctO2 tests. Select the tabs below to learn more about the clinical significance of pO2, SO2, and ctO2 tests.TitleTextpO2Tab TitleTextPurpose pO2 refers to physically dissolved oxygen in the blood. Because the intracellular measurement of the oxygen pressure is impossible, arterial pO2 becomes the standard for clinical evaluation of oxygen status. The pO2(a) measurement indicates the oxygen pressure in arterial blood and reflects the pressure which transports the oxygen from one place to the next due to the pressure difference and is not a measurement of the O2 content.   Based on Henry’s law, the quantity of a gas dissolved at a constant temperature in a unit of fluid is directly proportional to its partial pressure. The oxygen quantity soluble in plasma is 0.023 mL/mL .With respect to the pO2 in the alveoli, the dissolved quantity is calculated according to (0.023/760) x 100 = 0.003 mL of O2/mL of plasma, i.e. 0.3 percent by volume with respect to 100 mL of plasma. The solubility of oxygen in blood is so poor that no adequate oxygen supply of the organism would be guaranteed without the binding of O2 to hemoglobin (transports 200 mL/L, i.e. about 70 times the quantity). Nevertheless, this status has a major biological significance. Before gases enter into a chemical bond, they must diffuse to the reaction partners (erythrocyte, hemoglobin) in dissolved form. Each O2/CO2 molecule substituted in the lungs or tissue will have to have passed the status of physical solution first.    Clinical Significance The partial pressure of oxygen in arterial blood is a parameter for the ability of the lungs to enrich the blood with oxygen, thus evaluating changes in pulmonary function. This parameter has major significance for the evaluation of the degree of oxygen saturation in a patient, in particular with respect to the degree of hypoxemia (lack of oxygen in arterial blood).    Reference Range The laboratory reference range of pO2 in arterial blood in a healthy adult at sea level is normally 70 – 100 mmHg (9.5 – 13.3 kPa). But the pO2 depends on a number of factors, including: Age Newborns:  40 – 70 mmHg (5.3 – 9.3 kPa) People aged 50 and up experience a deterioration of the pulmonary function and hence a reduction of the “regular” pO2 value of ~ 1 mmHg (~ 0.13 kPa) per year (rule of thumb: pO2 [mmHg] = 102 – 0.33 x years of age. pO2 [kPA] = 13.6 – 0.044 x years of age) Stress: the pO2 rises as a result of hyperventilation (pCO2 decreases, pH rises). Position-dependent (subject to the same withdrawal site): in young adults in a sitting position: approximately 90 – 98 mmHg, in a supine position: 85 – 95 mmHg, while sleeping: 70 – 85 mmHg. When determining the pO2, the strong “age dependence” of the analyte should be taken into account, as mentioned above. In subjects over the age of 65, a decrease of the pO2 to below 60 mmHg is not considered dramatic. Note: In medicine, the conventional unit mmHg is still widely used instead of the S.I. unit Pascal. The conversion factors are as follows: 1 mmHg = 133.3 Pa 1 Pascal = 7.5 x 103 mmHg      Interpreting Results Elevated values: Risk of oxygen toxicosis (damaging the lungs) caused by free oxygen radicals (in newborns and premature babies, the arterial pO2 should not exceed 75 mmHg).  Decreased values: Inadequate oxygen uptake in the lungs (examination of the pulmonary function) If the pO2 is below approximately 40 mmHg, the subject is expected to experience unconsciousness.      sO2Tab TitleTextPurpose The “measured” oxygen saturation sO2 indicates the ratio of oxygenated (O2-bound) hemoglobin to oxygenizable (O2-bindable) hemoglobin. O2SAT vs. sO2 O2SAT: Calculates oxygen saturation via empirical equation which approximately describes the gradient of the oxygen dissociation curve. The parameters temperature (T), pH, pO2, pCO2, cHb are used in this equation; it does not take into account any other Hb fractions.   sO2: O2 saturation measured by means of the co-oximeter indicates the ratio of oxygenated (O2-bound) hemoglobin to oxygenizable (O2-bindable) hemoglobin. In the presence of non-oxygenizable hemoglobin derivatives or 2,3-diphosphoglycerate, it deviates from FO2Hb (and O2SAT).      Clinical Significance Oxygen saturation sO2 allows the evaluation of the oxygenation and dissociation of the oxyhemoglobin and is an indicator for the capability of the lungs to supply the blood with oxygen. It would make more sense to call it “partial O2 saturation”, where the term “partial” is meant to emphasize that only the O2Hb and HHb fractions are used in the calculation.      Reference Range > 96%    Interpreting Results Elevated values: Adequate oxygen transport capacity Possible risk of hyperoxia  Decreased values: Deteriorated oxygen uptake Right shift of the ODC    ctO2Tab TitleTextPurpose ctO2 (O2ct, OXYGEN CONTENT, OXYGEN CONCENTRATION) The oxygen concentration of the blood (B), referred to as total oxygen content in some regions, includes both hemoglobin-bound and physically dissolved oxygen. It is calculated according to the following formula: ctO2 (B) = FO2Hb x cHb x 1.39 + 0.0031 x pO2 bound O2 + dissolved O2 Sometimes, the following term is used: ctO2 (Hb) = FO2Hb x cHb x 1.39 It only takes into account the oxygen content of hemoglobin. Particularly in patients with very low hemoglobin concentrations, patients undergoing overpressure therapy or oxygen therapy, the dissolved oxygen can account for a significant share of the oxygen content and hence for the oxygen transport.    Clinical Significance The oxygen content of the blood reflects the effects of changes in the arterial pO2, the hemoglobin concentration and hemoglobin affinity for oxygen and includes all components involved in the oxygen supply.     Reference Range 20 mL/dL    Interpreting Results Elevated values: With regular pO2: cause for high cHb (cardiac stress)  Decreased values: Risk of reduced oxygen supply of the tissue (hypoxia) Further diagnostic procedures: Examine the lactate value With regular pO2: cause for decreased cHb or presence of non-oxygenizable hemoglobin When complete, select the X in the upper-right corner to close the window and continue.     Total Hemoglobin and Hemoglobin Derivatives Learn more about total hemoglobin and hemoglobin derivative tests. Select the tabs below to learn about the purpose and clinical significance of total hemoglobin (cHb) and hemoglobin derivative tests (oxyHb, deoxyHb, COHb, and MetHb).TitleTextcHbTab TitleTextPurpose Hemoglobin Concentration (total hemoglobin) Total hemoglobin (cHb) is the sum of all measured hemoglobin fractions and hence is a measurement for potential oxygen transport capacity.    Clinical Significance cHb is used to evaluate oxygen transport as well as anemias. However, a regular hemoglobin concentration does not necessarily guarantee a regular oxygen transport capacity. Dyshemoglobins in high concentrations significantly reduce this ability. Moreover, non-oxygenizable hemoglobins (dyshemoglobins) can be recorded in the total hemoglobin concentration via co-oximetry.    Reference Range Females: 12 – 16 g/dL (7.5 – 9.9 mmoL/L) Males: 14 – 18 g/dL (8.7 – 11.2 mmoL/L)    Interpreting Results Elevated values: High blood viscosity (cardiac stress) Polycythemia Dehydration Chronic lung/heart disease Living at high altitudes Trained athletes  Decreased values: (Anemia) Hemolysis Hemorrhages Blood thinning Reduced erythrocyte production    FO2HbTab TitleTextPurpose Oxyhemoglobin Fraction  FO2Hb calculates the ratio of oxygenated (O2- bound) hemoglobin to total hemoglobin and takes into account the sum of all measured hemoglobin fractions.    Clinical Significance While the regular range of the COHb fraction is around < 2%, values of up to 10% are found in heavy smokers, people living close to a major road in a large city or heavy industry workers. The affinity of  hemoglobin to CO is approximately 300 times higher than the one of oxygen to hemoglobin. Significant deviations between the sO2 values and FO2Hb are expected particularly in burn victims.    Reference Range > 96%    Interpreting Results Elevated (regular) values: Adequate oxygen transport capacity Potential risk of hyperoxia  Decreased values: Deteriorated oxygen uptake Presence of non-oxygenizable hemoglobins (dyshemoglobin) Right shift of the ODC    FHHbTab TitleTextPurpose Deoxyhemoglobin Fraction FHHb refers to the ratio of oxygenizable, not oxygen-charged hemoglobin with respect to the total hemoglobin.    Clinical Significance The parameter is used to calculate the partial saturation sO2.    Reference Range 0.0 – 5.0%       Interpreting Results N/A    FMetHbTab TitleTextPurpose Methemoglobin Fraction In MetHb, bivalent iron is oxidized to trivalent iron; therefore, it is no longer capable of a reversible oxygen bond.    Clinical Significance High methemoglobin concentrations prevent and inhibit the oxygen transporting ability of hemoglobin and can cause hypoxias and cyanosis.    Reference Range < 1.5%       Interpreting Results Elevated values In congenital methemoglobinemia (various forms) Due to exposure to toxic substances (nitrates, nitrites, aniline dyes and their derivatives) Due to diagnostic or therapeutic exposure (certain local anesthetics such as Prilocaine, Resorcine, Phenacetine, Nitroglycerin, Nitro.-containing substances)    FCOHbTab TitleTextPurpose Carboxyhemoglobin Fraction COHb refers to the hemoglobin linked to carbon monoxide via a covalent bond, blocking the bonding site for oxygen. The hemoglobin affinity to carbon monoxide is 300 times greater than to oxygen. The “elimination” of the carbon monoxide from the hemoglobin bond can be achieved faster under high partial oxygen pressures than under regular pressure conditions. CO-elimination – the greater the pressure of the administered oxygen, the faster CO is eliminated from the Hb-bond.    Clinical Significance High carboxyhemoglobin concentrations prevent and inhibit the oxygen transporting ability of hemoglobin and can cause hypoxias and cyanosis.     Reference Range < 2%       Interpreting Results Elevated values: In smokers and burn victims Due to household, industrial and agricultural exposure When complete, select the X in the upper-right corner to close the window and continue.      Er zijn twee manieren om de kwaliteitscontrole te analyseren: automatisch en handmatig. Automatische QC maakt gebruik van de AQC cartridge die is geïnstalleerd op de analyser en is voorgeprogrammeerd om QC analyseren op een vooraf bepaald schema. Handmatige QC kan worden geanalyseerd middels QC ampullen of spuit. Mogelijk wordt u gevraagd om ampul QC te analyseren door een vooraf bepaalde schema. Pathophysiological influences on oxygen supply vary greatly. The most common impairments to oxygen status and the associated conditions include: impaired cardiac/metabolic function impaired pulmonary function (impaired O2 uptake) impaired blood transport function (impaired O2 supply) Impaired Cardiac/Metabolic Function Learn more about impaired cardiac/metabolic function. Impaired Cardiac/Metabolic Function Impaired cardiac/metabolic function refers to: shock/collapse due to reduced venous reflux impaired stimulus formation or stimulus conduction (tachycardia, arrhythmia, atrial flutter and atrial fibrillation cause a decrease in cardiac output) elevated pressure and volume load due to heart defects, right/left shunt (venous blood is mixed directly with arterial blood while bypassing the lungs) cardiomyopathies, myocarditis, toxic myocardial impairments When complete, select the X in the upper-right corner to close the window and continue. Impaired O2 Uptake Learn more about impaired pulmonary function (impaired O2 uptake). Impaired O2 Uptake Impaired O2 uptake refers to: Ventilation (impaired respiratory mechanism) restrictive (impairment of lung volume or elasticity and associated limitation of the gas exchange surface): pulmonary fibrosis, pulmonary resection obstructive (congestion/narrowing of the respiratory system causing impaired air flow): stenosis of the upper respiratory tract (nasopharyngeal region), bronchial asthma Perfusion (impaired perfusion) right/left shunts (venous-arterial bypasses) due to cardiac malformation (heart defects) reduced pulmonary tissue due to surgery impaired perfusion due to acute and chronic pulmonary embolisms Distribution (impaired gas transfer) ventilation of non-perfused alveoli (pulmonary embolism) perfusion of non-ventilated alveoli (shunt due to pneumonia) Diffusion (difficult gas transfer between blood and lungs) enlarged diffusion distance (pulmonary edema, pulmonary fibrosis) When complete, select the X in the upper-right corner to close the window and continue. Impaired O2 Supply Learn more about impaired blood transport function (impaired O2 supply). Impaired O2 supply refers to: Hypoxia (↓pO2—reduced partial pressure of oxygen in blood), e.g. due to lack of oxygen in the air (high altitudes; the pO2 is reduced by half every 5,500 m) Hypoxemia (↓ctO2—reduced oxygen concentration per volume unit of blood ) Hypoxygenation (↓sO2—reduced blood saturation) Arterial hypoxia (pO2 too low) always requires arterial hypoxygenation (sO2 too low) – sO2 is determined by the bonding curve of pO2 – which in turn is expressed as hypoxemia (ctO2 too low). The correlation of the parameters pO2, sO2 (FO2Hb) and ctO2 is illustrated in the chart. All impairments of the cardio-pulmonary gas exchange mentioned above cause a decrease in arterial pO2 and lead to hypoxia (decreased ctO2) as a result. Example of hypoxic hypoxemia-68 year old male with pneumonia pH = 7.36 pCO2 = 43.2 mmHg pO2 = 68.4 mmHg↓ cHb = 14.3 g/dL ctO2 = 17.5 mL/dL↓ sO2 = 87.5%↓ The oxygen binding capacity of hemoglobin decreases with elevated COHb and MetHb concentrations, manifesting itself in a left shift of the O2 dissociation curve and an increase of the O2 affinity of the intact hemoglobin. The result is hypoxygenation and toxic hypoxemia. Likewise, the use of stored blood can cause a left shift of the ODC due to the decreased 2,3 DPG concentration, resulting in elevated O2 affinity (the anaerobic glycolysis of erythrocytes causes the degradation of 2,3 DPG, the O2 affinity in stored blood increases strongly during the first week).   Example of toxic hypoxemia-40 year old male with smoke poisoning pH = 7.40 pCO2 = 40.0 mmHg pO2 = 100.0 mmHg cHb = 15.7 g/dL ctO2 = 12.7 mL/dL↓ sO2 = 99.8% FCOHb = 42.8%↑ FO2Hb = 56.6%↓ This example highlights the difference between sO2 and FO2Hb. At 99.8%, the saturation (sO2) is excellent; but taking into account the COHb share, the FO2Hb at 56.6% is severely decreased and requires treatment.  Anemias with various causes (e.g. hemorrhagic anemia, iron deficiency anemia, impaired hemoglobin or hemoglobin synthesis, hemolytic anemia) impair the oxygen supply and cause anemic hypoxemia. This causes a right shift of the ODC, decreased O2 affinity, resulting in increased oxygen extraction in the tissue due to an increase in 2,3-DPG.   Example of anemic hypoxemia-75 year old female with hemorrhagic anemia pH = 7.40 pCO2 = 40.0 mmHg pO2 = 80.0 mmHg cHb = 9.0 g/dL↓ ctO2 = 12.4 mL/dL↓ sO2 = 97.0% When complete, select the X in the upper-right corner to close the window and continue. Key parameters that help physicians assess a patient’s electrolytes include: sodium potassium chloride calcium anion gap How does dialysis affect potassium levels? Learn more about how dialysis affects potassium levels. How does dialysis affect potassium levels? Renal insufficiency in dialysis patients leads to elevated potassium concentrations in the plasma. Values of 6.0 mmol/L and more are common. A further increase causes a decrease in the cardiac output as a result of reduced heart rate (bradycardia). Vital organs are no longer adequately perfused. The adrenal gland secretes adrenaline as an emergency reaction to elevate the blood pressure. However, the response of the hyperkalemic heart to adrenaline is immediate ventricular fibrillation and cardiac arrest. After dialysis, the potassium level is approximately 2 to 3 mmol/L. Consequently, potassium is the most important electrolyte in dialysis. When complete, select the X in the upper-right corner to close the window and continue. Electrolyte Tests Learn the purpose and clinical significance of these tests. Select the tabs below to learn the purpose and clinical significance of each electrolyte test.TitleTextNa+Tab TitleTextTest Purpose Na+ is the most important cation in extracellular fluid (blood plasma and interstitial space). It plays a central role in the regulation of the body’s fluid volume. In this context, it is responsible for maintaining the osmolarity (rough estimate: Na+ [mmol/L] x 2 = osmolarity of plasma in mmol/L). Two regulating hormones, aldosterone and adiuretin (ADH) influence the renal function and hence the sodium balance. Aldosterone stimulates the kidneys to reabsorb Na+, while ADH stimulates the kidneys to reabsorb water.   Clinical Significance Sodium is mainly responsible for regulation of body fluids, maintenance of electrical potential in muscle cells and control of cellular membrane permeability. Disorders of sodium metabolism are the result of inadequate sodium intake or output, frequently in connection with disorders of water metabolism. Both hypo-and hypernatremia can cause clouding of consciousness, seizures and vomiting.   Reference Range 135 – 145 mmol/L Alarm limits < 125 and > 155 mmol/L   Interpreting Results Elevated values (Hypernatremia) Hypertonic impairment of the electrolyte metabolism: the osmolarity (osmotic pressure) of the plasma increases as a result of reduced water intake or increased water output. Hypertonic dehydration (lack of water) caused by:        •  inadequate fluid intake in seriously ill patients or        •  high loss of water, e.g. in diabetes mellitus/insipidus, watery diarrhea, serious           febrile illnesses Hypertonic hyperhydration (sodium surplus exceeds water surplus)        •  infusion with hypertonic sodium chloride solutions or        •  hyperaldosteronism (Conn syndrome: Na+ retention.)   Interpreting Results (contd)Decreased values (Hyponatremia) Most common electrolyte shift (< 130 mmol/L) Hypotonic impairment of the electrolyte metabolism: decreased plasma osmolarity Hypotonic dehydration (sodium loss exceeds lack of water) caused by: loss of salt in patients with renal illnesses (impaired NaClresorption in the loop of Henle), diuretics (renal loss of NaCl and water), vomiting or diarrhea (gastrointestinal loss of water), excessive sweating, inadequate electrolyte supply under infusion therapy Hypotonic hyperhydration (water surplus), infusion with electrolyte-free glucose solutions, polydipsia, renal and cardiac insufficiency In the two following cases, the sodium concentration in the serum does not indicate an impairment of the water metabolism: Isotonic dehydration (concomitant with lack of water, causing a reduction in the osmotically active substances) due to loss of isotonic body fluids (diarrhea, vomiting, blood loss)Isotonic hyperhydration (increased ex-tracellular fluid volume) due to excess supply of isotonic solutions in illnesses with generalized formation of edema such as cardiac and renal insufficiency.Other Facts Important In serious losses of water, a sodium value within regular range may simulate normal sodium content in the body. Conversely, a decreased sodium concentration as a result of serious hyperhydration (renal, cardiac insufficiency) may simulate a lack of sodium that is not actually present.   K+Tab TitleTextTest Purpose Potassium is the most important intracellular cation in the human body. It maintains cellular resting membrane potential and osmotic pressure and plays a significant role in electrical events involving excitable tissue (muscles, especially the heart muscle). Potassium is responsible for the fluid content (osmotic pressure) in cells, because it is most prevalent there. The concentration of potassium is very high (155 mmol/L) inside a cell and very low (4 mmol/L) outside it. The serum potassium value does not reflect the intracellular potassium supply of the body.   Clinical Significance The regulation of potassium metabolism is by far less adaptable than that of sodium. As a result, the body compensates potassium imbalances comparatively poorly. Due to the important function of potassium, any impairments of K+ metabolism, irrespective of the direction (hyper- and hypokalemia) are always life-threatening. Disorders can be caused by inadequate K+ supply or output or shift between the extra- and intracellular spaces. The control of the potassium levels is especially important for patients suffering from cardiac arrhythmia or acute renal insufficiency and in those scheduled to undergo surgery or receive diuretic treatment as well as patients on digoxin monitoring and dialysis.   Reference Range 3.6 – 4.8 mmol/L  Alarm limits < 2.5 and > 6.5 mmol/L   Interpreting Results Elevated values (Hyperkalemia) Impairment of vital muscle functions: heart muscle (arrhythmia, ventricular fibrillation, cardiac arrest), intestinal muscles (spasms), respiratory muscles (paralysis)   Excess K+ or decreased K+ output:        •  renal failure (acute and chronic) with oliguria/anuria        •  incorrect infusion therapy (massive administration of solutions containing K+),            medications (Heparin, Digoxin, Succinylcholine, potassium-saving diuretics)        •  mineral corticoid deficiency within the scope of adrenal gland insufficiency K+ distribution disorders:        •  respiratory/metabolic acidosis        •  serious tissue destruction with K+ release from the cells, hemolysis   Interpreting Results (contd)Decreased values (Hypokalemia) Impairment of vital muscle functions: heart muscle (tachycardia, cardiac arrest), intestinal muscles (paralysis, ileus), respiratory muscles (paralysis), renal function (renal acidosis). Differentiating between K+ deficiency and K+ shift is important for therapeutic reasons. K+ loss or deficiency: undernourishment in anorexic patients and alcoholics gastrointestinal: loss of K+ containing digestive juices due to vomiting, diarrhea, laxative abuse, potassium-poor infusion renal: diuretics, renal tubular acidosis, renal illnesses with increased salt output additional diagnostic procedures:  examine the chloride levels (hyperchloridemia). hyperaldosteronism cutaneous: extensive burns Impaired K+ distribution: respiratory / metabolic alkalosis elevated insulin concentration elevated catecholamine concentration pernicious (vitamin B12 deficiency) anemia Other Facts Important Like sodium, potassium concentration in the serum depends on the size of the electrolyte-free space. Due to the large reference range, the clinical significance for the potassium determination is even smaller. When interpreting potassium values, the acid-base metabolism should be taken into account because the potassium levels are closely related to it (influence on the potassium distribution between inner and outer space of the cell). Potassium losses In case of potassium loss, e.g. due to diarrhea, serum potassium content can quickly be compensated by means of the storage inside the cells. This process is associated with the risk that a relevant potassium deficiency in the cells is not determined for a long time because the serum potassium levels are regular. Similarly, potassium deficiency in the intracellular space (ICS) can be compensated with the inflow of H+ ions; this results in alkalosis in the plasma, while acidosis is present in the ICS.   Ca++Tab TitleTextTest Purpose 99% of the calcium content (approximately 1 kg) is in bone in crystalline form as calcium hydroxylapatite. Approximately 50% of the remaining is located in the extracellular space (ECS) in ionized form (1.25 mmol/L); only this fraction is biologically active and integrated in the normal regulation. 35% is bound to protein (mainly albumin and globulin), while 15% is complex-bound (citrate, lactate, phosphate, bicarbonate). Calcium plays an important role in the electromechanical coupling in the cell (conversion of nerve impulses into muscular activities) and regulates the membrane permeability of sodium and potassium (ATPase). Moreover, it plays a key role in coagulation, in enzymatic activities and the secretion of hormones such as adrenaline. This broad range of responsibilities requires an extensive control of this ion with multiple security levels. Hormones (parathormone, calcitonin), acid-base metabolism, vitamin D metabolism and phosphate metabolism affect serum calcium levels.   The concentration of calcium in the cell is very low (0.001 mmol/L). At an overall concentration of 2.5 mmol/L in the space outside the cells, the concentration gradient of calcium is the greatest of all ions in the cellular wall. Therefore, it flows into the cell with minimal changes in the permeability of the cellular wall, giving the signal for important and various functional changes in the cell. Clinical Significance Impairments of calcium metabolism occur due to an imbalance between calcium intake and output or due to pathological alterations of calcium deposits in the skeleton. Ionized calcium level of patients in intensive care must be carefully monitored, especially if they require blood transfusions, because the anticoagulants (citrates) contained in the blood concentrate bind calcium, thus lowering the level of ionized calcium in the blood. This can lead to cardiac or neuromuscular disorders.   Reference Range 1.15 – 1.35 mmol/L (ionized) Alarm limits < 0.9 and > 1.75 mmol/L 2.20 – 2.65 mmol/L (overall) Alarm limits < 1.7 and > 3.5 mmol/L      Interpreting Results Elevated values (Hypercalcemia) 80% of serious hypercalcemias are due to osteolysis associated with malignant tumors (bone metastases) or primary hyperparathyroidism (pPHT). The Ca2+ release exceeds the Ca++ bonding in:        •  primary hyperparathyroidism        •  tumors (especially in breast, lung, prostate and kidney cancer)        •  prolonged restraint (e.g. due to pelvic fractures) Loss of fluid (diarrhea, alcohol, vomiting) Increased Ca++ uptake due to:        •  vitamin A and D overdose        •  intake of special drugs (Lithium, antiestrogens, certain diuretics)        •  sarcoidosis        •  Morbus Addison (Addison's Disease) Chronic hypercalcemias can lead to calcifications in different organs and formation of renal calculus.   Interpreting Results (contd)Decreased values (Hypocalcemia) Decreased Ca2+ supply due to:•  hypoalbuminia vitamin D deficiency or reduced vitamin D effect intake of special drugs (antiepileptic substances, certain diuretics) The Ca2+ bonding exceeds the Ca++ release in: pseudo hypoparathyroidism acute pancreatitis Ca2+ loss due to: chronic renal insufficiency chronic pancreatitis (impaired calcium reabsorption) Extreme deficiency (below 0.8 mmol/L) causes muscle cramps (tetany).Other Facts IMPORTANT:   If the plasma pH changes, the affinity of proteins to calcium changes too. In other words, the ratio of ionized calcium in plasma changes based on pH. To obtain a clear indication of the ionized calcium, it is recommended to print out the value calculated for pH 7.4 in addition to the measured calcium value. The total calcium concentration in serum is directly dependent on the albumin concentration. The total calcium concentration decreases in illnesses associated with hypoalbuminia (cirrhosis of the liver or nephrotic syndrome). However, the biologically more important ionized form remains unaffected in this “pseudohypocalcemia”. For this reason, it is preferable to measure the ionized calcium.   Cl-Tab TitleTextTest Purpose Chloride is the most important anion in body fluids. It occurs mainly in extra-cellular spaces. Together with a host of other factors, it regulates water distribution within the spaces in the body. Chloride is the counter-ion to sodium. Its metabolism is therefore closely related to that of sodium: both are ingested as common salt (NaCl) with food and secreted together via the kidneys. Therefore, the change is usually identical.   Clinical Significance Chloride metabolism is usually impaired to the same extent as sodium metabolism and is determined by impairments of the sodium and water balance. Isolated chloride deviations are found in disorders of acid-base metabolism. Bicarbonate and chloride concentrations change conversely because chloride is replaced by bicarbonate during the renal output. Here, chloride is required to calculate the anion gap.   Reference Range 95 – 105 mmol/L Alarm limits   <80 and > 118 mmol/L   Interpreting Results Elevated values (Hyperchloridemia)  Hypertonic impairment of electrolyte metabolism (elevated plasma osmolarity due to reduced water intake or increased loss of water) Hypertonic dehydration (water deficiency) due to: inadequate fluid supply in very ill patients high loss of water, e.g. in diabetes mellitus/insipidus, chronic watery diarrhea (chloride retention in the kidneys to compensate the bicarbonate loss metabolic acidosis, hypokalemia), serious febrile illnesses Hypertonic hyperhydration (excess sodium exceeds overhydration) due to: infusion with hypertonic sodium chloride solutions or hyperaldosteronism (Conn syndrome: Na+ retention Renal tubular acidosis Further diagnostic procedures: examine the potassium levels (hyper- or hypokalemia, depending on the type) Hyperventilation (respiratory alkalosis → compensatory chloride retention in the kidneys → metabolic acidosis) Interpreting Results (contd)Decreased values (Hypochloridemia) Generally identical symptoms as described for sodium Hypotonic dehydration (the sodium and chloride loss exceeds the water deficiency) due to Loss of salt in patients with kidney disease (impaired NaCl reabsorption in the Henle loop), diuretics (renal loss of NaCl and water) Vomiting or diarrhea (gastrointestinal chloride-rich loss of water) Excessive sweating Inadequate electrolyte supply during infusion therapy Hypotonic hyperhydration (overhydration) infusion with electrolyte-free glucose solutions polydipsy renal or cardiac insufficiency Metabolic alkalosis (hyperaldosteronism, Cushing syndrome, ACTH forming tumors, Bartter syndrome) Further diagnostic procedures: examine the potassium levels (hypokalemia) Symptoms may include thirst, drowsiness, water deposit in tissue and tendency to collapse (similar to sodium deficiency).Other Facts IMPORTANT If the specimen is measured by means of coulometry or indirect ISE, hyperproteinemia or hyperlipidemia can cause “pseudohypochloridemia due to the small reference interval of chloride. Conversely, hypoproteinemia and hypolipidemia can cause “pseudohyperchloridemia. The determination of chloride by means of ion-selective methods without diluting the specimen is dependent on the water content of the specimen and allows the proper interpretation.   Anion GapTab TitleTextTest Purpose Anion gap = [Na+] - ([Cl-] + [HCO=3-]) The anion gap refers to the difference between cations and anions. It is used to measure the routinely not determined and not determinable anions (mainly negatively charged plasma proteins, phosphate, sulphate and organic acid residues such as lactate, acetoacetate‚ beta-hydroxybutyrate).   Clinical Significance Although it is not a sensitive or specific procedure, the determination of the anion gap has achieved a firm position in emergency and intensive care within the scope of the differential diagnosis of metabolic acidosis. In particular, it is possible to distinguish life-threatening metabolic acidosis due to intoxication from other clinical symptoms.   Reference Range 8 – 16 mmol/L   Interpreting Results Metabolic acidosis with enlarged anion gap Diabetic acidosis (primarily acetoacetate due to lipolysis) Alcoholic acidosis (primarily beta-hydroxybutyrate due to lipolysis) Lactacidosis (due to shock or Biguanide therapy) Uremia (retention of organic acids from the metabolism) Intoxication Salicylate (combined metabolic acidosis and respiratory alkalosis) Methanol:  Formiate Ethylenglycole: Glycolate and Oxalate (crystals in the urine) Metabolic acidosis with regular anion gap (hyperchloridemic metabolic acidosis) Diarrhea (hypokalemia) Primary metabolic acidosis: renal tubular acidosis (hyper- or hypokalemia, depending on the type) Primary respiratory alkalosis with secondary metabolic acidosis (e.g. hyperventilation) Therapy with carboanhydrase inhibitors Ureterosigmoidostomy (hypokalemia)   Other Facts IMPORTANT The anion gap can be reduced under concomitant pronounced hypercalcemia or high bromide concentrations (abuse of bromium-containing barbiturates). When complete, select the X in the upper-right corner to close the window and continue.   Key parameters that help physicians assess a patient’s metabolic functions include: Glucose Lactate Hyperglycemia and Hyperlactatemia Learn more about hyperglycemia and hyperlactatemia. Depending on the type of insulin deficiency, hyperglycemia can lead to ketoacidotic diabetic coma or hyperosmolar diabetic coma. Hyperlactatemia can lead to lactate acidotic coma. Ketoacidotic diabetic coma > 400 mg of glucose/dL of blood or > 22.2 mmol/L Due to the absolute insulin deficiency in type I diabetics, hyperglycemia under inadequate blood glucose control or an acute serious crisis can lead to ketoacidotic diabetic coma. Because the hormone insulin is absent, which feeds glucose into the cells and generates energy reservoirs, a compensatory build-up of fatty acids takes place to provide energy. The ketone bodies generated during this process cause metabolic acidosis (elevated acetoacetate, beta-hydroxybutyrate levels in the blood with simultaneous drop in pH, Kussmaul’s breathing, acetone odor, exsiccosis). Further diagnostic procedures: enlarged anion gap, decreased bicarbonate levels, blood pH of < 7.37, pCO2 < 35 mmHg, increased osmolarity: up to approximately 350 mosm/kg, ketone bodies in the serum and urine are severely elevated, glucose levels in the urine are elevated. Hyperosmolar diabetic coma usually > 1,000 mg of glucose/dL of blood or > 55.5 mmol/L The relative insulin deficiency in type II diabetics can lead to hyperglycemia and hyperosmolar (non-ketoacidotic) diabetic coma, if left untreated. The elevated osmotic dieresis associated with this condition results in exsiccosis. In most patients, the insulin levels are measurable. Extreme dehydration, hypovolemia and hyperosmolarity lead to tissue hypoxia, anaerobic metabolism and ultimately to the possible lactacidosis. Further diagnostic procedures: blood pH 7.37 – 7.45, pCO2 35 – 46 mmHg, regular to slightly elevated ketone bodies in the serum and urine, elevated glucose in the urine, severely elevated osmolarity: > 350 mosm/kg. The typical findings in diabetic coma are summarized in chart shown here. Non-diabetic causes: reduced glucose tolerance due to a major surgical procedure or trauma (stress situation) as a result of the inhibited insulin secretion and/or increased glucose supply caused by the release of catecholamines (Adrenaline and Noradrenaline) and Glucocorticoids hyperglycemias as a result of reduced glucose tolerance in intensive care patients due to the use of Suprarenin® and, to a lesser extent, Arterenol®. The body compensates this situation by increasing the renal output to reduce the glucose level. This can lead to dehydration and loss of electrolytes. Further diagnostic procedures: electrolytes, especially potassium (decreased) Lactate acidotic coma In diabetics, the rare complication of lactate acidotic coma is not caused directly by diabetic metabolic disorders, but in connection with the anti-diabetic therapy using Biguanides. In this case, the pH, pCO2 and bicarbonate values are decreased and the anion gap increased, while the blood glucose is regular-to-low. Significant lactacidosis in lactate concentration of > 45 mg/dL of blood (5.0 mmol/L) blood pH of < 7.25 When complete, select the X in the upper-right corner to close the window and continue. Diabetes Mellitus Learn more about diabetes. An elevated blood glucose concentration (hyperglycemia) over an extended time usually indicates an insufficient concentration or action of insulin and is referred to as diabetes mellitus. We generally distinguish between two basic types of this disease: in type I diabetes mellitus, the pancreas lost its ability to produce insulin due to genetic disorders or as a result of infections. Glucose cannot be absorbed into the cells and the blood glucose levels remain elevated, as shown in the diagram. Type I diabetics (approximately 10% of all diabetics) therefore rely in exogenous insulin applications. in type II diabetes mellitus, the Islets of Langerhans in the pancreas produce insulin, but the body’s cells are incapable of "recognizing" insulin. The cause for this "insulin resistance" can be excess food supply across an extended period of time with concomitant genetic predisposition. The consequence is again an elevated blood glucose concentration with simultaneously elevated blood insulin concentration. Approximately 90% of all diabetics are type II diabetics; a majority of them also suffer from high blood pressure, elevated blood lipids and overweight ("metabolic syndrome"). Glucose is metabolized by the insulin antagonists glucagon, cortisol and adrenaline. These hormones have a blood glucose-elevating effect by catabolism of the glycogen stored in the liver and releasing glucose to the blood (glycogenolysis). Increased glucose requirements, e.g. due to illnesses and physical or mental stress, can be directly balanced this way. The concentration ratio between glucagon and insulin is characteristic for the status of the organism with respect to its nutritional and energy storage status: after eating (reabsorption phase), the glucagon/insulin ratio is low (a lot of insulin), the excess amount of glucose is stored. During the post-reabsorption phase, the ratio is high (less insulin), the storage is emptied again. When complete, select the X in the upper-right corner to close the window and continue. Interpreting Glucose Results Learn more about interpreting glucose results. Note the following when interpreting glucose test results: Capillary venous differences As expected, glucose concentration is higher in arterial blood than in venous. The extent of the capillary-venous differences is subject to significant fluctuations: while differences from “not measurable” to approximately 10 mg/dL or 0.6 mmol/L occur in fasting measurements, the values in capillary blood can be 50% higher than in the venous blood after food intake (postprandial) or after an oral glucose tolerance test. Differences between plasma/serum and whole blood In blood specimens, glucose is dissolved in the aqueous component. Erythrocytes have a water content of 71%, while it is 93% for plasma. This leads to a difference of 12% between the glucose value in plasma and in whole blood with a regular hematocrit. The relation and conversion of the two values is illustrated with the following equation: [Glucose]Whole blood = [Glucose]Plasma x [1.0 - (0.0024 x hematocrit [%])] If the whole blood specimen of a patient has a glucose value of 100 mg/dL (5.6 mmol/L), 112 mg/dL (6.3 mmol/L) are measured in the plasma specimen. A correlation of these two measured values that is as close as possible can only be measured in fasting status. Interferences If given at therapeutic concentrations, most medications do not cause interference. The first chart shows some substances that do not affect the glucose measurement. The respective specified concentrations result in a deviation of less than 6 mg/dL (0.3 mmol/L) with respect to the recovery of the glucose concentration. The second chart contains a list of substances which may affect the glucose measurement. When complete, select the X in the upper-right corner to close the window and continue. Interpreting Lactate Results Learn more about interpreting lactate results.  Note the following when interpreting lactate test results: Take into account the hepatic and renal functions. Although the basal values in patients with an impaired function of these organs are regular, their lactate clearance is reduced.   Lactate should not be considered as an individual value but in the overall clinical context. This applies in particular to the perfusion disorders applicable to the main area of indication, but also to inadequate metabolization (impaired uptake in the liver) regional deficiencies (surgical field, sepsis, shunts) and increased lactate output into the circulation, e.g. due to limited blood flow (wash-out effect). Leukocytosis can increase the lactate concentration by a maximum of 2.7 mg/dL (0.3 mmol/L). Interferences The first chart lists substances which do not affect the lactate measurement. In the specified concentrations, these compounds produce an error of less than 6 mg/dL (0.7 mmol/L) with respect to the recovery of the lactate concentration. The second chart lists the substances which can affect the lactate measurement. When complete, select the X in the upper-right corner to close the window and continue. Metabolic Function Tests Learn about the purpose and clinical significance of glucose and lactate tests. Select the tabs below to learn the purpose and clinical significance of glucose and lactate tests.TitleTextGlucoseTab TitleTextPurpose Glucose is the most important molecule in carbohydrate metabolism and is fed into the cells as a most significant energy supplier. The glucose concentration in the blood is affected by a number of factors, primarily by the nutrition: the blood glucose concentration increases as a result of food intake. The hormone insulin is secreted as a direct reaction to the increase. It plays an important role in the regulation of the blood glucose concentration: the blood glucose concentration is decreased as a result of the promotion of glycogenesis (glycogen formation from glucose) and increase of the cell permeability for glucose.    Clinical Significance The determination of the blood glucose concentration is helpful for the diagnosis of a number of metabolic diseases. Due to the constant increase in diseases of the carbohydrate metabolism and improved quality of analytical procedures, the blood glucose concentration remains to be the most commonly determined parameter both in the central (laboratory) and local (wards) area of the clinic.     Reference Range Regular range in adults: 70 – 100 mg/dL (3.89 – 5.55 mmol/L) in capillary whole blood 70 – 115 mg/dL (3.9 – 6.38 mmol/L) in venous plasma    Elevated Values Hyperglycemias (> 100 mg of glucose/dL of whole blood, postprandial > 160 mg/dL) can generally be triggered by:  Insulin deficiency Absolutely in type I diabetes mellitus (absent pancreatic insulin production) or Relative in type II diabetes mellitus (peripheral insulin resistance) Increased glucose intake Decreased glucose tolerance Post-aggression metabolism    Decreased Values Hypoglycemias (less than 70 mg/dL of whole blood or less than 3.9 mmol/L) are triggered by: Increased peripheral glucose requirement due to physical activities Insulin overdose/endogenic hyperinsulinism (Morbus Addison, hypopituitarism, Sulfonylurea therapy) Reduced hepatic gluconeogenesis (terminal cirrhosis of the liver, alcohol intoxication, poisoning) Further diagnostic procedures: elevated lactate, β-Hydroxybutyrate and free fatty acids in the blood, positive ketone bodies in the urine   Malabsorption Polycythemia vera (unbalanced glucose distribution between erythrocytes and plasma and/or excessive glycolysis caused by erythrocytes) Leukemia (excessive leukocytic glycolysis or glycolysis as a result of serious erythroblast propagation, e.g. in a hemolytic crisis) Dumping syndrome (gastrectomy). The body tries to compensate it through energy recovery from other substances (lypolysis). It increases the cerebral perfusion to protect the brain.    LactateTab TitleTextPurpose Lactate is an end product of the anaerobic glucose metabolism. It is normally formed during muscle contractions. During physical strain, lactate concentration increases significantly, the metabolite is transported to the liver via blood and metabolized. Under regular aerobic conditions, lactate is oxidized to pyruvate, which in turn is decomposed into CO2 and H2O during the next step. The lactate concentration in the blood is affected by the production rate, the metabolic rate and the oxygen availability in the cells.    Clinical Significance  The determination of the blood lactate concentration is helpful for the evaluation of the oxygen supply of the tissue and as an indicator in particular for the assessment of perfusion disorders and regional oxygen deficiencies. Elevated oxygen deficiency causes high lactate concentrations and may cause severe lactic acidosis.    Reference Range < 1.8 mmol/L Values of up to 15 mmol/L are tolerable with short-term strain (exercise). Values of more than 4 mmol/L for an extended period of time in intensive care patients are associated with a higher predicted mortality rate.    Elevated Values Hyperlactatemia  Impaired oxygen supply Hypoxic hypoxemia Cardiac decompensation Pulmonary insufficiency CO-poisoning Trauma/shock Metabolic causes Competitive sports (increased accumulation of pyruvate as a result of increased glycolysis due to muscle activities) Diabetic or alcoholic ketoacidosis (increased fatty acid metabolism) Sepsis, infections such as malaria, cholera Renal insufficiency, impaired hepatic function Medications (including Biguanidine, Salicylates, cocaine, Theophylline) and toxic substances (Cyanide, Methanol, Ethylene glycol, etc.) Further diagnostic procedures to evaluate the pathological quality of the hyperlactatemia: blood pH, bicarbonate, pCO2, pO2, anion gap, ketone body concentration in the serum/urine (not elevated in pure lactic acidosis), creatinine, urea.    Decreased Values N/A When complete, select the X in the upper-right corner to close the window and continue.     Regular Values Download and print a copy of Acid-Base Metabolism, Oxygen Status, Electrolyte and Water Metabolism, and Metabolic Function Tests. Download and print a copy of the Interdependence of the Parameters. These charts indicate which tests need to be measured to obtain values for calculated parameters. Select Next to continue. Every year, 14 million people die as a result of cardiovascular diseases. Cardiovascular disorders are responsible for 20% of all deaths worldwide. In the industrialized world, up to a staggering 50% of all deaths are associated with cardiovascular diseases. The main causes are coronary heart disease, cerebral vascular disorders and high blood pressure. The unspecific chest pain associated with heart disease requires an immediate evaluation to determine whether the “chest pain” is caused by cardiac problems, pulmonary embolism or if it is of a different nature. Quick assessment of the cause along with the corresponding introduction of treatment means lower morbidity and mortality for patients. With respect to the point of care, markers that meet the following criteria are preferable: Broad diagnostic window allowing early diagnosis within the first 2–6 hours after the start of the symptoms as well as late diagnosis after 7 or more days. High cardiac specificity Proven clinical benefits High test quality, sensitive, quick, easy to handle, cost-efficient Cardiac Marker Test & D-Dimer Tests Learn about troponin, B-type natriuretic peptides, C-reactive protein, and D-dimer tests. Select the tabs below to learn more about troponin, B-type natriuretic peptides, C-reactive protein, and D-dimer tests.TitleTextTroponinTab TitleTextDescription Tiny cardiomyocyte necroses can be identified with troponins. In some patients with instable angina pectoris and regular ck-mb levels, elevated troponin values were found to indicate cellular necrosis. The prognosis for troponin-positive patients is comparably poor compared to the one for patients with infarction. The causes for elevated troponin levels include:  Myocardial infarction Pulmonary embolism Contusio cordis Myocarditis Cardiosurgical procedures  Uses Possible uses of troponin cardiac marker: Early AMI diagnosis (<6h) Confirmation of the AMI diagnosis Retrospective diagnosis of the AMI (up to 9 days) Diagnosis of the AMI in patients with multiple trauma, disorders of the skeleton and muscles, renal function impairment Definition of the infarction size Re-infarction diagnosis Prognosis/risk stratification for patients with instable    B-typeTab TitleTextDescription B-type natriuretic peptide (BNP) is a substance secreted from the ventricles or lower chambers of the heart in response to changes in pressure that occur when heart failure develops and worsens.      Uses NT-proBNP and its main indications: Diagnosis to exclude heart failure in case of suspicious symptoms (e.g. dyspnoea) because of the poor prognostic values Objective classification of the severity of the heart failure Differential diagnosis of cardiac/pulmonary disorders in patients with acute dyspnoea Prognosis and risk stratification for acute coronary syndromes and heart failure Monitoring of the therapeutic effect, based on the marker profile after therapeutic intervention    C-reactiveTab TitleTextDescription Elevated levels of a range of plasma proteins, including C-reactive protein, are observed in acute phase reactions. CRP measurements are useful for the determination and evaluation of infections, tissue injuries, inflammation and accompanying diseases. The determination of highly-sensitive CRP (hsCRP) is a suitable risk marker for the identification of subjects with an increased risk for cardiovascular disease. Combined with traditional clinical laboratory tests of acute coronary syndrome, hsCRP measurements can be used as independent marker for the prognosis of relapsing events in patients with stable coronary disorders or acute coronary syndromes.    Uses Possible uses of C-reactive protein cardiac marker: Prognosis/risk stratification for patients with instable angina Myocarditis, endocarditis, pericarditis    D-dimerTab TitleTextDescription A positive D-dimer test indicates the presence of an abnormally high level of fibrin degradation products, which indicate there has been significant clot (thrombus) formation and breakdown.    Uses D-dimers now play a central role in diagnostic procedures to: exclude thromboembolism (DVD: deep leg vein thrombosis; PE: pulmonary embolism) follow-up of the diagnostic procedures for consumption coagulopathy When complete, select the X in the upper-right corner to close the window and continue.