Acid Base Balance Part 2 PDF

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Summary

Base Excess- Calculated parameter from pH and pCO2. The amount of acid required to restore 1L of blood back to normal pH at a PCO2 of 40 mmHg. - Normally, the base excess should be 0-2, and abnormal results reflect a metabolic disturbance. SBE is normal in uncompensated respiratory acidosis or alkal...

Description

MLSC-3111, Clinical Biochemistry II Base Excess -

Calculated parameter from pH and pCO2. The amount of acid required to restore 1L of blood back to normal pH at a PCO2 of 40 mmHg. Normally, the base excess should be 0-2, and abnormal results reflect a metabolic disturbance. SBE is normal in uncompensated respiratory acidosis or alkalosis. An SBE greater than 2 is metabolic alkalosis from excessive bicarbonate. An SBE less than -2 is metabolic acidosis from insufficient bicarbonate.

Oxygen Status Testing -

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Ventilation, the mechanical process of moving air in and out of the lungs. Chemoreceptors in the brain’s respiratory centre detect pH changes to stimulate or depress breathing. Respiration, the exchange of gasses between the atmosphere and the capillaries of the pulmonary function. The exchange of O2 and CO2 occurs across the alveolar membrane through a concentration gradient. Hypoxia, deficiency of oxygen being delivered to the tissues. Causes anaerobic respiration which makes lactic acid to cause metabolic acidosis and tissue death. Anoxia, close to total absence of oxygen being delivered to the tissue. Hypoxemia, decreased oxygen content in the blood. Caused by impaired blood oxygenation or low Hb. Respiratory Failure, failure of the lungs to adequately perform pulmonary gas exchange. The delivery of oxygen to the tissues cells occurs via synergy of respiratory and cardiovascular systems. Consists of three events: o Uptake, oxygen goes into the blood from alveolar diffusion o Transport, delivery of oxygen through the blood into the tissues o Release, oxygen is released from Hb into the tissue A disturbance in any of these steps will lead to poor oxygenation. The three oxygen status tests are oxygen uptake, oxygen transport and oxygen release.

Uptake -

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pO2, pressure exerted by oxygen in a mixture of gasses which represents dissolved O2. It is a direct measurement. pO2 represents only 1-2% of all the oxygen in the blood but is a key parameter for assessing adequacy of blood oxygenation. pO2 also provides means for diagnosing respiratory failure and it is defined as a pO2 lower than 60 mmHg. It also provides means for monitoring supplemental oxygen therapy. sO2, the percent of all functional hemoglobin that is bound to O2. Represents 98-99% of all oxygen in the blood. Increasing pO2 leads to more O2 bound to Hb (uptake) and less O2 dissolved in the plasma.

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For optimum oxygenation of blood, the blood must contain enough functional Hb and the Hb must be more than 95% saturated with O2. To achieve sO2 greater than 0.95, pO2 must be greater than 80 mmHg. If both pO2 and sO2 are normal, there is no Hb related disorder.

Transport -

Hb is considered a parameter for O2 transport. O2Hb, oxygenated hemoglobin that is reversible. HHB, deoxygenated hemoglobin that is not bound to O2 but able to bind to O2 if available. It is not a functional hemoglobin in terms of O2 transport. Dyshemoglobin, result from interference of O2 binding and are considered incapable of binding to O2 (CoHb, MetHb or SHb). THb, the sum of O2Hb, HHb and dysfunctional Hb.

Co-Oximetry -

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A spectrophotometric determination of O2Hb, etc. Able to identify Hb variants by taking Abs readings at numerous wavelengths (6-128 wavelengths). Determines the THb as well as each Hb fraction. Used to measure THb, O2Hb, HHb and dyshemoglobin Co-Oximetry is not standard for all ABG analyzers. The analyzer prepares hemolysate from whole blood, usually via ultrasonic vibration in a cuvette. Miscalibration, lipemia (and other spectral-interfering samples) and incomplete lysing of RBCS cause interferences. Often lipemia is missed on AGB analysis because the sample comes mixed in a syringe. CoHb, formed through reversible binding of carbon monoxide to Hb. CO has an affinity for Hb that is 240X greater than that of O2. Inhaled CO can cause this binding and severe hypoxia. Normal CoHb is less than 0.03, but smokers can have their normal up to 0.08. A cherry red colour of blood samples is indicative of high COHb. Elevated levels of CoHb are toxic. >0.60 produces a loss of consciousness and >0.80 causes convulsion and death. fCoHb, fraction of THb present as CoHb calculated by (cCoHb/ctHb) x 100. MetHb, Hb in which ferrous iron (Fe2+) is oxidized to ferric iron (Fe3+). Hb is unable to bind to O2 as iron is in an oxidized rather than a reduced state. A chocolate brown coloured sample is usually indicative of high MetHb. This is reversible by methemoglobin reductases in RBCs or by other reducing agents. Most likely high MetHb is caused by exposure to oxidative drugs. Sometimes is also congenital. Acute causes of high MetHb are treated with Methylene Blue to accelerate the activity of the reductase system. The normal MetHb reference range is 0.004 – 0.015. fMetHb = (cMetHb/ctHb x 100).

MLSC-3111, Clinical Biochemistry II -

SulfHb, stable compound formed from irreversible linkage of sulfur to Hb. Very rare but appears after exposure to sulfanomides, phenacetin, acetanilide and TNT. Samples have a greenish pigment if they are high in SHb and SHb is ineffective for O2 transport. SHb remains in the RBCs until they die. May cause the creation of Heinz bodies and high levels can cause anoxia and cyanosis.

Blood Gas Tests for O2Hb -

FO2Hb, the fraction of oxygenated hemoglobin to all Hbs. Estimated sO2, calculated from pH, pO2, and Hb using the equation based on the oxygen dissociation curve. The co-oximeter gives us a more accurate report of how much Hb is bound to oxygen. In the absence of dysHbs in the blood, sO2 and fO2Hb should be similar. In the presence of dysHbs in the blood, fO2Hb will be lower than the sO2. Pulse Oximeters, estimate sO2 via measurements at only two wavelengths to detect O2Hb and HHb.

Oxygen Released to Tissues -

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To utilize transported oxygen it must be released to the peripheral tissues. A decreased O2 affinity promotes release to tissues while an increase in affinity promotes O2 binding. CO2, Acid, 2,3-DPG, Exercise and Temperature (CADET) will all affect Hb affinity to O2. Metabolic processes in tissues causes increased temperature, CO2 production, lactic acid and 2,3-DPG in RBCs. These conditions will lower the affinity of O2 to Hb. Hb affinity to O2 is key to evaluating the blood’s ability to release O2 into the tissues. p50, the pO2 at which 50% of Hb is bound to O2. An increased p50 will cause a decreased affinity (right shift) between Hb and O2 (increased O2 release in the tissues). A decreased p50 will cause an increased affinity (left shift) between Hb and O2 (increased O2 uptake in the lungs). Lactic Acidosis, due to inadequate oxygen uptake in the lungs or the reduced blood flow to the tissues. Results in anaerobic respiration and lactic acid production to lower the blood pH. Lactate Testing, used as a marker for poor tissue perfusion. It is also a good prognostic indicator of patient outcome, since an increase lactate result is associated with morbidity and mortality. Lactate samples are usually collected in NaFl tubes on ice to reduce RBC metabolism. Lactate can be done on ABG analyzers or routine chem analyzers. Should be considered STAT and require immediate processing.

Sample Collection

MLSC-3111, Clinical Biochemistry II

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ABG samples are collected ideally from the radial artery (thumb side of the wrist). The modified Allen’s test checks for proper collateral circulation to the hands. Patients should be at rest for 5 minutes and ventilatory changes should be unchanged for at least 20 minutes. This will ensure the patient is in a steady state of ventilation for representative results. Complications of ABG punctures include: o Hematomas, more common in ABG punctures than venipuncture. o Arteriospasm, usually temporary constriction of an artery from an involuntary response to pain. A completely closed artery can lead to gangrene from hypoxia in the hand tissue after artery constriction. Modified Allen’s Test will prevent this. o Thrombus Formation, can occur on the inside of the arterial wall during puncture and may result in a occlusion. o Bleeding, can occur in patients coagulation disorders. o Sepsis, can occur if the puncture site was not properly cleansed. o Nerve Damage, can be due to improper puncture technique in deep tissue areas with nerves. Cellular metabolism still goes on after collection. pCO2 and cLac can increase while pO2, cGLU and pH can decrease as time goes on without analyzing. Temperature, increased temperature decreases pO2, increases pCO2 (4%/degree) and decreases pH (0.015 units/degree). These changes occur if the sample isn’t processed ASAP. Not all patients are at a body temperature of 37 degrees. This can be corrected for using algorithms during analysis to find out what would be expected at the patient’s body temperature. Only pH, pCO2 and pO2 are corrected for temperature. pH temperature adjustment is reciprocal to patient temperature (high temp needs a lowered pH). pCO2 and pO2 adjustments are done in the same direction as the temperature. Transport, a sample of ABG must be transported in an ice slurry and is acceptable up to one hour if placed in the slurry and 30 minutes after the time of collection. However, CLSI recommends no ice because it shouldn’t take an hour to analyze an ABG. Storage, ABG samples are good for 30 minutes with no ice, 30-60 minutes on ice and rejected at >60 minutes. Metabolically active WBCs and thrombocytes also can affect test results. High levels of WBCs in leukemic patients can result in falsely lowered pO2. Room Air Contamination, air bubbles in the sample mean room air contamination. This can cause pCO2 to decrease (CO2 escapes into the air), pH to increase and pO2 to increase or decrease (depending on the samples original pO2). Anaerobic collection is essential for ABG collections. Air bubbles must be expelled from the syringe ASAP after aspiration. Samples should not be mixed with heparin or cooled when a bubble is present.

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Plastics syringes when stored on ice cause an increased permeability of room air O2 through the plastic resulting in pO2 errors. O2 solubility increases at a lower temperature. Samples Collected in glass syringes on ice slurry may yield acceptable blood gas analyzers for up to 2h after collection. Insufficient mixing can cause the heparin to not get throughout the sample, resulting in blood clots. Heparin only prevents clotting and cannot reverse clotting. Clots can lower THb and therefor all parameters relying on THb will be affected. Micro clots can form in as soon as 10 seconds. If a sample is received and it is visibly clotted, reject it and request a new collection. Inadequate mixing prior to analysis results in an inhomogeneous sample error on the machine. A syringe is stated to contain 50 IU/mL of heparin when filled with 1.5 mL of blood. Overfilling means low heparin leading to clots and underfilling means too much heparin and alters electrolyte concentrations. The addition of 10% of venous blood to an arterial sample can produce a drop in pO2 greater than 25%. Can occur if a vein is also punctured when arterial blood was collected. Three levels of QC for pH, pCO2 and pO2 are run. Level one is for acidosis, two is for normal and three is for alkalosis....