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Original Article Correlation Between Peripheral Venous And Arterial Blood Gas Measurements In Patients Admitted To The Intensive Care Unit: A Single-center Study

Original Article Correlation Between Peripheral Venous And Arterial Blood Gas Measurements In Patients Admitted To The Intensive Care Unit: A Single-center Study

Introduction The acid–base and respiratory status of critical patients are commonly ascertained by means of arterial blood gas (ABG) analysis. Nevertheless, the test can cause patients to experience discomfort, and its associated complications include arterial injury, thrombosis or embolization, hematoma, aneurysm formation, and reflex sympathetic dystrophy [1,2]. A further drawback for health care providers is the possibility of a needle stick injury when performing an ABG. A comparatively safer procedure is venous blood gas (VBG) analysis, which poses fewer risks to both the patients and health care professionals. VBG may eventually take the place of ABG analysis in determining acid–base status. In contrast to earlier studies, which questioned the precision of VBG values [3–5], more recent evidences indicate a concurrence of ABG and VBG values [6–14]. However, as far as we can determine, the correlation between all parameters typically used in arterial and peripheral VBG samples as found in a broad population of intensive care unit (ICU) patients has not been studied previously. An earlier study investigated whether the similarities between ABG and VBG values are sufficient for the respiratory and dynamic acid–base conditions. For this evaluation, each patient provided multiple paired ABG and VBG samples during the length of their ICU treatment. The purpose of this study was to investigate the correlation of ABG and peripheral VBG samples for all common parameters (bicarbonate, total CO2, pH, and PCO2) in an ICU patient population exhibiting a variety of pathologies. Specific attention was given to the analysis of each patient's multiple paired arterial and venous samples. Methods A single-center, prospective trial was performed from April 2010 to September Continue reading >>

Vbg Versus Abg

Vbg Versus Abg

OVERVIEW Venous blood gases (VBG) are widely used in the emergency setting in preference to arterial blood gases (ABG) as a result of research published since 2001 The weight of data suggests that venous pH has sufficient agreement with arterial pH for it to be an acceptable alternative in clinical practice for most patients Nevertheless acceptance of this strategy has been limited by some specialties and maybe inappropriate in some settings; for instance there is no data to confirm that this level of agreement is maintained in shock states or mixed acid-base disturbances Clinically acceptable limits of agreement for blood gas parameters remains poorly defined ARTERIAL BLOOD GAS PROS AND CONS Advantages gold standard test for determining the arterial metabolic millieu (pH, PaCO2, HCO3) can determine PaO2 Disadvantages pH, PCO2 (if normocapnic), HCO3 and base excess from a VBG are usually adequate for clinical decision making SpO2 is usually sufficient for clinical decision making unless pulse oximetry is unreliable for other reasons (e.g. shock state, poor pick up) painful (should be performed with local anaesthetic in conscious patients) increased risk of bleeding and hematoma risk of pseudo aneurysm and AV fistula infection nerve injury digital ischemia injury to staff delays in care serial exams may be needed venous sampling may better represent the tissue milieu CORRELATION BETWEEN VBG AND ABG pH Good correlation pooled mean difference: +0.035 pH units pCO2 good correlation in normocapnia non-correlative in severe shock 100% sensitive in detecting arterial hypercarbia in COPD exacerbations using cutoff of PaCO2 45 mmHg and laboratory based testing (McCanny et al, 2012), i.e. if VBG PCO2 is normal then hypercapnia ruled out (PaCO2 will be normal), though this conflic Continue reading >>

Use Of Sodium Bicarbonate And Blood Gas Monitoring In Diabetic Ketoacidosis: A Review

Use Of Sodium Bicarbonate And Blood Gas Monitoring In Diabetic Ketoacidosis: A Review

Use of sodium bicarbonate and blood gas monitoring in diabetic ketoacidosis: A review Department of Internal Medicine, Eastern Virginia Medical School, Norfolk, VA 23501, United States Medicine Service, Hampton Veterans Affairs Medical Center, Hampton, VA 23667, United States. ude.smve@eslesseh Author contributions: All authors equally contributed to this paper with literature review and analysis, drafting and critical revision and editing, and final approval of the final version. Correspondence to: Sean E Hesselbacher, FCCP, MD, Assistant Professor, Medicine Service, Hampton Veterans Affairs Medical Center, 100 Emancipation Drive, Hampton, VA 23667, United States. ude.smve@eslesseh Telephone: +1-757-7229961 Fax: +1-757-7283187 Received 2018 Jul 22; Revised 2018 Aug 30; Accepted 2018 Oct 9. Copyright The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved. This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. This article has been cited by other articles in PMC. Diabetic ketoacidosis (DKA) is a severe and too-common complication of uncontrolled diabetes mellitus. Acidosis is one of the fundamental disruptions stemming from the disease process, the complications of which are potentially lethal. Hydration and insulin administration have been the cornerstones of DKA therapy; however, adjunctive treatments such as the use of sodium bicarbonate and p Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

4 Evaluation 5 Management Defining features include hyperglycemia (glucose > 250mg/dl), acidosis (pH < 7.3), and ketonemia/ketonuria Leads to osmotic diuresis and depletion of electrolytes including sodium, magnesium, calcium and phosphorous. Further dehydration impairs glomerular filtration rate (GFR) and contributes to acute renal failure Due to lipolysis / accumulation of of ketoacids (represented by increased anion gap) Compensatory respiratory alkalosis (i.e. tachypnea and hyperpnea - Kussmaul breathing) Breakdown of adipose creates first acetoacetate leading to conversion to beta-hydroxybutyrate Causes activation of RAAS in addition to the osmotic diuresis Cation loss (in exchange for chloride) worsens metabolic acidosis May be the initial presenting of an unrecognized T1DM patient Presenting signs/symptoms include altered mental status, tachypnea, abdominal pain, hypotension, decreased urine output. Perform a thorough neurologic exam (cerebral edema increases mortality significantly, especially in children) Assess for possible inciting cause (especially for ongoing infection; see Differential Diagnosis section) Ill appearance. Acetone breath. Drowsiness with decreased reflexes Tachypnea (Kussmaul's breathing) Signs of dehydration with dry mouth and dry mucosa. Perform a thorough neurologic exam as cerebral edema increases mortality significantly, especially in children There may be signs from underlying cause (eg pneumonia) Differential Diagnosis Insulin or oral hypoglycemic medication non-compliance Infection Intra-abdominal infections Steroid use Drug abuse Pregnancy Diabetic ketoacidosis (DKA) Diagnosis is made based on the presence of acidosis and ketonemia in the setting of diabetes. Bicarb may be normal due to compensatory and contraction alcoholosis so the Continue reading >>

How To Read A Venous Blood Gas (vbg) - Top 5 Tips

How To Read A Venous Blood Gas (vbg) - Top 5 Tips

Share on Facebook Share on Twitter Arterial blood gas analysers are designed to measure multiple components in the arterial blood. The readout from the machine quotes normal values based on the assumption that the sample analysed is arterial (an ABG). There is currently a plague of ‘venous’ blood gases (VBG) in clinical practice. A VBG is obtained by placing a venous sample in the arterial blood gas analyser. VBGs are popular as it is far less painful for the patient to obtain a venous sample compared to an arterial sample. In addition, obtaining ABGs carries well known risks. VBGs are useful if you know how to interpret them and have a knowledge of their limitations. An ABG has a number of uses, the VBG can be substituted for some of these uses but not for others. 1) Assessment of oxygenation status The pO2 on a VBG bears no relationship to the paO2. The VBG is of no value in assessing oxygenation status. 2) Assessment of hypercarbia In patients with COPD we need to detect the presence of CO2 retention. This has an important impact on treatment. If the pCO2 on the VBG is above the normal arterial range (ie >45 mmHg, >6 kPa) the patient has CO2 retention. (100% sensitivity reported, so, at least in studies, it does not appear to miss any cases) However, the absolute value of pCO2 on the VBG above this range correlates poorly with the paCO2 and cannot be used to monitor the response to treatment in a CO2 retainer. 3) Assessment of pH status This is probably where the VBG is of most use but there are still limitations. The venous pH correlates well with the arterial pH. The venous pH tends to be more acidic than the arterial pH. Add 0.035 to the venous pH to estimate the arterial pH. In conditions such as DKA, it is probably reasonable to follow the pH response to tre Continue reading >>

Lab Test

Lab Test

Measurement of serum chloride concentrations for the assessment of certain disorders manifesting with electrolyte abnormalities. This test is performed as part of multiphasic testing for what is usually called "electrolytes." By itself, this test does not provide much information, but with interpretation of the other electrolytes, chloride can given an indication of acid-base balance and hydration status. Neonates, Cord Blood: 96-104 mEq/L (96-104 mmol/L) Neonates, 0 to 30 days: 98-113 mEq/L (98-113 mmol/L) Children, older than 30 days: 98-107 mEq/L (98-107 mmol/L) *(PDR) Adult/elderly: 98-106 mEq/L or 98-106 mmol/L Child: 90-110 mEq/L Newborn: 96-106 mEq/L Premature infant: 95-110 mEq/L Critical Values: < 80 or > 115 mEq/L Hypokalemia - high serum chloride levels with hypokalemia are usually associated with low serum bicarbonate levels and may reflect either metabolic acidosis (e.g., diarrhea renal tubular acidosis) or respiratory alkalosis (e.g., cirrhosis, sepsis salicylate poisoning). Low serum chloride levels with hypokalemia are usually associated with increased serum bicarbonate and metabolic alkalosis, suggesting diuretic use, vomiting, hyperaldosteronism, or abuse of licorice or laxatives as the etiology of hypokalemia. Initial evaluation and monitoring of diabetic ketoacidosis (DKA)- chloride measurement is used to calculate plasma anion gap. Hyperchloremic normal anion gap metabolic acidosis is present on admission in about 10% of patients with DKA and is present in nearly al patients after resolution of Ketonemia. During treatment, severity of hyperchloremia can be exacerbated by excessive administration of 0.9% sodium chloride for hydration. Metabolic acidosis - an elevated serum chloride level occurs in Hyperchloremic acidosis, a metabolic acidosis in whic Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Snap Shot A 12 year old boy, previously healthy, is admitted to the hospital after 2 days of polyuria, polyphagia, nausea, vomiting and abdominal pain. Vital signs are: Temp 37C, BP 103/63 mmHg, HR 112, RR 30. Physical exam shows a lethargic boy. Labs are notable for WBC 16,000, Glucose 534, K 5.9, pH 7.13, PCO2 is 20 mmHg, PO2 is 90 mmHg. Introduction Complication of type I diabetes result of ↓ insulin, ↑ glucagon, growth hormone, catecholamine Precipitated by infections drugs (steroids, thiazide diuretics) noncompliance pancreatitis undiagnosed DM Presentation Symptoms abdominal pain vomiting Physical exam Kussmaul respiration increased tidal volume and rate as a result of metabolic acidosis fruity, acetone odor severe hypovolemia coma Evaluation Serology blood glucose levels > 250 mg/dL due to ↑ gluconeogenesis and glycogenolysis arterial pH < 7.3 ↑ anion gap due to ketoacidosis, lactic acidosis ↓ HCO3- consumed in an attempt to buffer the increased acid hyponatremia dilutional hyponatremia glucose acts as an osmotic agent and draws water from ICF to ECF hyperkalemia acidosis results in ICF/ECF exchange of H+ for K+ moderate ketonuria and ketonemia due to ↑ lipolysis β-hydroxybutyrate > acetoacetate β-hydroxybutyrate not detected with normal ketone body tests hypertriglyceridemia due to ↓ in capillary lipoprotein lipase activity activated by insulin leukocytosis due to stress-induced cortisol release H2PO4- is increased in urine, as it is titratable acid used to buffer the excess H+ that is being excreted Treatment Fluids Insulin with glucose must prevent resultant hypokalemia and hypophosphatemia labs may show pseudo-hyperkalemia prior to administartion of fluid and insulin due to transcellular shift of potassium out of the cells to balance the H+ be Continue reading >>

End-tidal Capnography Can Be Useful For Detecting Diabetic Ketoacidosis, Monitoring Copd

End-tidal Capnography Can Be Useful For Detecting Diabetic Ketoacidosis, Monitoring Copd

End-Tidal Capnography Can be Useful for Detecting Diabetic Ketoacidosis, Monitoring COPD by Katrina DAmore, DO, MPH, Justin McNamee, DO, and Terrance McGovern, DO, MPH End-tidal capnography has gained momentum over the years as a standard for monitoring patients undergoing procedural sedation in the emergency department, with a level B recommendation coming out of ACEPs clinical policy regarding procedural sedation in 2014.1 It can identify hypoventilation earlier than other monitoring tools we have at our disposal in the emergency department, but its utility doesnt end there. It can quickly and efficiently answer clinical questions beyond that of sufficient ventilation. Are the chest compressions being performed on your cardiac arrest inadequate? Should you stop resuscitation efforts? Is your hyperglycemic diabetic in diabetic ketoacidosis (DKA)? Is that nasogastric tube in the stomach? End-tidal capnography can lend insight to these questions that emergency physicians encounter on a daily basis. End-tidal carbon dioxide (EtCO2) sensibly correlates with the pathophysiology of those and many other disease processes and can help guide decision making on your next shift. Capnography offers an indirect method to detect metabolic acidosis. EtCO2 measurements have been shown to closely estimate arterial partial pressure of carbon dioxide (pCO2) in healthy patients and also in the presence of metabolic derangements such as acidosis. The end-tidal capnogram is separated into four separate phases (see Figure 1). Phase 0 begins during the inhalation phase of the respiratory cycle and the capnogram drops precipitously from its peak level at the end of expiration. Once the patient begins to exhale (phase I), the initial expired air is predominantly dead space with little expired Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus.[1] Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness.[1] A person's breath may develop a specific smell.[1] Onset of symptoms is usually rapid.[1] In some cases people may not realize they previously had diabetes.[1] DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances.[1] Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids.[1] DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies.[3] DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine.[1] The primary treatment of DKA is with intravenous fluids and insulin.[1] Depending on the severity, insulin may be given intravenously or by injection under the skin.[3] Usually potassium is also needed to prevent the development of low blood potassium.[1] Throughout treatment blood sugar and potassium levels should be regularly checked.[1] Antibiotics may be required in those with an underlying infection.[6] In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.[1][6] Rates of DKA vary around the world.[5] In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% a year.[1][5] DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>

Exam Shows Diffuse Abdominal Tenderness With Guarding.

Exam Shows Diffuse Abdominal Tenderness With Guarding.

A 14 y/o female is brought to the emergency department by her mother after being found unresponsive at home. She had been ill the day before with nausea and vomiting, but was not running a fever. Her parents had kept her home from school that day. When her mother came home at lunchtime to check on her, she was very lethargic and not responding coherently. By the time she arrived at the hospital, she had to be brought in to the ED on a gurney. Initial evaluation showed O2 sat 100% on room air, pulse 126, respirations 30, BP 92/68, temperature 101.2 F. She appears pale, mucous membranes are dry and she only responds to painful stimuli. Exam shows diffuse abdominal tenderness with guarding. Differential diagnosis? What initial treatment would you suggest? What labs would you order? Any xrays or additional studies? CBC WBC 23,500 Hgb 14.2 g/dL Hct 45% Platelets 425,000 BMP Sodium 126 Potassium 5.2 Chloride 87 CO2 <5 BUN 32 Creatinine 1.5 Glucose 1,376 Arterial Blood Gases pH 7.19 Po2 100 mm Hg HCO3 7.5 mmo/L Pco2 20 mm Hg Sao2 98% (room air) Urine Specific gravity 1.015 Ketones 4+ Leukocytes few Glucose 4+ Nitrates 0 RBCs many Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. DKA occurs mostly in type 1 diabetics. It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Symptoms and signs of DKA Nausea & vomiting Abdominal pain--particularly in children Lethargy and somnolence Kussmaul respirations Hypotension Tachycardia Fruity breath Continue reading >>

Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Go to: Pathogenesis In both DKA and HHS, the underlying metabolic abnormality results from the combination of absolute or relative insulin deficiency and increased amounts of counterregulatory hormones. Glucose and lipid metabolism When insulin is deficient, the elevated levels of glucagon, catecholamines and cortisol will stimulate hepatic glucose production through increased glycogenolysis and enhanced gluconeogenesis4 (Fig. 1). Hypercortisolemia will result in increased proteolysis, thus providing amino acid precursors for gluconeogenesis. Low insulin and high catecholamine concentrations will reduce glucose uptake by peripheral tissues. The combination of elevated hepatic glucose production and decreased peripheral glucose use is the main pathogenic disturbance responsible for hyperglycemia in DKA and HHS. The hyperglycemia will lead to glycosuria, osmotic diuresis and dehydration. This will be associated with decreased kidney perfusion, particularly in HHS, that will result in decreased glucose clearance by the kidney and thus further exacerbation of the hyperglycemia. In DKA, the low insulin levels combined with increased levels of catecholamines, cortisol and growth hormone will activate hormone-sensitive lipase, which will cause the breakdown of triglycerides and release of free fatty acids. The free fatty acids are taken up by the liver and converted to ketone bodies that are released into the circulation. The process of ketogenesis is stimulated by the increase in glucagon levels.5 This hormone will activate carnitine palmitoyltransferase I, an enzyme that allows free fatty acids in the form of coenzyme A to cross mitochondrial membranes after their esterification into carnitine. On the other side, esterification is reversed by carnitine palmitoyltransferase I Continue reading >>

Abg’s—it’s All In The Family

Abg’s—it’s All In The Family

By Cyndi Cramer, BA, RN, OCN, PCRN RealNurseEd.com 3.0 Contact Hour Self Learning Module Objectives: Identify the components of the ABG and their normal ranges Interpret ABG values and determine the acid base abnormality given Identify the major causes of acid base abnormalities Describe symptoms associated with acid base abnormalities Describe interventions to correct acid base abnormalities Identify the acceptable O2 level per ABG and Pulse Oximetry Identify four causes of low PaO2 The Respiratory System (Acid); CO2 is a volatile acid If you increase your respiratory rate (hyperventilation) you "blow off" CO2 (acid) therefore decreasing your CO2 acid—giving you ALKLAOSIS If you decrease your respiratory rate (hypoventilation) you retain CO2 (acid) therefore increasing your CO2 (acid)—giving you ACIDOSIS The Renal System (Base); the kidneys rid the body of the nonvolatile acids H+ (hydrogen ions) and maintain a constant bicarb (HCO3). Bicarbonate is the body’s base You have Acidosis when you have excess H+ and decreased HCO3- causing a decrease in pH. The Kidneys try to adjust for this by excreting H+ and retaining HCO3- base. The Respiratory System will try to compensate by increasing ventilation to blow off CO2 (acid) and therefore decrease the Acidosis. You have Alkalosis when H+ decreases and you have excess (or increased) HCO3- base. The kidneys excrete HCO3- (base) and retain H+ to compensate. The respiratory system tries to compensate with hypoventilation to retain CO2 (acid) To decrease the alkalosis Compensation The respiratory system can effect a change in 15-30 minutes The renal system takes several hours to days to have an effect. RESPIRATORY ACIDOSIS: pH < 7.35 (Normal: 7.35 - 7.45) CO2 > 45 (Normal: 35 – 45) 1. Causes: Hypoventilation a. Depressio Continue reading >>

Tips From Other Journals

Tips From Other Journals

Diabetic ketoacidosis consists of elevated blood glucose, measurable ketone bodies and metabolic acidosis. Arterial blood gas determination is considered essential in the initial evaluation of patients with suspected diabetic ketoacidosis. Arterial blood sampling is painful, may be technically difficult and must be done in addition to venous sampling when testing for electrolytes and other values. The general correlation between arterial and venous pH measurements is well established, although this correlation has not been studied in patients with diabetic ketoacidosis. Brandenburg and Dire prospectively studied the relationship between arterial and venous blood gas values in the initial evaluation of patients with suspected diabetic ketoacidosis. Thirty-eight patients with 44 episodes of diabetic ketoacidosis who presented to an emergency department with blood glucose levels greater than 250 mg per dL (13.9 mmol per L), urine dipstick results positive for ketones and clinical suspicion of diabetic ketoacidosis were included in the study. Arterial and venous samples were obtained as temporally close to each other as possible for blood gas analysis. The mean difference between arterial and venous pH values was 0.03 (range: 0 to 0.11). Arterial and venous pH results, arterial and venous bicarbonate measurements and arterial bicarbonate and serum carbon dioxide results were also closely correlated. The authors conclude that the peripheral venous pH measurement is a valid and reliable substitute for arterial pH in patients with diabetic ketoacidosis. A potential disadvantage of using venous determinations to determine the presence of diabetic ketoacidosis is that it may be more difficult to detect when mixed acid-base disturbances are present, since venous blood values may Continue reading >>

Abg (arterial Blood Gas)

Abg (arterial Blood Gas)

Arterial Blood Gas analysis typically measures: And may include: These measurements are often used to evaluate oxygenation of the tissues and pulmonary function. pH is a measurement of the acidity of the blood, reflecting the number of hydrogen ions present. Lower numbers mean more acidity; higher number mean more alkalinity. pH is Elevated (more alkaline, higher pH) with: Hyperventilation Anxiety, pain Anemia Shock Some degrees of Pulmonary disease Some degrees of Congestive heart failure Myocardial infarction Hypokalemia (decreased potassium) Gastric suctioning or vomiting Antacid administration Aspirin intoxication pH is Decreased (more acid, lower pH) with: Strenuous physical exercise Obesity Starvation Diarrhea Ventilatory failure More severe degrees of Pulmonary Disease More severe degrees of Congestive Heart Failure Pulmonary edema Cardiac arrest Renal failure Lactic acidosis Ketoacidosis in diabetes pCO2 (Partial Pressure of Carbon Dioxide) reflects the the amount of carbon dioxide gas dissolved in the blood. Indirectly, the pCO2 reflects the exchange of this gas through the lungs to the outside air. Two factors each have a significant impact on the pCO2. The first is how rapidly and deeply the individual is breathing: Someone who is hyperventilating will "blow off" more CO2, leading to lower pCO2 levels Someone who is holding their breath will retain CO2, leading to increased pCO2 levels The second is the lungs capacity for freely exchanging CO2 across the alveolar membrane: With pulmonary edema, there is an extra layer of fluid in the alveoli that interferes with the lungs' ability to get rid of CO2. This leads to a rise in pCO2. With an acute asthmatic attack, even though the alveoli are functioning normally, there may be enough upper and middle airway obstru Continue reading >>

Blood Gas Test

Blood Gas Test

What Is a Blood Gas Test? A blood gas test measures the amount of oxygen and carbon dioxide in the blood. It may also be used to determine the pH of the blood, or how acidic it is. The test is commonly known as a blood gas analysis or arterial blood gas (ABG) test. Your red blood cells transport oxygen and carbon dioxide throughout your body. These are known as blood gases. As blood passes through your lungs, oxygen flows into the blood while carbon dioxide flows out of the blood into the lungs. The blood gas test can determine how well your lungs are able to move oxygen into the blood and remove carbon dioxide from the blood. Imbalances in the oxygen, carbon dioxide, and pH levels of your blood can indicate the presence of certain medical conditions. These may include: kidney failure heart failure uncontrolled diabetes hemorrhage chemical poisoning a drug overdose shock Your doctor may order a blood gas test when you’re showing symptoms of any of these conditions. The test requires the collection of a small amount of blood from an artery. It’s a safe and simple procedure that only takes a few minutes to complete. A blood gas test provides a precise measurement of the oxygen and carbon dioxide levels in your body. This can help your doctor determine how well your lungs and kidneys are working. This is a test that is most commonly used in the hospital setting to determine the management of acutely ill patients. It does not have a very significant role in the primary care setting, but may be used in a pulmonary function lab or clinic. Your doctor may order a blood gas test if you’re showing symptoms of an oxygen, carbon dioxide, or pH imbalance. The symptoms can include: shortness of breath difficulty breathing confusion nausea These symptoms may be signs of certain Continue reading >>

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