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 >>
Metabolic Acidosis Treatment & Management
Approach Considerations Treatment of acute metabolic acidosis by alkali therapy is usually indicated to raise and maintain the plasma pH to greater than 7.20. In the following two circumstances this is particularly important. When the serum pH is below 7.20, a continued fall in the serum HCO3- level may result in a significant drop in pH. This is especially true when the PCO2 is close to the lower limit of compensation, which in an otherwise healthy young individual is approximately 15 mm Hg. With increasing age and other complicating illnesses, the limit of compensation is likely to be less. A further small drop in HCO3- at this point thus is not matched by a corresponding fall in PaCO2, and rapid decompensation can occur. For example, in a patient with metabolic acidosis with a serum HCO3- level of 9 mEq/L and a maximally compensated PCO2 of 20 mm Hg, a drop in the serum HCO3- level to 7 mEq/L results in a change in pH from 7.28 to 7.16. A second situation in which HCO3- correction should be considered is in well-compensated metabolic acidosis with impending respiratory failure. As metabolic acidosis continues in some patients, the increased ventilatory drive to lower the PaCO2 may not be sustainable because of respiratory muscle fatigue. In this situation, a PaCO2 that starts to rise may change the plasma pH dramatically even without a significant further fall in HCO3-. For example, in a patient with metabolic acidosis with a serum HCO3- level of 15 and a compensated PaCO2 of 27 mm Hg, a rise in PaCO2 to 37 mm Hg results in a change in pH from 7.33 to 7.20. A further rise of the PaCO2 to 43 mm Hg drops the pH to 7.14. All of this would have occurred while the serum HCO3- level remained at 15 mEq/L. In lactic acidosis and diabetic ketoacidosis, the organic anion can r Continue reading >>
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Respiratory Alkalosis
Abstract: Steady state blood CO2 levels remain relatively constant in compensated respiratory acidosis and alkalosis (i.e., CO2 in = CO2 out). Uncompensated respiratory alkalosis is associated with an increased blood pH, and a modestly decreased HCO3 – concentration. Renal compensation for respiratory alkalosis involves a decrease in HCO3 – reabsorption. The blood pH may be within the normal range in some mixed acid-base disorders. A mixed acid-base disturbance is indicated when the Pco2 and blood HCO3 – concentration are moving in opposite directions. Mixed acid-base distrubances can be additive, or subtractive. The bicarbonate buffer equation is shifted to the left in metabolic acidosis and respiratory alkalosis. Respiratory alkalosis can be due to either direct or reflex hypoxemic stimulation of the respiratory center, to pulmonary disease, or to excessive mechanical ventilation. Respiratory Alkalosis Respiratory alkalosis results from excessive ventilation (hyperventilation). In respiratory alkalosis, Pco2 falls, leading to an increase in pH (alkalosis). If the alkalosis persists for more than 12 hours, the alkalosis may be partially compensated by decreased renal H+ excretion. During respiratory alkalosis, HCO3− may fall acutely owing to equilibration with depleted CO2. There is a 2 mEq/L decrease in HCO3− per 10 mm Hg decrease Pco2 that is chemical and not part of the renal compensation. Common causes of respiratory alkalosis include hyperventilation from voluntary effort (anxiety) or stimulation of central respiratory centers secondary to meningitis or a fever. 2 Respiratory Alkalosis Respiratory alkalosis is associated with an increase in pH and a decrease in pCO2. a Causes of Respiratory Alkalosis Respiratory alkalosis is due to hyperventilation, whic Continue reading >>
Partially Compensated Vs. Fully Compensated Abgs Practice
This is an NCLEX practice question on partially compensated vs fully compensated ABGs. This question provides a scenario about arterial blood gas results. As the nurse, you must determine if this is a respiratory or metabolic problem, alkalosis or acidosis along with if it is uncompensated, partially or fully compensated based on the results. This question is one of the many questions we will be practicing in our new series called “Weekly NCLEX Question”. So, every week be sure to tune into our YouTube Channel for the NCLEX Question of the Week. More NCLEX Weekly Practice Questions. To solve ABGs problems, I like to use the Tic Tac Toe method. If you are not familiar with this method, please watch my video on how to solve arterial blood gas problems with this method. The Tic Tac Toe method makes solving ABG problems so EASY. However, if the ABG values are partially or fully compensated you must take it a step further by analyzing the values further with this method, which is the purpose of this review. My goal is to show you how to use the Tic Tac Toe method for partially and fully compensated interpretation. So let’s begin: NCLEX Practice Questions on Partially vs. Fully Compensated ABGs Problem 1 A patient has the following arterial blood gas results: blood pH 7.43, PaCO2 28 mmHg, and HCO3 18 mEq/L. This is known as: A. Partially compensated respiratory alkalosis B. Fully compensated metabolic acidosis C. Partially compensated respiratory acidosis D. Fully compensated respiratory alkalosis The first thing you want to do is to pull from your memory bank the normal values for arterial blood gases. Here they are: <-Acid Base-> pH: 7.35-7.45 (less than 7.35 ACID & greater than 7.45 ALKALOTIC) PaCO2: 45-35 (greater than 45 ACID & less than 35 ALKALOTIC)** HCO3: 22-26 Continue reading >>
Abg Interpreter
pH CO2 HCO3 Result appears in here. Normal Arterial Blood Gas Values pH 7.35-7.45 PaCO2 35-45 mm Hg PaO2 80-95 mm Hg HCO3 22-26 mEq/L O2 Saturation 95-99% BE +/- 1 Four-Step Guide to ABG Analysis Is the pH normal, acidotic or alkalotic? Are the pCO2 or HCO3 abnormal? Which one appears to influence the pH? If both the pCO2 and HCO3 are abnormal, the one which deviates most from the norm is most likely causing an abnormal pH. Check the pO2. Is the patient hypoxic? I used Swearingen's handbook (1990) to base the results of this calculator. The book makes the distinction between acute and chronic disorders based on symptoms from identical ABGs. This calculator only differentiates between acute (pH abnormal) and compensated (pH normal). Compensation can be seen when both the PCO2 and HCO3 rise or fall together to maintain a normal pH. Part compensation occurs when the PCO2 and HCO3 rise or fall together but the pH remains abnormal. This indicates a compensatory mechanism attempted to restore a normal pH. I have not put exact limits into the calculator. For example, it will perceive respiratory acidosis as any pH < 7.35 and any CO2 > 45 (i.e. a pH of 1 and CO2 of 1000). These results do not naturally occur. pH PaCO2 HCO3 Respiratory Acidosis Acute < 7.35 > 45 Normal Partly Compensated < 7.35 > 45 > 26 Compensated Normal > 45 > 26 Respiratory Alkalosis Acute > 7.45 < 35 Normal Partly Compensated > 7.45 < 35 < 22 Compensated Normal < 35 < 22 Metabolic Acidosis Acute < 7.35 Normal < 22 Partly Compensated < 7.35 < 35 < 22 Compensated Normal < 35 < 22 Metabolic Alkalosis Acute > 7.45 Normal > 26 Partly Compensated > 7.45 > 45 > 26 Compensated Normal > 45 > 26 Mixed Disorders It's possible to have more than one disorder influencing blood gas values. For example ABG's with an alkale Continue reading >>
Respiratory Acidosis
Respiratory acidosis is an abnormal clinical process that causes the arterial Pco2 to increase to greater than 40 mm Hg. Increased CO2 concentration in the blood may be secondary to increased CO2 production or decreased ventilation. Larry R. Engelking, in Textbook of Veterinary Physiological Chemistry (Third Edition) , 2015 Respiratory acidosis can arise from a break in any one of these links. For example, it can be caused from depression of the respiratory center through drugs or metabolic disease, or from limitations in chest wall expansion due to neuromuscular disorders or trauma (Table 90-1). It can also arise from pulmonary disease, card iog en ic pu lmon a ryedema, a spira tion of a foreign body or vomitus, pneumothorax and pleural space disease, or through mechanical hypoventilation. Unless there is a superimposed or secondary metabolic acidosis, the plasma anion gap will usually be normal in respiratory acidosis. Kamel S. Kamel MD, FRCPC, Mitchell L. Halperin MD, FRCPC, in Fluid, Electrolyte and Acid-Base Physiology (Fifth Edition) , 2017 Respiratory acidosis is characterized by an increased arterial blood PCO2 and H+ ion concentration. The major cause of respiratory acidosis is alveolar hypoventilation. The expected physiologic response is an increased . The increase in concentration of bicarbonate ions (HCO3) in plasma ( ) is tiny in patients with acute respiratory acidosis, but is much larger in patients with chronic respiratory acidosis. Respiratory alkalosis is caused by hyperventilation and is characterized by a low arterial blood PCO2 and H+ ion concentration. The expected physiologic response is a decrease in . As in respiratory acidosis, this response is modest in patients with acute respiratory alkalosis and much larger in patients with chronic respir Continue reading >>
5.5 Metabolic Acidosis - Compensation
Acid-Base Physiology 5.5.1 Hyperventilation Compensation for a metabolic acidosis is hyperventilation to decrease the arterial pCO2. This hyperventilation was first described by Kussmaul in patients with diabetic ketoacidosis in 1874. The metabolic acidosis is detected by both the peripheral and central chemoreceptors and the respiratory center is stimulated. The initial stimulation of the central chemoreceptors is due to small increases in brain ISF [H+]. The subsequent increase in ventilation causes a fall in arterial pCO2 which inhibits the ventilatory response. Maximal compensation takes 12 to 24 hours The chemoreceptor inhibition acts to limit and delay the full ventilatory response until bicarbonate shifts have stabilised across the blood brain barrier. The increase in ventilation usually starts within minutes and is usually well advanced at 2 hours of onset but maximal compensation may take 12 to 24 hours to develop. This is �maximal� compensation rather than �full� compensation as it does not return the extracellular pH to normal. In situations where a metabolic acidosis develops rapidly and is short-lived there is usually little time for much compensatory ventilatory response to occur. An example is the acute and sometimes severe lactic acidosis due to a prolonged generalised convulsion: this corrects due to rapid hepatic uptake and metabolism of the lactate following cessation of convulsive muscular activity, and hyperventilation due to the acidosis does not occur. The expected pCO2 at maximal compensation can be calculated from a simple formula The arterial pCO2 at maximal compensation has been measured in many patients with a metabolic acidosis. A consistent relationship between bicarbonate level and pCO2 has been found. It can be estimated from the Continue reading >>
Metabolic Acidosis - Endocrine And Metabolic Disorders - Msd Manual Professional Edition
By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincents Ascension Health, Birmingham Metabolic acidosis is primary reduction in bicarbonate (HCO3), typically with compensatory reduction in carbon dioxide partial pressure (Pco2); pH may be markedly low or slightly subnormal. Metabolic acidoses are categorized as high or normal anion gap based on the presence or absence of unmeasured anions in serum. Causes include accumulation of ketones and lactic acid, renal failure, and drug or toxin ingestion (high anion gap) and GI or renal HCO3 loss (normal anion gap). Symptoms and signs in severe cases include nausea and vomiting, lethargy, and hyperpnea. Diagnosis is clinical and with ABG and serum electrolyte measurement. The cause is treated; IV sodium bicarbonate may be indicated when pH is very low. Metabolic acidosis is acid accumulation due to Increased acid production or acid ingestion Acidemia (arterial pH < 7.35) results when acid load overwhelms respiratory compensation. Causes are classified by their effect on the anion gap (see Table: Causes of Metabolic Acidosis ). Lactic acidosis (due to exogenous toxins) Toluene (initially high gap; subsequent excretion of metabolites normalizes gap) HIV nucleoside reverse transcriptase inhibitors Biguanides (rare except with acute kidney injury) Normal anion gap (hyperchloremic acidosis) Renal tubular acidosis , types 1, 2, and 4 The most common causes of a high anion gap metabolic acidosis are Ketoacidosis is a common complication of type 1 diabetes mellitus (see diabetic ketoacidosis ), but it also occurs with chronic alcoholism (see alcoholic ketoacidosis ), undernutrition, and, to a lesser degree, fasting. In these conditions, the body converts from glucose metabolism to free fatty acid (F Continue reading >>
Metabolic Alkalosis - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition
(Video) Overview of Buffering and the Henderson-Hasselbalch Equation By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincents Ascension Health, Birmingham Metabolic alkalosis is primary increase in bicarbonate (HCO3) with or without compensatory increase in carbon dioxide partial pressure (Pco2); pH may be high or nearly normal. Common causes include prolonged vomiting, hypovolemia, diuretic use, and hypokalemia. Renal impairment of HCO3 excretion must be present to sustain alkalosis. Symptoms and signs in severe cases include headache, lethargy, and tetany. Diagnosis is clinical and with arterial blood gas and serum electrolyte measurement. The underlying condition is treated; oral or IV acetazolamide or hydrochloric acid is sometimes indicated. Metabolic alkalosis is bicarbonate (HCO3) accumulation due to Intracellular shift of hydrogen ion (H+as occurs in hypokalemia ) Regardless of initial cause, persistence of metabolic alkalosis indicates that the kidneys have increased their HCO3 reabsorption, because HCO3 is normally freely filtered by the kidneys and hence excreted. Volume depletion and hypokalemia are the most common stimuli for increased HCO3 reabsorption, but any condition that elevates aldosterone or mineralocorticoids (which enhance sodium [Na] reabsorption and potassium [K] and hydrogen ion [H+] excretion) can elevate HCO3. Thus, hypokalemia is both a cause and a frequent consequence of metabolic alkalosis. The most common causes of metabolic alkalosis are Volume depletion (particularly when involving loss of gastric acid and chloride [Cl] due to recurrent vomiting or nasogastric suction) Among other causes (see Table: Causes of Metabolic Alkalosis ) are disorders that cause Continue reading >>
Perfecting Your Acid-base Balancing Act
When it comes to acids and bases, the difference between life and death is balance. The body’s acid-base balance depends on some delicately balanced chemical reactions. The hydrogen ion (H+) affects pH, and pH regulation influences the speed of cellular reactions, cell function, cell permeability, and the very integrity of cell structure. When an imbalance develops, you can detect it quickly by knowing how to assess your patient and interpret arterial blood gas (ABG) values. And you can restore the balance by targeting your interventions to the specific acid-base disorder you find. Basics of acid-base balance Before assessing a patient’s acid-base balance, you need to understand how the H+ affects acids, bases, and pH. An acid is a substance that can donate H+ to a base. Examples include hydrochloric acid, nitric acid, ammonium ion, lactic acid, acetic acid, and carbonic acid (H2CO3). A base is a substance that can accept or bind H+. Examples include ammonia, lactate, acetate, and bicarbonate (HCO3-). pH reflects the overall H+ concentration in body fluids. The higher the number of H+ in the blood, the lower the pH; and the lower the number of H+, the higher the pH. A solution containing more base than acid has fewer H+ and a higher pH. A solution containing more acid than base has more H+ and a lower pH. The pH of water (H2O), 7.4, is considered neutral. The pH of blood is slightly alkaline and has a normal range of 7.35 to 7.45. For normal enzyme and cell function and normal metabolism, the blood’s pH must remain in this narrow range. If the blood is acidic, the force of cardiac contractions diminishes. If the blood is alkaline, neuromuscular function becomes impaired. A blood pH below 6.8 or above 7.8 is usually fatal. pH also reflects the balance between the p Continue reading >>
Easy Way To Interpret Abg Values
ABG values can be very intimidating! Its hard to remember all the different normal values, what they mean, and which direction theyre supposed to be going. With so much information, its super easy to get mixed up and make a stupid mistake on an exam, even when you really DO know how to interpret ABGs. In this article, Im focusing more on the How to, rather than understanding whats going on with the A&P, which Ive already done in previous articles. If you want to understand whythese steps work (which you should do anyway to become a great nurse!),take some time to review my articles on Respiratory Imbalances and Metabolic Imbalances . Heres my 7-step method to interpreting ABGs. We have three puzzle pieces to put together: B)uncompensated, partially compensated, or compensated 1) Across the top of your page, write down the normal values for the three most important ABG lab results: pH (7.35-7.45), PaCO2 (35-45), and HCO3 (22-26). 2) Underneath pH, draw arrows to remind you which direction is acidic (down), and which direction is basic (down). 3) UnderneathPaCO2, and HCO3, draw arrows to remind you what abnormally high and low values would do to the bodys pH. When youre done, your page should look something like this: So far, we havent even looked at the question yet, were just trying to prevent any stupid mistakes!! 4) Now you can finally look at the patients ABG values. Check the pH and decide if the value is normal, high, or low. 4a) If the pH is normal, check PaCO2, and HCO3. If they are both normal, then you patient is fine and you can stop here. But if one or both of these values is abnormal, then continue to step 5. 5) Identify if the patient has alkalosis or acidosis. 5a) If the pH is abnormal, then compare it to the arrows you wrote at the top of your paper and Continue reading >>
Base Excess
In physiology, base excess and base deficit refer to an excess or deficit, respectively, in the amount of base present in the blood. The value is usually reported as a concentration in units of mEq/L, with positive numbers indicating an excess of base and negative a deficit. A typical reference range for base excess is −2 to +2 mEq/L.[1] Comparison of the base excess with the reference range assists in determining whether an acid/base disturbance is caused by a respiratory, metabolic, or mixed metabolic/respiratory problem. While carbon dioxide defines the respiratory component of acid-base balance, base excess defines the metabolic component. Accordingly, measurement of base excess is defined, under a standardized pressure of carbon dioxide, by titrating back to a standardized blood pH of 7.40. The predominant base contributing to base excess is bicarbonate. Thus, a deviation of serum bicarbonate from the reference range is ordinarily mirrored by a deviation in base excess. However, base excess is a more comprehensive measurement, encompassing all metabolic contributions. Definition[edit] Pathophysiology sample values BMP/ELECTROLYTES: Na+ = 140 Cl− = 100 BUN = 20 / Glu = 150 K+ = 4 CO2 = 22 PCr = 1.0 \ ARTERIAL BLOOD GAS: HCO3− = 24 paCO2 = 40 paO2 = 95 pH = 7.40 ALVEOLAR GAS: pACO2 = 36 pAO2 = 105 A-a g = 10 OTHER: Ca = 9.5 Mg2+ = 2.0 PO4 = 1 CK = 55 BE = −0.36 AG = 16 SERUM OSMOLARITY/RENAL: PMO = 300 PCO = 295 POG = 5 BUN:Cr = 20 URINALYSIS: UNa+ = 80 UCl− = 100 UAG = 5 FENa = 0.95 UK+ = 25 USG = 1.01 UCr = 60 UO = 800 PROTEIN/GI/LIVER FUNCTION TESTS: LDH = 100 TP = 7.6 AST = 25 TBIL = 0.7 ALP = 71 Alb = 4.0 ALT = 40 BC = 0.5 AST/ALT = 0.6 BU = 0.2 AF alb = 3.0 SAAG = 1.0 SOG = 60 CSF: CSF alb = 30 CSF glu = 60 CSF/S alb = 7.5 CSF/S glu = 0.4 Base excess Continue reading >>
Uncompensated, Partially Compensated, Or Combined Abg Problems
Arterial Blood Gas (ABG) analysis requires in-depth expertise. If the results are not understood right, or are wrongly interpreted, it can result in wrong diagnosis and end up in an inappropriate management of the patient. ABG analysis is carried out when the patient is dealing with the following conditions: • Breathing problems • Lung diseases (asthma, cystic fibrosis, COPD) • Heart failure • Kidney failure ABG reports help in answering the following questions: 1. Is there acidosis or alkalosis? 2. If acidosis is present, whether it is in an uncompensated state, partially compensated state, or in fully compensated state? 3. Whether acidosis is respiratory or metabolic? ABG reports provide the following descriptions: PaCO2 (partial pressure of dissolved CO2 in the blood) and PaO2 (partial pressure of dissolved O2 in the blood) describe the efficiency of exchange of gas in the alveolar level into the blood. Any change in these levels causes changes in the pH. HCO3 (bicarbonate in the blood) maintains the pH of the blood within normal range by compensatory mechanisms, which is either by retaining or increasing HCO3 excretion by the kidney. When PaCO2 increases, HCO3 decreases to compensate the pH. The following table summarizes the changes: ABG can be interpreted using the following analysis points: Finding acidosis or alkalosis: • If pH is more it is acidosis, if pH is less it is alkalosis. Finding compensated, partially compensated, or uncompensated ABG problems: • When PaCO2 is high, but pH is normal instead of being acidic, and if HCO3 levels are also increased, then it means that the compensatory mechanism has retained more HCO3 to maintain the pH. • When PaCO2 and HCO3 values are high but pH is acidic, then it indicates partial compensation. It means t Continue reading >>
8-step Guide To Abg Analysis: Tic-tac-toe Method
An arterial blood gas (ABG) is a blood test that measures the acidity (pH) and the levels of oxygen and carbon dioxide in the blood . Blood for an ABG test is taken from an artery whereas most other blood tests are done on a sample of blood taken from a vein. This test is done to monitor several conditions that can cause serious health complications especially to critically ill individuals. Every day, a lot of nursing and medical students assigned in acute areas encounter ABG results, which they may not necessarily be able to interpret with its knotty aspect. They struggle over the interpretation of its measurements, but they are not especially complicated nor difficult if you understand the basic physiology and have a step by step process to analyze and interpret them. There may be various tips and strategies to guide you, from mnemonics, to charts, to lectures, to practice, but this article will tell you how to interpret ABGs in the easiest possible way. And once you have finished reading this, youll be doing actual ABG analysis in the NCLEX with fun and excitement! Here are the steps: Know the normal and abnormal ABG values when you review the lab reports. Theyre fairly easy to remember: for pH, the normal value is 7.35 to 7.45; 35-45 for paCO2; and 22-26 for HCO3. Remember also this diagram and note that paCO2 is intentionallyinverted for the purpose of this method. 2. Determine if pH is under acidosis or alkalosis Next thing to do is to determine the acidity or alkalinity of the blood through the value of pH. The pH level of a healthy human should be between 7.35 to 7.45. The human body is constantly striving to keep pH in balance. 3. Determine if acid-base is respiratory or metabolic Next thing you need to determine is whether the acid base is Respiratory or Meta Continue reading >>
Blood Gas Analysis For Bedside Diagnosis
Department of Oral and Maxillofacial Surgery, Post Graduate Institute of Dental Sciences, Rohtak, Haryana, India Address for correspondence: Dr. Virendra Singh, Department of Oral and Maxillofacial Surgery, Post Graduate Institute of Dental Sciences, Pt. B.D. Sharma University of Health Sciences, Rohtak, Haryana - 124 001, India. E-mail: ni.oc.oohay@1hgnisardnerivrd Author information Copyright and License information Disclaimer Copyright : National Journal of Maxillofacial Surgery This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This article has been cited by other articles in PMC. Arterial blood gas is an important routine investigation to monitor the acid-base balance of patients, effectiveness of gas exchange, and the state of their voluntary respiratory control. Majority of the oral and maxillofacial surgeons find it difficult to interpret and clinically correlate the arterial blood gas report in their everyday practice. This has led to underutilization of this simple tool. The present article aims to simplify arterial blood gas analysis for a rapid and easy bedside interpretation. In context of oral and maxillofacial surgery, arterial blood gas analysis plays a vital role in the monitoring of postoperative patients, patients receiving oxygen therapy, those on intensive support, or with maxillofacial trauma with significant blood loss, sepsis, and comorbid conditions like diabetes, kidney disorders, Cardiovascular system (CVS) conditions, and so on. The value of this analysis is limited by the understanding of the basic physiology and ability of the surgeon Continue reading >>
