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Mixed Acidosis Abg

Interpretation Of Arterial Blood Gas

Interpretation Of Arterial Blood Gas

Go to: Introduction Arterial blood gas (ABG) analysis is an essential part of diagnosing and managing a patient’s oxygenation status and acid–base balance. The usefulness of this diagnostic tool is dependent on being able to correctly interpret the results. Disorders of acid–base balance can create complications in many disease states, and occasionally the abnormality may be so severe so as to become a life-threatening risk factor. A thorough understanding of acid–base balance is mandatory for any physician, and intensivist, and the anesthesiologist is no exception. The three widely used approaches to acid–base physiology are the HCO3- (in the context of pCO2), standard base excess (SBE), and strong ion difference (SID). It has been more than 20 years since the Stewart’s concept of SID was introduced, which is defined as the absolute difference between completely dissociated anions and cations. According to the principle of electrical neutrality, this difference is balanced by the weak acids and CO2. The SID is defined in terms of weak acids and CO2 subsequently has been re-designated as effective SID (SIDe) which is identical to “buffer base.” Similarly, Stewart’s original term for total weak acid concentration (ATOT) is now defined as the dissociated (A-) plus undissociated (AH) weak acid forms. This is familiarly known as anion gap (AG), when normal concentration is actually caused by A-. Thus all the three methods yield virtually identical results when they are used to quantify acid–base status of a given blood sample.[1] Continue reading >>

Uncompensated, Partially Compensated, Or Combined Abg Problems

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 >>

A Primer On Arterial Blood Gas Analysis By Andrew M. Luks, Md(cont.)

A Primer On Arterial Blood Gas Analysis By Andrew M. Luks, Md(cont.)

Step 4: Identify the compensatory process (if one is present) In general, the primary process is followed by a compensatory process, as the body attempts to bring the pH back towards the normal range. If the patient has a primary respiratory acidosis (high PCO2 ) leading to acidemia: the compensatory process is a metabolic alkalosis (rise in the serum bicarbonate). If the patient has a primary respiratory alkalosis (low PCO2 ) leading to alkalemia: the compensatory process is a metabolic acidosis (decrease in the serum bicarbonate) If the patient has a primary metabolic acidosis (low bicarbonate) leading acidemia, the compensatory process is a respiratory alkalosis (low PCO2 ). If the patient has a primary metabolic alkalosis (high bicarbonate) leading to alkalemia, the compensatory process is a respiratory acidosis (high PCO2 ) The compensatory processes are summarized in Figure 2. (opens in a new window) Important Points Regarding Compensatory Processes There are several important points to be aware of regarding these compensatory processes: The body never overcompensates for the primary process. For example, if the patient develops acidemia due to a respiratory acidosis and then subsequently develops a compensatory metabolic alkalosis (a good example of this is the COPD patient with chronic carbon dioxide retention), the pH will move back towards the normal value of 7.4 but will not go to the alkalemic side of normal This might result in a pH of 7.36, for example but should not result in a pH such as 7.44 or another value on the alkalemic side of normal. If the pH appears to "over-compensate" then an additional process is at work and you will have to try and identify it. This can happen with mixed acid-base disorders, which are described further below. The pace of co Continue reading >>

Metabolic Acidosis Workup: Approach Considerations, Laboratory Evaluation, Complete Blood Count

Metabolic Acidosis Workup: Approach Considerations, Laboratory Evaluation, Complete Blood Count

Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FASN more... Often the first clue to metabolic acidosis is a decreased serum HCO3- concentration observed when serum electrolytes are measured. Remember, however, that a decreased serum [HCO3-] level can be observed as a compensatory response to respiratory alkalosis. An [HCO3-] level of less than 15 mEq/L, however, almost always is due, at least in part, to metabolic acidosis. The only definitive way to diagnose metabolic acidosis is by simultaneous measurement of serum electrolytes and arterial blood gases (ABGs) , which shows pH and PaCO2 to be low; calculated HCO3- also is low. (For more information, see Metabolic Alkalosis .) A low serum HCO3- and a pH of less than 7.40 upon ABG analysis confirm metabolic acidosis. Go to Pediatric Metabolic Acidosis and Emergent Management of Metabolic Acidosis for complete information on these topics. The diagnosis is made by evaluating serum electrolytes and ABGs. A low serum HCO3- and a pH of less than 7.40 upon ABG analysis confirm metabolic acidosis. The anion gap (AG) should be calculated to help with the differential diagnosis of the metabolic acidosis and to diagnose mixed disorders. In general, a high-AG acidosis is present if the AG is greater than 10-12 mEq/L, and a non-AG acidosis is present if the AG is less than or equal to 10-12 mEq/L. It is important to note that the AG decreases by 2.5 mEq for every 1 g/dL decrease in serum albumin. If the AG is elevated, the osmolar gap should be calculated by subtracting the calculated serum osmolality from the measured serum osmolality. Ethylene glycol and methanol poisoning increase the AG and the osmolar gap. Acetone, produced by decarboxylation of acetoacetate, can also raise serum osmolalit Continue reading >>

Abg: Respiratory Acidosis/metabolic Alkalosis

Abg: Respiratory Acidosis/metabolic Alkalosis

Home / ABA Keyword Categories / A / ABG: Respiratory acidosis/metabolic alkalosis ABG: Respiratory acidosis/metabolic alkalosis A combined respiratory acidosis / metabolic alkalosis will result in elevated PaCO2 and serum bicarbonate. Which process is the primary disorder (e.g. primary respiratory acidosis with metabolic compensation versus primary metabolic alkalosis with respiratory compensation) is dependent on the pH in an acidotic patient, the acidosis is primary (and the alkalosis is compensatory) and vice versa. Compensation behaves in accordance with the following rules: Metabolic Acidosis: As bicarbonate goes from 10 to 5, pCO2 will bottom out at 15. pCO2 = 1.5 x [HCO3-] + 8 (or pCO2 = 1.25 x [HCO3-]) Metabolic Alkalosis: compensation here is less because CO2 is driving force for respiration. pCO2 = 0.7 x [HCO3-] + 21 (or pCO2 = 0.75 x [HCO3-]) Acutely: [HCO3-] = 0.1 x pCO2 or pH = 0.008 x pCO2 Chronically: [HCO3-] = 0.4 x pCO2 or pH = 0.003 x pCO2 Respiratory Alkalosis: Metabolic compensation will automatically be retention of chloride (i.e., hyperchloremic, usually referred to as loss of bicarb although it is the strong ion difference that matters). If you have an anion gap, then youve automatically got a little bit of an acidosis on top of the compensation (because the compensation should be a NON-gap acidotic process. Acutely: [HCO3-] = 0.2 x pCO2 (or pH = 0.008 x pCO2) Chronically: [HCO3-] = 0.4 x pCO2 (or pH = 0.017 x pCO2) Continue reading >>

Delta Ratio - Wikipedia

Delta Ratio - Wikipedia

Delta ratio is a formula that can be used to assess elevated anion gap metabolic acidosis and to evaluate whether a mixed acid base disorder ( metabolic acidosis ) is present. The anion gap (AG) is calculated first and if an anion gap is present, results in either a high anion gap metabolic acidosis (HAGMA) or a normal anion gap acidosis (NAGMA). A low anion gap is usually an oddity of measurement, rather than a clinical concern. The equation for calculating the Delta Ratio is: (AG 12) ___________ (24 - [HCO3]) [1] and reflects either an increase in the anion gap or a decrease in the bicarbonate concentration ( [HCO3] ). [2] 2. 0.4 - 0.8 due to a mixed NAGMA + HAGMA 4. >2.0 due to a mixed HAGMA + metabolic alkalosis (or pre-existing compensated respiratory acidosis) Results 2 and 4 are the ones which have mixed acid-base disorders. Results 1. and 4. are oddities, mathematically speaking: Result 1: if there is a normal anion gap acidosis, the [ AG - 12 ] part of the equation will be close to zero, the delta ratio will be close to zero and there is no mixed acid-base disorder. Your calculations can stop here. A normal anion gap acidosis (NAGMA) has more to do with a change in [Cl]) or [HCO3] concentrations. So the AG doesnt change; but to maintain electrical equilibrium, if [Cl] goes up, [HCO3] must come down. Hence, hyperchloremia always causes a metabolic acidosis as [HCO3] must fall; alternatively, if the [HCO3] rises, the [Cl] must fall. For a list of the common causes of this change in bicarbonate or chloride, see normal anion gap acidosis . Results 2-4 all involve HAGMAs. A high anion gap metabolic acidosis usually occurs because of an increase in anions. So in the equation: it is the [A] that is the cause. For a list of the common anions responsible, see high anio Continue reading >>

Abg Interpretation

Abg Interpretation

Arterial blood gas (ABG) interpretation is something many medical students find difficult to grasp (we’ve been there). We’ve created this guide, which aims to provide a structured approach to ABG interpretation whilst also increasing your understanding of each results relevance. The real value of an ABG comes from its ability to provide a near immediate reflection of the physiology of your patient, allowing you to recognise and treat pathology more rapidly. To see how to perform an arterial blood gas check out our guide here. If you want to put your ABG interpretation skills to the test, check out our ABG quiz here. Normal ranges pH: 7.35 – 7.45 PaCO2: 4.7-6.0 kPa PaO2: 11-13 kPa HCO3-: 22-26 mEg/L Base excess: -2 to +2 mmol/L Patient’s clinical condition Before getting stuck into the details of the analysis, it’s important to look at the patient’s current clinical status, as this provides essential context to the ABG result. Below are a few examples to demonstrate how important context is when interpreting an ABG. A normal PaO2 in a patient on high flow oxygen – this is abnormal as you would expect the patient to have a PaO2 well above the normal range with this level of oxygen therapy A normal PaCO2 in a hypoxic asthmatic patient – a sign they are tiring and need ITU intervention A very low PaO2 in a patient who looks completely well, is not short of breath and has normal O2 saturations – likely a venous sample Oxygenation (PaO2) Your first question when looking at the ABG should be “Is this patient hypoxic?” (because this will kill them long before anything else does). PaO2 should be >10 kPa on air in a healthy patient If the patient is receiving oxygen therapy their PaO2 should be approximately 10kPa less than the % inspired concentration / FiO Continue reading >>

American Thoracic Society - Interpretation Of Arterial Blood Gases (abgs)

American Thoracic Society - Interpretation Of Arterial Blood Gases (abgs)

Interpretation of Arterial Blood Gases (ABGs) Chief, Section of Pulmonary, Critical Care & Sleep Medicine Bridgeport Hospital-Yale New Haven Health Assistant Clinical Professor, Yale University School of Medicine (Section of Pulmonary & Critical Care Medicine) Interpreting an arterial blood gas (ABG) is a crucial skill for physicians, nurses, respiratory therapists, and other health care personnel. ABG interpretation is especially important in critically ill patients. The following six-step process helps ensure a complete interpretation of every ABG. In addition, you will find tables that list commonly encountered acid-base disorders. Many methods exist to guide the interpretation of the ABG. This discussion does not include some methods, such as analysis of base excess or Stewarts strong ion difference. A summary of these techniques can be found in some of the suggested articles. It is unclear whether these alternate methods offer clinically important advantages over the presented approach, which is based on the anion gap. Step 1: Assess the internal consistency of the values using the Henderseon-Hasselbach equation: If the pH and the [H+] are inconsistent, the ABG is probably not valid. Step 2: Is there alkalemia or acidemia present? Remember: an acidosis or alkalosis may be present even if the pH is in the normal range (7.35 7.45) You will need to check the PaCO2, HCO3- and anion gap Step 3: Is the disturbance respiratory or metabolic? What is the relationship between the direction of change in the pH and the direction of change in the PaCO2? In primary respiratory disorders, the pH and PaCO2 change in opposite directions; in metabolic disorders the pH and PaCO2 change in the same direction. Decrease in [HCO3-] = 5( PaCO2/10) to 7( PaCO2/10) If the observed compensa Continue reading >>

Abg Interpreter

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 >>

Arterial Blood Gases - Indications And Interpretation

Arterial Blood Gases - Indications And Interpretation

Severely unwell patients from any cause - affects prognosis. Arterial blood can be obtained by direct arterial puncture most usually at the wrist (radial artery). Alternatives to the radial artery include the femoral and brachial artery - both of which are usually used in emergency settings. The dorsalis pedis artery and ulnar artery may also be used. It is important to ensure good collateral circulation (see below), as there is a theoretical risk of thrombus occlusion. If multiple samples are required then an indwelling arterial cannula can be placed. Allow the patient to titrate with the oxygen for 5-10 minutes (30 minutes if they have chronic obstructive pulmonary disease (COPD)) before taking a sample. If the radial artery is to be used, perform Allen's test to confirm collateral blood flow to the hand. Elevate the hand and make a fist for approximately 30 seconds. Apply pressure over the ulnar and the radial arteries occluding both (keep the hand elevated). Release pressure on the ulnar artery and look for perfusion of the hand (this takes under eight seconds). If there is any delay then it may not be safe to perform radial artery puncture. Explain the procedure to the patient - it is painful. If there is time then local anaesthesia can be used. ABG syringes usually come prepacked and are heparinised. Some contain a vacuum and thus the plunger does not always need to be pulled. (Check with your department as to which they use). The wrist is extended - a pillow under the hand may improve comfort. Palpate the artery and hold fingers firmly over the pulsation. Then introduce the needle at a 45 angle slowly with the bevel facing upwards, aiming for the point of maximum pulsation. Once you hit the artery, try to obtain at least a 1 ml sample. Once you have taken your s Continue reading >>

Acid-base Disorders - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition

Acid-base Disorders - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition

(Video) Overview of Acid-Base Maps and Compensatory Mechanisms By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincents Ascension Health, Birmingham Acid-base disorders are pathologic changes in carbon dioxide partial pressure (Pco2) or serum bicarbonate (HCO3) that typically produce abnormal arterial pH values. Acidosis refers to physiologic processes that cause acid accumulation or alkali loss. Alkalosis refers to physiologic processes that cause alkali accumulation or acid loss. Actual changes in pH depend on the degree of physiologic compensation and whether multiple processes are present. Primary acid-base disturbances are defined as metabolic or respiratory based on clinical context and whether the primary change in pH is due to an alteration in serum HCO3 or in Pco2. Metabolic acidosis is serum HCO3< 24 mEq/L. Causes are Metabolic alkalosis is serum HCO3> 24 mEq/L. Causes are Respiratory acidosis is Pco2> 40 mm Hg (hypercapnia). Cause is Decrease in minute ventilation (hypoventilation) Respiratory alkalosis is Pco2< 40 mm Hg (hypocapnia). Cause is Increase in minute ventilation (hyperventilation) Compensatory mechanisms begin to correct the pH (see Table: Primary Changes and Compensations in Simple Acid-Base Disorders ) whenever an acid-base disorder is present. Compensation cannot return pH completely to normal and never overshoots. A simple acid-base disorder is a single acid-base disturbance with its accompanying compensatory response. Mixed acid-base disorders comprise 2 primary disturbances. Compensatory mechanisms for acid-base disturbances cannot return pH completely to normal and never overshoot. Primary Changes and Compensations in Simple Acid-Base Disorders 1.2 mm Hg decrease in Pco2 for every 1 mmol/L decrease in HC 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 >>

More Abg Examples - Resus

More Abg Examples - Resus

This is an elderly man with vomiting for 3 days, who presents with tachycardia. It would be expected that there be a metabolic alkalosis with loss of gastric contents. His pH shows an alkalosis and he has raised bicarb. He is hypokalaemic and hypocloraemic, with a raised BSL. The Na is low, when corrected for increased BSL it is 134. With this metabolic alkalosis the expected pCO2 is (0.9 x HCO3) + 16 = 43. The actual pCO2 is 28.5. Therefore this is a mixed picture ofMetabolic and Respiratory Alkalosis i.e.,he has his metabolic alkalosis but is also breathing up more than he should. Expected Aa gradient is age/4 +4 = 22.5 so a very high Aa gradient indicating a V/Q mismatch, or diffusion defect. So when we think of causes, take both things into account- the vomiting and the Aa. Pneumonia(although afebrile- elderly may be) A 21 year old man is brought in by his father with a one week history of vomiting. He has not been able to keep any food down. He has been diagnosed with Hashimotos thyroiditis by his local doctor 4 months previously. Today his blood pressure is 90/48 and pulse rate 104. These are his venous blood gas results: Is it acidosis or alkalosis? ACIDOSIS What is the primary cause? Given the low HCO3 and the not so high pCO2 it isMETABOLIC ACIDOSIS. Expected pCO2 is [(1.5xHCO3) +8]+2 i.e.., [(~30) + 8]+2 = 38-39 sothere is adequate compensation Na -(Cl + HCO3) = 108-(72 + 19) = 17 so raised anion gap metabolic acidosis. (reference is 8-16) Is there any other process going on? Look at the delta gap. change in AG/change in HCO3 = 17-12(use 12 as the expected AG)/24-19(24 is the expected HCO3) = 5/5 = 1 so this is a pure anion gap metabolic acidosis. ( Given what I say below, I might have also expected a normal anion gap metabolic acidosis) The Na is very low an Continue reading >>

Simple Method Of Acid Base Balance Interpretation

Simple Method Of Acid Base Balance Interpretation

A FOUR STEP METHOD FOR INTERPRETATION OF ABGS Usefulness This method is simple, easy and can be used for the majority of ABGs. It only addresses acid-base balance and considers just 3 values. pH, PaCO2 HCO3- Step 1. Use pH to determine Acidosis or Alkalosis. ph < 7.35 7.35-7.45 > 7.45 Acidosis Normal or Compensated Alkalosis Step 2. Use PaCO2 to determine respiratory effect. PaCO2 < 35 35 -45 > 45 Tends toward alkalosis Causes high pH Neutralizes low pH Normal or Compensated Tends toward acidosis Causes low pH Neutralizes high pH Step 3. Assume metabolic cause when respiratory is ruled out. You'll be right most of the time if you remember this simple table: High pH Low pH Alkalosis Acidosis High PaCO2 Low PaCO2 High PaCO2 Low PaCO2 Metabolic Respiratory Respiratory Metabolic If PaCO2 is abnormal and pH is normal, it indicates compensation. pH > 7.4 would be a compensated alkalosis. pH < 7.4 would be a compensated acidosis. These steps will make more sense if we apply them to actual ABG values. Click here to interpret some ABG values using these steps. You may want to refer back to these steps (click on "linked" steps or use "BACK" button on your browser) or print out this page for reference. Step 4. Use HC03 to verify metabolic effect Normal HCO3- is 22-26 Please note: Remember, the first three steps apply to the majority of cases, but do not take into account: the possibility of complete compensation, but those cases are usually less serious, and instances of combined respiratory and metabolic imbalance, but those cases are pretty rare. "Combined" disturbance means HCO3- alters the pH in the same direction as the PaCO2. High PaCO2 and low HCO3- (acidosis) or Low PaCO2 and high HCO3- (alkalosis). Continue reading >>

Acid Base Disorders

Acid Base Disorders

Arterial blood gas analysis is used to determine the adequacy of oxygenation and ventilation, assess respiratory function and determine the acid–base balance. These data provide information regarding potential primary and compensatory processes that affect the body’s acid–base buffering system. Interpret the ABGs in a stepwise manner: Determine the adequacy of oxygenation (PaO2) Normal range: 80–100 mmHg (10.6–13.3 kPa) Determine pH status Normal pH range: 7.35–7.45 (H+ 35–45 nmol/L) pH <7.35: Acidosis is an abnormal process that increases the serum hydrogen ion concentration, lowers the pH and results in acidaemia. pH >7.45: Alkalosis is an abnormal process that decreases the hydrogen ion concentration and results in alkalaemia. Determine the respiratory component (PaCO2) Primary respiratory acidosis (hypoventilation) if pH <7.35 and HCO3– normal. Normal range: PaCO2 35–45 mmHg (4.7–6.0 kPa) PaCO2 >45 mmHg (> 6.0 kPa): Respiratory compensation for metabolic alkalosis if pH >7.45 and HCO3– (increased). PaCO2 <35 mmHg (4.7 kPa): Primary respiratory alkalosis (hyperventilation) if pH >7.45 and HCO3– normal. Respiratory compensation for metabolic acidosis if pH <7.35 and HCO3– (decreased). Determine the metabolic component (HCO3–) Normal HCO3– range 22–26 mmol/L HCO3 <22 mmol/L: Primary metabolic acidosis if pH <7.35. Renal compensation for respiratory alkalosis if pH >7.45. HCO3 >26 mmol/L: Primary metabolic alkalosis if pH >7.45. Renal compensation for respiratory acidosis if pH <7.35. Additional definitions Osmolar Gap Use: Screening test for detecting abnormal low MW solutes (e.g. ethanol, methanol & ethylene glycol [Reference]) An elevated osmolar gap (>10) provides indirect evidence for the presence of an abnormal solute which is prese Continue reading >>

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