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Mixed Respiratory And Metabolic Acidosis Causes

Metabolic Acidosis Treatment & Management: Approach Considerations, Type 1 Renal Tubular Acidosis, Type 2 Renal Tubular Acidosis

Metabolic Acidosis Treatment & Management: Approach Considerations, Type 1 Renal Tubular Acidosis, Type 2 Renal Tubular Acidosis

Metabolic AcidosisTreatment & Management Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FASN more... 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 whi Continue reading >>

Mixed Acid-base Disorders, Hydroelectrolyte Imbalance And Lactate Production In Hypercapnic Respiratory Failure: The Role Of Noninvasive Ventilation

Mixed Acid-base Disorders, Hydroelectrolyte Imbalance And Lactate Production In Hypercapnic Respiratory Failure: The Role Of Noninvasive Ventilation

Mixed Acid-Base Disorders, Hydroelectrolyte Imbalance and Lactate Production in Hypercapnic Respiratory Failure: The Role of Noninvasive Ventilation 1 Fondazione Eleonora Lorillard Spencer Cenci, Sapienza University of Rome, Rome, Italy, 2 Laboratory of Biostatistics, Department of Biomedical Science, University G. d'Annunzio of Chieti-Pescara, Chieti, Italy, University of Pittsburgh, United States of America Conceived and designed the experiments: CT FDS VC AR. Performed the experiments: FDS VC AP GP. Analyzed the data: MDN. Contributed reagents/materials/analysis tools: CT FDS VC GP AP AR. Wrote the paper: CT FDS VC MDN GP AP AR. Received 2011 Oct 9; Accepted 2012 Mar 12. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. This article has been cited by other articles in PMC. Hypercapnic Chronic Obstructive Pulmonary Disease (COPD) exacerbation in patients with comorbidities and multidrug therapy is complicated by mixed acid-base, hydro-electrolyte and lactate disorders. Aim of this study was to determine the relationships of these disorders with the requirement for and duration of noninvasive ventilation (NIV) when treating hypercapnic respiratory failure. Sixty-seven consecutive patients who were hospitalized for hypercapnic COPD exacerbation had their clinical condition, respiratory function, blood chemistry, arterial blood gases, blood lactate and volemic state assessed. Heart and respiratory rates, pH, PaO2 and PaCO2 and blood lactate were checked at the 1st, 2nd, 6th and 24th hours after starting NIV. Nine patients were transferred to the intensive care unit. NIV was perf 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 >>

Mixed Acid-base Disorders.

Mixed Acid-base Disorders.

1. Vet Clin North Am Small Anim Pract. 1989 Mar;19(2):307-26. (1)Department of Small Animal Clinical Sciences, University of Minnesota College of Veterinary Medicine, St. Paul. Mixed acid-base disturbances are combinations of two or more primary acid-basedisturbances. Mixed acid-base disturbances may be suspected on the basis offindings obtained from the medical history, physical examination, serumelectrolytes and chemistries, and anion gap. The history, physical examination,and serum biochemical profile may reveal disease processes commonly associatedwith acid-base disturbances. Changes in serum total CO2, serum potassium andchloride concentrations, or increased anion gap may provide clues to theexistence of acid-base disorders. Blood gas analysis is usually required toconfirm mixed acid-base disorders. To identify mixed acid-base disorders, bloodgas analysis is used to identify primary acid-base disturbance and determine ifan appropriate compensatory response has developed. Inappropriate compensatoryresponses (inadequate or excessive) are evidence of a mixed respiratory andmetabolic disorder. The anion gap is also of value in detecting mixed acid-basedisturbances. In high anion gap metabolic acidosis, the change in the anion gapshould approximate the change in serum bicarbonate. Absence of this relationship should prompt consideration of a mixed metabolic acid-base disorder. Finding anelevated anion gap, regardless of serum bicarbonate concentration, suggestsmetabolic acidosis. In some instances, elevated anion gap is the only evidence ofmetabolic acidosis. In patients with hyperchloremic metabolic acidosis, increasesin the serum chloride concentration should approximate the reduction in the serumbicarbonate concentration. Significant alterations from this relationsh 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 >>

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 >>

Acidbase Disturbances In Intensive Care Patients: Etiology, Pathophysiology And Treatment

Acidbase Disturbances In Intensive Care Patients: Etiology, Pathophysiology And Treatment

Acidbase disturbances in intensive care patients: etiology, pathophysiology and treatment Center for Critical Care Nephrology, CRISMA Center, Department of Critical Care Medicine Correspondence and offprint requests to: John A. Kellum; E-mail: [email protected] Search for other works by this author on: Center for Critical Care Nephrology, CRISMA Center, Department of Critical Care Medicine Nephrology Dialysis Transplantation, Volume 30, Issue 7, 1 July 2015, Pages 11041111, Mohammed Al-Jaghbeer, John A. Kellum; Acidbase disturbances in intensive care patients: etiology, pathophysiology and treatment, Nephrology Dialysis Transplantation, Volume 30, Issue 7, 1 July 2015, Pages 11041111, Acidbase disturbances are very common in critically ill and injured patients as well as contribute significantly to morbidity and mortality. An understanding of the pathophysiology of these disorders is vital to their proper management. This review will discuss the etiology, pathophysiology and treatment of acidbase disturbances in intensive care patientswith particular attention to evidence from recent studies examining the effects of fluid resuscitation on acidbase and its consequences. acidbase physiology , acidosis , alkalosis , anion gap , strong ion difference The modern intensive care unit is a place where complex acidbase and electrolyte disorders are common, with one study, showing that 64% of critically ill patients have acute metabolic acidosis [ 1 ]. Although it is generally believed that most cases of acidbase derangement are mild and self-limiting, extremes of blood pH in either direction, especially when happening quickly, can have significant multiorgan consequences. Advances in evaluating acidbase balance have helped in understanding the impact of fluids in the critic Continue reading >>

Combined Respiratory And Metabolic Acidosis Caused By Bronchospasm In Anaphylactic Shock

Combined Respiratory And Metabolic Acidosis Caused By Bronchospasm In Anaphylactic Shock

Zieliński J. · Koziorowski A. From the Department of Internal Medicine (Prof. Dr. B. Jochweds) and Department of Pathophysiology (Dr. A. Koziorowski), Institute of Tuberculosis, Warszawa Authors’ address: Dr. Jan Zielinski and Dr. Antoni Koziorowski, Instytut Gruzlicy, Klinika Chorób Wewnetrznych, Plocka 26, Warszawa (Poland) 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 >>

Recognizing Mixed Acid Base Disturbances - Acvim 2008 - Vin

Recognizing Mixed Acid Base Disturbances - Acvim 2008 - Vin

A proper understanding of the terms acidosis, alkalosis, acidemia, and alkalemia is necessary to differentiate simple from mixed acid base disorders.1 Acidosis and alkalosis refer to the pathophysiologic processes that cause net accumulation of acid or alkali in the body, whereas acidemia and alkalemia refer specifically to the pH of extracellular fluid. In acidemia, the extracellular fluid pH is less than normal and the [H+] is higher than normal. In alkalemia, the extracellular fluid pH is higher than normal and the [H+] is lower than normal. Due to the effectiveness of compensatory mechanisms, animals can have acidosis or alkalosis but not acidemia or alkalemia. For example, a dog with chronic respiratory alkalosis may have a blood pH that is within the normal range. Such a patient has alkalosis, but does not have alkalemia. The primary acid base disorders are divided into metabolic and respiratory disturbances: metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. The Henderson-Hasselbach equation in its clinically relevant form emphasizes the relationship between the metabolic and respiratory systems in determining extracellular fluid pH: Traditionally, the kidneys have been considered responsible for regulation of the metabolic component (blood bicarbonate concentration, [HCO3-]) and the lungs for regulation of the respiratory component (partial pressure of CO2, [pCO2]). In this form, the Henderson-Hasselbach equation makes it clear that the pH of extracellular fluid is determined by the ratio of the bicarbonate concentration and pCO2. Each primary (metabolic or respiratory) acid base disturbance is accompanied by a secondary (opposing) response in the other system (respiratory or metabolic). Blood pH is returned nearly, but no Continue reading >>

Chapter 61. Acidbase Disorders

Chapter 61. Acidbase Disorders

Matzke GR. Matzke G.R. Matzke, Gary R.Chapter 61. AcidBase Disorders. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey L. DiPiro J.T., Talbert R.L., Yee G.C., Matzke G.R., Wells B.G., Posey L Eds. Joseph T. DiPiro, et al.eds. Pharmacotherapy: A Pathophysiologic Approach, 8e New York, NY: McGraw-Hill; 2011. Accessed April 28, 2018. Matzke GR. Matzke G.R. Matzke, Gary R.. "Chapter 61. AcidBase Disorders." Pharmacotherapy: A Pathophysiologic Approach, 8e DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey L. DiPiro J.T., Talbert R.L., Yee G.C., Matzke G.R., Wells B.G., Posey L Eds. Joseph T. DiPiro, et al. New York, NY: McGraw-Hill, 2011, The kidney plays a central role in the regulation of acidbase homeostasis through the excretion or reabsorption of filtered bicarbonate (HCO3), the excretion of metabolic fixed acids, and generation of new HCO3. Metabolic acidosis and metabolic alkalosis are generated by a primary change in the serum bicarbonate concentration. In metabolic acidosis, bicarbonate is lost or a nonvolatile acid is gained, whereas metabolic alkalosis is characterized by a gain in bicarbonate or a loss of nonvolatile acid. Arterial blood gases, along with serum electrolytes, physical findings, medical and medication history, and the clinical condition of the patient, are the primary tools to determine the cause of an acidbase disorder and to design and monitor a course of therapy. Renal tubular acidosis refers to a group of disorders characterized by impaired tubular renal acid handling despite normal or near-normal glomerular filtration rates. These patients often present with hyperchloremic metabolic acidosis. Respiratory compensation for a primary metabolic acidosis begins rapidly (within 1530 minutes) but does not reach a steady state fo Continue reading >>

Acid–base Imbalance

Acid–base Imbalance

Acid–base imbalance is an abnormality of the human body's normal balance of acids and bases that causes the plasma pH to deviate out of the normal range (7.35 to 7.45). In the fetus, the normal range differs based on which umbilical vessel is sampled (umbilical vein pH is normally 7.25 to 7.45; umbilical artery pH is normally 7.18 to 7.38).[1] It can exist in varying levels of severity, some life-threatening. Classification[edit] A Davenport diagram illustrates acid–base imbalance graphically. An excess of acid is called acidosis or acidemia and an excess in bases is called alkalosis or alkalemia. The process that causes the imbalance is classified based on the cause of the disturbance (respiratory or metabolic) and the direction of change in pH (acidosis or alkalosis). This yields the following four basic processes: process pH carbon dioxide compensation metabolic acidosis down down respiratory respiratory acidosis down up renal metabolic alkalosis up up respiratory respiratory alkalosis up down renal Mixed disorders[edit] The presence of only one of the above derangements is called a simple acid–base disorder. In a mixed disorder more than one is occurring at the same time.[2] Mixed disorders may feature an acidosis and alkosis at the same time that partially counteract each other, or there can be two different conditions affecting the pH in the same direction. The phrase "mixed acidosis", for example, refers to metabolic acidosis in conjunction with respiratory acidosis. Any combination is possible, except concurrent respiratory acidosis and respiratory alkalosis, since a person cannot breathe too fast and too slow at the same time... Calculation of imbalance[edit] The traditional approach to the study of acid–base physiology has been the empirical approach. Continue reading >>

Acid-base Disturbance: A Comprehensive Flowchart-based Diagnostic Approach

Acid-base Disturbance: A Comprehensive Flowchart-based Diagnostic Approach

Received October 10, 2014; Accepted Date: February 28, 2015; Published Date: March 04, 2015 Citation: Ali AA, Abdullah AM, Jaber AS (2015) Acid-Base Disturbance: A Comprehensive Flowchart-based Diagnostic Approach. Emerg Med (Los Angel) 5:245. doi:10.4172/2165-7548.1000245 Copyright: 2015 Ali AA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Approaching acid-base disturbances is considered a medical problem among healthcare practitioners. Practicewise, system-based approach should be used to simplify the diagnosis and facilitate management. Flowcharts are considered education tools that can organize thoughts and standardize care. Using a flowchart approach make the practitioners solve any complex acid-base disturbance and facilitate the teaching of such topic. Acid-base; Metabolic; Respiratory; Acidosis; Alkalosis; Anion gap; Osmol gap; Flowchart The acid-base homeostasis is carefully balanced through a delicate series of interactions which involve organs such as the lungs and kidneys, as well as a complex system of buffers. Optimal body function and metabolic systems are kept in check by maintaining a normal pH (7.35-7.45) of arterial blood. Values less then <7.35 are termed acidemia, whereas values more than >7.45 are referred to as alkalemia. Any disorder that lowers the pH to <7.35 is called acidosis, while a disorder that increases the pH >7.45 is called alkalosis [ 1 - 3 ]. The Henderson-Hasselbalch equation describes the Regulation of the systemic pH by means of metabolic and respiratory components [ 4 ]: The equation demonstrates that the pH is determined by bicarbona Continue reading >>

Types Of Disturbances

Types Of Disturbances

The different types of acid-base disturbances are differentiated based on: Origin: Respiratory or metabolic Primary or secondary (compensatory) Uncomplicated or mixed: A simple or uncomplicated disturbance is a single or primary acid-base disturbance with or without compensation. A mixed disturbance is more than one primary disturbance (not a primary with an expected compensatory response). Acid-base disturbances have profound effects on the body. Acidemia results in arrythmias, decreased cardiac output, depression, and bone demineralization. Alkalemia results in tetany and convulsions, weakness, polydipsia and polyuria. Thus, the body will immediately respond to changes in pH or H+, which must be kept within strict defined limits. As soon as there is a metabolic or respiratory acid-base disturbance, body buffers immediately soak up the proton (in acidosis) or release protons (alkalosis) to offset the changes in H+ (i.e. the body compensates for the changes in H+). This is very effective so minimal changes in pH occur if the body is keeping up or the acid-base abnormality is mild. However, once buffers are overwhelmed, the pH will change and kick in stronger responses. Remember that the goal of the body is to keep hydrogen (which dictates pH) within strict defined limits. The kidney and lungs are the main organs responsible for maintaining normal acid-base balance. The lungs compensate for a primary metabolic condition and will correct for a primary respiratory disturbance if the disease or condition causing the disturbance is resolved. The kidney is responsible for compensating for a primary respiratory disturbance or correcting for a primary metabolic disturbance. Thus, normal renal function is essential for the body to be able to adequately neutralize acid-base abnor Continue reading >>

Acid-base Disturbances In Children, Acidosis, Alkalosis

Acid-base Disturbances In Children, Acidosis, Alkalosis

Acid-base disturbances in children, Acidosis, Alkalosis Acid-base disturbances in children, Acidosis, Alkalosis The pH of the blood is controlled via three systems: chemical buffering, respiratory function, and renal function. Acidosis means a clinical disturbance in which there is an increase in plasma acidity, whether due to increased production by the tissues, loss of buffering ability or decreased clearance by the kidneys. A multitude of problems, congenital and acquired, can result in metabolic acidosis. The hallmark of a metabolic acidosis is a low serum HCO3 level. Metabolic alkalosis means the patient has an elevated HCO3, most typically seen with administration of loop diuretics. A respiratory acidosis means an increase in the partial pressure of carbon dioxide in the blood (PaCO2) due to inadequate respiration. Respiratory alkalosis typically occurs in response to a metabolic stimulus, such as hyperammonemia (seen in urea cycle defects) or diabetic ketoacidosis (DKA). Metabolic and respiratory mechanisms affect the acid-base state. The relationship between the pH and PaCO2 is dependent upon the plasma bicarbonate-plasma carbonic acid pool. To estimate the effect of pH change, for every 10 mmHg PaCO2, the pH will change by approximately 0.08; for example, if the PaCO2 rises to 50 from a normal 40 mmHg, then the expected pH will be approximately 7.32, or decreased by 0.08. 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 CO2 defines the respiratory component of acid-base balance, base excess defines the metabolic component. To generalize, a metabolic acidosis will have a low serum HCO3 and a respiratory acidosis will Continue reading >>

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