Acid-base Disorders In Patients With Chronic Obstructive Pulmonary Disease: A Pathophysiological Review
Acid-Base Disorders in Patients with Chronic Obstructive Pulmonary Disease: A Pathophysiological Review Department of Internal Medicine and Systemic Diseases, University of Catania, 95100 Catania, Italy Received 29 September 2011; Accepted 26 October 2011 Copyright 2012 Cosimo Marcello Bruno and Maria Valenti. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The authors describe the pathophysiological mechanisms leading to development of acidosis in patients with chronic obstructive pulmonary disease and its deleterious effects on outcome and mortality rate. Renal compensatory adjustments consequent to acidosis are also described in detail with emphasis on differences between acute and chronic respiratory acidosis. Mixed acid-base disturbances due to comorbidity and side effects of some drugs in these patients are also examined, and practical considerations for a correct diagnosis are provided. Chronic obstructive pulmonary disease (COPD) is a major public health problem. Its prevalence varies according to country, age, and sex. On the basis of epidemiologic data, the projection for 2020 indicates that COPD will be the third leading cause of death worldwide and the fifth leading cause of disability [ 1 ]. About 15% of COPD patients need admission to general hospital or intensive respiratory care unit for acute exacerbation, leading to greater use of medical resources and increased costs [ 2 5 ]. Even though the overall prognosis of COPD patients is lately improved, the mortality rate remains high, and, among others, acid-base disorders occurring in these subjects can affect the outcome. The aim of this pa Continue reading >>
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 >>
Respiratory Acidosis
(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 Respiratory acidosis is primary increase in carbon dioxide partial pressure (Pco2) with or without compensatory increase in bicarbonate (HCO3); pH is usually low but may be near normal. Cause is a decrease in respiratory rate and/or volume (hypoventilation), typically due to CNS, pulmonary, or iatrogenic conditions. Respiratory acidosis can be acute or chronic; the chronic form is asymptomatic, but the acute, or worsening, form causes headache, confusion, and drowsiness. Signs include tremor, myoclonic jerks, and asterixis. Diagnosis is clinical and with ABG and serum electrolyte measurements. The cause is treated; oxygen (O2) and mechanical ventilation are often required. Respiratory acidosis is carbon dioxide (CO2) accumulation (hypercapnia) due to a decrease in respiratory rate and/or respiratory volume (hypoventilation). Causes of hypoventilation (discussed under Ventilatory Failure ) include Conditions that impair CNS respiratory drive Conditions that impair neuromuscular transmission and other conditions that cause muscular weakness Obstructive, restrictive, and parenchymal pulmonary disorders Hypoxia typically accompanies hypoventilation. Distinction is based on the degree of metabolic compensation; carbon dioxide is initially buffered inefficiently, but over 3 to 5 days the kidneys increase bicarbonate reabsorption significantly. Symptoms and signs depend on the rate and degree of Pco2 increase. CO2 rapidly diffuses across the blood-brain barrier. Symptoms and signs are a result of high CO2 concentrations and low pH in the CNS and any accompanying hypoxemia. Acute (or acutely wor Continue reading >>
Case 5 Answers - Arterial Blood Gas - Clinical Respiratory Diseases & Critical Care Medicine, Seattle - Med 610 - University Of Washington School Of Medicine
A 68 year-old man with a history of very severe COPD (FEV1 ~ 1.0L, <25% predicted) and chronic carbon dioxide retention (Baseline PCO2 58) presents to the emergency room complaining of worsening dyspnea and an increase in the frequency and purulence of his sputum production over the past 2 days. His oxygen saturation is 78% on room air. Before he is place on supplemental oxygen, a room air arterial blood gas is drawn and reveals: pH 7.25, PCO2 68, PO2 48, HCO3- 31 The patient has a high PCO2 (respiratory acidosis) and a high bicarbonate (metabolic alkalosis). The combination of the low pH and the high PCO2 tells us that the respiratory acidosis is the primary process. The metabolic alkalosis is the compensatory process. The pH is still low despite this metabolic compensation Summary: Primary respiratory acidosis with compensatory metabolic alkalosis. The alveolar-arterial oxygen difference is 17 mmHg. This value is elevated, suggesting that the hypoxemia is due to either shunt or areas of low V/Q (the more likely explanation in a patient with COPD) and cannot be explained by hypoventilation alone. The patient has very severe COPD and chronic carbon dioxide retention. As a result, you expect that at baseline, they will have a chronic respiratory acidosis (his baseline PCO2 was 58) with a compensatory metabolic alkalosis. In this case, the clinical history suggests the patient is in an exacerbation. When the patient presents to the ER, his PCO2 is elevated above his baseline. Because this is an acute change, the bicarbonate has not had time to adjust and the pH falls. This case is, therefore, an example of an acute on chronic respiratory acidosis. Continue reading >>
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Emdocs.net Emergency Medicine Educationhow To Crush Abgs - Emdocs.net - Emergency Medicine Education
Stepwise Approach w/ interpretations found below. You wont need to look anywhere else unless you want to do the Stewart Acid Base Approach. Step 1: 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-, anion gap, and Albumin Step 2: 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. Chronic => for every PaC02 increase of 10 mmhg, ph drops by .03 Acute => for every paC02 increase of 10 mmhg, ph drops by .08 Chronic => Decrease of PaC02 by 10 mmHg, pH increase by .03 Acute => Decrease of PaC02 by 10 mmHg, pH increase by .08 Step 3: Is there appropriate compensation for the primary disturbance? Usually, compensation does not return the pH to normal (7.35 7.45). If the observed compensation is not the expected compensation, it is likely that more than one acid-base disorder is present. Metabolic Acidosis: PaC02 = 1.5 (HC03) + 8 +/- 2 Acute Respiratory Acidosis: Increase in HC03 = Change in PaC02/10 +/- 3 Chronic Respiratory Acidosis (3-5 Days) Increase in HC03 = 3.5 (Change PaC02/10) Metabolic Alkalosis: Increase in PaC02 = .6 (Change in Bicarb) Acute Respiratory Alkalosis: Decease in Bicarb = 2 (Change PaC02/10) Chronic Respiratory Alkalosis: Decrease in Bicarb = 5(Change in PaC02/10) to 7(Change in PaC02/10) A normal anion gap is approximately 12 meq/L. Correct for albumin. Correct for Alb: (2.5) (4-pts Alb) + AG. Super important in the Unit. If the anion gap is elevated, consider calculating the Continue reading >>
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 >>
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Arterial Blood Gas - Abg - Interpretation | Almostadoctor
Most commonly cause by diarrhoea . In diarrhoea , there is a loss of K+ into the GI tract. This causes K+ to leave cells, and enter the bloodstream in an attempt to keep K+ levels normal. In order to maintain the electrical charge of the cell, H+ is then taken up by the cell. Normal kidneys are very effective at excreting bicarbonate. Diuretics prevent the re-absorption of sodium from the renal tubule, and thus they promote sodium loss. The normal mechanism for recovering this sodium , involves an exchange with bicarbonate, and thus the ability of the renal tubule to excret bicarbonate is reduced. May also be cause by too much bicarbonate (sometimes iatrogenic) or ingestion of other alkaline substances. Metabolic acidosis is the most common and the most complex of the acid base disturbances. There are a wide variety of causes, which can be differentiated with the help of the anion gap. This is used to help diagnose acid base disorders. It is usually used in suspected cases ofmetabolic acidosis. It can either be normal, or raised. Low anion gap does not usually occur. Anions are negatively charged ions.The two most common ones in the human body are chloride and bicarbonate. Anions are hard to measure accurately.The anion gap is thedifference between the number of measured anions, and the number of unmeasured anions. Negatively chargedproteinsmake up most of the unmeasured anions in a normal individual, and the main one is albumin. And thus in a normal individual, there is an anion gap of 4-16, made up mostly of albumin.Some causes of metabolic acidosis, do not produce a large number of unmeasured anions, and the anion gap doesnt increase. This isnormal anion gap metabolic acidosis NAGMA Some causes of metabolic acidosis produce a large number of both measured (e.g. HCO3 Continue reading >>
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Changes In Arterial Blood Gas Values
CONDITION: Acute Alveolar Hyperventilation Acute Alveolar Hyperventilation is ventilation in excess of needs and the blood gas values would show the following: We can use the formulas given on the previous page to determine if the following blood gas changes are appropriate for acute alveolar hyperventilation / respiratory alkalosis RULE: Each 1 mm Hg in PaCO2 should give 0.01 in pH When the PaCO2 < 40 mmHg the expected pH = 7.40 + (40 mm Hg measured PaCO2)0.01 Expected change matches actual. This indicates that the changes in the blood gas would be primarily due to PaCO2 and therefore would be an acute respiratory or ventilatory disturbance. RULE: Each 5 mm Hg in PaCO2 should HCO3 by 1 mEq Verifying that the changes in bicarb are tied to the changes in PaCO2 and not due to renal compensation by elimination of bicarb. pH IN NORMAL RANGE BUT ON ACID SIDE OF 7.40 (7.35 - 7.39) Would be identified as a fully compensated respiratory acidosis We can evaluate the following for compensation by looking at the expected pH in relation to the measured PaCO2 RULE: Each 1 mm Hg in PaCO2 should give 0.006 in pH When the PaCO2 is > 40, the expected pH = 7.40 - (measured PaCO2 40 mm Hg)0.006 This indicates that there is compensation as the pH of 7.38 is not as low as expected. RULE: Each 10 mm Hg in PaCO2 should HCO3 by 1 mEq Indicates that the elevated HCO3 is higher than expected and is the result of renal retention. ACUTE CONDITIONS SUPERIMPOSED ON CHRONIC VENTILATORY FAILURE CONDITION:Acute Alveolar Hyperventilation on Chronic Ventilatory Failure Can be confused with partially compensated metabolic alkalosis where the elevated PaCO2 would be related due to hypoventilation, not hyperventilation that has actually caused a much higher initial PaCO2 to be reduced. Assess oxygenated st Continue reading >>
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Irocket Learning Module: Intro To Arterial Blood Gases, Pt. 1
Acute vs. Chronic Respiratory Disturbances Remember respiratory processes alter the blood pH by changing the carbon dioxide levels. When CO2 accumulates in the blood (elevated PaCO2), as when a person hypoventilates, acid builds up and the pH decreases. This is called respiratory acidosis. Similarly, with increased CO2 elimination (low PaCO2), as when a person hyperventilates, the amount of acid in the blood decreases and the pH increases. This is called respiratory alkalosis. Primary respiratory disturbances can be acute or chronic. Near drowning, asthma attack, respiratory arrest, drug overdose, upper airway obstruction, panic attack Emphysema, chronic bronchitis, high altitude travel, neuromuscular disease When anaylzing an ABG of a person with a primary respiratory disturbance, it is important to determine if the problem is acute or chronic. For example, acute respiratory acidosis is associated with an abrupt and sometimes significant decline in pH; it is a sign of possible acute respiratory failure that requires urgent intervention. However, chronic respiratory failure occurs over weeks to months to years. The acidosis associated with it is mild because the kidney has had time to re-adjust for additional bicarbonate retention. For acute respiratory disturbances, each change in the PaCO2 of 10 mm Hg from 40 mm Hg ("normal") is accompanied by a pH shift of 0.08 units. For example, if the PaCO2 acutely rises to 50 mm Hg, we would expect to see a lowering of the pH 0.08 units, from 7.40 to 7.32. Similarily, if the PaCO2 acutely decreases to 30 mm Hg, we would expect to see an elevation of the pH, from 7.40 to 7.48. Continue reading >>
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Chapter 39. Acute-on-chronic Respiratory Failure
Chapter 39. Acute-on-Chronic Respiratory Failure Ivor S. Douglas; Gregory A. Schmidt; Jesse B. Hall Douglas IS, Schmidt GA, Hall JB. Douglas I.S., Schmidt G.A., Hall J.B. Douglas, Ivor S., et al.Chapter 39. Acute-on-Chronic Respiratory Failure. In: Hall JB, Schmidt GA, Wood LH. Hall J.B., Schmidt G.A., Wood L.H. Eds. Jesse B. Hall, et al.eds. Principles of Critical Care, 3e New York, NY: McGraw-Hill; 2005. Accessed April 15, 2018. Douglas IS, Schmidt GA, Hall JB. Douglas I.S., Schmidt G.A., Hall J.B. Douglas, Ivor S., et al.. "Chapter 39. Acute-on-Chronic Respiratory Failure." Principles of Critical Care, 3e Hall JB, Schmidt GA, Wood LH. Hall J.B., Schmidt G.A., Wood L.H. Eds. Jesse B. Hall, et al. New York, NY: McGraw-Hill, 2005, Acute-on-chronic respiratory failure (ACRF) occurs when relatively minor, although often multiple, insults cause acute deterioration in a patient with chronic respiratory insufficiency. ACRF is usually seen in patients known to have severe chronic obstructive pulmonary disease (COPD), but occasionally it manifests as cryptic respiratory failure or postoperative ventilator dependence in a patient with no known lung disease. The wide variety of causes of ACRF may be compartmentalized into causes of incremental load, diminished neuromuscular competence, or depressed drive, superimposed on a limited ventilatory reserve. Intrinsic positive end-expiratory pressure (PEEPi) is a central contributor to the excess work of breathing in patients with ACRF. The most important therapeutic interventions are administration of oxygen, bronchodilators, and corticosteroids, and noninvasive positive pressure ventilation (NIPPV). NIPPV can be used in most patients to avoid intubation and has been shown to improve survival. The decision to intubate a patient with Continue reading >>
Respiratory Acidosis
DEFINITION Respiratory acidosis = a primary acid-base disorder in which arterial pCO2 rises to an abnormally high level. PATHOPHYSIOLOGY arterial pCO2 is normally maintained at a level of about 40 mmHg by a balance between production of CO2 by the body and its removal by alveolar ventilation. PaCO2 is proportional to VCO2/VA VCO2 = CO2 production by the body VA = alveolar ventilation an increase in arterial pCO2 can occur by one of three possible mechanisms: presence of excess CO2 in the inspired gas decreased alveolar ventilation increased production of CO2 by the body CAUSES Inadequate Alveolar Ventilation central respiratory depression drug depression of respiratory centre (eg by opiates, sedatives, anaesthetics) neuromuscular disorders lung or chest wall defects airway obstruction inadequate mechanical ventilation Over-production of CO2 -> hypercatabolic disorders Malignant hyperthermia Thyroid storm Phaeochromocytoma Early sepsis Liver failure Increased Intake of Carbon Dioxide Rebreathing of CO2-containing expired gas Addition of CO2 to inspired gas Insufflation of CO2 into body cavity (eg for laparoscopic surgery) EFFECTS CO2 is lipid soluble -> depressing effects on intracellular metabolism RESP increased minute ventilation via both central and peripheral chemoreceptors CVS increased sympathetic tone peripheral vasodilation by direct effect on vessels acutely the acidosis will cause a right shift of the oxygen dissociation curve if the acidosis persists, a decrease in red cell 2,3 DPG occurs which shifts the curve back to the left CNS cerebral vasodilation increasing cerebral blood flow and intracranial pressure central depression at very high levels of pCO2 potent stimulation of ventilation this can result in dyspnoea, disorientation, acute confusion, headache, Continue reading >>
The Abcs Of Abgs: Blood Gas Analysis
A systematic and step-wise process based upon pH shift is the key to correct interpretation and application of arterial blood gas results In a previous article, “The Pitfalls of Arterial Blood Gases” (RT, April 2013), I described how simple pre-analytical, analytical, and post-analytical errors can produce arterial blood gas test results (ABGs) that are of little or no value, and perhaps even dangerous. In this article, I will assume that we have avoided all of those pitfalls and and will discuss how to interpret valid ABG results. (Some of the foundational information in this article is necessary for those new to interpreting. I encourage more experienced practitioners to bear with me.) This article will not attempt to discuss all of the possible causes or disease states that could relate to the results. Neither will it attempt to go into the interpretation of electrolytes or co-oximetry results. Adequate review of these subjects could require—in fact, have required—whole textbooks, and are beyond the scope of this article. What Is Normal? To interpret ABGs, we first need to know the normal values for the various analytes. Where do these normal values come from? They mostly come from collected results of volunteers or study subjects who appear to have uncompromised lungs and gas exchange. Researchers plotted the results of the various parameters, found the collective center of the bell-shaped curve of data, and declared the results shown in Table 1. Whichever range you and your facility prefer, it is important to think in terms of a normal range, not a single, specific, always “normal” value—except when it comes to pH for interpreting acid-base balance. We will get to why shortly. It is also vital to remember that the aggregate “normal” value is a con Continue reading >>
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Respiratory Acidosis
Practice Essentials Respiratory acidosis is an acid-base balance disturbance due to alveolar hypoventilation. Production of carbon dioxide occurs rapidly and failure of ventilation promptly increases the partial pressure of arterial carbon dioxide (PaCO2). [1] The normal reference range for PaCO2 is 35-45 mm Hg. Alveolar hypoventilation leads to an increased PaCO2 (ie, hypercapnia). The increase in PaCO2, in turn, decreases the bicarbonate (HCO3–)/PaCO2 ratio, thereby decreasing the pH. Hypercapnia and respiratory acidosis ensue when impairment in ventilation occurs and the removal of carbon dioxide by the respiratory system is less than the production of carbon dioxide in the tissues. Lung diseases that cause abnormalities in alveolar gas exchange do not typically result in alveolar hypoventilation. Often these diseases stimulate ventilation and hypocapnia due to reflex receptors and hypoxia. Hypercapnia typically occurs late in the disease process with severe pulmonary disease or when respiratory muscles fatigue. (See also Pediatric Respiratory Acidosis, Metabolic Acidosis, and Pediatric Metabolic Acidosis.) Acute vs chronic respiratory acidosis Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (ie, >45 mm Hg) with an accompanying acidemia (ie, pH < 7.35). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal or near-normal pH secondary to renal compensation and an elevated serum bicarbonate levels (ie, >30 mEq/L). Acute respiratory acidosis is present when an abrupt failure of ventilation occurs. This failure in ventilation may result from depression of the central respiratory center by one or another of the foll Continue reading >>
Respiratory Acidosis
Respiratory acidosis is a medical emergency in which decreased ventilation (hypoventilation) increases the concentration of carbon dioxide in the blood and decreases the blood's pH (a condition generally called acidosis). Carbon dioxide is produced continuously as the body's cells respire, and this CO2 will accumulate rapidly if the lungs do not adequately expel it through alveolar ventilation. Alveolar hypoventilation thus leads to an increased PaCO2 (a condition called hypercapnia). The increase in PaCO2 in turn decreases the HCO3−/PaCO2 ratio and decreases pH. Terminology[edit] Acidosis refers to disorders that lower cell/tissue pH to < 7.35. Acidemia refers to an arterial pH < 7.36.[1] Types of respiratory acidosis[edit] Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (over 6.3 kPa or 45 mm Hg) with an accompanying acidemia (pH <7.36). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal blood pH (7.35 to 7.45) or near-normal pH secondary to renal compensation and an elevated serum bicarbonate (HCO3− >30 mm Hg). Causes[edit] Acute[edit] Acute respiratory acidosis occurs when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of the central respiratory center by cerebral disease or drugs, inability to ventilate adequately due to neuromuscular disease (e.g., myasthenia gravis, amyotrophic lateral sclerosis, Guillain–Barré syndrome, muscular dystrophy), or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD) exacerbation. Chronic[edit] Chronic respiratory acidosis may be secondary to many disorders, including COPD. Hypoventilation Continue reading >>
9.3 Bedside Rules For Assessment Of Compensation
The method of assessing acid-base disorders discussed here uses a set of six rules which are used primarily to assess the magnitude of the patients compensatory response. These rules are now widely known and are soundly based experimentally. These rules are used at Step 4 of the method of Systematic Acid-Base Diagnosis outlined in Section 9.2.- (You should read section 9.1 & 9.2 before this section.) These rules are called 'bedside rules' because that can be used at the patient's bedside to assist in the assessment of the acid-base results. The rules should preferably be committed to memory - with practice this is not difficult. A full assessment of blood-gas results must be based on a clinical knowledge of the individual patient from whom they were obtained and an understanding of the pathophysiology of the clinical conditions underlying the acid-base disorder. Do not interpret the blood-gas results as an intellectual exercise in itself. It is one part of the overall process of assessing and managing the patient. A set of blood-gas and electrolyte results should NOT be interpreted without these initial clinical details. They cannot be understood fully without knowledge of the condition being diagnosed. Diagnosing a metabolic acidosis, for example, is by itself, often of little clinical use. What is really required is a more specific diagnosis of the cause of the metabolic acidosis (eg diabetic ketoacidosis, acute renal failure, lactic acidosis) and to initiate appropriate management. The acid-base analysis must be interpreted and managed in the context of the overall clinical picture. The snapshot problem: Are the results 'current'? Remember also that a set of blood gas results provides a snapshot at a particular point in time and the situation may have changed since Continue reading >>
