diabetestalk.net

Compensatory Mechanism For Respiratory Acidosis

Respiratory Acidosis

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 >>

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 >>

Respiratory Compensation

Respiratory Compensation

Metabolic Acidosis Respiratory compensation for metabolic disorders is quite fast (within minutes) and reaches maximal values within 24 hours. A decrease in Pco2 of 1 to 1.5 mm Hg should be observed for each mEq/L decrease of in metabolic acidosis.27 A simple rule for deciding whether the fall in Pco2 is appropriate for the degree of metabolic acidosis is that the Pco2 should be equal to the last two digits of the pH. For example, compensation is adequate if the Pco2 decreases to 28 when the pH is 7.28. Alternatively, the Pco2 can be predicted by adding 15 to the observed (down to a value of 12). Although reduction in Pco2 plays an important role in correcting any metabolic acidosis, evidence suggests that it may in some respects be counterproductive because it inhibits renal acid excretion. Fetoplacental Elimination of Metabolic Acid Load Fetal respiratory and renal compensation in response to changes in fetal pH is limited by the level of maturity and the surrounding maternal environment. However, although the placentomaternal unit performs most compensatory functions,3 the fetal kidneys have some, although limited, ability to contribute to the maintenance of fetal acid–base balance. The most frequent cause of fetal metabolic acidosis is fetal hypoxemia owing to abnormalities of uteroplacental function or blood flow (or both). Primary maternal hypoxemia or maternal metabolic acidosis secondary to maternal diabetes mellitus, sepsis, or renal tubular abnormalities is an unusual cause of fetal metabolic acidosis. Pregnant women, at least in late gestation, maintain a somewhat more alkaline plasma environment compared with that of nonpregnant control participants. This pattern of acid–base regulation in pregnant women is present during both resting and after maximal e Continue reading >>

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

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 2011 Sep 29; Accepted 2011 Oct 26. Copyright 2012 C. M. Bruno and M. 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. This article has been cited by other articles in PMC. 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 Continue reading >>

Disorders Of Acid-base Balance

Disorders Of Acid-base Balance

Module 10: Fluid, Electrolyte, and Acid-Base Balance By the end of this section, you will be able to: Identify the three blood variables considered when making a diagnosis of acidosis or alkalosis Identify the source of compensation for blood pH problems of a respiratory origin Identify the source of compensation for blood pH problems of a metabolic/renal origin Normal arterial blood pH is restricted to a very narrow range of 7.35 to 7.45. A person who has a blood pH below 7.35 is considered to be in acidosis (actually, physiological acidosis, because blood is not truly acidic until its pH drops below 7), and a continuous blood pH below 7.0 can be fatal. Acidosis has several symptoms, including headache and confusion, and the individual can become lethargic and easily fatigued. A person who has a blood pH above 7.45 is considered to be in alkalosis, and a pH above 7.8 is fatal. Some symptoms of alkalosis include cognitive impairment (which can progress to unconsciousness), tingling or numbness in the extremities, muscle twitching and spasm, and nausea and vomiting. Both acidosis and alkalosis can be caused by either metabolic or respiratory disorders. As discussed earlier in this chapter, the concentration of carbonic acid in the blood is dependent on the level of CO2 in the body and the amount of CO2 gas exhaled through the lungs. Thus, the respiratory contribution to acid-base balance is usually discussed in terms of CO2 (rather than of carbonic acid). Remember that a molecule of carbonic acid is lost for every molecule of CO2 exhaled, and a molecule of carbonic acid is formed for every molecule of CO2 retained. Figure 1. Symptoms of acidosis affect several organ systems. Both acidosis and alkalosis can be diagnosed using a blood test. Metabolic Acidosis: Primary Bic Continue reading >>

Compensated Respiratory Acidosis

Compensated Respiratory Acidosis

Definition In a compensated respiratory acidosis, although the PCO2 is high, the pH is within normal range. The kidneys compensate for a respiratory acidosis by tubular cells reabsorbing more HCO3 from the tubular fluid, collecting duct cells secreting more H+ and generating more HCO3, and ammoniagenesis leading to increased formation of the NH3 buffer. Compensated respiratory acidosis is typically the result of a chronic condition, the slow nature of onset giving the kidneys time to compensate. Common causes of respiratory acidosis include hypoventilation due to: Respiratory depression (sedatives, narcotics, CVA, etc.) Respiratory muscle paralysis (spinal cord injury, Guillan-Barre, residual paralytics). Chest wall disorders (flail chest, pneumothorax) Lung parenchyma disorders (ARDS, pneumonia, COPD, CHF, aspiration) Abdominal distension (laporoscopic surgery, ascites, obesity, etc.). Subspecialty Keyword history Similar Keyword: Respiratory acidosis: Compensation Sources Miller’s Anesthesia, 7th ed. Ch. 49. PubMed Continue reading >>

Response To Disturbances

Response To Disturbances

The body tries to minimize pH changes and responds to acid-base disturbances with body buffers, compensatory responses by the lungs and kidney (to metabolic and respiratory disturbances, respectively) and by the kidney correcting metabolic disturbances. Body buffers: There are intracellular and extracellular buffers for primary respiratory and metabolic acid-base disturbances. Intracellular buffers include hemoglobin in erythrocytes and phosphates in all cells. Extracellular buffers are carbonate (HCO3–) and non-carbonate (e.g. protein, bone) buffers. These immediately buffer the rise or fall in H+. Compensation: This involves responses by the respiratory tract and kidney to primary metabolic and respiratory acid-base disturbances, respectively. Compensation opposes the primary disturbance, although the laboratory changes in the compensatory response parallel those in the primary response. This concept is illustrated in the summary below. Respiratory compensation for a primary metabolic disturbance: Alterations in alveolar ventilation occurs in response to primary metabolic acid-base disturbances. This begins within minutes to hours of an acute primary metabolic disturbance. Note that complete compensation via this mechanism may take up to 24 hours. Renal compensation for a primary respiratory disturbance: Here, the kidney alters excretion of acid (which influences bases as well) in response to primary respiratory disturbances. This begins within hours of an acute respiratory disturbance, but take several days (3-5 days) to take full effect. Correction of acid-base changes: Correction of a primary respiratory acid-base abnormality usually requires medical or surgical intervention of the primary problem causing the acid-base disturbance, e.g. surgical relief of a colla Continue reading >>

Respiratory Acidosis

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 >>

Renal Compensation

Renal Compensation

Chronic Carbon Dioxide Retainer Renal compensation of respiratory acidosis is by increased urinary excretion of hydrogen ions and resorption of HCO3−. This relatively slow process occurs over several days. Slowly, pH reaches low normal values, but HCO3− levels and BE are increased. This is the situation of the patient with chronic respiratory failure. Pulmonary patients usually have chronic obstructive pulmonary disease or restrictive pulmonary disease, or they are morbidly obese. Increased Co2 stores are the rule, and the normal respiratory drive to Paco2 is obtunded. This group of patients is sensitive to O2 supplementation because respiratory drive is predominantly determined by hypoxemia. Patients with a Pao2 in the mid-50s and a Paco2 at the same level usually receive home O2 treatment, initially at night to reduce pulmonary hypertension and to relieve dyspnea. When the chronic Co2 retainer develops an acute respiratory problem and pH levels fall to less than 7.20, noninvasive ventilatory assistance is usually indicated. Fetoplacental Elimination of Metabolic Acid Load Fetal respiratory and renal compensation in response to changes in fetal pH is limited by the level of maturity and the surrounding maternal environment. However, although the placentomaternal unit performs most compensatory functions,3 the fetal kidneys have some, although limited, ability to contribute to the maintenance of fetal acid–base balance. The most frequent cause of fetal metabolic acidosis is fetal hypoxemia owing to abnormalities of uteroplacental function or blood flow (or both). Primary maternal hypoxemia or maternal metabolic acidosis secondary to maternal diabetes mellitus, sepsis, or renal tubular abnormalities is an unusual cause of fetal metabolic acidosis. Pregnant women, a Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Respiratory Acidosis is a pathophysiological category of acidosis and refers to those acidoses caused by primary disturbances in ventilation. Although ventilatory defects can cause significant decreases in the blood pH, renal compensatory mechanisms can largely correct the pH over several days. The fundamental cause of all respiratory acidoses is insufficient alveolar ventilation, resulting in an increase in the partial pressure of arterial carbon dioxide (PaCO2). Increased PaCO2 results in an misalignment of the Henderson-Hasselbalch Equation for the bicarbonate buffer which largely determines the pH of the extracellular fluid. Mathematically, the reduced ECF pH results from an increase in the ratio between PaCO2 relative to the ECF concentration of bicarbonate ([HCO3-]). More colloquially, deficiencies in alveolar ventilation result in an inability of the lungs to "Breathe Off" gaseous CO2 which is immediately converted to carbonic acid H2CO3 in the extracellular fluid. H2CO3 immediately releases a free hydrogen ion (H+) which serves to reduce the ECF pH, thus causing acidosis. Respiratory Acidoses can be compensated by the actions of the kidneys which serve to realign the bicarbonate buffer Henderson-Hasselbalch Equation over a period of several days. As described in Renal Response to Acid-Base Imbalance, the kidneys respond to acidosis by secreting free hydrogen ions in the urine, synthesizing novel bicarbonate which is added to the ECF, and reducing any urinary excretion of bicarbonate. By secreting acid in the urine, the kidneys may slightly reduce the PaCO2 over several days. However, the most important renal contribution is the synthesis of novel bicarbonate and reduction in urinary bicarbonate excretion which serve to slowly increase the ECF bicarbonate concent Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

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 .) 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 following: Central nervous system disease or drug-induced r Continue reading >>

Ch 3 Obj 9 Flashcards | Quizlet

Ch 3 Obj 9 Flashcards | Quizlet

noncarbonic acids increase or bicarbonate is lost from the extracellular fluid. compensatory mechanisms for metabolic acidosis the buffer systems compensate for the excess acid and attempt to maintain the arterial pH within a normal range. Buffering by bicarbonate lowers the serum value of this ion. The respiratory system compensates for a metabolic acidosis as the reduced pH stimulates hyperventilation lowering Paco2 and the amount of H2CO3 circulating in the blood occurs when ventilation is depressed. Carbon dioxide is retained, increasing H+ and producing acidosis. Carbon dioxide excess is called hypercapnia. compensatory mechanisms for respiratory acidosis Renal compensation is effective and is established over several days. The acidosis produced from CO2 retention stimulates the kidney to secrete hydrogen ion and regenerate bicarbonate. Occurs when bicarbonate is increased, usually caused by excessive loss of metabolic acids. compensatory mechanisms for metabolic alkalosis respiratory compensation for metabolic alkalosis occurs when the elevated pH inhibits the respiratroy center. the rate and depth of ventilation are decreased, causing retention of carbon dioxide. the ratio of HCO3 to H2CO3 is reduced toward normal. Continue reading >>

Acid-base Balance

Acid-base Balance

1. Compensatory mechanisms of acid-base balance: respiratory acidosis and alkalosis and metabolic acidosis and alkalosis 2. Compensatory mechanisms for Metabolic Acidosis The body regulates the acidity of the blood by four buffering mechanisms: • Bicarbonate buffering system • Intracellular buffering system • Respiratory compensation • Renal compensation 3. Bicarbonate buffering system  The bicarbonate buffering system is an important buffer system in the acid-base homeostasis.  In this system, carbon dioxide (CO2) combines with water to form carbonic acid (H2CO3), which in turn rapidly dissociates to form hydrogen ions and bicarbonate (HCO3- )  The carbon dioxide - carbonic acid equilibrium is catalyzed by the enzyme carbonic 4. Intracellular buffering  by absorption of hydrogen atoms by various molecules, including proteins, phosphates and carbonate in bone. 5. Respiratory Compensation of Metabolic Acidosis  is a mechanism by which plasma pH can be altered by varying the respiratory rate. It is faster than renal compensation, but has less ability to restore normal values  In the case of Metabolic Acidosis chemoreceptors sense a deranged acid-base system, and there is increased breathing 6. Renal Compensation of Metabolic Acidosis  the kidney produces and excretes ammonium (NH4+) and monophosphate, generating bicarbonate in the process while clearing acid 7. Compensatory mechanisms for Metabolic Alkalosis  2 Buffering mechanisms : Renal compensation Respiratory compensation 8.  Respiratory compensation - occurs mainly in the lungs, which retain CO2 through slower breathing, or hypoventilation (respiratory compensation). CO2 is then consumed toward the formation of the carbonic acid intermediate, thus decreasing pH. The decrease in [H+ Continue reading >>

4.5 Respiratory Acidosis - Compensation

4.5 Respiratory Acidosis - Compensation

Acid-Base Physiology 4.5.1 The compensatory response is a rise in the bicarbonate level This rise has an immediate component (due to a resetting of the physicochemical equilibrium point) which raises the bicarbonate slightly. Next is a slower component where a further rise in plasma bicarbonate due to enhanced renal retention of bicarbonate. The additional effect on plasma bicarbonate of the renal retention is what converts an "acute" respiratory acidsosis into a "chronic" respiratory acidosis. As can be seen by inspection of the Henderson-Hasselbalch equation (below), an increased [HCO3-] will counteract the effect (on the pH) of an increased pCO2 because it returns the value of the [HCO3]/0.03 pCO2 ratio towards normal. pH = pKa + log([HCO3]/0.03 pCO2) 4.5.2 Buffering in Acute Respiratory Acidosis The compensatory response to an acute respiratory acidosis is limited to buffering. By the law of mass action, the increased arterial pCO2 causes a shift to the right in the following reaction: CO2 + H2O <-> H2CO3 <-> H+ + HCO3- In the blood, this reaction occurs rapidly inside red blood cells because of the presence of carbonic anhydrase. The hydrogen ion produced is buffered by intracellular proteins and by phosphates. Consequently, in the red cell, the buffering is mostly by haemoglobin. This buffering by removal of hydrogen ion, pulls the reaction to the right resulting in an increased bicarbonate production. The bicarbonate exchanges for chloride ion across the erythrocyte membrane and the plasma bicarbonate level rises. In an acute acidosis, there is insufficient time for the kidneys to respond to the increased arterial pCO2 so this is the only cause of the increased plasma bicarbonate in this early phase. The increase in bicarbonate only partially returns the extracel Continue reading >>

Acid-base Disturbance In Copd

Acid-base Disturbance In Copd

Summarized from Bruno M, Valenti M. Acid-base disorders in patients with chronic obstructive pulmonary disease: A pathophysiological review. J Bomedicine and Biotechnology (2012) Article ID 915150 8 pages ( available at :) Arterial blood gases are frequently useful in the clinical management of patients with chronic obstructive pulmonary disease (COPD) to assess both oxygenation and acid-base status. A recent review article focuses on disturbance of acid-base in these patients, which occurs in advanced disease when pulmonary gas exchange is so compromised that the rate of carbon dioxide production in the tissues exceeds the rate of carbon dioxide elimination by the lungs. The article begins with an explanation of how the resulting carbon dioxide accumulation in blood leads to respiratory acidosis, the acid-base disturbance that commonly occurs in advanced COPD. An important distinction is made between acute and chronic respiratory acidosis; compensation is less effective in the former. Then follows a detailed description of the several renal mechanisms involved in the compensatory response to chronic respiratory acidosis. Although this mitigates the acidosis to a considerable extent, it often does not result in normalisation of pH. The deleterious effects of acidosis are enumerated and the authors also briefly review the epidemiological study that links severity of acidosis to poorer outcome among COPD patients. The significance of renal compensatory mechanisms is highlighted again in the discussion of the co-existence of renal failure in patients with COPD who to a greater or lesser extent lack these mechanisms and thereby have worse acidosis and poorer outcome. Many COPD patients with respiratory acidosis are suffering other conditions or prescribed drugs that affect Continue reading >>

More in ketosis