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What Is The Primary Abnormality In Respiratory Acidosis?

Respiratory Acidosis

Respiratory Acidosis

What is respiratory acidosis? Respiratory acidosis is a condition that occurs when the lungs can’t remove enough of the carbon dioxide (CO2) produced by the body. Excess CO2 causes the pH of blood and other bodily fluids to decrease, making them too acidic. Normally, the body is able to balance the ions that control acidity. This balance is measured on a pH scale from 0 to 14. Acidosis occurs when the pH of the blood falls below 7.35 (normal blood pH is between 7.35 and 7.45). Respiratory acidosis is typically caused by an underlying disease or condition. This is also called respiratory failure or ventilatory failure. Normally, the lungs take in oxygen and exhale CO2. Oxygen passes from the lungs into the blood. CO2 passes from the blood into the lungs. However, sometimes the lungs can’t remove enough CO2. This may be due to a decrease in respiratory rate or decrease in air movement due to an underlying condition such as: There are two forms of respiratory acidosis: acute and chronic. Acute respiratory acidosis occurs quickly. It’s a medical emergency. Left untreated, symptoms will get progressively worse. It can become life-threatening. Chronic respiratory acidosis develops over time. It doesn’t cause symptoms. Instead, the body adapts to the increased acidity. For example, the kidneys produce more bicarbonate to help maintain balance. Chronic respiratory acidosis may not cause symptoms. Developing another illness may cause chronic respiratory acidosis to worsen and become acute respiratory acidosis. Initial signs of acute respiratory acidosis include: headache anxiety blurred vision restlessness confusion Without treatment, other symptoms may occur. These include: sleepiness or fatigue lethargy delirium or confusion shortness of breath coma The chronic form of Continue reading >>

Why Measure Blood Gases? A Three-part Introduction For The Novice. Part 2.

Why Measure Blood Gases? A Three-part Introduction For The Novice. Part 2.

Why measure blood gases? A three-part introduction for the novice. Part 2. Why measure blood gases? A three-part introduction for the novice. Part 2. Arterial blood gases (ABG), a clinical test that involves measurement of the pH of arterial blood and the amount of oxygen and carbon dioxide dissolved in arterial blood, is routinely used in the diagnosis and monitoring of predominantly critically/acutely ill patients being cared for in hospital emergency rooms and intensive care units. The test allows assessment of two related physiological functions: pulmonary gas exchange and acid-base homeostasis. This is the second of three articles intended to explain the clinical value of ABG to those with little or no experience of the test. The first article focused on the physiological aspects that underpin an understanding of patient ABG results. The concepts of pH, acid, base and buffer were explained, and the parameters generated during ABG were defined and related to pulmonary gas exchange and acid-base homeostasis. In this second article attention turns to the clinical significance of abnormal ABG results, specifically abnormality in three ABG parameters (pH, pCO2(a) and bicarbonate) that determine patient acid-base status. A major focus of the article will be an explanation of the four classes of acid-base disturbance: respiratory acidosis, metabolic acidosis, respiratory alkalosis and metabolic alkalosis. The causes and physiological consequence of each of these disturbances will be discussed. Reference (normal) range for the blood gas parameters under discussion here: pH 7.35-7.45 pCO2(a) 4.7-6.0 kPa (35-45 mmHg) Bicarbonate 22-28 mmol/L DISTURBANCE OF ACID-BASE HOMEOSTASIS - GENERAL CONSIDERATION Disturbance of acid-base homeostasis is characterized by abnormality in o Continue reading >>

The Four Primary Disturbances Of Acid-base Balance

The Four Primary Disturbances Of Acid-base Balance

Primary Respiratory Acidosis initiating event: V�A (hypoventilation) chronic obstructive pulmonary disease (COPD) weak respiratory muscles (neuromuscular diseases) barbiturate poisoning (central nervous system depression) resultant effects: CO2 retention PaCO2, [H+] and pH compensations: 2� metabolic alkalosis HCO3- retention via PaCO2 effect on renal proximal tubules Primary Respiratory Alkalosis initiating event: V�A (hyperventilation) salicylate intoxication (over-aggressive aspirin therapy) hyperexcitability psychogenic paroxysmal hyperventilation ("brown paper bag" therapy) artificial ventilation resultant effects: CO2 elimination PaCO2, [H+] and pH compensations: 2� metabolic acidosis HCO3- retention via reverse PaCO2 effect on renal proximal tubules Primary Metabolic Acidosis initiating events: renal and extrarenal diabetes mellitus and ketoacidosis (larger than normal anion gap) severe shock or heart failure and lactic acidosis (larger than normal anion gap) diarrhea and loss of bicarbonate ions (normal anion gap) renal tubular acidosis and retention of hydrogen ions (normal anion gap) resultant effects: [H+] and/or [HCO3-], pH compensations: 2� respiratory alkalosis (with renal participation if possible) CO2 elimination via acid drive on ventilation Kussmaul respiration (characteristic deep labored breathing) Primary Metabolic Alkalosis initiating events: renal and extrarenal chronic potassium ion depletion (aggressive diuretic therapy, hyperaldosteronism) protracted vomiting (pyloric obstruction, gastric ulcers) and loss of gastric acids dehydration and depletion of extracellular fluid volume (contraction alkalosis) resultant effects: [H+] and/or [HCO3-], pH urine pH will be paradoxically low (acidic) if there is chronic depletion of potassium ions c Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Causes of respiratory acidosis include: Diseases of the lung tissue (such as pulmonary fibrosis, which causes scarring and thickening of the lungs) Diseases of the chest (such as scoliosis) Diseases affecting the nerves and muscles that signal the lungs to inflate or deflate Drugs that suppress breathing (including powerful pain medicines, such as narcotics, and "downers," such as benzodiazepines), often when combined with alcohol Severe obesity, which restricts how much the lungs can expand Obstructive sleep apnea Chronic respiratory acidosis occurs over a long time. This leads to a stable situation, because the kidneys increase body chemicals, such as bicarbonate, that help restore the body's acid-base balance. Acute respiratory acidosis is a condition in which carbon dioxide builds up very quickly, before the kidneys can return the body to a state of balance. Some people with chronic respiratory acidosis get acute respiratory acidosis because an illness makes their condition worse. Continue reading >>

Acid-base Disorders - Endocrine And Metabolic Disorders - Msd Manual Professional Edition

Acid-base Disorders - Endocrine And Metabolic Disorders - Msd Manual Professional Edition

By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincents Ascension Health, Birmingham 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 HCO3 0.60.75 mm Hg increase in Pco2 for every 1 mmol/L increase i 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 >>

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 >>

Intro To Arterial Blood Gases, Part 2

Intro To Arterial Blood Gases, Part 2

Arterial Blood Gas Analysis, Part 2 Introduction Acute vs. Chronic Respiratory Disturbances Primary Metabolic Disturbances Anion Gap Mixed Disorders Compensatory Mechanisms Steps in ABG Analysis, Part II Summary Compensatory Mechanisms Compensation refers to the body's natural mechanisms of counteracting a primary acid-base disorder in an attempt to maintain homeostasis. As you learned in Acute vs. Chronic Respiratory Disturbances, the kidneys can compensate for chronic respiratory disorders by either holding on to or dumping bicarbonate. With Chronic respiratory acidosis: Chronic respiratory alkalosis: the kidneys hold on to bicarbonate the kidneys dump bicarbonate With primary metabolic disturbances, the respiratory system compensates for the acid-base disorder. The lungs can either blow off excess acid (via CO2) to compensate for metabolic acidosis, or to a lesser extent, hold on to acid (via CO2) to compensate for metabolic alkalosis. With Metabolic acidosis: Metabolic alkalosis: ventilation increases to blow off CO2 ventilation decreases to hold on to CO2 The body's response to metabolic acidosis is predictable. With metabolic acidosis, respiration will increase to blow off CO2, thereby decreasing the amount of acid in the blood. Recall that with metabolic acidosis, central chemoreceptors are triggered by the low pH and increase the drive to breathe. For now, it is only important to learn (qualitatively) that there is a predictable compensatory response to metabolic acidosis. Later, during your 3rd or 4th year rotations, you might learn how to (quantitatively) determine if the compensatory response to metabolic acidosis is appropriate by using the Winter's Formula. The body's response to metabolic alkalosis is not as complete. This is because we would need to hypov Continue reading >>

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 >>

Respiratory Acidosis

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 >>

Respiratory Acidosis

Respiratory Acidosis

LABORATORY TESTS The following lab tests can be used to interpret and explain acidosis and alkalosis conditions. All are measured on blood samples. 1. pH: This measures hydrogen ions - Normal pH = 7.35-7.45 2. pCO2= Partial Pressure of Carbon Dioxide: Although this is a pressure measurement, it relates to the concentration of GASEOUS CO2 in the blood. A high pCO2 may indicate acidosis. A low pCO2 may indicate alkalosis. 3. HCO3- = Bicarbonate: This measures the concentration of HCO3- ion only. High values may indicate alkalosis since bicarbonate is a base. Low values may indicate acidosis. 4. CO2 = Carbon Dioxide Content: This is a measure of ALL CO2 liberated on adding acid to blood plasma. This measure both carbon dioxide dissolved and bicarbonate ions and is an older test. Do not confuse with pCO2 Typically, dissolved carbon dioxide = l.2-2.0 mmoles/L and HCO3- = 22-28 mmoles/L Therefore, although it is listed as CO2 content, the lab test really reflects HCO3- concentration. Respiratory Acidosis .ABNORMAL pH IN THE BODY: ACIDOSIS AND ALKALOSIS: INTRODUCTION: Normal blood pH is maintained between 7.35 and 7.45 by the regulatory systems. The lungs regulate the amount of carbon dioxide in the blood and the kidneys regulate the bicarbonate. When the pH decreases to below 7.35 an acidosis condition is present. Acidosis means that the hydrogen ions are increased and that pH and bicarbonate ions are decreased. A greater number of hydrogen ions are present in the blood than can be absorbed by the buffer systems. Alkalosis results when the pH is above 7.45. This condition results when the buffer base (bicarbonate ions) is greater than normal and the concentration of hydrogen ions are decreased. Both acidosis and alkalosis can be of two different types: respiratory and metabol Continue reading >>

4.7 Respiratory Acidosis - Assessment

4.7 Respiratory Acidosis - Assessment

The arterial pCO2 value is used to quantify the magnitude of the alteration in alveolar ventilation (assuming CO2 production is constant and inspired pCO2 is negligible). The arterial pCO2 alone is not satisfactory for assessing the magnitude of a respiratory acidosis in some cases. In particular, coexisting metabolic acid-base disorders cause compensatory changes in pCO2 and these must be accounted for. The best available quantitative index of the magnitude of a respiratory acidosis is the difference between the 'actual' pCO2 and the 'expected' pCO2 Actual pCO2 - the measured value obtained from arterial blood gas analysis. Expected pCO2 - the value of pCO2 that we calculate would be present taking into account the presence of any metabolic acid-base disorder. If there is no metabolic acid-base disorder then a pCO2 of 40 mmHg is taken as the reference point - ie we would use 40mmHg as the expected pCO2 The reason we have to allow for a metabolic acid-base disorder is that the pCO2 value changes from 40mmHg due solely to the body's compensatory ventilatory response to a metabolic acidosis or alkalosis so just using a value of 40mmHg as normal would be wrong and lead us to incorrect conclusions. With an acute metabolic acidosis, the body responds by increasing alveolar ventilation. This response is compensatory because hyperventilation results in a decrease in arterial pCO2 which tends to return the arterial pH towards 7.4 partially correcting the acute deviation of plasma pH from normal. The value of pCO2 at maximal compensation can be predicted using a simple bedside 'rule of thumb' and this calculated value is the 'expected' pCO2 which we use to compare with the 'actual'(measured) pCO2 value. If a metabolic disorder is present, we can calculate (using a simple formul Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Respiratory acidosis is an abnormal clinical process that causes the arterial Pco2 to increase to greater than 40 mm Hg. Increased CO2 concentration in the blood may be secondary to increased CO2 production or decreased ventilation. Larry R. Engelking, in Textbook of Veterinary Physiological Chemistry (Third Edition) , 2015 Respiratory acidosis can arise from a break in any one of these links. For example, it can be caused from depression of the respiratory center through drugs or metabolic disease, or from limitations in chest wall expansion due to neuromuscular disorders or trauma (Table 90-1). It can also arise from pulmonary disease, card iog en ic pu lmon a ryedema, a spira tion of a foreign body or vomitus, pneumothorax and pleural space disease, or through mechanical hypoventilation. Unless there is a superimposed or secondary metabolic acidosis, the plasma anion gap will usually be normal in respiratory acidosis. Kamel S. Kamel MD, FRCPC, Mitchell L. Halperin MD, FRCPC, in Fluid, Electrolyte and Acid-Base Physiology (Fifth Edition) , 2017 Respiratory acidosis is characterized by an increased arterial blood PCO2 and H+ ion concentration. The major cause of respiratory acidosis is alveolar hypoventilation. The expected physiologic response is an increased . The increase in concentration of bicarbonate ions (HCO3) in plasma ( ) is tiny in patients with acute respiratory acidosis, but is much larger in patients with chronic respiratory acidosis. Respiratory alkalosis is caused by hyperventilation and is characterized by a low arterial blood PCO2 and H+ ion concentration. The expected physiologic response is a decrease in . As in respiratory acidosis, this response is modest in patients with acute respiratory alkalosis and much larger in patients with chronic respir Continue reading >>

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 >>

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 >>

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