diabetestalk.net

Respiratory Acidosis Pathophysiology

Respiratory Acidosis: Causes And Regulation

Respiratory Acidosis: Causes And Regulation

This lesson will discuss an important relationship between the kidneys and the lungs and how both of them play a role in respiratory acidosis. We'll also discuss some of the major causes of respiratory acidosis. Mutualistic Relationships A mutualistic relationship refers typically to a couple of different species of animals helping one another out. Take, for example, the birds that clean an alligator's teeth. The alligator gets a free dental exam, no insurance necessary, and the birds get a nice meal. It's really weird in a way that a bird and a reptile would rely on one another. They are just so different in terms of their size, function, and appearance, but their relationship is nonetheless very important. Well, the kidneys have a relationship with the lungs that is equally weird but important. I mean, the lungs are much bigger, look totally different, and don't seem to be related to the kidneys at all! But these two organ systems are in a very important mutualistic relationship, only one fourth of which can be discussed in this lesson. A Couple of Important Terms Before we get to everything, I want to clarify some terms. 'Acidemia' refers to an abnormally low pH of the blood. pH is inversely proportional to the concentration of H+ (hydrogen ions, aka protons). Hydrogen ions confer acidity upon a substance. So if we raise the concentration of hydrogen, we actually lower the pH. Acidemia is a result of acidosis. 'Acidosis' refers to a pathological state or process that leads to acidemia. We'll be using these terms later, so keep them in mind. To help remember that acid has a low pH, just think about the fact that gastric acid sits 'down' in your stomach. Therefore, something acidic moves 'down' the pH scale. Respiratory Acidosis Okay, with that out of the way for a bit 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 >>

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 >>

Respiratory Acidosis

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 Pathophysiology

Respiratory Acidosis Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Vamsikrishna Gunnam M.B.B.S [2] Respiratory acidosis is an result of imbalance between acid-base due to alveolar hypoventilation .The normal range is 35-45 mm Hg for PaCO2.Increase in the production of carbon dioxide due to failure of ventilation results in sudden increase of the partial pressure of arterial carbon dioxide (PaCO2) above the normal range. Alveolar hypoventilation is one of the cause to increased PaCO2which is is called hypercapnia . Hypercapnia and respiration acidosis occur while impairment in air flow happens and the elimination of carbon dioxide by the respiratory system is much less than the production of carbon dioxide in the tissues .Respiratory acidosis encountered in the emergency department and inpatient patients, as well as in intensive care unit s and postoperative patients. Metabolism in the body tissues rapidly generates a big quantity of volatile acids which are like eg carbon dioxid e and nonvolatile acid. [1] The metabolism of fats and carbohydrates ends up in the formation of a huge quantity of carbon dioxide . The carbon dioxide combines with water to form carbonic acid (H2CO3). The lungs excrete the unstable fraction via ventilation , and generally acid accumulation does not occur. A considerable alteration in ventilation that affects elimination of carbon dioxide can cause a respiratory acid-base disease. The partial arterial pressure of carbon dioxide ( PaCO2 ) is normally maintained in between 35-45 mm Hg. Continue reading >>

Respiratory Acidosis.

Respiratory Acidosis.

Abstract Respiratory acidosis, or primary hypercapnia, is the acid-base disorder that results from an increase in arterial partial pressure of carbon dioxide. Acute respiratory acidosis occurs with acute (Type II) respiratory failure, which can result from any sudden respiratory parenchymal (eg, pulmonary edema), airways (eg, chronic obstructive pulmonary disease or asthma), pleural, chest wall, neuromuscular (eg, spinal cord injury), or central nervous system event (eg, drug overdose). Chronic respiratory acidosis can result from numerous processes and is typified by a sustained increase in arterial partial pressure of carbon dioxide, resulting in renal adaptation, and a more marked increase in plasma bicarbonate. Mechanisms of respiratory acidosis include increased carbon dioxide production, alveolar hypoventilation, abnormal respiratory drive, abnormalities of the chest wall and respiratory muscles, and increased dead space. Although the symptoms, signs, and physiologic consequences of respiratory acidosis are numerous, the principal effects are on the central nervous and cardiovascular systems. Treatment for respiratory acidosis may include invasive or noninvasive ventilatory support and specific medical therapies directed at the underlying pathophysiology. Continue reading >>

Respiratory Acidosis: Causes, Symptoms, And Treatment

Respiratory Acidosis: Causes, Symptoms, And Treatment

Respiratory acidosis develops when air exhaled out of the lungs does not adequately exchange the carbon dioxide formed in the body for the inhaled oxygen in air. There are many conditions or situations that may lead to this. One of the conditions that can reduce the ability to adequately exhale carbon dioxide (CO2) is chronic obstructive pulmonary disease or COPD. CO2 that is not exhaled can shift the normal balance of acids and bases in the body toward acidic. The CO2 mixes with water in the body to form carbonic acid. With chronic respiratory acidosis, the body partially makes up for the retained CO2 and maintains acid-base balance near normal. The body's main response is an increase in excretion of carbonic acid and retention of bicarbonate base in the kidneys. Medical treatment for chronic respiratory acidosis is mainly treatment of the underlying illness which has hindered breathing. Treatment may also be applied to improve breathing directly. Respiratory acidosis can also be acute rather than chronic, developing suddenly from respiratory failure. Emergency medical treatment is required for acute respiratory acidosis to: Regain healthful respiration Restore acid-base balance Treat the causes of the respiratory failure Here are some key points about respiratory acidosis. More detail and supporting information is in the main article. Respiratory acidosis develops when decreased breathing fails to get rid of CO2 formed in the body adequately The pH of blood, as a measure of acid-base balance, is maintained near normal in chronic respiratory acidosis by compensating responses in the body mainly in the kidney Acute respiratory acidosis requires emergency treatment Tipping acid-base balance to acidosis When acid levels in the body are in balance with the base levels in t 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 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 >>

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 Alkalosis

Respiratory Alkalosis

(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 alkalosis is a primary decrease in carbon dioxide partial pressure (Pco2) with or without compensatory decrease in bicarbonate (HCO3); pH may be high or near normal. Cause is an increase in respiratory rate or volume (hyperventilation) or both. Respiratory alkalosis can be acute or chronic. The chronic form is asymptomatic, but the acute form causes light-headedness, confusion, paresthesias, cramps, and syncope. Signs include hyperpnea or tachypnea and carpopedal spasms. Diagnosis is clinical and with ABG and serum electrolyte measurements. Treatment is directed at the cause. (See also Acid-Base Regulation , Acid-Base Disorders , and Hyperventilation Syndrome .) Respiratory alkalosis is a primary decrease in Pco2 (hypocapnia) due to an increase in respiratory rate and/or volume (hyperventilation). Ventilation increase occurs most often as a physiologic response to hypoxia (eg, at high altitude), metabolic acidosis , and increased metabolic demands (eg, fever) and, as such, is present in many serious conditions. In addition, pain and anxiety and some CNS disorders (eg, stroke, seizure [post-ictal]) can increase respirations without a physiologic need. Distinction is based on the degree of metabolic compensation. Excess HCO3 is buffered by extracellular hydrogen ion (H+) within minutes, but more significant compensation occurs over 2 to 3 days as the kidneys decrease H+ excretion. Pseudorespiratory alkalosis is low arterial Pco2 and high pH in mechanically ventilated patients with severe metabolic acidosis due to poor systemic perfusion (eg, cardiogenic shock, during CPR). Pseu 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 >>

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 >>

Respiratory Acidosis

Respiratory Acidosis

Acid-base balance disturbance from alveolar hypoventilation Rapid production of carbon dioxide Failure of ventilation increases partial pressure of arterial carbon dioxide (PaCO2) Respiratory acidosis can be acute or chronic In acute respiratory acidosis: PaCO2 is > 45 mm Hg with accompanying acidemia (pH < 7.35) In chronic respiratory acidosis: PaCO2 is > 45 mm HG with normal/near-normal pH (renal compensation) and serum bicarbonate levels > 30 mEq/L Treatment directed at underlying disorder/pathophysiologic process Caution: too-rapid correction of hypercapnia can result in metabolic alkalemia CSF alkalization can result in seizures Due to alveolar hypoventilation from any cause CNS depression causing impaired ventilation most common cause Lung diseases causing abnormal alveolar gas exchange usually don't cause hypoventilation Stimulate ventilation and hypocapnia 2 degrees to hypoxia Hypercapnia only occurs if severe disease, respiratory muscle fatigue Accompanying acidemia (can be severe) Only acute compensatory response is intracellular buffering CNS: CVA, infection, trauma, tumor Pulmonary: PNA, COPD, PTX, PE. Pulmonary edema, Smoke inhalation Neuromuscular disease (myasthenia gravis, ALS, Guillain-Barre) Airway Obstruction: Foreign body, edema Increased dead space ventilation (from increased V/Q mismatch) Decreased diaphragm function (from fatigue and hyperinflation) Obesity hypoventilation syndrome (Pickwickian Syndrome) Severe restrictive ventilatory processes (interstitial fibrosis, thoracic deformities) Usually that of underlying disease Depends on rate of hypercapnia development Slowly developing hypercapnia (mild-moderate) - minimal symptoms When PCO2 > 70 [SI: > 9.3 kPa] acutely Confusion, somnolence, obtundation (CO2 narcosis) Mental status may be depresse Continue reading >>

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 >>

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 >>

More in ketosis