{"id":7697,"date":"2024-12-05T16:18:04","date_gmt":"2024-12-05T21:18:04","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathology\/chapter\/respiratory-acidosis\/"},"modified":"2025-11-11T23:45:12","modified_gmt":"2025-11-12T04:45:12","slug":"respiratory-acidosis","status":"publish","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathology\/chapter\/respiratory-acidosis\/","title":{"raw":"Respiratory Acidosis","rendered":"Respiratory Acidosis"},"content":{"raw":"<div class=\"textbox textbox--learning-objectives\"><header class=\"textbox__header\">\r\n<p class=\"textbox__title\">Learning Objectives<\/p>\r\n\r\n<\/header>\r\n<div class=\"textbox__content\">\r\n\r\nBy the end of this section, you will be able to:\r\n<ul>\r\n \t<li>Define respiratory acidosis.<\/li>\r\n \t<li>Explain the relationship between respiration and blood pH.<\/li>\r\n \t<li>Identify causes of respiratory acidosis.<\/li>\r\n<\/ul>\r\n<\/div>\r\n<\/div>\r\n<h2>Respiratory Acidosis<\/h2>\r\nRespiratory acidosis is a condition where the lungs cannot remove enough CO<sub>2<\/sub>. As a result, the retained CO<sub>2<\/sub> will be converted to carbonic acid, leading to increased acidity in the blood.\r\n<h2>Causes of Respiratory Acidosis<\/h2>\r\nRespiratory Acidosis is caused primarily by hypoventilation which means insufficient CO<sub>2<\/sub> is being exhaled. CO<sub>2<\/sub> is normally a byproduct of aerobic respiration to create ATP in order to meet metabolic demands. If the CO<sub>2<\/sub> is not excreted in the lungs, then it begins to build up in the bloodstream. If we look back to our bicarbonate buffer equilibrium equation we will remember that, as CO<sub>2<\/sub> levels rise the amount of carbonic acid made by carbon anhydrase will also increase, more protons will be released into the serum, and pH will lower (more acid).\r\n\r\nHypoventilation can be caused by CNS depression that affects the respiratory centres causing slow and\/or shallow breathing (e.g. brain injury or medication\/drug use).\r\n\r\nHypoventilation can also be caused by inefficient ventilation causing CO<sub>2<\/sub> retention. Any condition which impairs the diaphragm from fully expanding or contracting will lead to insufficient CO<sub>2<\/sub> being exhaled (e.g. obesity). Similarly, anything which prolongs exhalation - whether due to obstruction or lack of lung compliance as is the case of chronic obstructive pulmonary disease - will lead to hypoventilation\r\n\r\nCO<sub>2<\/sub> retention can also be a result of a physical blockage of CO<sub>2<\/sub> leaving the respiratory system. Exudates in the alveolar space physically prevent alveolar gas exchange thus making it difficult for CO<sub>2<\/sub> from being eliminated (e.g. Pulmonary edema, Pneumonia).\r\n<h2>Clinical Manifestations of Respiratory Acidosis<\/h2>\r\nAs the root cause of respiratory acidosis is CO<sub>2<\/sub> retention and hypoventilation, the signs and symptoms will be predominantly respiratory in nature. In the case of hypoventilation, an abnormally low respiratory rate will be seen with possible shallow breaths. In the case of alveolar exudates causing CO<sub>2<\/sub> retention, coughing would be present. Upon auscultation, exudate manifest as audible crackles. Inefficient ventilation may also be heard as wheezes as exhalation is passing through a narrowed and\/or blocked airway.\r\n<h2>Consequences of Acidosis<\/h2>\r\n<h3>Decreased Hemoglobin Affinity for Oxygen<\/h3>\r\nAcidosis causes hypoxemia by reducing hemoglobin binding affinity for oxygen through what is known as the Bohr effect. As the environment around hemoglobin becomes saturated in hydrogen ions the hydrogen ions begin to cause conformational changes in hemoglobin. The hemoglobin that exists in these conditions is known as 'taut hemoglobin'. When taut hemoglobin goes through a capillary in the alveoli the O<sub>2<\/sub> concentration is so great that often it will bind some oxygen. When it reaches the tissues however it readily disassociates the oxygen in favour of binding to protons. This poses a barrier to proper perfusion.<sup>[1][3]<\/sup>\r\n<h3>Acidotic Changes to Vessel Tone<\/h3>\r\nAcidotic state often causes increased sympathetic tone - possibly as a way for the body to promote excretion of acid. The end result is increased cardiac output and vasoconstriction in peripheral vessels. Conversely, acidosis will cause vasodilation of cerebral capillaries which can lead to increased intracranial pressure. <sup>[2]<\/sup>\r\n<h2>Compensation<\/h2>\r\nThe renal system should attempt to compensate by reabsorption of HCO<sub>3<\/sub><sup>-<\/sup> at the proximal convoluted tubule to balance pH. <sup>[3]<\/sup> . In the distal tubule, H<sup>+<\/sup> and NH4<sup>+<\/sup> are excreted by increasing action of the sodium hydrogen antiporter: sodium is reabsorbed out of the solute in exchange for protons which are then excreted to compensate for the acidity. Urinary excretion of HCO<sub>3<\/sub><sup>-<\/sup> under normal conditions is negligible.<sup>[2]<\/sup>\r\n<h1>References<\/h1>\r\n<ol>\r\n \t<li style=\"list-style-type: none\">\r\n<ol>\r\n \t<li><span style=\"color: #000000\" data-darkreader-inline-color=\"\"><a href=\"https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK526028\/\">Physiology, Bohr Effect <\/a><\/span><\/li>\r\n \t<li><span style=\"color: #000000\" data-darkreader-inline-color=\"\"><a style=\"color: #000000\" href=\"https:\/\/doi.org\/10.1007\/978-3-031-25810-7\" data-darkreader-inline-color=\"\"> Fluid, Electrolyte and Acid-Base Disorders: Clinical Evaluation and Management <\/a><\/span><\/li>\r\n \t<li><span style=\"color: #000000\" data-darkreader-inline-color=\"\"><a style=\"color: #000000\" href=\"https:\/\/pressbooks.bccampus.ca\/pathology\/chapter\/acute-kidney-injury-chapter-overview\/\" data-darkreader-inline-color=\"\"> Acute Kidney Injury<\/a><\/span><\/li>\r\n<\/ol>\r\n<\/li>\r\n<\/ol>","rendered":"<div class=\"textbox textbox--learning-objectives\">\n<header class=\"textbox__header\">\n<p class=\"textbox__title\">Learning Objectives<\/p>\n<\/header>\n<div class=\"textbox__content\">\n<p>By the end of this section, you will be able to:<\/p>\n<ul>\n<li>Define respiratory acidosis.<\/li>\n<li>Explain the relationship between respiration and blood pH.<\/li>\n<li>Identify causes of respiratory acidosis.<\/li>\n<\/ul>\n<\/div>\n<\/div>\n<h2>Respiratory Acidosis<\/h2>\n<p>Respiratory acidosis is a condition where the lungs cannot remove enough CO<sub>2<\/sub>. As a result, the retained CO<sub>2<\/sub> will be converted to carbonic acid, leading to increased acidity in the blood.<\/p>\n<h2>Causes of Respiratory Acidosis<\/h2>\n<p>Respiratory Acidosis is caused primarily by hypoventilation which means insufficient CO<sub>2<\/sub> is being exhaled. CO<sub>2<\/sub> is normally a byproduct of aerobic respiration to create ATP in order to meet metabolic demands. If the CO<sub>2<\/sub> is not excreted in the lungs, then it begins to build up in the bloodstream. If we look back to our bicarbonate buffer equilibrium equation we will remember that, as CO<sub>2<\/sub> levels rise the amount of carbonic acid made by carbon anhydrase will also increase, more protons will be released into the serum, and pH will lower (more acid).<\/p>\n<p>Hypoventilation can be caused by CNS depression that affects the respiratory centres causing slow and\/or shallow breathing (e.g. brain injury or medication\/drug use).<\/p>\n<p>Hypoventilation can also be caused by inefficient ventilation causing CO<sub>2<\/sub> retention. Any condition which impairs the diaphragm from fully expanding or contracting will lead to insufficient CO<sub>2<\/sub> being exhaled (e.g. obesity). Similarly, anything which prolongs exhalation &#8211; whether due to obstruction or lack of lung compliance as is the case of chronic obstructive pulmonary disease &#8211; will lead to hypoventilation<\/p>\n<p>CO<sub>2<\/sub> retention can also be a result of a physical blockage of CO<sub>2<\/sub> leaving the respiratory system. Exudates in the alveolar space physically prevent alveolar gas exchange thus making it difficult for CO<sub>2<\/sub> from being eliminated (e.g. Pulmonary edema, Pneumonia).<\/p>\n<h2>Clinical Manifestations of Respiratory Acidosis<\/h2>\n<p>As the root cause of respiratory acidosis is CO<sub>2<\/sub> retention and hypoventilation, the signs and symptoms will be predominantly respiratory in nature. In the case of hypoventilation, an abnormally low respiratory rate will be seen with possible shallow breaths. In the case of alveolar exudates causing CO<sub>2<\/sub> retention, coughing would be present. Upon auscultation, exudate manifest as audible crackles. Inefficient ventilation may also be heard as wheezes as exhalation is passing through a narrowed and\/or blocked airway.<\/p>\n<h2>Consequences of Acidosis<\/h2>\n<h3>Decreased Hemoglobin Affinity for Oxygen<\/h3>\n<p>Acidosis causes hypoxemia by reducing hemoglobin binding affinity for oxygen through what is known as the Bohr effect. As the environment around hemoglobin becomes saturated in hydrogen ions the hydrogen ions begin to cause conformational changes in hemoglobin. The hemoglobin that exists in these conditions is known as &#8216;taut hemoglobin&#8217;. When taut hemoglobin goes through a capillary in the alveoli the O<sub>2<\/sub> concentration is so great that often it will bind some oxygen. When it reaches the tissues however it readily disassociates the oxygen in favour of binding to protons. This poses a barrier to proper perfusion.<sup>[1][3]<\/sup><\/p>\n<h3>Acidotic Changes to Vessel Tone<\/h3>\n<p>Acidotic state often causes increased sympathetic tone &#8211; possibly as a way for the body to promote excretion of acid. The end result is increased cardiac output and vasoconstriction in peripheral vessels. Conversely, acidosis will cause vasodilation of cerebral capillaries which can lead to increased intracranial pressure. <sup>[2]<\/sup><\/p>\n<h2>Compensation<\/h2>\n<p>The renal system should attempt to compensate by reabsorption of HCO<sub>3<\/sub><sup>&#8211;<\/sup> at the proximal convoluted tubule to balance pH. <sup>[3]<\/sup> . In the distal tubule, H<sup>+<\/sup> and NH4<sup>+<\/sup> are excreted by increasing action of the sodium hydrogen antiporter: sodium is reabsorbed out of the solute in exchange for protons which are then excreted to compensate for the acidity. Urinary excretion of HCO<sub>3<\/sub><sup>&#8211;<\/sup> under normal conditions is negligible.<sup>[2]<\/sup><\/p>\n<h1>References<\/h1>\n<ol>\n<li style=\"list-style-type: none\">\n<ol>\n<li><span style=\"color: #000000\" data-darkreader-inline-color=\"\"><a href=\"https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK526028\/\">Physiology, Bohr Effect <\/a><\/span><\/li>\n<li><span style=\"color: #000000\" data-darkreader-inline-color=\"\"><a style=\"color: #000000\" href=\"https:\/\/doi.org\/10.1007\/978-3-031-25810-7\" data-darkreader-inline-color=\"\"> Fluid, Electrolyte and Acid-Base Disorders: Clinical Evaluation and Management <\/a><\/span><\/li>\n<li><span style=\"color: #000000\" data-darkreader-inline-color=\"\"><a style=\"color: #000000\" href=\"https:\/\/pressbooks.bccampus.ca\/pathology\/chapter\/acute-kidney-injury-chapter-overview\/\" data-darkreader-inline-color=\"\"> Acute Kidney Injury<\/a><\/span><\/li>\n<\/ol>\n<\/li>\n<\/ol>\n","protected":false},"author":1076,"menu_order":8,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":["callen05-y6watyomw8","jen-2-8b3ju00vg8"],"pb_section_license":""},"chapter-type":[],"contributor":[264,349],"license":[],"class_list":["post-7697","chapter","type-chapter","status-publish","hentry","contributor-callen05-y6watyomw8","contributor-jen-2-8b3ju00vg8"],"part":7690,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters\/7697","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/users\/1076"}],"version-history":[{"count":25,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters\/7697\/revisions"}],"predecessor-version":[{"id":9811,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters\/7697\/revisions\/9811"}],"part":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/parts\/7690"}],"metadata":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters\/7697\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/media?parent=7697"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapter-type?post=7697"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/contributor?post=7697"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/license?post=7697"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}