The Pathophysiology of Acid Base Imbalances
Michelle Hornsby
NUR 347 Pathophysiology for Professional Nursing Practice
University of Alabama At Birmingham
1a.
The pathophysiology for respiratory acidosis is a disturbance of the arterial carbon dioxide levels within the body and well as a decreased arterial bicarbonate level. A disturbance in these to arterial values leads to an decrease in the pH. Chemoreceptors within pons and medulla are responsible for control ventilation and managing carbon dioxide, oxygen and pH levels within the body. These receptors are sensitive to changes in the pH level. When ventilation is disrupted it causes hypercapnia and acid-base imbalance are likely to develop. This particular imbalance is most commonly brought on by hypoventilation which leads to the production of more carbon dioxide that the body can eliminate causing a retention in carbon dioxide. (Patel & Sharma, 2018)
The pathophysiology for respiratory alkalosis is an increase in the arterial blood pH levels above 7.45. Secondary to an increased pH you are likely to see a decrease in carbon dioxide levels. Carbon dioxide levels are regulated through respiration and ventilation just as with respiratory acidosis. Respiratory alkalosis is most commonly caused by hyperventilation; however this can be brought on by many different causes: CNS causes, hypoxemic causes, pulmonary causes, and iatrogenic causes . (Brinkman & Sharma, 2018)
The pathophysiology for metabolic acidosis is characterized by a decrease in serum bicarbonate resulting in a decrease in blood pH. The decrease in serum bicarbonate levels are brought on by an increase in hydrogen ions resulting in a HCO3 less than 24 mEq/L. The many causes of metabolic acidosis are classified into for main mechanisms: increased production of acid, decreased excretion of acid, acid ingestion, and renal or gastrointestinal (GI) bicarbonate losses (Kraut & Madias, 2010)
The pathophysiology of metabolic alkalosis is characterized as acid loss which can be brought on by multiple causes. Metabolic alkalosis is characterized as an increase in the body’s serum bicarbonate levels leading to a pH greater than 7.45 secondary to a metabolic process. There are a multiple disease processes that can induce metabolic alkalosis by causes a shift in the number of hydrogen ions circulating within the body. This can be classified using the same 4 mechanisms that can cause metabolic acidosis: decreased production of acid, increase in the exception of acid, renal hydrogen loss or gastrointestinal hydrogen loss (Brinkman & Sharma, 2018)
1b.
A disease/condition that causes respiratory acidosis is COPD. This disease can cause chronic carbon dioxide retention resulting in hypercapnia and hypoventilation. Respiratory acidosis is depicted by the following partially compensated arterial blood gas results: pH: 7.28, pCO2: 55, HCO3:27. In respiratory acidosis, compensation occurs via two body systems the first being pH changes initiate a cellular buffering response that elevates bicarbonate levels which occurs over minutes to hours. The renal system compensates over several days by excreting carbonic acid and reabsorbing bicarbonate within the body (Patel & Sharma, 2018).
A disease/condition that causes respiratory alkalosis is asthma. This disease is usually characterized by hyperventilation within an acute asthma exacerbation. This disease is usually depicted by the following partially compensated arterial blood gas results: pH 7.49, PCO2, 24, HCO3: 21. In respiratory alkalosis, compensation occurs via two body systems: changes in the bicarbonate buffer system offers a slight decrease in HCO3 levels. Renal systems compensates further by causing a retention of acid and excretion of bicarbonate ions (Brinkman & Sharma, 2018).
A disease/condition that causes metabolic acidosis is diabetic ketoacidosis. Metabolic acidosis is depicted by the following partially compensated arterial blood gas results: pH 7.30, PCO2 25, HCO3: 18. In metabolic acidosis, compensation occurs via respiratory system initially by increasing ventilation to blow off excess carbon dioxide to decrease the amount of acid in the blood. While bicarbonate reabsorption is increased. The kidneys also excrete carbonic acid as a compensatory mechanism in metabolic acidosis (Kraut & Madais, 2010).
A disease/condition that causes metabolic alkalosis prolonging vomiting. Metabolic alkalosis is depicted by the following partially compensated arterial blood gas results: pH: 7.50, PCO2: 50 HCO: 27. In metabolic alkalosis, compensation occurs via respiratory system which leads to alveolar hypoventilation to rise carbon dioxide levels to diminish the change in the pH. Carbon dioxide is the reabsorbed as carbonic acid; while the kidneys excret excess bicarbonate. (Brinkman & Sharma, 2018)
1c.
The electrolyte potassium is increased in acidosis. The electrolyte calcium is decreased in alkalosis.
1d.
The electrolyte potassium is increased in acidosis because…. The electrolyte calcium is decreased in alkalosis because acid secretion through the kidneys that is influences a shift of potassium from intracellular to extracellular causing an increase in serum potassium. Calcium binding to albumin is dependent on serum pH in severe alkalosis ionized calcium is decreased due to the increased binding of calcium to albumin (Goyal & Bhijimi, 2017)
2a. One function of the liver is to produce proteins that are important to blood clotting. A sign/symptom that commonly occurs as a consequence of this first liver dysfunction is bleeding or bruising easily (2018). A second function of the liver is to help break down old or damaged blood cells this function leads to an increase in the production of bilirubin. A sign/symptom commonly occurs as a consequence of this liver dysfunction is jaundice in the eyes and skin. This is due to the decreased ability to bind with bile within the live. A third function of the liver is to break down fats and produce energy; the liver cells change amino acids in food so they can be used to produce energy. Ammonia is a by-product of this conversion. The liver converts ammonia into urea. A sign/symptoms commonly occurs as a consequence of this liver dysfunction is increased ammonia levels which can lead to alteration in mental status (Bowen).
2b. The pathophysiology of the first sign/symptom the liver synthesizes clotting factors necessary for coagulation. The liver dysfunction causes an increase in bleeding and bruising. The pathophysiology of the second sign/symptom the body the function of the liver is to help break down old or damaged blood cells causing an increase in bilirubin in the blood. Bilirubin is formed when hemoglobin is broken down. The bilirubin is carried to the liver where it binds to bile. When bilirubin can not be eliminated quickly enough bilirubin builds up in the blood causing deposits in the skin resulting in jaundice. The pathophysiology of the third sign/symptom is the liver breaks down amino acids to use for energy. This process releases a by-product, ammonia. The liver is responsible for converting ammonia into urea to be excreted in the urine (2018).
2c. Liver dysfunction causes abnormal lab values. This first dysfunction of the liver results in an abnormal serum vitamin k of 0.015 ng/ml. Some patients may show normal levels of vitamin K but impaired blood clotting can be seen with levels as low as 0.5 ng/ml. The second dysfunction of the liver results in an abnormal total bilirubin serum lab value of 1.6 mg/dL. The third dysfunction of the liver results in an abnormal serum ammonia level of 80 u/dL.
References
Alcohol-related liver disease. (2018, October 08). Retrieved November 12, 2018, from Https://nhs.uk/conditions/alcohol-related-liver-disease-arld/symptoms/
Bowen, R. (Ed.). (n.d.). Metabolic Functions of The Liver. Retrieved November 12, 2018, from https://www.vivo.colostate/edu/hbooks/pathophysiology/digestion/liver/metabolic.html
Brinkman, J. E., & Sharma, S. (2018, January 19). Physiology, Alkalosis, Metabolic. Retrieved October 29, 2018, from https://www.ncbi.nlm.nih.gov/books/NBK482291/#_NBK482291_pubdet_
Brinkman, J. E., & Sharma, S. (2018, January 27). Physiology, Alkalosis, Repiratory. Retrieved October 29, 2018, from Https://ncbi/nvm.nih.gov/books/NBK482117/
Goyal, A., & Bhimiji, S. S. (2017, April 25). Hypocalcemia. Retrieved October 29, 2018, from Https://www.ncbi.nlm.nih.gov/books/NBK430912/#_NBK430912_pubdet_
Kraut, J. A., & Madias, N. E. (2010). Metabolic acidosis: Pathophysiology, diagnosis, and management. Retrieved October 29, 2018, from https://www.ncbi.nlm.nih.gov.m/pubmed/20308999/#fft
Patel, S., & Sharma, S. (2018, January 25). Physiology, Acidosis, Respiratory. Retrieved November 5, 2018, from https://www.ncbi.nlm.nih.gov/books/NBK482430/#_NBK482430_pubdet_
How does the liver work? (2016, August 22). Retrieved November 12, 2018, from Https://www.ncbi.nlm.nih.gov/books/NBK279393/?report reader#NBK279393_pubdet_