Metabolic acidosis and alkalosis
The normal pH range for systemic arterial blood is between 7.35 and 7.45. Any levels that drop below a pH of 7.35 is a condition known as acidosis. Any levels that rise above a pH of 7.45 is known as alkalosis. Acidosis can depress the central nervous system, which if severe enough, can lead to death. Alkalosis can overly excite the central nervous system causing muscle spasms, convulsions, and even death. Either end of the spectrum can result in an unwanted outcome. This Assignment will require you to look at four conditions: respiratory acidosis, respiratory alkalosis, metabolic acidosis and metabolic alkalosis.
-Define each condition by including the levels of PCO2 or HCO3- and the pH levels.
Identify at least three or more common causes for each condition.
-Describe the compensatory mechanism for each condition in detail; include whether the kidneys or lungs assist.
-Describe treatment mechanisms for each condition when the regular compensatory mechanisms are not working well.
-Describe how older age may compromise the acid-base balance processes. Be sure to include any changes associated with the kidneys and the lungs.Basic Writing Expectations:-Paper should be at least 800 words, not counting the title or reference pages, answering all questions listed above.
-Include a title page, double space, font size 12 pt. Times New Roman.
-A minimum of at least 4 credible peer reviewed sources should be used.
-Use APA style for all citations.
-Make certain that your paper is free of grammar and spelling errors.Refer to Assignment rubric located in the course Syllabus and scoring guide located in Doc Sharing for additional guidance.
Metabolic acidosis and alkalosis
The blood pH is controlled by the respiratory function, renal function and the chemical buffering. When there is an increase in plasma acidity, the condition is referred to as Acidosis. This condition is as a result of the low ability to buffer, reduced function of the kidneys or increases production of acid in the tissues. Congenital and acquired problems result in this metabolic acidosis. The indicator of the condition is a reduced level of HCO3in the serum. The opposite of this condition is the metabolic alkalosis. This condition means an elevated level of HCO3. Metabolic alkalosis can be seen with the use of loop diuretics. The renal and respiratory system compensate for acidosis. To regulate the acidity in the system, the depth of breathing and increased respiratory rate facilitate respiratory alkalosis and therefore the metabolic acidosis is partially buffered (DuBose, 2016).
Extreme acidosis result to lethargy, cardiovascular instability, and altered mental status. The major symptoms of lactic acidosis include Ataxia, seizures, and lethargy, poor feeding, developmental delay, poor feeding, altered mental status, deafness and optic nerve atrophy. Metabolic alkalosis occurs when the body gains a lot of bases or loses much of the body acidity. This metabolic alkalosis is caused by overuse of diuretics, antacids, vomiting causing electrolyte loss, laxatives, alcohol abuse and ingestion of bicarbonate. Metabolism process in the body produces acidic products that alter the pH of body fluids. Carbon dioxide which is a by-product of metabolism combines with H2O to form acid. Lactic acid produced after anaerobic metabolism and lipid metabolism resulting to fatty acids contributed to the change in body acidity. These acidic products are eliminated to control pH homeostasis. When the process of the elimination takes place rapidly, the resulting condition is alkalosis while failure to remove these products cause acidosis (Angus, 2016). The side effects of acidosis in the body affect the functionality of the central nervous system. A fall of pH below 7.35 results to malfunctioning of the central nervous system. An individual with acidosis becomes comatose and disoriented as the condition worsen. An increase alkalosis causes hyperexitability of central nervous system (IMRP, 2004).
ExtremeMetabolic acidosis is treated by administration of sodium bicarbonate. This medication improves the acidosis status but does not treat or alter the causes of the acidosis. The administration of the bicarbonate, however, has side effects, hypernatremia result from over usage of the bicarbonate. In situations where HCO2 (CO2) load is unwanted, Tromenthamine (THAM) is given to buffer (DuBose, 2016). For patients with DKA, bicarbonate medication is not recommended except when the acidosis is extremely high. Usage of bicarbonate in DKA result in the growth of cerebral edema. In the instances of alkalosis, RTA 2(proximal) is given to respond as the buffer. Citrate or sodium bicarbonate may be used by the patient. Once the alkali administration has begun, potassium supplements should be given to the patient to increased urine potassium losses. A case of alkalosis may be treated by the use of thiazide diuretics, this enhances reabsorption of bicarbonates but this treatment has side effects of potassium loss in the body. For metabolic alkalosis, the medics should eliminate or reduce the diuretic use if possible and in the case of vomiting anti-emetics or PPI may be useful (Sabatini, 1994).
Respiratory acidosis and alkalosis
Respiratory alkalosis is caused by the excessive airing of the lungs. Hyperventilation of the lungs decreases the amount of CO2 in the body fluid which in return increase the pH level. As the level of carbon dioxide decrease, less carbonic acid is formed by the reaction of hydrogen ions with bicarbonate ions. If the pH level of body fluid goes beyond 7.35 then symptoms of alkalosis become clear. Respiratory alkalosis is characterized by low PCO2 and HCO3. Respiratory acidosis result when lungs have paralyzed ability to remove carbon dioxide from the body (Stockwell, 2017). Excessive accumulation of the CO2 cause increased acidity in the body fluid. The acidosis results from decreased arterial pH(less than 7.36) increased PCO2 and elevated levels of HCO3.
Respiratory alkalosis is caused by insufficient carbon dioxide in the bloodstream. Is can also be caused by high fever, liver diseases, lack of oxygen, hyperventilation of the lungs which is brought by anxiety, touring high altitudes zones and lung diseases. Respiratory acidosis results from depression resulting from obesity and poliomyelitis, inadequate alveolar ventilation, muscle disorders, lungs infections, for example, pulmonary edema and over production of CO2. Intake of carbon dioxide from expired gases cause respiratory acidosis (Stockwell, 2017).
Respiratory acidosis cause increased H+ and lower body pH, the body counteracts this State by increasing the level of HCO3- to match the reduced PCO2. This means the ratio of the PCO2 and the HCO3- is maintained at a balance (Stockwell, 2017). The buffering ensure the level of acidity is constant and rate of acid excretion is improved. The respiratory alkalosis is regulated by decreasing level amount of renal acid excreted from the body and buffering the cells from high pH. The body reduces the HCO3- in order to lower the level of the PCO2 and therefore reduce the pH level. The kidney reduces the rate of secretion of hydrogen in the instance of persistent respiratory alkalosis (Angus, 2016).
Respiratory alkalosis is treated by teaching how to hold breath during training or exercising and treating the cause such as the diuretics. Pathophysiologic can be used to treat hypercapnia. Respiratory alkalosis patients can be given antidepressants or administered conservative treatments like rebreathing into a polythene bag. Beta-adrenergic blockers can be used to regulate the lungs hyperventilation (Sabatini, 1994).
Older age acid-base balance processes
As people advance in age, the respiratory and renal function depreciated thus interfering with base-acid balance in the body. When respiratory and renal system performances slow down, the carbon dioxide removal process slow down. The kidney experience reduced blood flow with age thus lower antidiuretic hormone this interfere with its ability to maintain the electrolyte –fluid balance. The impaired abilities of kidneys and lungs, therefore, inhibit base-acid imbalance reparation (Angus, 2016).
Angus, D. S. (2016). Respiratory Alkalosis. Retrieved from University of Connecticut: http://fitsweb.uchc.edu/student/selectives/TimurGraham/Etiology_Respiratory_Alkalosis.html
DuBose, T. (2016). Chapter 47. Acidosis and Alkalosis. Retrieved from McGraw-Hill Global Education: http://accessmedicine.mhmedical.com/content.aspx?bookid=331§ionid=40726770&jumpsectionID=40731164
IMRP. (2004). Evaluation of Acid-Base Disorders. Retrieved from http://www.ucdenver.edu/academics/colleges/medicalschool/departments/medicine/intmed/imrp/CURRICULUM/Documents/Evaluation%20of%20Acid%20Base%20Disorders.pdf
Sabatini, S. (1994). Effect of respiratory acidosis and respiratory alkalosis on renal transport enzymes. Retrieved from ncbi: https://www.ncbi.nlm.nih.gov/pubmed/8092253
Stockwell, J. (2017). Acid-base disturbances in children, Acidosis, Alkalosis. Retrieved from Journal of Family Practise: http://www.mdedge.com/jfponline/dsm/8819/critical-care/acid-base-disturbances-children-acidosis-alkalosis