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Alkalosisis the result of a process reducinghydrogen ionconcentration ofarterialblood plasma(alkalemia). In contrast toacidemia(serum pH 7.35 or lower), alkalemia occurs when the serum pH is higher than normal (7.45 or higher). Alkalosis is usually divided into the categories ofrespiratory alkalosisandmetabolic alkalosisor a combined respiratory/metabolic alkalosis.[1]
| Alkalosis | |
|---|---|
| Specialty | Endocrinology |
Signs and symptoms
editMetabolic alkalosis is usually accompanied bylow blood potassium concentration,causing, e.g., muscular weakness,muscle pain,and muscle cramps (from disturbed function of the skeletal muscles), and muscle spasms (from disturbed function of smooth muscles).
It may also causelow blood calcium concentration.As the blood pH increases, bloodtransport proteins,such asalbumin,become more ionized into anions. This causes the free calcium present in blood to bind more strongly with albumin. If severe, it may causetetany.
Causes
editRespiratory alkalosis is caused byhyperventilation,[2]resulting in a loss ofcarbon dioxide.Compensatory mechanisms for this include release of hydrogen ion from tissue buffers and excretion ofbicarbonatein the kidneys, both of which lower bloodpH.[3]Hyperventilation-induced alkalosis can be seen in several deadlycentral nervous systemdiseases such asstrokesorRett syndrome.[2]
InMcArdle disease(glycogen storage disease type V), the inability to utilize muscle glycogen leads to a shortage of ATP during exercise and subsequent exercise-induced prematuremuscle fatigue,muscle cramps, muscle pain (myalgia), inappropriate rapid heart rate response to exercise (tachycardia), rapid depletion of phosphocreatine, insufficient ATP production, increased ADP and AMP, increased rise in venous ammonia (from thepurine nucleotide cycle), increased epinephrine (adrenaline), increased plasma free fatty acids (lipolysis), increased venous pH (alkalosis), rapid (tachypnea) and commonly (approx. 50%) also heavy breathing (hyperpnea), that is exercise hyperventilation.[4][5][6][7][8][9]During exercise, due to the inability to utilize muscle glycogen as a substrate for ATP synthesis, plasma lactate does not significantly rise (and may fall below) compared to resting levels; consequently, McArdle disease individuals do not experience lactic acidosis.[7]The rise in venous pH (alkalosis), may be due to increased ammonia production,[10]increased epinephrine, and/or increased oxygen demand for oxidative phosphorylation of blood borne substrates (free fatty acids and blood glucose).[8][6]
Metabolic alkalosis can be caused by repeated vomiting,[2]resulting in a loss ofhydrochloric acidin the stomach contents. Severedehydration,and the consumption ofalkali,[3]are other causes. It can also be caused by administration of diuretics[2]and endocrine disorders such asCushing's syndrome.Compensatory mechanism for metabolic alkalosis involve slowed breathing by the lungs to increaseserumcarbon dioxide,[2]a condition leaning toward respiratoryacidosis.As respiratory acidosis often accompanies the compensation for metabolic alkalosis, and vice versa, a delicate balance is created between these two conditions.
See also
editReferences
edit- ^Mosby's Paramedic Textbook – Mick J. Sanders
- ^abcdeYee AH, Rabinstein AA (February 2010). "Neurologic presentations of acid-base imbalance, electrolyte abnormalities, and endocrine emergencies".Neurol Clin.28(1): 1–16.doi:10.1016/j.ncl.2009.09.002.PMID19932372.
- ^abNorman G. Levinsky (1987).Eugene Braunwald;et al. (eds.).Harrison's Principles of Internal Medicine(11 ed.). McGraw-Hill. pp. 212–214.ISBN0-07-100134-4.
- ^Zange, Jochen; Grehl, Torsten; Disselhorst-Klug, Catherine; Rau, Günter; Müller, Klaus; Schröder, Rolf; Tegenthoff, Martin; Malin, Jean-Pierre; Vorgerd, Matthias (June 2003)."Breakdown of adenine nucleotide pool in fatiguing skeletal muscle in McArdle's disease: a noninvasive 31P-MRS and EMG study".Muscle & Nerve.27(6): 728–736.doi:10.1002/mus.10377.ISSN0148-639X.PMID12766985.
- ^Kitaoka, Yu (2014-02-25)."McArdle Disease and Exercise Physiology".Biology.3(1): 157–166.doi:10.3390/biology3010157.ISSN2079-7737.PMC4009758.PMID24833339.
- ^abRodriguez-Lopez, Carlos; Santalla, Alfredo; Valenzuela, Pedro L.; Real-Martínez, Alberto; Villarreal-Salazar, Mónica; Rodriguez-Gomez, Irene; Pinós, Tomàs; Ara, Ignacio; Lucia, Alejandro (February 2023)."Muscle glycogen unavailability and fat oxidation rate during exercise: Insights from McArdle disease".The Journal of Physiology.601(3): 551–566.doi:10.1113/JP283743.ISSN1469-7793.PMC10099855.PMID36370371.
- ^abØrngreen, Mette Cathrine; Jeppesen, Tina Dysgaard; Taivassalo, Tanja; Hauerslev, Simon; Preisler, Nicolai; Heinicke, Katja; Haller, Ronald G.; Vissing, John; van Hall, Gerrit (August 2015)."Lactate and Energy Metabolism During Exercise in Patients With Blocked Glycogenolysis (McArdle Disease)".The Journal of Clinical Endocrinology and Metabolism.100(8): E1096–1104.doi:10.1210/jc.2015-1339.ISSN1945-7197.PMID26030324.
- ^abHagberg, J. M.; Coyle, E. F.; Carroll, J. E.; Miller, J. M.; Martin, W. H.; Brooke, M. H. (April 1982)."Exercise hyperventilation in patients with McArdle's disease".Journal of Applied Physiology: Respiratory, Environmental and Exercise Physiology.52(4): 991–994.doi:10.1152/jappl.1982.52.4.991.ISSN0161-7567.PMID6953061.
- ^Hagberg, J. M.; King, D. S.; Rogers, M. A.; Montain, S. J.; Jilka, S. M.; Kohrt, W. M.; Heller, S. L. (April 1990)."Exercise and recovery ventilatory and VO2 responses of patients with McArdle's disease".Journal of Applied Physiology.68(4): 1393–1398.doi:10.1152/jappl.1990.68.4.1393.ISSN8750-7587.PMID2347781.
- ^"Metabolic disease in neonates: Initial metabolic tests for suspected metabolic disease".Safer Care Victoria.
External links
edit- IUPAC,Compendium of Chemical Terminology,2nd ed. (the "Gold Book" ) (1997). Online corrected version: (2006–) "alkalosis".doi:10.1351/goldbook.A00221