Alkalosis


Article Author:
Moushumi Sur


Article Editor:
Ankur Shah


Editors In Chief:
Kranthi Sitammagari
Mayank Singhal


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Trevor Nezwek
Radia Jamil
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes


Updated:
8/4/2019 11:56:51 AM

Introduction

Alkalosis is an abnormal pathophysiological condition characterized by the buildup of excess base or alkali in the body. It results in an abnormally high serum pH (arterial pH greater than 7.45), which is termed alkalemia and forms one end of the spectrum of acid-base disorders. There is generally a loss of hydrogen ions (H) or an excess of bicarbonate ions (OH), and multiple factors can cause either of these. In general, alkalosis is less life-threatening than acidosis, but severe electrolyte derangements can accompany alkalosis due to transcellular shifts, and this can result in rare but severe clinical disorders. Alkalosis can be either respiratory or metabolic in origin, but metabolic alkalosis is far more common than respiratory causes.

Etiology

The etiology of alkalosis can subdivide into metabolic and respiratory causes:

Metabolic

  1. Excess loss of hydrogen ion—this occurs primarily due to gastric losses (prolonged and severe gastric aspiration, excessive emesis of gastric contents as in pyloric stenosis, congenital chloridorrhea).[1][2]
  2. Increased bicarbonate in the extracellular compartment—this occurs due to excess enteral intake of bicarbonate or alkali (milk-alkali syndrome) or increased parenteral intake of citrate or acetate. Increased renal reabsorption of bicarbonate can also cause metabolic alkalosis (severe hypokalemia, primary hyperaldosteronism, Cushing syndrome, Bartter syndrome, Gitelman syndrome, toxic ingestion of licorice, excessive chloruretic diuretic use).[3][4][5]
  3. Diuretic-induced alkalosis—diuretics (loop and thiazide) that block sodium and chloride reabsorption can cause increased bicarbonate absorption at the proximal tubule leading to increased serum bicarbonate concentration, also called as contraction alkalosis.

Respiratory

  1. Low production of CO2—hypometabolic conditions like severe coma, particularly when supported by mechanical ventilation.
  2. Excess pulmonary loss of CO2—this results in alkalosis when the production of CO2 in the body is normal (psychogenic hyperventilation, iatrogenic hyperventilation in patients on assisted mechanical ventilation or extracorporeal membrane oxygenation, early stages of salicylate overdose due to overstimulation of the respiratory center).[6]

Epidemiology

Among the various acid-base disorders, metabolic alkalosis is the most frequently occurring derangement in hospitalized patients, with an incidence of 51% in this group.[7] Respiratory alkalosis is also commonly seen in the hospitalized patient population. Prevalence has shown to be 22.5 to 44.7% in large inpatient studies in the US.[7][8] An Italian study has shown a prevalence of 24% respiratory alkalosis at the time of admission.[9]

The incidence of mixed respiratory and metabolic alkalosis is estimated to be around 29%.

There does not appear to be a significant gender distribution to alkalosis, except in the case of infantile pyloric stenosis where there is an overwhelming male predominance noted.[10]

Pathophysiology

The body has a robust buffering system that acts to minimize pH change in the initial stages of acid-base derangements. When these buffering systems are overwhelmed, alkalosis may result.

The kidney attempts to maintain normal acid-base balance by the dual mechanisms of bicarbonate reabsorption, mainly in the proximal tubule, and bicarbonate production in the distal nephron. Reabsorption of bicarbonate is mediated by a Na-H antiporter and also by the H (+)-ATPase (adenosine triphosphate-ase). Influences on bicarbonate reabsorption include effective arterial blood volume, glomerular filtration rate, chloride, and potassium concentrations in the serum. In conditions resulting in respiratory alkalosis, the kidney acts to both decrease bicarbonate reabsorption and bicarbonate production as a compensatory mechanism. This process helps maintain the pH of the extracellular compartment to neutralize the effect of the low pCO2 that is the primary derangement of respiratory alkalosis. However, the complex buffering mechanisms of the kidneys may take several days to achieve full effect, with an eventual expected fall of bicarbonate by 4-5 mmol/L for every 10 mm Hg fall in pCO2.

On the other hand, respiratory depression resulting in increased PaCO2 occurs promptly and predictably to buffer the alkalemia resulting from metabolic conditions (while this is variable, expectations are that there will be a 0.5 mm Hg increase in PaCO2 per 1 mmol/L increase in HCO). Alkalemia also causes a shift in the oxyhemoglobin dissociation curve towards the left, thus increasing hemoglobin's affinity for oxygen, and decreasing oxygen release to the tissues.

When the intake of potassium is suboptimal, this can correlate with metabolic alkalosis due to intracellular sodium as well as proton levels rising and a consequent depression in aldosterone levels.[11] When protons shift into the cellular compartment, metabolic alkalosis ensues; this is followed by respiratory center depression of respiratory drive and ultimately, purging of bicarbonate by the kidney.

Histopathology

There are no specific histopathological features that are pathognomonic for alkalosis. However, the primary cause of alkalosis may be established by histopathological studies, especially when related to kidney disorders. 

History and Physical

Alkalosis can present with a myriad of symptoms and signs, based on the etiology of alkalosis, respiratory versus metabolic, and the primary condition leading to the alkalosis. 

Metabolic alkalosis can have central nervous system manifestations ranging from confusion to coma, peripheral neuropathic symptoms of tremor, tingling and numbness, muscle weakness and twitching, and arrhythmias, in particular when associated with hypokalemia and hypocalcemia.[12] Nonhypochloremic metabolic alkalosis associates with hypertension and is usually the result of syndromes of excess mineralocorticoid production. These generally correlate with signs of volume expansion, hypertension, and hypokalemia.[13] Persistent and projectile, non-bilious emesis in a two to six week old, otherwise well-appearing infant is a hallmark presentation of pyloric stenosis.

Respiratory alkalosis can have associated syncope, tremors, and signs of hyperventilation along with chest pain and dyspnea.[14]

Evaluation

A blood gas analysis, preferably arterial, is needed to establish alkalosis and whether it appears to be metabolic or respiratory in origin. Ancillary blood tests are necessary; these are serum chemistries with electrolytes, blood urea nitrogen, creatinine. While the bicarbonate concentration being high can indicate the possibility of metabolic alkalosis but is not confirmatory as both the carbon dioxide concentration as well as the concentration of H+ ions will affect the presence or absence of alkalosis. Hence, a blood gas estimate of pH and pCO2 is also needed. However, in mixed acid-base disorders, complex calculations are necessary to establish multiple disturbances and whether they are primary and/or coexistent abnormalities or compensatory buffering mechanisms.[13]

Associated electrolyte abnormalities need to be identified, including hypochloremia, hypokalemia, and hypocalcemia. An EKG may be necessary to evaluate for arrhythmias. Urine chemistry is required to assess the kidney's response to the alkalosis. Hypertension requires assessment and other tests for hyperaldosteronism when indicated. Volume depletion also requires evaluation as a coexisting condition. 

Respiratory alkalosis, when associated with hypoxia or an increased alveolar-arterial (A-a) gradient, requires a search for a cause of the hypoxia. However, pulmonary embolism may cause respiratory alkalosis without associated hypoxia and must be ruled out before attributing hyperventilation to pain or anxiety. 

Treatment / Management

The appropriate management of alkalosis rests on prompt identification followed by management of the primary etiology of the alkalosis and the type (metabolic, respiratory, or mixed). Specific etiologies like pyloric stenosis need surgical correction while excessive ingestion of alkali will respond to restriction of excess intake. Alkalosis associated with conditions of excess aldosterone may need hormonal correction or replacement along with treatment of associated hypertension. Correction of chloride responsive alkalosis caused by volume depletion is possible by replenishment of extracellular volume. Electrolyte disturbances associated with alkalosis such as hypokalemia and hypocalcemia are the chief causes of clinical deterioration in the patient and must undergo correction before the onset of life-threatening complications. Slow acid administration or dialysis with low bicarbonate baths may be necessary for emergent situations.[15]

Treatment of respiratory alkalosis primarily targets correcting the hyperventilation (primary or iatrogenic) and apart from anxiety and pain treatment, it sometimes also requires adjustment of mechanical ventilation with intentional hypercapnia.[14]

Differential Diagnosis

Since alkalosis has a broad spectrum of manifestations, the differential diagnosis for its wide range of signs and symptoms can be confusing. Associated electrolyte disturbances can also complicate the diagnosis, like hypochloremia, hypokalemia, and hypocalcemia. 

Prognosis

Alkalosis, whether respiratory or metabolic, is usually compensated by the body's innate buffering mechanisms in the acute and subacute phase. When the alkalosis is uncorrected or chronic, the buffering mechanisms may become overwhelmed, and this may lead to a poor prognosis. Prognosis depends on associated problems of volume depletion, electrolyte, and hormonal disturbances and varies based on primary etiology of the alkalosis.

Patients with metabolic alkalosis have been found to have increased ICU length of stay, more days on mechanical ventilation and higher hospital mortality. An increase of 5-mEq/l in the serum bicarbonate level over 30 mEq/l correlated with an odds ratio of 1.21 for hospital mortality. The association between metabolic alkalosis and mortality occurs independently of the etiology of alkalosis.[16]

Complications

Alkalosis can lead to life-threatening arrhythmias (atrial and ventricular tachyarrhythmias), especially when associated with hypokalemia and hypocalcemia. These associated electrolyte abnormalities can also cause carpopedal spasms, muscle weakness, and altered mental status.

Consultations

Depending upon the primary etiology of the alkalosis, consultation may be necessary with various subspecialties. A nephrological consult may be needed to elucidate the cause of metabolic alkalosis and management. A cardiologist and an endocrinologist may be able to help with blood pressure control and hormonal correction in conditions of hyperaldosteronism. The patient may require admission under the care of an intensivist for severe electrolyte correction. Infants with pyloric stenosis will need surgical evaluation and correction.  

Deterrence and Patient Education

Patients require education about the significance of severe alkalosis and the primary etiology that is causing their alkalosis. Patients and families need to understand the link between causes of alkalosis such as anxiety disorders, severe emesis or excessive alkali ingestion, and resultant alkalosis.   

Pearls and Other Issues

Alkalosis is a common finding in hospitalized patients but is rarely life-threatening in itself. While the body's buffering systems initially correct alkalosis, ongoing alkalosis may cause clinical problems due to associated electrolyte disturbances.

Enhancing Healthcare Team Outcomes

Managing alkalosis requires an interprofessional team of healthcare professionals that includes a nurse, laboratory technologists, pharmacist, and several physicians in different specialties. 

Immediately upon identifying alkalosis, the primary clinician is responsible for coordinating the care, which includes the following[17]:

  • Ordering serial blood gas analysis, blood, and urine chemistries. [Level V]
  • Monitor the patient for signs and symptoms of neuromuscular depression, cardiac arrhythmias, hypertension, and volume depletion.
  • Performing various maneuvers to help limit the severity of alkalosis and boost the body's buffering mechanisms.
  • Consult with the pharmacist about the correct dose and method of correcting electrolyte abnormalities.
  • Consult with a nephrologist on further management, which may include dialysis.
  • Consult with the radiologist about imaging tests to evaluate the causes of persistent emesis.
  • Consult with the intensivist about ICU care and monitoring while in hospital.
  • Nurses monitoring the patient with metabolic alkalosis should be aware of the potential complications, including arrhythmias and promptly inform members of the team.

The management of alkalosis does not stop with correction of alkalosis. Once the patient achieves a stable state, one has to determine how and why the patient became alkalotic and also determine risk factors for recurrence of alkalosis. The morbidity and mortality of alkalosis in hospitalized patients are significant,[16][18] [Level III]

Only by working as an interprofessional team can the morbidity of alkalosis be decreased. This process will include ongoing monitoring by the nursing staff, who will alert the attending regarding any change in status. The pharmacist can perform medication reconciliation, as well as being involved in the ordering and administration rate of fluids, bicarbonate, and other pharmaceutical measures to correct alkalosis. Their expertise should be used as a tool by the clinicians managing the case, in a collaborative interprofessional effort with the primary aim of achieving optimal patient outcomes. [Level V]


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Alkalosis - Questions

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A 24-year-old male develops an extreme right lower quadrant pain and is brought to the emergency department by her family. The clinical findings are consistent with acute appendicitis, and he underwent an appendectomy a few hours ago. Post-operatively, the patient is complaining of significant pain and is also noted to be tachypneic with a respiratory rate of 30 per minute. Blood workup, including, serum phosphorus, magnesium, and bicarbonate, was ordered in this patient. The lab results revealed low serum bicarbonate consistent with the patient's clinical condition causing respiratory alkalosis due to severe pain. Given the patient's current status, which of the following electrolyte also drops in respiratory alkalosis?



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A 12-year-old female with Rett's syndrome presents to the emergency department with symptoms of fever, cough and runny nose. On exam, she is found to have a heart rate of 88/min and a respiratory rate of 28/min with signs of a carpopedal spasm. Her blood gas shows a pH of 7.46, pCO2 of 29 and p02 of 95. Which of the following serum findings will be most likely seen?



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A 2-week-old full-term boy is brought to the emergency department with the complaints of forceful, projectile, non-bilious vomiting after each feed for the last three days. On examination, he appears irritable but otherwise well-appearing and sucks down vigorously on a bottle. However, he promptly throws up the formula within minutes. Which of the following is the most likely result expected on the patient's arterial blood gas?



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A patient with congestive heart failure has been prescribed loop diuretics that he has been taking for the last two months. His provider recently recommended an increase in his diuretic regimen based on signs of pulmonary edema on his chest x-ray. He also ordered an arterial blood gas analysis that reveals a pH of 7.45, pCO2 of 60 mmHg and bicarbonate level of 42 mEq/L. Which of the following is the most likely underlying acid-base disorder?



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A 68-year-old male with a history of emphysema, hypertension, and osteoporosis has been admitted to the hospital for pneumonia. Initial chemistry studies reveal a sodium level of 143 meq/L, a chloride level of 102 meq/L, a potassium level of 2.8 meq/L, and a bicarbonate level of 42. Which of the following best explains the elevated bicarbonate level in this patient?



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A 2-year-old patient is recovering in the intensive care unit after a tumor resection surgery on her left femur. She is currently intubated and mechanically ventilated with settings of tidal volume 6 ml/kg, ventilation rate of 25/min, PEEP of 5 cmH2O, and FiO2 of 60%. She starts waking up on postoperative day 1 and reaching for her mother. She is afebrile, heart rate is 136/min, blood pressure is 120/86 mmHg, respiratory rate is 32/min and SpO2 of 100%. A venous blood gas reveals a pH of 7.47, pCO2 of 32, pO2 of 88. Which of the following would be the most appropriate ventilatorsetting change to make at this time?



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Alkalosis - References

References

HOWE CT,LEQUESNE LP, PYLORIC STENOSIS: THE METABOLIC EFFECTS. The British journal of surgery. 1964 Dec;     [PubMed]
STRODER J,BLENNEMANN H, METABOLIC ALKALOSIS IN PYLORIC STENOSIS. Lancet (London, England). 1964 Oct 24;     [PubMed]
Medarov BI, Milk-alkali syndrome. Mayo Clinic proceedings. 2009 Mar;     [PubMed]
Koni I,Takeda R, [Acid-base disturbance in adrenal and parathyroid diseases]. Nihon rinsho. Japanese journal of clinical medicine. 1992 Sep;     [PubMed]
Khanna A,Kurtzman NA, Metabolic alkalosis. Respiratory care. 2001 Apr;     [PubMed]
Laffey JG,Kavanagh BP, Hypocapnia. The New England journal of medicine. 2002 Jul 4;     [PubMed]
Hodgkin JE,Soeprono FF,Chan DM, Incidence of metabolic alkalemia in hospitalized patients. Critical care medicine. 1980 Dec;     [PubMed]
Mazzara JT,Ayres SM,Grace WJ, Extreme hypocapnia in the critically ill patient. The American journal of medicine. 1974 Apr;     [PubMed]
Palange P,Carlone S,Galassetti P,Felli A,Serra P, Incidence of acid-base and electrolyte disturbances in a general hospital: a study of 110 consecutive admissions. Recenti progressi in medicina. 1990 Dec;     [PubMed]
To T,Wajja A,Wales PW,Langer JC, Population demographic indicators associated with incidence of pyloric stenosis. Archives of pediatrics     [PubMed]
Jones JW,Sebastian A,Hulter HN,Schambelan M,Sutton JM,Biglieri EG, Systemic and renal acid-base effects of chronic dietary potassium depletion in humans. Kidney international. 1982 Feb;     [PubMed]
Dhondup T,Qian Q, Acid-Base and Electrolyte Disorders in Patients with and without Chronic Kidney Disease: An Update. Kidney diseases (Basel, Switzerland). 2017 Dec;     [PubMed]
Seifter JL,Chang HY, Disorders of Acid-Base Balance: New Perspectives. Kidney diseases (Basel, Switzerland). 2017 Jan;     [PubMed]
Hopper K, Respiratory Acid-Base Disorders in the Critical Care Unit. The Veterinary clinics of North America. Small animal practice. 2017 Mar;     [PubMed]
Pahari DK,Kazmi W,Raman G,Biswas S, Diagnosis and management of metabolic alkalosis. Journal of the Indian Medical Association. 2006 Nov;     [PubMed]
Libório AB,Noritomi DT,Leite TT,de Melo Bezerra CT,de Faria ER,Kellum JA, Increased serum bicarbonate in critically ill patients: a retrospective analysis. Intensive care medicine. 2015 Mar;     [PubMed]
Batlle D,Chin-Theodorou J,Tucker BM, Metabolic Acidosis or Respiratory Alkalosis? Evaluation of a Low Plasma Bicarbonate Using the Urine Anion Gap. American journal of kidney diseases : the official journal of the National Kidney Foundation. 2017 Sep;     [PubMed]
Hamdi H,Hassanian-Moghaddam H,Hamdi A,Zahed NS, Acid-base disturbances in acute poisoning and their association with survival. Journal of critical care. 2016 Oct;     [PubMed]

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