What intervention does the nurse provide to prevent respiratory alkalosis in the patient with?

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Introduction

Respiratory alkalosis is 1 of the 4 basic classifications of blood pH imbalances. Normal human physiological pH is 7.35 to 7.45. A decrease in pH below this range is acidosis, an increase above this range is alkalosis. Respiratory alkalosis is by definition a disease state where the body’s pH is elevated to greater than 7.45 secondary to some respiratory or pulmonary process.[1]

Etiology

Before going into details about pathology and this disease process, some background information about the physiological pH buffering process is important. The primary pH buffer system in the human body is the HCO3/CO2 chemical equilibrium system. Where:

• H + HCO3 <----> H2CO3 <----> CO2 + H2O

HCO3 functions as an alkalotic substance. CO2 (carbon dioxide) functions as an acidic substance. Therefore, Increases in HCO3 (bicarbonate) or decreases in CO2 will make blood more alkalotic. The opposite is also true where decreases in HCO3 or an increase in CO2 will make blood more acidic. CO2 levels are physiologically regulated by the pulmonary system through respiration, whereas the HCO3 levels are regulated through the renal system with reabsorption rates. Therefore, respiratory alkalosis is a decrease in serum CO2. While it is theoretically possible to have decreased CO2 production, in every scenario this illness is a result of hyperventilation where CO2 is breathed away.[2][3][4]

Epidemiology

Respiratory alkalosis is the most common acid-base abnormality with no discrimination between genders. The exact frequency and distribution of disease are dependent upon the etiology. Likewise, the morbidity and mortality rates are dependent on the etiology of the disease.[5]

Pathophysiology

In almost every scenario, respiratory alkalosis is induced by a process involving hyperventilation. These include central causes, hypoxemic causes, pulmonary causes, and iatrogenic causes. Central sources are a head injury, stroke, hyperthyroidism, anxiety-hyperventilation, pain, fear, stress, drugs, medications such as salicylates, and various toxins. Hypoxic stimulation leads to hyperventilation in an attempt to correct hypoxia at the expense of a CO2 loss. Pulmonary causes include pulmonary embolisms, pneumothorax, pneumonia, and acute asthma or COPD exacerbations. Iatrogenic causes are primarily due to hyperventilation in intubated patients on mechanical ventilation.[6][7]

Respiratory alkalosis may be an acute process or a chronic process. These are determined based on the level of metabolic compensation for the respiratory disease. Excess HCO3 levels are buffered to reduce levels and maintain a physiological pH through the renal decrease of H secretion and increasing HCO3 secretion; however, this metabolic process occurs over the course of days whereas respiratory disease can adjust CO2 levels in minutes to hours. Therefore, acute respiratory alkalosis is associated with high bicarbonate levels since there has not been sufficient time to lower the HCO3 levels and chronic respiratory alkalosis is associated with low to normal HCO3 levels.[8][1][9]

History and Physical

Since the primary cause of all respiratory alkalosis etiologies is hyperventilation, many patients present with complain to shortness of breath. The exact history and physical exam findings are highly variable as there are many pathologies that induce the pH disturbance. These may include acute onset dyspnea, fever, chills, peripheral edema, orthopnea, weakness, confusion, light-headedness, dizziness, anxiety, chest pain, wheezing, hemoptysis, trauma, history of central line catheter, recent surgery, history of thromboembolic disease, history of asthma, history of COPD, acute focal neurological signs, numbness, paresthesia, abdominal pain, nausea, vomiting, tinnitus, or weight loss.

Physical exam findings may be just as varied depending on etiology to include fever, tachycardia, tachypnea, diaphoresis, hyper or hypotension, altered mental status, productive or non-productive cough, wheezing, rales, crackles, cardiac murmur or arrhythmia, jugular venous distension, meningeal signs, focal neurological loss, Trousseau sign, Chvostek sign, jaundice, melena, hematochezia, hepatosplenomegaly, or there may be no definitive signs at all.[10][11]

Evaluation

With a wide preliminary differential diagnosis list, evaluation should always begin with a thorough history and physical exam to focus diagnostic considerations. In all cases, arterial blood gas is necessary to diagnose the pH imbalance. Serum electrolytes should be measured with particular attention to sodium, potassium, and calcium levels as aberrations in these may lead to further complication. Magnesium and phosphate are also essential to measure. In hypoxic patients, it is important to calculate the A-a gradient to determine the etiology and further diagnosis. If the A-a gradient is wide, be suspicious of pulmonary embolism and appropriately work up the patient. A chest x-ray is important in all patients as it helps discern an anatomical or infectious cause and may rule in/out pulmonary edema. If there is a clinical reason for it, chest CT can play a vital role in achieving a diagnosis. If there is appropriate clinical suspicion for neurological insult, CT or MRI of the head may be appropriate along with lumbar puncture for WBC, glucose, and protein analysis.[1][12][13]

Treatment / Management

Treatment of metabolic alkalosis is targeted at treating the underlying pathology. In anxious patients, anxiolytics may be necessary. In infectious disease, antibiotics targeting sputum or blood cultures are appropriate. In embolic disease, anticoagulation is necessary. Ventilator support may be necessary for patients with acute respiratory failure, acute asthma, or acute, chronic obstructive pulmonary disease (COPD) exacerbation if they show signs of respiratory fatigue. In ventilator controlled patients, it may be necessary to reevaluate their ventilator settings to reduce respiratory rate. If hyperventilation is intentional, monitor the arterial or venous blood gas values closely. In severe cases, pH may be directly reduced using acidic agents. However, this is not routinely done.[14][15][16]

Differential Diagnosis

Other possibilities include:

• Asthma exacerbation

• Atrial fibrillation

• Atrial flutter

• Atrial tachycardia

• Bacterial pneumonia

• Bacterial sepsis

• Community-acquired pneumonia

• COPD exacerbation

• Head trauma

• Heatstroke

• Hyperthyroidism and thyrotoxicosis

• Idiopathic pulmonary fibrosis

• Meningitis

• Metabolic acidosis

• Metabolic alkalosis

• Myocardial infarction

• Panic disorder

• Pneumothorax

• Pulmonary edema

• Pulmonary embolism

• Salicylate toxicity

• Theophylline toxicity

• Viral pneumonia

Prognosis

Respiratory alkalosis in itself is not a life-threatening diagnosis. However, the prognosis is variable depending on etiology.

Pearls and Other Issues

Respiratory alkalosis is a pathology that is secondary to hyperventilation.

Hyperventilation typically occurs in response to an insult such as hypoxia, metabolic acidosis, pain, anxiety, or increased metabolic demand.

Respiratory alkalosis in itself is not life-threatening; however, the underlying etiology may be. Always look for and treat the source of the illness. Interventions to reduce pH directly are typically not necessary as there is no mortality benefit to this therapy.

Enhancing Healthcare Team Outcomes

Respiratory alkalosis is easy to diagnose but its management can be difficult; the key is to find the cause. Because there are many causes of respiratory alkalosis, the condition is best managed by an interprofessional team that includes an internist, primary care provider, nurse practitioner, pulmonologist, mental health nurse and a pain specialist.

Treatment of metabolic alkalosis is targeted at treating the underlying pathology. If hyperventilation is intentional, monitor the arterial or venous blood gas values closely. In severe cases, pH may be directly reduced using acidic agents. However, this is not routinely done. Hyperventilation typically occurs in response to an insult such as hypoxia, metabolic acidosis, pain, anxiety, or increased metabolic demand.

Respiratory alkalosis in itself is not life-threatening; however, the underlying etiology may be. Always look for and treat the source of the illness. Interventions to reduce pH directly are typically not necessary as there is no mortality benefit to this therapy.

Review Questions

References

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Raphael KL, Murphy RA, Shlipak MG, Satterfield S, Huston HK, Sebastian A, Sellmeyer DE, Patel KV, Newman AB, Sarnak MJ, Ix JH, Fried LF., Health ABC Study. Bicarbonate Concentration, Acid-Base Status, and Mortality in the Health, Aging, and Body Composition Study. Clin J Am Soc Nephrol. 2016 Feb 05;11(2):308-16. [PMC free article: PMC4741040] [PubMed: 26769766]

Hamdi H, Hassanian-Moghaddam H, Hamdi A, Zahed NS. Acid-base disturbances in acute poisoning and their association with survival. J Crit Care. 2016 Oct;35:84-9. [PubMed: 27481740]

Junod AF. [Physiopathology of chronic respiratory insufficiency]. Schweiz Med Wochenschr. 1980 Dec 13;110(50):1896-1901. [PubMed: 6782666]

Gardner WN. The pathophysiology of hyperventilation disorders. Chest. 1996 Feb;109(2):516-34. [PubMed: 8620731]

Castro D, Patil SM, Keenaghan M. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Sep 20, 2021. Arterial Blood Gas. [PubMed: 30725604]

Piekutowska-Abramczuk D, Rutyna R, Czyżyk E, Jurkiewicz E, Iwanicka-Pronicka K, Rokicki D, Stachowicz S, Strzemecka J, Guz W, Gawroński M, Kosierb A, Ligas J, Puchala M, Drelich-Zbroja A, Bednarska-Makaruk M, Dąbrowski W, Ciara E, Książyk JB, Pronicka E. Leigh syndrome in individuals bearing m.9185T>C MTATP6 variant. Is hyperventilation a factor which starts its development? Metab Brain Dis. 2018 Feb;33(1):191-199. [PMC free article: PMC5769826] [PubMed: 29116603]

Morel J, Gergelé L, Dominé A, Molliex S, Perrot JL, Labeille B, Costes F. The venous-arterial difference in CO2 should be interpreted with caution in case of respiratory alkalosis in healthy volunteers. J Clin Monit Comput. 2017 Aug;31(4):701-707. [PubMed: 27287759]

Park JJ, Choi DJ, Yoon CH, Oh IY, Lee JH, Ahn S, Yoo BS, Kang SM, Kim JJ, Baek SH, Cho MC, Jeon ES, Chae SC, Ryu KH, Oh BH., KorHF Registry. The prognostic value of arterial blood gas analysis in high-risk acute heart failure patients: an analysis of the Korean Heart Failure (KorHF) registry. Eur J Heart Fail. 2015 Jun;17(6):601-11. [PubMed: 26096207]

Fujii N, Kashihara M, Kenny GP, Honda Y, Fujimoto T, Cao Y, Nishiyasu T. Carotid chemoreceptors have a limited role in mediating the hyperthermia-induced hyperventilation in exercising humans. J Appl Physiol (1985). 2019 Feb 01;126(2):305-313. [PubMed: 30382804]

Batlle D, Chin-Theodorou J, Tucker BM. Metabolic Acidosis or Respiratory Alkalosis? Evaluation of a Low Plasma Bicarbonate Using the Urine Anion Gap. Am J Kidney Dis. 2017 Sep;70(3):440-444. [PMC free article: PMC5572668] [PubMed: 28599903]

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