Respiratory acidosis and alkalosis

Kundan Mittal; HK Aggarwal; N Rungta; Vinayak Patki

doi:10.4103/jpcc.jpcc_20_21

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CLINICAL UPDATE

Year : 2021 | Volume : 8 | Issue : 3 | Page : 161-166

Respiratory acidosis and alkalosis

Kundan Mittal¹, HK Aggarwal², N Rungta³, Vinayak Patki⁴
¹ Department of Pedaitrics, Pt B D Sharma, PGIMS, Rohtak, Haryana, India
² Department of Medicine and Nephrology, Pt B D Sharma, PGIMS, Rohtak, Haryana, India
³ Department of Critical Care Medicine, JNU Hospital, Jaipur, Rajasthan, India
⁴ Department of Pediaitric Critical Care, Advanced Pediatric Critical Care, Wanless Hospital, Miraj, Maharashtra, India

Date of Submission	25-Feb-2021
Date of Decision	12-Mar-2021
Date of Acceptance	22-Mar-2021
Date of Web Publication	21-May-2021

Correspondence Address:
Dr. Kundan Mittal
Pt B D Sharma, PGIMS, Rohtak, Haryana
India

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jpcc.jpcc_20_21

Abstract

Respiratory illnesses and failure are common in pediatric population compared to adults due to anatomical and physiological differences in respiratory system. Respiratory acidosis is commonly seen in intensive care settings and needs immediate attention. Treatment depends on underlying pathology and mechanical ventilation. Respiratory alkalosis is least common only mainly iatrogenic or child is hyperventilating.

Keywords: Respiratory acidosis, respiratory alkalosis, respiratory failure

How to cite this article:
Mittal K, Aggarwal H K, Rungta N, Patki V. Respiratory acidosis and alkalosis. J Pediatr Crit Care 2021;8:161-6

How to cite this URL:
Mittal K, Aggarwal H K, Rungta N, Patki V. Respiratory acidosis and alkalosis. J Pediatr Crit Care [serial online] 2021 [cited 2023 Jun 2];8:161-6. Available from: http://www.jpcc.org.in/text.asp?2021/8/3/161/316596

Respiratory Acidosis

A 10-year-old female child brought history road-side accident. Child was sitting unstrained in front seat. On arrival child was unconscious, respiratory rate was 8/min, jerky, oxygen saturation in room air 88%, Pulses were weak, extremities cold, 112/min, blood pressure 84/54 mmHg, no evidence of external bleed. Child was immediately intubated and mechanically ventilated. Mode of ventilation was ACMV (volume control), FiO₂ 100%, rate 16/min, inspiratory time 0.6 seconds, PEEP 5, trigger sensitivity 2 L/min. Her ABG revealed pH 7.30, PaO₂ 58, PCO₂ 80, HCO₃−28.

Objectives

Defining the respiratory acidosis
Etiology of respiratory acidosis
Clinical features
Management of acute and chronic respiratory acidosis.

To ensure normal functions of cellular enzymes body pH is regulated very tightly (7.35–7.45). Similarly, cell pH is also regulated between 7.0 and 7.3 depending on cell type. Normal PCO₂ of around 40 mmHg is regulated by alveolar ventilation and PCO₂ level is further maintained by CO₂ production (metabolism of carbohydrates and fats), transport (plasma and red blood cells [RBCs]), excretion (alveolar ventilation), and central nervous system (central and peripheral chemoreceptors, medulla and pons and respiratory muscles). When carbohydrate is metabolized 1 mmol of CO₂ is produced by consuming 1 mmol of oxygen (RQ 1) and less CO₂ is produced when fats utilize the oxygen (RQ 0.7). The production of CO₂ varies in different conditions in different organs of body. As soon as PCO₂ rises, the pH falls. This is immediately (within minutes) buffered by nonbicarbonate buffers (hemoglobin, plasma proteins and phosphate) so that HCO₃ − is not used. The acute non-bicarbonate buffer response is completed within 10–15 min, and steady-state persists for 1 h and if hypercapnia continues for >12 h, the kidneys generate additional HCO₃⁻. Respiratory acidosis can be classified acute (<12 h) or chronic (>3–5 days) types depending on duration. Acute and chronic hypercapnia are associated with hypoxemia. It should be clear that CO₂ per se is not acidic but combines with water inside blood. Carbon dioxide is major stimulus of ventilation and for every 1 mmHg PCO₂, the minute ventilation rises 1-4 L. Rise in PCO₂ is associated with fall in arterial PaO₂ since sum of partial pressure of gases in alveoli must remain equal to atmospheric pressure thus hypoxemia is more prominent than hypercapnia (CO₂ diffuses more quickly i.e., 20 times than oxygen and oxygen cannot be taken up by fully saturated hemoglobin in normal segment of lung). Hypoxemia stimulates ventilation when PaO₂ is 50-60 mmHg. Falling PCO₂ and rising pH also blunt the hypoxemic response. Hypoxemia and normocapnia in child with asthma reflects severe attack. Small rise in CO₂ in patient with intrinsic lung disease reflects severe dysfunction. Acute respiratory acidosis is associated with rise in catecholamines, glucocorticoids, aldosterone, renin and antidiuretic hormone (ADH) leading to water and sodium retention. Cardiac manifestations in such patients are due to hypoxia (alveolar hypoventilation) and electrolyte (associated metabolic acidosis) disturbances.

Compensatory response:

Acute (10 min) =1 mEq in bicarbonate for every 10 mmHg in PCO₂

OR HCO₃⁻= 0.1 x PCO₂

Chronic (3-5 days) =3.5 mEq in bicarbonate for every 10 mmHg in PCO₂

OR HCO₃⁻= 0.4 x PCO₂

Acute respiratory disorders:

Δ ↓ pH + 0.008 × Δ ↑ PCO₂

Chronic respiratory disorders

Δ ↓ pH + 0.003 × Δ ↑ PCO₂

Acute respiratory acidosis: D H⁺/DPCO₂ > 0.7

Acute on chronic respiratory acidosis: D H⁺/DPCO₂ 0.3–0.7

Chronic respiratory acidosis: D H⁺/DPCO₂ < 0.3

H⁺ =24 (PCO₂/HCO₃⁻)

If pH is normal then directional PCO₂ will classify respiratory disorder
If pH and bicarbonate and carbon dioxide are in opposite direction, defect is of respiratory origin [Table 1].
Bicarbonate usually increase up to 45 mEq/L and beyond this suspect mixed disorder.

Table 1: Compensatory response

Click here to view

Hypercapnia may result due to over production, decreased alveolar ventilation, impaired gas exchange, decreased respiratory center response, chest wall and respiratory muscles abnormalities. Thus, any pathology involving central nervous, system, neuromuscular diseases, spinal cord injury, foreign body aspiration, laryngospasm, obstructive sleep apnea, acute respiratory distress syndrome (ARDS), pulmonary edema, severe asthma, metabolic alkalosis, chest wall defects, massive pleural effusion, pneumothorax, airway obstruction, increased work of breathing, and ventilatory/gas exchange defects, drugs like opiates, organophosphate poisonings, sepsis, shock, electrolyte abnormalities, multiorgan failure, tetanus, status epilepticus, extreme obesity, increase glucose load in diet, cardiac arrest, Guillain-Barre' syndrome, poliomyelitis, tetanus, myasthenia crisis, neuromuscular blockers use, diaphragm paralysis, iatrogenic hypoventilation, permissive hypercapnia, and inappropriate ventilatory settings (minute ventilation [RR X TV], tidal volume set or generated [peak inspiratory pressure (PIP) in pressure mode] may be low <6 mL/kg), rate set is low or trigger sensitivity is high, pressure support may be less for supported breaths, flow set may be low or inspiratory time may not be age appropriate] are associated with increased blood carbon dioxide level.

Symptoms and Signs of Hypercapnia

Symptoms and signs are as a result of sympathetic stimulation, peripheral vasodilatation, cerebral vasodilatation, cerebral depression, and decreased diaphragm contractility and endurance.

Nausea, vomiting, irritability, confusion, raised intracranial pressure (ICP) (increase blood volume and vascular pressure), cerebral vasodilatation, papilledema
Increase in heart rate, blood pressure, cardiac output, arrhythmias and coronary vessels dilatation are due to sympathetic over activity
Initial renal vasodilatation and followed by vasoconstriction if PCO₂ >70 mmHg. Renin-angiotensin and ADH secretion may also increase.
Increase gastric acid production
Respiratory muscle fatigue due to decrease diaphragmatic contractility and endurance
Shift of oxygen-dissociation curve to right in acute phase and back towards normal side in chronic phase due to decrease in 2,3-DPG level in RBC's
Secondary polycythemia in chronic cases
Hypercapnia is associated with hypoxemia and usually seen early as partial pressure of gases in alveoli must equal to atmospheric pressure. Patient hyperventilate to excrete carbon dioxide but oxygen saturation is 100% so no more oxygen is taken up
Decreased glucose uptake by peripheral tissues and inhibit anaerobic glycolysis
In chronic cases respiratory center become less sensitive to PCO₂.

Types of Respiratory Failure

Type I (hypoxemic respiratory failure): PaO₂ is <60 mmHg (<8KPA) and normal or increased CO_2, or SPO₂ <92%

Ventilation/perfusion mismatch
Shunt
Alveolar hypoventilation
Diffusion defect
Perfusion/diffusion impairment: Hepatic failure, right to left intracardiac shunt
Decreased inspired O2

Type II (Hypercapnic Respiratory Failure or Pump or Ventilatory): PCO₂ is elevated >50 mmHg with or without hypoxemia

₂

5 mmHg: Hot hands
10 mmHg: Rapid bounding pulse, small pupils
15 mmHg: Engorged fundal veins, confusion or drowsiness, muscular twitching
30 mmHg: Depressed tendon reflexes, depressed extensor plantar responses, and coma
40 mmHg: Papilledema

Insidious exposure
Increased CO₂ production
Impaired respiratory control
Impaired respiratory efforts
Increased work of breathing.

Type III (Per-operative Respiratory Failure): Functional residual capacity falls below closing capacity as a result of atelectasis. Various contributing factors are general anesthesia, pain, supine posture and depressed cough reflex.
Type IV (Shock with hypoperfusion): Perfusion increased to respiratory muscles and resulting in decreased coronary perfusion.
Mixed Type: Mix of Type I and Type II
Acute on chronic respiratory failure
Chronic respiratory failure: Near normal pH >7.30, HCO₃⁻>32, PCO₂ >60

Investigations

General investigations

ABG: ABG will reveal raised PCO₂, fall in pH and compensatory increase in HCO₃⁻, slight increase in sodium, potassium, phosphate and decrease in chloride level. Also measure calcium and magnesium level (slight increase level may be observed). Normal anion gap is reported in respiratory acidosis
Urine: pH <5.5
Chest radiography and electrocardiography
Complete blood count (CBC), Bronchoscopy, pulmonary function tests
Alveolar-arterial oxygen difference will help in differentiating between lung parenchymal diseases and extrapulmonary disorders.

Type I: Complete history, physical examination, ABG on room air, A-a gradient, pulse oximetry, chest X-ray, CBC, Electrolytes and blood glucose, HRCT, VQ scan.

Type II: Chest X-ray, pulse oximetry, ABG in room air.

Treatment:

Objectives are to eliminate CO₂, decrease CO₂ production, correcting pH tolerating hypercapnia and correct the underlying pathology
Secure airway: Intubate the child if in coma or altered sensorium, PCO₂ >80, pH <7.10, poor respiratory efforts, hemodynamically unstable and ARDS
Administer oxygen to correct hypoxemia. Avoid excessive oxygen in chronic hypercapnia to prevent CNS depression (maintain PO₂ 60–70 mmHg and saturation 88%–93%)
Assisted ventilation: Mechanical ventilation is not required in conscious and hemodynamically stable children. Noninvasive ventilation (BiPAP) may be used in children who are hemodynamically stable, conscious and able to handle secretions. Increase IPAP by 2 (If issue is ventilation) and if oxygenation is concern, increase EPAP by 2 and IPAP also by same value). Usually maintain difference between IPAP and EPAP of five and measure PCO₂ after every hour.

Invasive ventilation

Indications:

Cardio-respiratory arrest, impending respiratory arrest
Respiratory muscle fatigue
Severe hypercapnic respiratory failure
Refractory hypoxemia not responding to non-invasive ventilation
Severe metabolic acidosis
Glasgow Coma Scale <8
Unable to protect airway.

The initial ventilatory settings depend on patient body weight, disease process, patho-physiology and laboratory studies. The initial settings are just guidelines and have to be modified depending on patho-physiological changes and improvement of patient.

Many ventilators ask for patient weight, age, leak and tubal compensation, sigh breath, inspiratory limbs etc., Most of the present-day ventilator will blink light for setting parameters once the mode of ventilation is selected. In pediatric population pressure-controlled ventilation is preferred mode of ventilation. Initially children are put on A/CMV or SIMV mode. In this mode we have to set the Ti time. Flow is automatically adjusted. In some situation we may set PRVC/VTPC mode, a dual control mode, where set tidal volume is delivered by adjusting pressure within limits.

Initial Ventilator Settings: We may have to ventilate four types of lung pathology (normal lung, restrictive, or obstructive diseased pathology, or diffusion defect). Depending on pathology settings are adjusted.

PCV: Assist Control: RR (physiological), PIP 20, PEEP 5, FiO₂ 100%, Pressure or flow trigger, monitor PIP to adjust TV 6-8 mL/kg/IBW.

VCV: Assist Control: RR, TV 6-8 mL/kg/IBW, PEEP 5, FiO₂ 100%, decelerating waveform.

SIMV (PCV or VCV): Set SIMV rate and pressure support to get tidal volume of 6-8 mL/kg/IBW. Rest of parameters will remain same depending on mode.

Adjust FiO₂ based on saturation and PaO₂
Adjust PEEP depending on hypoxemia
Adjust PIP and PS for tidal volume.
Role of sodium bicarbonate is limited to few cases only. Sodium bicarbonate infusion is harmful in patient with pulmonary edema. It can increase CO₂ production and more over it has no effect on central nervous system. Metabolic alkalosis is another issue once PCO₂ turns towards normal. Associated metabolic alkalosis may be treated using normal saline therapy and discontinuing diuretics
Antibiotics, bronchodilators, steroids as per condition
Avoid high carbohydrate diet in mechanically ventilated child
Avoid sedatives and neuro-suppressants
Control excessive CO₂ production (control fever, avoid high carbohydrate diet, overfeeding, use of fat reach diet, hypothermia)
Treatment of chronic respiratory acidosis includes addressing underlying etiology, adequate oxygenation (PaO₂ 60-70 mmHg and oxygen saturation 88-93%), treatment of infections, bronchodilator therapy, diet modification to reduce CO₂ production.

Respiratory Alkalosis

A 12-year-old male child, a known case of asthma brought with acute exacerbation of asthma for the last 6 h following acute respiratory tract infection. He was already on inhaled bronchodilator and corticosteroids. On examination respiratory rate 38/min with increased work of breathing, oxygen saturation 92% in room air, heart rate 112/min, blood pressure 1110/70. His ABG report is pH 7.5, PCO₂ 20 mmHg, PaO₂ 72 mmHg, HCO₃ − 18 mEq/L, Serum sodium 134 mEq/L, K + 3.4 mEq/L, Cl 98 mEq/L, CBC (TLC 16400. cmm, P80, L18).

Objectives

Defining respiratory alkalosis
Etiology of respiratory alkalosis
Management of child with respiratory alkalosis

Respiratory alkalosis is characterized by primarily decrease in PCO₂ (<35 mmHg in setting of alkalemia) and increase in pH >7.45. Primary hypocapnia reflects hyperventilation and secondary hypocapnia is in response to metabolic acidosis. Compensatory response to respiratory alkalosis is decrease in serum bicarbonate level. Respiratory alkalosis may be as a result of increased alveolar ventilation or decreased CO₂ production or combination of both. Respiratory alkalosis can be acute or chronic depending upon the duration.

Compensatory Changes

Acute (10 min) =2 mEq ↓ in bicarbonate for every 10 mmHg ↓ in PCO₂

HCO₃⁻=0.2 x PCO₂

Chronic = 5 mEq ↓ in bicarbonate for every 10 mmHg ↓ in pCO₂

HCO₃⁻=0.5 x PCO₂

Acute respiratory alkalosis: ↑ΔpH = 0.01 x ↓ΔPCO2

↓ΔH⁻ =0.75 x ↓ΔPCO2

H⁻ = (0.75 x PCO₂) +10

Chronic respiratory alkalosis: ↑ΔpH = 0.0003 x ↓ΔPCO2

↓ΔH⁻ =0.75 x ↓ΔPCO2

H⁻ = (0.3 x PCO₂) +28

Etiology

Respiratory alkalosis is common in anxiety, pain, central hyperventilation, high altitude, fever, encephalopathy, meningitis, cerebral edema, severe anemia, hypotension (tachypnea, hypoxia), tissue hypoxia, congestive cardiac failure, cold shock, pneumonia, acute asthma exacerbation, pulmonary embolism, pulmonary edema, pneumothorax, interstitial lung disease (hypocapnia and hypoxemia), hemodialysis, acidosis, inappropriate ventilatory settings (high rate, tidal volume), salicylate toxicity, xanthine (hyperventilation) toxicity, gram-negative sepsis (fever, hypotension and hypoxemia), hepatic failure (cerebral hypoxia, increased level of ammonia and progesterone), heat stroke, sepsis (fever, hypotension, hypoxemia).

Clinical signs and symptoms are basically seen in acute phase which include various neurological [decrease in cerebral blood flow (PCO₂ between 15 and 20 mmHg is associated with 45% decrease in blood flow), seizure, confusion, tingling sensation in limb, decrease in ICP and intraocular pressure, generalized slowing and high voltage EEG, and ionized calcium level], cardiovascular (decrease blood pressure, cardiac output, coronary blood flow, myocardial oxygen supply, cardiac arrhythmias, increased peripheral resistance, decrease tissue perfusion), metabolic effects (increased lactate production, decrease plasma volume, serum sodium, potassium, phosphate, ionized calcium, increased binding of calcium to albumin and chloride level), hypoxemia, shift of ODC to left, increased affinity to oxygen, increased oxygen uptake and decreased oxygen release to tissues, increased 2, 3-DPG level and hemoconcentration due to shift in plasma. In acute phase urinary pH is >7.0 and in chronic respiratory alkalosis it is <6.0. In chronic respiratory alkalosis urinary SID is also increased.

Diagnosis

Detailed history including medications, physical examination, blood gas analysis, CBC, serum electrolytes, chest X-ray, blood culture and other tests performed to know the etiology of respiratory alkalosis. Serum bicarbonate may fall up to 12 mEq/L and always consider associated metabolic acidosis if value falls below 12.^{[1],[2],[3],[4],[5],[6],[7],[8],[9],[10],[11]}

Treatment

Respiratory alkalosis is not a benign condition and needs correction of primary etiology.

If the patient is on mechanical ventilator appropriate ventilatory adjustment is made. We may also use sedatives to decrease respiratory derive
May correct pH using chloride rich fluid tolerating hypocapnia
Hypoxia is treated by proving supplementary oxygen
Rebreathe in paper mask or plastic bag in children with anxiety induced hyperventilation
In suspected salicylate toxicity perform forced diuresis, urine alkalinization and dialysis
Bronchodilators in child with acute exacerbation of asthma
Diuretics in case of pulmonary edema
Beta blockers and antithyroid medications in child with hyperthyroidism.

Pseudo-Respiratory Alkalosis

Arterial hypocapnia associated with circulatory shock characterized by raised mixed venous carbon dioxide but normal or decreased arterial carbon dioxide due to decreased delivery to lung and increased pulmonary transient time.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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