Respiratory alkalosis

Respiratory alkalosis
ICD-10	E87.3
ICD-9	276.3
DiseasesDB	406

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Madhu Sigdel M.B.B.S.[2] Priyamvada Singh, M.D. [3], Eiman Ghaffarpasand, M.D. [4]

Overview

Acid-base status of an organism is determined by the extracellular fluid (ECF) hydrogen ion concentration [H+] since pH is equal to minus log of [H+] i.e. pH = -log[H+]. Normal pH of human blood is 7.40 (7.35-7.45). Acidosis raises ECF [H+] thereby lowering pH whereas alkalosis lowers ECF [H+] thereby raising pH of the ECF. Respiratory alkalosis is an acid-base disorder, primarily a decrease in partial pressure of carbon dioxide in arterial blood means PaCo2 [normal PaCo2 is 40 mm Hg on average with range between 35-45mm Hg (4.7-6.0kPa)] with or without compensatory decrease in serum bicarbonate [HCO3-] (normal bicarbonate is 22-30mEq/L in arterial blood gas analysis) and pH being alkaline (normal pH of blood is 7.35-7.45).

Pathophysiology

Production of CO2 in body tissues by intracellular metabolic process (from oxidation of fat, carbohydrate and carbon skeleton of amino acids in normal metabolic process produces carbon dioxide and water) and elimination of CO2 through lungs are in equilibrium under normal physiology. CO2 in body tissues from normal metabolic process enters blood in the tissues because its local partial pressure in tissues is greater than the partial pressure in blood flowing through the tissues due to property of gases to diffuse from high pressure to low pressure. Flowing blood transports the CO2 to the lungs, where it diffuses into the alveoli and then to the atmosphere by pulmonary ventilation. The reversible combination of CO2 with water in the red blood cells under the influence of carbonic anhydrase enzyme forms carbonic acid (H2CO3) which dissociates into hydrogen and bicarbonate ions (H+ and HCO3−) ions. HCO3− diffuse from the red blood cells into the plasma, while chloride ions diffuse into the red blood cells to take their place (chloride shift). Hence, most of tissue CO2 is brought to lungs as plasma venous bicarbonate ions that accounts for about 70 percent of the CO2 transported from the tissues to the lungs. Remaining CO2 is transported as carbaminohemoglobin (23%) and as dissolved CO2 in fluids of blood(7%).

Respiratory alkalosis in almost all cases results from increased alveolar respiration (hyperventilation) leading to decrease in blood carbon dioxide concentration measured as PaCO2. This leads to decreased hydrogen ion [H+] and bicarbonate [HCO3-] concentrations. Decreased [H+] leads to increase in pH leading to alkalosis.

Compensation in respiratory alkalosis

compensation for respiratory alkalosis is mostly mediated through plasma buffers and proteins (eg. hemoglobin in RBC, plasma proteins) in acute stage and by kidneys in chronic compensatory stage.

Acute compensatory stage

• Starts within minutes to hours and mediated by body's non-bicarbonate buffers (hemoglobin, intracellular proteins and phosphates, plasma proteins) and it consists of cellular uptake of HCO3- and buffered by intracellular phosphates and proteins
• For every PaCO2 decrease of 10 mm Hg, serum bicarbonate decreases by 1-2mEq/L
• Change in pH is unpredictable

Chronic compensatory stage

• Renal mediated process where reduction in PaCO2 leads to decreased renal tubular H+ secretion. Within the renal tubular cells, CO2, under the influence of carbonic anhydrase enzyme, combines with H2O to form carbonic acid (H2CO3), which then dissociates into HCO3- and H+. Alkalosis inhibits carbonic anhydrase activity, resulting in reduced H+ secretion into the renal tubule. As a result, there is not enough H+ in the renal tubular fluid to react with all the filtered HCO3− from glomerular capillaries of the kidneys. Therefore, the HCO3− that cannot react with H+ is not reabsorbed and is excreted in the urine. This causes a decrease in urinary net acid excretion(mostly ammonium ions NH4+) and due to increased bicarbonate excretion, body's bicarbonate stores is reduced.
• Starts after 24-36 hours and renal compensation for sustained hypocapnia is complete in 36-72 hours
• For every PaCO2 decrease of 10 mm Hg, serum bicarbonate decreases by 5mEq/L
• pH in chronic compensation is near normal

Classification

There are two types of respiratory alkalosis: chronic and acute.

Acute respiratory alkalosis

• Lasting for less than 24-48 hours
• Increased levels of carbon dioxide are "blown off" by the lungs, which are hyperventilating.
• During acute respiratory alkalosis, the person may lose consciousness where the rate of ventilation will resume to normal.

Chronic respiratory alkalosis

• Lasting for longer than 24-48 hours
• For every 10 mM drop in pCO₂ in blood, there is a corresponding 5 mM of bicarbonate ion drop.
• The drop of 5 mM of bicarbonate ion is a compensation effect which reduces the alkalosis effect of the drop in pCO₂ in blood. This is termed metabolic compensation.

Risk Factors

Common Risk Factors

• Common risk factors in the development of respiratory alkalosis include:
  • Old age
  • Mechanical ventilation
  • Lung diseases
  • Hepatic failure
  • Infection
  • High altitude
  • Anxiety disorder
  • CNS infection

Less Common Risk Factors

• Less common risk factors in the development of respiratory alkalosis include:
  • Drugs
  • Poisoning

Causes

Tissue hypoxia (hypoxemia)

• Pneumonia
• Aspiration of foreign body, food or vomitus
• Pulmonary embolism
• Bronchospasm/laryngospasm (eg. in asthma)
• Drowning
• Anemia
• High altitude
• Cyanotic heart disease
• Circulatory failure or hypotension

Stimulation of chest receptors

• Pneumonia
• Asthma
• Pneumothorax/hemothorax
• Flail chest
• Cardiac failure
• Pulmonary edema (non-cardiogenic)
• Adult/infant respiratory distress syndrome
• Interstitial lung disease

Stimulators of central respiratory drive

• Pain
• Anxiety
• Fever
• High altitude
• Anemia
• Drugs like doxapram and large doses of aspirin (stimulate the respiratory center), Gallium nitrate, cocaine, catecholamines
• CNS causes, including stroke, subarachnoid haemorrhage, meningitis, encephalitis, CNS tumor
• Caffeine overdose and coffee abuse, methylxanthines (eg. theophyllin, aminophyllin)
• Progesterone

Systemic diseases

• Sepsis
• Liver failure
• Hyperthyroidism
• Pregnancy
• Iatrogenically during mechanical ventilation of patients
• Carbon monoxide poisoning
• Recovery from metabolic acidosis
• Heat exposure

Special considerations

• Sepsis or salicylate toxicity are the only single disorders that cause both an elevated anion gap metabolic acidosis and a respiratory alkalosis.
• Ischemia, infection or infarction of the central respiratory centers may result either respiratory acidosis (decreased respiratory drive) or respiratory alkalosis (increased respiratory drive)
• Asthma, and Pneumonia can also present with either repiratory alkalosis or acidosis. Asthma typically presents with a respiratory alkalosis, however as the patient tires, respiratory acidosis may occur.
• Pulmonary embolus can be a life threatening condition and often presents as respiratory alkalosis.
• Progesterone is sometimes used as a respiratory stimulant in obstructive sleep apnea and hypoventilation.
• Respiratory alkalosis is the most common acid base abnormality in critically ill patients.

Differential Diagnosis

Abbreviations: ABG (arterial blood gas); ACE (angiotensin converting enzyme); BMI (body mass index); CBC (complete blood count); CSF (cerebrospinal fluid); CXR (chest X-ray); DOE (dyspnea on exercise); ECG (electrocardiogram); FEF (forced expiratory flow rate); FEV1 (forced expiratory volume); FVC (forced vital capacity); JVD (jugular vein distention); MCV (mean corpuscular volume); Plt (platelet); RV (residual volume); SIADH (syndrome of inappropriate antidiuretic hormone); TSH (thyroid stimulating hormone); Vt (tidal volume); WBC (white blood cell);

Organ system			Diseases	Clinical manifestations													Diagnosis					Other features
				Symptoms								Physical exam
				Loss of consciousness	Agitation	Weight loss	Fever	Chest pain	Cough	Orthopnea	DOE	Cyanosis	Clubbing	JVD	Peripheral edema	Auscultation	CBC	ABG	Imaging	Spirometry	Gold standard
Acute Dyspnea	Respiratory system	Chest and Pleura, Lower airway	Asthma attack	-	+	-	-	+/-	+	-	-	+	-	-	-	Wheeze	↑ Eosinophil	Respiratory alkalosis	Normal	↓ FEV1, PEF	Physical exam and Spirometry	Chest pain
			COPD exacerbation	-	+	-	+	+	+	+	-	+	+/-	+/-	+/-	Wheeze, Rhonchi, and Crackles	↑WBC, ↑RBC	Respiratory alkalosis	Hyperexpansion	↓ FEV1/FVC	Clinical assessment	Acute exacerbations of chronic bronchitis (AECB)
			Pneumonia	-	-	-	+	+	+	-	-	-	-	-	-	Wheeze, Rhonchi, and Crackles	↑WBC, neutrophilia	Respiratory alkalosis	Lobar consolidation	Normal	Chest X-ray and CT Scan	productive cough
			Pneumothorax	-	-	-	-	+	-	-	-	-	-	+/-	-	Diminished breath sounds	Normal	↓O2, ↑CO2	Radiolucency without lung marking	↓Vt	CXR and Chest CT scan	Tracheal deviation
			Pulmonary embolism	-	-	-	-	+	-	-	+/-	-	-	-	-	Normal	Normal	Respiratory alkalosis	Normal	Normal	Pulmonary CT angiography	Pleuritic chest pain
			Rib fractures (flail chest)	-	+	-	-	+	-	-	-	-	-	-	-	Normal	Normal	Respiratory alkalosis	Fracture marks	Normal	Chest X-ray	Pneumothorax
	Cardiovascular system		Acute myocardial ischemia	+/-	+	-	+/-	+	-	+	+	-	-	-	-	Normal	Normal	Respiratory alkalosis	Normal	Normal	Cardiac troponin I	Nausea and vomiting, Positive pertinent risk factors, such as hypertension, diabetes, and smoking
			Acute heart failure	+/-	+	-	-	+/-	+	+/-	+	+	-	+	+	S3	Normal	Respiratory alkalosis	↑ Cardiothoracic ratio	↓Vt	B-type natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP)	Excessive sweating, high blood pressure
			Tachyarrhythmia	+/-	+	-	-	+/-	-	-	-	-	-	-	-	High pulse rate	Normal	Respiratory alkalosis	Normal	Normal	ECG	Palpitation
			Pulmonary edema	+/-	+	-	+	+	+	+	+	+	+	+	+	Basal crackle	Normal	Respiratory alkalosis	Bat wing pattern, air bronchograms	↓Vt, ↑RV	Cardiac Catheterization	Tachypnea
	Central nervous system		Encephalitis	+	+	-	+	-	-	-	-	-	-	-	-	Normal	↑WBC, neutrophilia	Respiratory alkalosis	Normal	Normal	CSF PCR	Confusion
			Traumatic brain injury	+	+/-	-	-	-	-	-	-	-	-	-	-	Normal	Normal	Respiratory alkalosis	Intracerebral hemorrhage	Normal	Brain CT scan	Lucid interval
	Toxic/Metabolic		Salicylate poisoning	+	-	-	-	-	-	-	-	+	-	-	-	Normal	Normal	Metabolic acidosis, Respiratory alkalosis	Normal	Normal	Blood test	Vomiting, Tinnitus, Confusion, Hyperthermia
	Systemic		Pregnancy	-	-	-	-	+/-	-	-	-	-	-	-	+	Normal	↑WBC, RBC	Respiratory alkalosis	Normal	↓Vt, ↑RV	βhCG	Missed period, Hyperemesis
			Sepsis	+/-	-	-	+	-	-	-	-	-	-	-	-	Normal	↑WBC, neutrophilia	Respiratory alkalosis	Normal	Normal	SIRS criteria	Chills, Confusion
Organ system			Diseases	Clinical manifestations													Diagnosis					Other features
				Symptoms								Physical exam
				Loss of consciousness	Agitation	Weight loss	Fever	Chest pain	Cough	Orthopnea	DOE	Cyanosis	Clubbing	JVD	Peripheral edema	Auscultation	CBC	ABG	Imaging	Spirometry	Gold standard
Chronic Dyspnea	Respiratory system	Chest and Pleura, Lower airway	Bronchial asthma	-	+	+/-	-	+/-	+	-	-	+	+	-	-	Wheeze	↑ Eosinophil	Respiratory alkalosis, Metabolic acidosis	Pulmonary hyperinflation, Bronchial wall thickening	↓ FEV1/FVC	Spirometry before and after bronchodilator	Paroxysmal respiratory distress
			COPD	-	-	+/-	-	-	+	+	+	+	+	+	+/-	Expiratory wheeze	↑ RBC	Respiratory alkalosis, Metabolic acidosis	↑ Bronchovascular markings, Cardiomegaly	↓ FEV1/FVC	Physical exam and Spirometry	Heavy smoking history
			Emphysema	-	-	-	-	-	+/-	-	-	+	+	-	-	Expiratory wheeze, Hyperinflation	Normal	Respiratory alkalosis, Metabolic acidosis	Flattening of diaphragm, vertical heart	↓ FEV1/FVC	Physical exam and Spirometry	Barrel chest
	Toxic/Metabolic		Metabolic acidosis	-	-	+	-	-	-	-	-	-	-	-	-	Normal	Normal	Metabolic acidosis, Respiratory alkalosis	Normal	Normal	ABG	Confusion, Vomiting
	Systemic		Anxiety	+	+	+	-	+/-	+/-	-	-	-	-	-	-	Normal	Normal	Respiratory alkalosis	Normal	Normal	Psychological interview	Sweating, Palpitation

History and Symptoms

• Symptoms of respiratory alkalosis depends upon duration of disease and underlying diseases. Symptoms of acute respiratory alkalosis are related to decrease blood carbon dioxide levels (PaCO2) that leads to reduced cerebral blood flow resulting from vasoconstriction of cerebral vessels. Most of the symptoms arise when PaCO2 falls below 30 mm Hg.

History

Patients with respiratory alkalosis may have a positive history of:

• Anxiety disorders or primary neurologic diseases
• Lung or liver diseases
• Critical illness with mechanical ventilation

Common Symptoms

Common symptoms of acute respiratory alkalosis include:

• Light-headedness
• Syncope
• Confusion
• Seizure
• Peripheral and circumoral paresthesia and cramp
• Chest pain and shortness of breath are seen in patients hyperventilating due to pain or anxiety
• Chronic respiratory alkalosis is generally well tolerated without apparent clinical symptoms

• Signs include:
  • Carpopedal spasm due to tetany as a result of decreased levels of ionized calcium in the blood (ionized calcium [Ca++] are driven inside cells in exchange for hydrogen ion [H+] as compensatory mechanism to correct pH) with no fall in total serum calcium level. Alkalosis also increases protein-bound fraction of calcium reducing free calcium.

Physical Examination

• Physical examination findings of patients with respiratory alkalosis is related to the underlying causes.

Appearance of the Patient

• Patients with acute respiratory alkalosis usually appear anxious in primary hyperventilation syndrome, OR are ill appearing in mechanically ventilation whereas are comfortable in chronic respiratory alkalosis.

Vital Signs

• High-grade / low-grade fever
• Tachycardia may be present
• Tachypnea or hyperpnea is present with both increase in respiratory rate and tidal volume
• Cheyne-Stokes type of breathing may be seen in upper pontine lesion or heart failure
• Low blood pressure in mechanically ventilated patients with respiratory alkalosis

Skin

• Cyanosis is present in hypoxic patient
• Jaundice may be present in liver disease

HEENT

• HEENT examination of patients with respiratory alkalosis is usually normal.

Neck

• Neck examination of patients with respiratory alkalosis is usually normal

Lungs

• Lungs are dull to percussion in hemothorax/hyperresonant in pneumothorax
• Fine/coarse crackles upon auscultation of the lung suggest interstitial lung disease/pneumonia as a cause of respiratory alkalosis

Heart

• Cardiovascular examination of patients with respiratory alkalosis is usually normal except in patients with coronary artery disease

Abdomen

Hepatomegaly and right upper quadrant tenderness may be seen in cirrhosis

Back

• Back examination of patients with respiratory alkalosis is usually normal.

Genitourinary

• Genitourinary examination of patients with respiratory alkalosis is usually normal

Neuromuscular

• Focal neurologic signs and depressed level of consciousness is seen in respiratory alkalosis of neurologic cause

Extremities

• Extremities examination of patients with respiratory alkalosis show positive Trousseau sign in acute hypocapnia as a result of tetany.

Approach to acid-base disorders

Check pH on ABG

pH<7.35=Acidosis

pH>7.45=Alkalosis

Check PaCO2

PaCO2 > 45mm Hg = Respiratory acidosis Primary cause: hypoventilation

PaCO2 Normal or < 35mm Hg = Metabolic acidosis

Check PaCO2

PaCO2 > 45mm Hg = Metabolic alkalosis

PaCO2 < 35mm Hg = Respiratory alkalosis Primary cause: hyperventilation

HCO3- > 29 eg. vomiting

Check HCO3-

Normal or slight decrease = Acute respiratory alkalosis eg. fever, panic attack

Decreased < 24 = Chronic respiratory alkalosis eg. Anemia, CNS causes

Laboratory Findings

• Arterial blood gas analysis(ABG):
  • It is the diagnostic test of choice for respiratory alkalosis
  • primary respiratory alkalosis has pH> 7.45, PaCO2 <35mm Hg or 4.7kPa while PaO2 is normal(>80mm Hg or 10.7kPa)
• Serum electrolytes: Decrease in [HCO3-],[Na+], [K+] and ionized [Ca++] are seen in acute hypocapnia due to intracellular shift whereas decreased [HCO3-] and hyperphosphatemia are seen in sustained hypocapnia.
• Other laboratory test and imaging studies that may be useful in respiratory alkalosis to find out the causes includes:
  • Urine pH and urinalysis
  • CBC: elevated WBC in sepsis
  • Blood/sputum/urine C/S: for sepsis
  • EKG and ECHO: for congestive heart failure
  • Drug screening test
  • Thyroid function test: to rule out hyperthyroidism
  • Liver function test: abnormal in hepatic causes
  • pulmonary function test: to rule out chest infections
  • V/Q scan: to rule out pulmonary embolism
  • Chest X-ray: for chest infection
  • CT scan: for pulmonary embolism
  • MRI brain: to rule out CNS cause of hyperventilation

Treatment

• Respiratory alkalosis is not a life threatening disorder, so treatment is directed at the underlying causes of the disorder.
  • patients with hyperventilation disorder (eg. anxiety, conversion disorder) are benefited from rebreathing mask.
  • High altitude sickness is treated with acetazolamide 250mg 12 hourly, Dexamethasone 4mg 6 hourly, oxygen therapy and descent to lower altitude in severe cases.
  • For critically ill patients on mechanical ventilation with respiratory alkalosis, tidal volume and respiratory rate needs to be decreased with adequate pain control.
  • Sedatives and antidepressants should not be used in cases of respiratory alkalosis.

Related Chapters

• Metabolic alkalosis
• Acid-base imbalance
• Metabolic acidosis
• Respiratory acidosis
• Anion gap
• Hypocalcemia