Hyperventilation is Defined as an Increase in Respiratory Rate and/or Tidal Volume, Resulting in the Elimination of More Carbon Dioxide than the Body Produces
Hyperventilation Results in Hypocapnia (Decreased Arterial pCO2) and Respiratory Alkalosis (at Least Initially, Until Renal Compensation Results in Bicarbonate Excretion with an Eventual Decrease in the pH Back Toward Normal) (see Respiratory Alkalosis)
Respiratory Alkalosis is Defined as an Acid-Base Disorder Characterized by a Decrease in Arterial pCO2 with an Associated Increase in Arterial pH (at Least Initially)
Note that a Patient Can Have a Respiratory Alkalosis without Being Alkalemic
Example
Due to Normal Compensatory Mechanisms, Chronic Respiratory Alkalosis Induces Metabolic (Predominantly Renal) Compensation (with a Progressive Decrease in Serum Bicarbonate Over Time), Culminating in Only Minimal/Absent Alkalemia
Hypoxemia-Induced Stimulation of Peripheral Chemoreceptors in the Carotid Bodies
However, the Degree of Hypoxemia-Induced Increase in Minute Ventilation is Modulated by Co-Existing pCO2 and pH, Mechanics of the Lung and Chest Wall, Genetic Factors, and the Overall Duration of Hypoxemia
The Increase in Minute Ventilation (VE) in Response to Decrease in pO2 is Non-Linear
The Most Pronounced Response is Observed with pO2 <60 mm Hg
The Increase in Minute Ventilation (VE) in Response to Decreased SaO2 is Relatively Linear
Clinical
On Mount Everest (Where pO2 is 27 mm Hg), the pCO2 is Decreased to 7.5 mm Hg (J Appl Physiol Respir Environ Exerc Physiol, 1983) [MEDLINE]
Hypoxemia-Induced Stimulation of Peripheral Chemoreceptors in the Carotid Bodies
However, the Degree of Hypoxemia-Induced Increase in Minute Ventilation is Modulated by Co-Existing pCO2 and pH, Mechanics of the Lung and Chest Wall, Genetic Factors, and the Overall Duration of Hypoxemia
The Increase in Minute Ventilation (VE) in Response to Decrease in pO2 is Non-Linear
The Most Pronounced Response is Observed with pO2 <60 mm Hg
The Increase in Minute Ventilation (VE) in Response to Decreased SaO2 is Relatively Linear
Pulmonary Disease (of Any Etiology Resulting in Hypoxemia)
Physiology
Hypoxemia-Induced Stimulation of Peripheral Chemoreceptors in the Carotid Bodies
However, the Degree of Hypoxemia-Induced Increase in Minute Ventilation is Modulated by Co-Existing pCO2 and pH, Mechanics of the Lung and Chest Wall, Genetic Factors, and the Overall Duration of Hypoxemia
The Increase in Minute Ventilation (VE) in Response to Decrease in pO2 is Non-Linear
The Most Pronounced Response is Observed with pO2 <60 mm Hg
The Increase in Minute Ventilation (VE) in Response to Decreased SaO2 is Relatively Linear
Stimulation of Peripheral and Central Chemoreceptors (and Increased Sensitivity of Peripheral Chemoreceptors to Hypoxia), Resulting in Increased Respiratory Drive
Increased Progesterone and Vasoactive Intestinal Peptide (VIP), Increased Brain Ammonia and Glutamine, and Hypoxemia from the Formation of Small Intrapulmonary Shunts (ie: Hepatopulmonary Syndrome), Resulting in Increased Respiratory Drive
Stimulation of Mechanical and Chemical Bronchopulmonary Receptors, Resulting in Increased Afferent Vagal Firing, Resulting in Increase in Respiratory Drive (and Cough and/or Bronchoconstriction)
Stimulation of Chest Wall Receptors (in Asthma, Pulmonary Fibrosis, and Chest Wall Disease), Resulting in Increased Respiratory Drive (and Dyspnea)
Stimulation of Mechanical and Chemical Bronchopulmonary Receptors, Resulting in Increased Afferent Vagal Firing, Resulting in Increase in Respiratory Drive (and Cough and/or Bronchoconstriction)
Stimulation of Mechanical and Chemical Bronchopulmonary Receptors, Resulting in Increased Afferent Vagal Firing, Resulting in Increase in Respiratory Drive (and Cough and/or Bronchoconstriction)
Stimulation of Chest Wall Receptors (in Asthma, Pulmonary Fibrosis, and Chest Wall Disease), Resulting in Increased Respiratory Drive (and Dyspnea)
Stimulation of Mechanical and Chemical Bronchopulmonary Receptors, Resulting in Increased Afferent Vagal Firing, Resulting in Increase in Respiratory Drive (and Cough and/or Bronchoconstriction)
Stimulation of Chest Wall Receptors (in Asthma, Pulmonary Fibrosis, and Chest Wall Disease), Resulting in Increased Respiratory Drive (and Dyspnea)
Stimulation of Mechanical and Chemical Bronchopulmonary Receptors, Resulting in Increased Afferent Vagal Firing, Resulting in Increase in Respiratory Drive (and Cough and/or Bronchoconstriction)
Stimulation of Chest Wall Receptors (in Asthma, Pulmonary Fibrosis, and Chest Wall Disease), Resulting in Increased Respiratory Drive (and Dyspnea)
Stimulation of Mechanical and Chemical Bronchopulmonary Receptors, Resulting in Increased Afferent Vagal Firing, Resulting in Increase in Respiratory Drive (and Cough and/or Bronchoconstriction)
Stimulation of Mechanical and Chemical Bronchopulmonary Receptors, Resulting in Increased Afferent Vagal Firing, Resulting in Increase in Respiratory Drive (and Cough and/or Bronchoconstriction)
Stimulation of Chest Wall Receptors (in Asthma, Pulmonary Fibrosis, and Chest Wall Disease), Resulting in Increased Respiratory Drive (and Dyspnea)
Stimulation of Mechanical and Chemical Bronchopulmonary Receptors, Resulting in Increased Afferent Vagal Firing, Resulting in Increase in Respiratory Drive (and Cough and/or Bronchoconstriction)
Stimulation of Mechanical and Chemical Bronchopulmonary Receptors, Resulting in Increased Afferent Vagal Firing, Resulting in Increase in Respiratory Drive (and Cough and/or Bronchoconstriction)
Stimulation of Mechanical and Chemical Bronchopulmonary Receptors, Resulting in Increased Afferent Vagal Firing, Resulting in Increase in Respiratory Drive (and Cough and/or Bronchoconstriction)
Stimulation of Peripheral and Central Chemoreceptors (or Direct Effect on Brainstem Respiratory Centers), Resulting in Increased Respiratory Drive
With Salicylates, Secondary Metabolic Acidosis Can Also Drive Respiration
Physiology
Hypocapnic Alkalosis is Synonymous with Respiratory Alkalosis (see Respiratory Alkalosis)
Acute Hypocapnia Results in the Immediate Development of Alkalosis
The Extracellular pH May Be Predicted on the Basis of the Henderson–Hasselbach Formula (see Acid-Base Physiology)
Sequence of Events
Initially, Hypocapnia in the Extracellular Fluid Results in an Immediate Decrease in the Intracellular FLuid Carbon Dioxide Concentration, Resulting in the Transfer of Chloride Ions from the Intracellular Fluid to Extracellular Fluid Compartment
The Chloride Ion Egress (Accompanied by a Decrease in the Concentrations of Bicarbonate Ions in the Extracellular Fluid) is Called “Tissue Buffering”)
Subsequently, There is Inhibition of Renal Tubular Reabsorption of Bicarbonate Ions within Minutes-Days
Over Time (and Assuming Normal Renal Function), the Serum Bicarbonate Ion Level Begins to Decrease and the pH Decreases Toward the Normal Value of 7.40 (i.e, a Hydrogen Ion Concentration of 40 nmol/L)
Mild Hypocapnia Generally Does Not Have Serious Clinical Effects in Healthy Persons
Clinical Manifestations Attributable to Acute Respiratory Alkalosis are More Common Than in Metabolic Alkalosis (see Metabolic Alkalosis)
Respiratory Alkalosis Probably Causes a Larger Change in Intracellular and Brain pH than Does Metabolic Alkalosis
Acute Respiratory Alkalosis Results in a Rapid Shift in Arterial pCO2, Which is Almost Immediately Transmitted Throughout the Total Body Water (Including the Intracellular Fluid Compartment, the Brain, and the Cerebrospinal Fluid)
This Accounts for the Characteristic Symptoms of Paresthesias, Carpopedal Spasm, and Lightheadedness Observed in Acute Respiratory Alkalosis
Metabolic Alkalosis-Associated Alterations in Blood bicarbonate Cause slower and Less Marked pH Changes within the Intracellular Fluid Compartment and Across the Blood Brain Barrier
Cardiovascular Manifestations
Arrhythmias
Epidemiology
Hypocapnia has Been Linked to the Development of Arrhythmias, Both in Critically Ill Patients and in Patients with Panic Disorder
Physiology
Arrhythmias are Likely Mediated by Alkalosis-Associated Electrophysiologic Effects on the Cardiac Conduction System (J Thorac Cardiovasc Surg, 1966) [MEDLINE]
May Also Be Mediated to Myocardial Ischemia (Although Specific Direct Myocardial Effects May Occur)
In Traumatic Brain Injury, Prophylactic Hyperventilation is Associated with Worse Outcome (and is Therefore, Not Recommended)
Physiology
Decreased Cerebral Oxygenation
Although Hyperventilation May Transiently Decrease Intracranial Pressure, it May Do so at the Expense of Cerebral Perfusion
Additionally, Hypocapnia May Exacerbate Secondary Brain Injury, Because Increased Cerebral Vascular Reactivity and Vasoconstriction Can Result in Decreased Regional Cerebral Blood Flow
In Ischemic Cerebrovascular Accident, Prophylactic Hyperventilation is Associated with Worse Outcome (and is Therefore, Not Recommended)
Physiology
The Beneficial Effects of Hypocapnia on Intracranial Pressure are Likely Outweighed by the Effects of a Decreased Oxygen Supply (Due to Decreased Cerebral Perfusion)
Postoperative Psychomotor Dysfunction
Epidemiology
Acute Hypocapnia is Common During General Anesthesia
Otherwise Healthy Patients Who are Subjected to Hypocapnia During General Anesthesia Have Been Found to Have Impaired Psychomotor Function for Up to 6 Days
Such Effects are Especially Pronounced in Older Patients
Seizures May Occur in the Setting of Hypocapnia (Lancet, 1998)[MEDLINE]
Physiology
Increased Neuronal Excitability, Seizure Activity, and Anaerobic Metabolism
Hypocapnic Potentiation of Seizure Activity, in Addition to Increasing Oxygen Demand, Augments Production of the Cytotoxic Excitatory Amino Acids Associated with Seizures
Hypocapnia May Also Induce Increased Neuronal Dopamine, which May Increase Risk of Seizures
Abnormal hyperventilation in patients with hepatic cirrhosis: role of enhanced chemosensitivity to carbon dioxide. Int J Cardiol. 2012 Jan 12;154(1):22-6. doi: 10.1016/j.ijcard.2010.08.066 [MEDLINE]
