section name header

Basics ⬇

Outline

BASICS

Definition!!navigator!!

  • Increase in blood PCO2
  • Homeostatic mechanisms maintain normal blood concentrations within a narrow range
  • Arterial concentrations in the range 35–42 mmHg
  • Venous concentrations in the range 43–49 mmHg

Pathophysiology!!navigator!!

  • CO2 is formed in all tissues during metabolic energy production and diffuses passively out of cells and into the blood in gaseous form
  • Most of this CO2 (65–70%) combines with water almost instantaneously to form carbonic acid, which then dissociates into HCO3– and H +
  • Most CO2 is transported in the blood as HCO3–. Some is bound to proteins, especially deoxygenated hemoglobin, and a small amount is dissolved directly into plasma
  • In the lungs, the reverse occurs, and CO2 passively diffuses out of capillaries into the alveoli
  • These 3 forms of CO2 exist in equilibrium in the blood, but PCO2 as measured by blood gases depends on the dissolved portion

  • The chemical components of the carbonic acid equilibrium are:

  • Alveolar CO2 then is removed mechanically by ventilation as air moves in and out of the lungs
  • Hypercapnia is present only when tissue production exceeds the capacity of normal lungs to eliminate CO2 or when components of the respiratory system are abnormal
  • Respiratory acidosis results from disease or alteration of the respiratory center in the brain, peripheral chemoreceptors that control respiration, mechanical components of respiration (chest wall, respiratory muscles), or the respiratory tract (airways, alveoli, pulmonary vasculature, lung parenchyma). This can result in hypoventilation, diffusion impairment, or V/Q mismatching
  • Because CO2 diffuses across alveolar membranes in direct proportion to ventilation, hypoventilation leads to increased blood CO2 concentration
  • Diffusion impairment (e.g. pneumonia) rarely results in hypercapnia given that CO2 diffuses very readily across alveolar membranes
  • Increased blood CO2 concentration develops as a compensatory response of the lungs to metabolic alkalosis

Systems Affected!!navigator!!

Respiratory

Genetics!!navigator!!

N/A

Incidence/Prevalence!!navigator!!

N/A

Geographic Distribution!!navigator!!

N/A

Signalment!!navigator!!

  • Any breed, age or sex
  • Neonatal foals with perinatal asphyxia
  • Anesthetized patients develop some degree of hypercapnia when breathing spontaneously
  • Because of their size, equids are predisposed to hypoventilation under anesthesia

Signs!!navigator!!

Historical Findings

  • Neonatal foals born from a dam with dystocia
  • Respiratory noise may be heard, especially with exercise, in cases of upper airway obstruction

Physical Examination Findings

  • None if minute ventilation is increased via increased tidal volume; if not, tachypnea may be present
  • Decreased respiratory rate or an apneustic breathing pattern may be present in neonatal foals with perinatal asphyxia
  • Decrease or absence of airway sounds may be found at auscultation in cases with damage or disease of the chest wall or thorax
  • Abnormal sounds may be present with pulmonary disease

Causes!!navigator!!

  • Upper airway obstruction leading to hypoventilation. Specific causes—nasal edema, cyst, mass, or infection of the paranasal sinuses, laryngeal or pharyngeal paralysis or inflammation, soft palate displacement, pharyngeal or epiglottal cysts, and tracheal masses or collapse
  • Hypoxia to the respiratory center of the brainstem in foals with perinatal asphyxia can cause hypoventilation
  • Injury or disease of the thorax, diaphragm, or pleura may restrict movement of the chest wall or respiratory muscles. Tension pneumothorax may rapidly lead to death
  • Large volumes of pleural or peritoneal fluid, as well as severe GI distention, may restrict diaphragmatic movement, leading to hypoventilation
  • Paresis or paralysis of the respiratory muscles can be seen with neurologic diseases such as botulism, tetanus, encephalitis, or head trauma
  • Respiratory muscle damage caused by box elder seeds (i.e. seasonal pasture myopathy)
  • Severe pneumonia, pulmonary edema, or acute respiratory distress syndrome can cause diffusion impairment
  • Premature foals with significant atelectasis (diffusion impairment) and weak thoracic muscles (hypoventilation)
  • Hypoventilation caused by muscle relaxation and decreased sensitivity of the respiratory center to CO2 occurs in all anesthetized horses. Heavy sedation also may produce temporary hypercapnia via muscle relaxation and respiratory center insensitivity
  • Pregnant animals are more prone to hypoventilation under general anesthesia because of abdominal distention from the pregnant uterus
  • Defective cellular metabolism of muscle is seen with malignant hyperthermia. This syndrome is very rare but has been seen in horses with inhalant anesthesia or succinyl choline administration. Abnormal metabolic processes in muscle cells are triggered, resulting in tremendous production of heat and CO2, such that elimination mechanisms are overwhelmed and respiratory acidosis results
  • Anaerobic exercise produces temporary respiratory acidosis because ventilation is limited when chest wall movement is linked to stride at high speeds

Risk Factors!!navigator!!

  • General anesthesia, heavy sedation
  • Pregnancy
  • Prolonged recumbency
  • History of malignant hyperthermia in related individuals
  • Prematurity, dystocia, asphyxia or sepsis, persistent fetal circulation, or pulmonary hypertension in neonates

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

  • Physiologic states or disease processes that present with tachypnea (e.g. fever, hyperthermia, excitement, anxiety, painful conditions, hypoxemia, metabolic acidosis, and CNS derangements)
  • Under anesthesia, tachypnea also may result from a light plane of anesthesia, hypoxemia, metabolic acidosis, or faulty anesthetic rebreathing systems
  • Compensatory hypercapnia secondary to metabolic alkalosis caused by upper GI obstruction, early large colon impaction or simple obstruction, or supplementation with HCO3– or other alkalinizing agent. pH in these cases is often still higher than normal because compensatory hypoventilation is limited once hypoxemia develops

Laboratory Findings!!navigator!!

Drugs That May Alter Laboratory Results

N/A

Disorders That May Alter Laboratory Results

  • With poor peripheral perfusion, results of blood gas analysis on samples taken from peripheral vessels may not reflect the overall systemic condition. Appropriate reference ranges must be used (venous vs. arterial)
  • Prolonged exposure to room air may alter PCO2 concentrations, because the sample equilibrates with the air
  • Cellular metabolism of red blood cells continues after sampling; if not measured quickly, PCO2 concentrations may be falsely elevated

CBC/Biochemistry/Urinalysis!!navigator!!

N/A

Other Laboratory Tests!!navigator!!

  • Arterial blood gas analysis is necessary to evaluate adequacy of ventilation and gas exchange and to document hypercapnia
  • Handheld analyzers are available and easy to use, and some require only small amounts of whole blood. Otherwise, pre-heparinized syringes are preferred or use syringes heparinized before sampling
  • Perform sampling anaerobically. Immediately evacuate any air bubbles, and cap the needle with a rubber stopper
  • Perform analysis within 15–20 min. If not possible, samples can be stored on ice, and results may be valid for 3–4 h when glass syringes or dedicated arterial blood gas syringes are used

Imaging!!navigator!!

N/A

Other Diagnostic Procedures!!navigator!!

  • Capnography or capnometry to measure CO2 indirectly from expired gases
  • Samples of end-tidal gases reflect arterial PCO2 concentrations, because this gas is essentially alveolar gas
  • Continuous monitoring of anesthetized or ventilated patients
  • V/Q mismatch is always present in anesthetized or recumbent patients, and end-tidal CO2 concentrations may underestimate arterial concentrations by ≅10–15 mmHg

Treatment ⬆ ⬇

TREATMENT

  • Emergency therapy occasionally may be necessary for upper airway obstructions (e.g. passage of a nasotracheal tube or tracheotomy). Stridor is usually present in affected horses
  • Definitive therapy for hypercapnia involves resolution of the primary disease process affecting ventilation, diffusion, or gas exchange
  • Avoid excessive anesthetic depth. If depth is adequate, controlled ventilation is necessary when hypoventilation persists and PaCO2 is > 60 mmHg
  • In neonates, postural therapy and coupage may improve gas exchange
  • With botulism or severe lung disease, treat hypercapnia with controlled ventilation

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

Caffeine

Respiratory stimulant (10 mg/kg PO loading dose followed by 2.5 mg/kg PO every 12 h) for foals with perinatal asphyxia that do not have ileus.

Doxapram

  • Respiratory stimulant (0.2–0.5 mg/kg IV or an infusion of 0.01–0.05 mg/kg/min) in foals with perinatal asphyxia or muscular weakness
  • Anesthetized patients who are breathing poorly may respond temporarily to its effects, but controlled ventilation, decreasing depth, and anesthetic reversal are more specific and appropriate therapies
  • Not indicated for healthy patients being weaned from controlled ventilation

Contraindications!!navigator!!

  • Controlled ventilation may cause barotrauma in foals with meconium aspiration
  • Partial obstruction of the small airways may lead to air trapping in alveoli, which may rupture

Precautions!!navigator!!

  • Monitor ventilated patients continuously for airway obstruction caused by accumulation of secretions, kinking of tubing, hoses, etc.
  • Oxygen toxicity can develop with inspired PO2 > 50% or if PaO2 > 100 mmHg is maintained for prolonged periods (10–12 h).

Possible Interactions!!navigator!!

N/A

Alternative Drugs!!navigator!!

N/A

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

Use serial arterial blood gas analyses or capnometry to assess adequacy of ventilation and monitor progress, especially during weaning from ventilation.

Prevention/Avoidance!!navigator!!

N/A

Possible Complications!!navigator!!

  • Respiratory acidosis lowers systemic pH and may affect ionization of protein-bound drugs
  • Acidosis decreases heart contractility and may cause or contribute to CNS depression
  • Hypercapnia and resultant acidosis predispose patients to cardiac arrhythmias, especially under general anesthesia
  • The PaCO2 concentration greatly affects cerebral blood flow and cerebrospinal fluid pressure
  • Severe or prolonged hypercapnia may contribute to brain damage or herniation in cases of head trauma

Expected Course and Prognosis!!navigator!!

Dependent on the underlying cause.

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Associated Conditions!!navigator!!

Disorders that result in metabolic alkalosis.

Age-Related Factors!!navigator!!

Neonates with perinatal asphyxia or prematurity.

Zoonotic Potential!!navigator!!

N/A

Pregnancy/Fertility/Breeding!!navigator!!

See Risk Factors.

Synonyms!!navigator!!

  • Hypercapnia
  • Hypercarbia

Abbreviations!!navigator!!

  • CNS = central nervous system
  • GI = gastrointestinal
  • PaCO2 = partial pressure of carbon dioxide in arterial blood
  • PaO2 = partial pressure of oxygen in arterial blood
  • PCO2 = partial pressure of carbon dioxide
  • PO2 = partial pressure of oxygen
  • V/Q = ventilation/perfusion

Suggested Reading ⬆ ⬇

Hall JE.Guyton and Hall: Textbook of Medical Physiology, 13e. Philadelphia, PA: Elsevier Inc., 2016:497–556.

Moens Y. Mechanical ventilation and respiratory mechanics during equine anesthesia. Vet Clin North Am Equine Pract 2013;29(1):51–67.

Palmer JE. Ventilatory support of the critically ill foal. Vet Clin North Am Equine Pract 2005;21(2):457–486.

Author(s) ⬆ ⬇

Author: Sara L. Connolly

Consulting Editor: Sandra D. Taylor

Acknowledgment: The author and editor acknowledge the prior contribution of Jennifer G. Adams.

Additional Further Reading ⬆

Click here for Additional Further Reading