Hypocarbia


Article Author:
Sandeep Sharma
Muhammad Hashmi


Article Editor:
Deepa Rawat


Editors In Chief:
Chaddie Doerr


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Trevor Nezwek
Radia Jamil
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes


Updated:
9/13/2019 1:49:09 PM

Introduction

Hypocarbia, also known as hypocapnia, is a decrease in alveolar and blood carbon dioxide (CO2) levels below the normal reference range of 35 mm Hg. CO2 is a metabolic product of the many cellular processes within the body when processing lipids, carbohydrates, and proteins. The primary organ systems responsible for regulating CO2 homeostasis are the pulmonary system and the renal system. Additionally, CO2 is regulated through the CO2/HCO3 pH buffering system. Aberrations that lead to hypocarbia typically also result in respiratory alkalosis.[1][2]

Etiology

At its root, hypocarbia is induced by either a decrease in CO2 production or an increase in CO2 loss.[3] Since metabolic demand does not typically decrease in a way that meaningfully adjusts CO2 levels into hypocarbic levels, the primary occurrence is a loss of CO2 via the pH buffering system or changes in the pulmonary system. The pulmonary system is highly efficient in its removal of CO2 from the body through gas diffusion. This requires a diffusion gradient from the high concentration arteriolar blood into the relatively low concentration environmental air. This gradient is maintained through continually washing away CO2 from the alveolar space, regardless of the absolute PACO2 concentration. As such, the CO2 gradients are developed and maintained where PaCO2 in arterial blood is directly proportional to the rate of CO2 metabolic production and inversely related to the rate of CO2 elimination by the lung via increased alveolar ventilation. Alveolar ventilation is the removal of alveolar air into the environment, defined as the expired minute volume that reaches the alveoli and is determined by minute ventilation and the ratio of dead space to tidal volume. Mathematically, this relationship is determined as:

  • PaCO2 = 0.863 x VCO2/ VA

and

  • VA = VE – VD

and

  • VE = RR x TV

and

  • TV = RR x dead-space volume

Where VCO2 is the metabolic production of CO2, VA is alveolar ventilation, VE is minute ventilation, VD is dead space ventilation, RR is the respiratory rate, and TV is tidal volume.[4]

Through these relationships, one can conclude that respiratory rate and tidal volume are the 2 components of ventilation that are physiologically or artificially controlled to moderate CO2 elimination. Subsequently, the etiologies that induce hypocarbia are any disease which increases ventilation rate or tidal volume. More commonly, the increased respiratory rate is the culprit. A wide variety of illnesses may induce this. In almost every scenario, hypocarbia is synonymous with respiratory alkalosis as they are both 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 chronic obstructive pulmonary disease (COPD) exacerbations. Iatrogenic causes are primarily due to hyperventilation in intubated patients on mechanical ventilation.[5][6]

Epidemiology

The frequency and distribution of illness is variable dependent on the exact etiology of the disease. Likewise, the morbidity and mortality are linked to the exact etiology of the inciting disease. In general, younger patients have better outcomes.

Pathophysiology

Hypocarbia is a result of hyperventilation. Increased ventilation to the alveolar space quickly removes gaseous CO2. This increases the diffusion gradient of CO2 from blood to alveoli. Subsequently, CO2 is more readily removed from the body. There are virtually no mechanisms outside of decreasing respiratory rate to regulate this loss.[7]

History and Physical

Since the primary cause of all hypocapnia etiologies is hyperventilation, many patients present with complain to shortness of breath. The exact history and physical exam findings are highly variable as many pathologies induce the respiratory change. 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 beyond hyperventilation.[8]

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 any pH imbalances. Serum electrolytes should be measured with 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.[9][10][9]

Treatment / Management

Treatment of hypocapnia is targeted at treating the underlying pathology to reduce the respiratory rate if possible. Historically treatment involved rebreathing into a paper bag to increase alveolar CO2. However, this has been shown to increase undesirable outcomes including mortality and is no longer recommended. 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 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 performed.[11]

Differential Diagnosis

  • Asthma Exacerbation
  • Atrial Fibrillation 
  • Atrial Flutter 
  • Atrial Tachycardia
  • Bacterial Pneumonia
  • Bacterial Sepsis
  • Community-Acquired Pneumonia
  • COPD Exacerbation
  • Head Trauma
  • Heatstroke
  • Hyperthyroidism and Thyrotoxicosis
  • Hyperventilation syndrome
  • Idiopathic Pulmonary Fibrosis
  • Meningitis
  • Metabolic Acidosis
  • Metabolic Alkalosis
  • Myocardial Infarction
  • Panic Disorder
  • Pneumothorax
  • Pulmonary Edema
  • Pulmonary Embolism
  • Salicylate Toxicity 
  • Theophylline Toxicity 
  • Viral Pneumonia[12]

Prognosis

Hypocapnia is relatively benign and well tolerated by patients, as such the prognosis is linked to the underlying etiology and response to treatment.

Pearls and Other Issues

Hypocarbia is typically resultant to hyperventilation.

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

Hypocarbia results in respiratory alkalosis.

Respiratory alkalosis 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.

Enhancing Healthcare Team Outcomes

Hypocarbia or hypocapnia, is a decrease in alveolar and blood carbon dioxide (CO2) levels below the normal reference range of 35 mm Hg. Aberrations lead to hypocarbia typically resulting in respiratory alkalosis. It is important for the interprofessional team to recognize this condition and report its presence to the team leader so that appropriate adjustments in care can be made. This will improve patient outcomes. [Level V]


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Hypocarbia - Questions

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At what level of PaCO2 is cerebral ischemia seen?



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Which of the following causes hypocarbia?



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What is the treatment for chronic hypocarbia ?



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Which direction does hypocarbia shift the oxyhemoglobin dissociation curve?



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Changes in which component of the respiratory system determines alveolar carbon dioxide levels?



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Which of the following can induce hypocarbia?



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Which of the following is a symptom of hypocarbia?



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A 42-year-old female with a history of morbid obesity, sleep apnea, asthma, smoker, and diabetes presents to the emergency department with shortness of breath since last 10 days, which has been progressively getting worse. The shortness of breath is associated with left lower side chest pain, which gets worse on taking a deep breath. The shortness of breath is also associated with dry cough and wheezing. She denies any recent travels, no sick contacts, no long car rides. She has used her albuterol inhaler for her symptoms without any help. She is compliant with her CPAP machine but is not able to use it for the last 8 days due to constant coughing. Her vital signs show an SpO2 of 79% on room air, pulse 130/min, blood pressure 142/70 mmHg, and respiratory rate 28/min. Physical examination reveals decreased breath sounds, left leg pedal edema. Initial labs are unremarkable. An EKG shows right bundle branch block, while troponins and BNP are elevated. Chest x-ray shows some basal atelectasis on the left lower lobe. An ABG shows pH 7.45, pCO2 35 mmHg and pO2 52 mmHg. Which of the following best explains her low pCO2?



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A 25-year-old female with a history of asthma presents to the emergency department with shortness of breath. She has had these symptoms for the past 4 days which has been progressively getting worse. She has used her albuterol inhaler and duo nebs repeatedly but they have not helped her. She smokes electronic cigarettes and drinks socially. Vital signs show blood pressure 142/70 mmHg, pulse 128/min, respiratory rate 24/min, and SpO2 92% on room air. She has severe diffuse expiratory wheezing. Chest x-ray shows hyperinflated lungs. Initial ABG shows as pH 7.45, pCO2 35 mmHg, HCO3 25 mmol/L and pO2 65 mmHg. She is admitted for an asthma exacerbation. Three hours, the patient is lethargic. A repeat ABG shows pH 7.4, pCO2 42 mmHg, HCO3 27 mmol/L, and pO2 80 mmHg. The patient quickly deteriorates and becomes unconscious. She is intubated and ventilated. A third blood gas shows pH 7.18, pCO2 66 mmHg, and pO2 58 mmHg. What was the most likely reason for her low pCO2 on her first blood gas, and why did it almost normalize on second blood gas?



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Hypocarbia - References

References

Slow V̇O<sub>2</sub> kinetics in acute hypoxia are not related to a hyperventilation-induced hypocapnia., Keir DA,Pollock M,Thuraisingam P,Paterson DH,Heigenhauser GJF,Rossiter HB,Kowalchuk JM,, Respiratory physiology & neurobiology, 2018 Feb 22     [PubMed]
Blood oxygen on Mount Everest., de Vries AP,Berend K,, The New England journal of medicine, 2009 Apr 30     [PubMed]
Hypocapnia., Brusilow SW,, The New England journal of medicine, 2002 Nov 7     [PubMed]
Hypocapnia., Laffey JG,Kavanagh BP,, The New England journal of medicine, 2002 Jul 4     [PubMed]
A mechanism of central sleep apnea in patients with heart failure., Javaheri S,, The New England journal of medicine, 1999 Sep 23     [PubMed]
Severe diabetic ketoacidosis complicated by hypocapnic seizure., Majid A,Wheeler BJ,, Endocrinology, diabetes & metabolism case reports, 2017     [PubMed]
A Quick Reference on Respiratory Alkalosis., Johnson RA,, The Veterinary clinics of North America. Small animal practice, 2017 Mar     [PubMed]
Altered mental status and complete heart block: an unusual presentation of aspirin toxicity., Aggarwal N,Kupfer Y,Chawla K,Tessler S,, BMJ case reports, 2013 Jun 10     [PubMed]
The venous-arterial difference in CO<sub>2</sub> should be interpreted with caution in case of respiratory alkalosis in healthy volunteers., Morel J,Gergelé L,Dominé A,Molliex S,Perrot JL,Labeille B,Costes F,, Journal of clinical monitoring and computing, 2017 Aug     [PubMed]
Stroev YI,Churilov LP, Hyperventilation Hypocapnia as The Leonardo da Vinci's Syndrome. Psychiatria Danubina. 2019 Mar;     [PubMed]
Sachan D,Goyal S, Association of Hypocapnia in Children with Febrile Seizures. Journal of pediatric neurosciences. 2018 Oct-Dec;     [PubMed]
Brinkman JE,Sharma S, Physiology, Respiratory Alkalosis 2019 Jan;     [PubMed]

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