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Related Concept Videos

Acute Respiratory Failure-II01:21

Acute Respiratory Failure-II

Type I Respiratory Failure, or hypoxemic respiratory failure, occurs when the partial pressure of oxygen (PaO2) in arterial blood falls below 60 mmHg while breathing room air without a corresponding increase in arterial carbon dioxide levels (PaCO2). This condition highlights a significant impairment in the lungs' capacity to oxygenate the blood.
The underlying physiological abnormalities that contribute to hypoxemic respiratory failure include:
Hyperpnea and Hyperventilation01:25

Hyperpnea and Hyperventilation

Hyperventilation refers to a higher-than-normal rate and depth of breathing, often associated with anxiety attacks. This excessive breathing surpasses the body's need to expel CO2, leading to a condition known as hypocapnia - an unusually low level of carbon dioxide in the blood. Hypocapnia can constrict cerebral blood vessels, reducing blood flow to the brain, which may result in dizziness or fainting. Early signs include tingling and muscle spasms in the hands and face, caused by falling...
Alterations in Respiration II01:30

Alterations in Respiration II

There are numerous types of normal and abnormal respiration. Based on ventilatory movements, breathing patterns are classified as regular, deep, or shallow. Examples include Biot's breathing, Cheyne-Stokes respiration, Kussmaul's breathing, hyperventilation, and hypoventilation. Each pattern is clinically significant and aids in evaluating patients.
In Biot's breathing, the respiratory rate and depth are irregular, alternating between periods of deep gasping and apnea. Common causes include...
Acute Respiratory Failure-III01:30

Acute Respiratory Failure-III

Hypercapnic respiratory failure, also known as Type 2 or ventilatory respiratory failure, is a severe condition characterized by the body's inability to effectively remove carbon dioxide (CO2) from the bloodstream. It leads to an arterial CO2 pressure (PaCO2) exceeding 45 mmHg and a blood pH above 7.35. This situation indicates that the body's ventilatory demand, or the ventilation needed to maintain normal PaCO2 levels, surpasses its supply or the maximum gas flow achievable without causing...
Acute Respiratory Failure-I01:21

Acute Respiratory Failure-I

Acute respiratory failure is a condition characterized by the inability of the lungs to perform their primary function: gas exchange. This failure leads to insufficient oxygen levels (hypoxemia) in the blood, elevated carbon dioxide levels (hypercapnia), or both, causing critical impairment in organ function.
Definition: It is defined by specific criteria based on blood gas measurements. Hypoxemia happens when the partial pressure of oxygen (PaO2) falls below 60 mmHg. At the same time,...
Atelectasis II: Pathophysiology01:10

Atelectasis II: Pathophysiology

Atelectasis develops when alveoli lose their air and collapse inward. Because lung tissue is naturally elastic, these air sacs shrink rather than remaining open. Collapsed alveoli are no longer ventilated, reducing their role in gas exchange. Blood flow may continue in these regions, creating a ventilation–perfusion mismatch. Clinical findings include decreased breath sounds, dullness to percussion, reduced chest expansion, and decreased tactile fremitus as sound transmission through collapsed...

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Late-onset hypoventilation without PHOX2B mutation or hypothalamic abnormalities.

Virginia D'Alessandro1, Thornton Mason, Michael N Pallone

  • 1Department of Pediatrics, Children's Hospital "Sor María Ludovica", La Plata, Buenos Aires, Argentina.

Journal of Clinical Sleep Medicine : JCSM : Official Publication of the American Academy of Sleep Medicine
|June 15, 2007
PubMed
Summary

Idiopathic central hypoventilation in children can present later in life without obesity or PHOX2B gene mutations. This case highlights the diverse causes of this rare respiratory disorder.

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Area of Science:

  • Pediatric Pulmonology
  • Genetics
  • Neurology

Background:

  • Idiopathic central hypoventilation (ICH) typically manifests in newborns with PHOX2B gene mutations.
  • Later-onset ICH is often associated with obesity and hypothalamic dysfunction.

Observation:

  • A 5-year-old boy presented with severe ICH.
  • He exhibited no signs of obesity or hypothalamic abnormalities.
  • Genetic testing revealed no PHOX2B gene mutation.

Findings:

  • This case represents a distinct phenotype of childhood ICH.
  • It challenges the established genetic and clinical associations for later-onset ICH.

Implications:

  • The findings suggest a broader spectrum of ICH etiology.
  • This underscores the need for considering multifactorial causes in diagnosing ICH.
  • Further research into non-PHOX2B related ICH is warranted.