Nasal congestion is marked by:
- a stuffy or runny nose
- sinus pain
- mucus buildup
- swollen nasal tissue
Blockage of upper airway
Blockage of the upper airway occurs when the upper breathing passages become narrowed or blocked, making it hard to breathe. Areas in the upper airway that can be affected are the windpipe (trachea), voice box (larynx), or throat (pharynx).
The airway can become narrowed or blocked due to many causes, including:
- Allergic reactions in which the trachea or throat swell closed, including allergic reactions to a bee sting, peanuts, antibiotics (such as penicillin), and blood pressure medicines (such as ACE inhibitors)
- Chemical burns and reactions
- Epiglottitis (infection of the structure separating the trachea from the esophagus)
- Fire or burns from breathing in smoke
- Infections of the upper airway area
- Injury to the upper airway area
- Peritonsillar abscess (collection of infected material near the tonsils)
- Poisoning from certain substances, such as strychnine
- Retropharyngeal abscess (collection of infected material in the back of the airway)
- Severe asthma attack
- Tracheomalacia (weakness of the cartilage that supports the trachea)
- Vocal cord problems
Even minor narrowing of the upper airway can cause breathing difficulties in a person with abnormal breathing rates at rest.
If your respiratory rate is in the normal range, 15 breathes per minute give or take 5, at rest, then this may not be a big problem, [aside from feeling stuffed up and feeling sick ].
If, like Paula, your respiratory rate is abnormal, low and deep at rest, then a narrowed airway and a stuffed nose will make breathing more shallow, yet remain abnormally slow [this is true of Paula] and this might result in hypercapnic respiratory failure. Even mild hypercapnic respiratory failure is not pleasant and may result in signs of hypercapnia.
Hypercapnia occurs in respiratory failure either secondary to lung disease (e.g. chronic obstructive pulmonary disease) or to mechanical problems such as neurological disease (e.g. myasthenia gravis). Clinically, hypercapnia presents with headache, papilloedema, mental slowing, drowsiness, confusion, coma and asterixis. The mechanism is unclear but thought to be due to a direct effect of carbon dioxide possibly on the hydrogen ion concentration (pH) of the CSF. Hypercapnia can be confirmed by measurement of PCO2 on an arterial bloodsample. Coma can occur with PCO2 > 9 kPa. Treatment is of the underlying cause and, once corrected, there is no prolonged cerebral damage Respiratory failure Biochemical aspects of neurological disease Paul Hart, … Min Htut, in Clinical Biochemistry: Metabolic and Clinical Aspects (Third Edition), 2014
Hypercapnia causes cerebral vasodilation which causes intracranial pressure to increase, which in turn can cause brain swelling [edema].
Thus nonspecific neurological signs of mental slowing and mental confusion and dyspnea [the unpleasant sensation of difficulty breathing] occur and are indistinguishable from major depression.
Treatment of hypercapnia and treatment of major depression are not the same.
It is important to discover which ailment the patient is suffering from.
Measuring respiratory rate at rest will differentiate one from the other.
It is that simple.
Inflammation of the brain and permanent ventilatory mechanical injury limiting homeostatic control over pH of the brain can result in the sensation of suffocation [which is very unpleasant] and mental and motor slowing which the patient cannot explain not only because they have become impaired but also because these effects are impossible to describe as they are so very distressing and so very completely abnormal as to defy description.
May it never happen to you, says Paula, because you won’t know what hit you and no one else will suspect [without measuring your minute ventilation. [minute ventilation is described in previous blogposts].