11.carbon monoxide Flashcards
etiology on carbon monoxide poisoning
1.) arises from the incomplete combustion of fuel sources such as petroleum and naphtha.
2.) sources of CO exposure include urban traffic, heating facilities, and
industrial processes.
3.) risk industries such as miners,
firefighters, and
metal and chemical workers
pathogenesis in CO poisoning
Inhalation of carbon monoxide, a colorless and odorless gas,
leads to its rapid absorption through the alveolar-capillary membrane.
CO competes with oxygen (O2) for binding sites on hemoglobin, forming carboxyhemoglobin (Carboxy-Hb) with a significantly higher affinity for Fe2+.
This leads to the displacement of O2, resulting in hypoxemia and hypoxia of vital organs such as the brain and heart.
Additionally, CO inhibits mitochondrial oxidative phosphorylation,
impairing ATP synthesis and further exacerbating tissue hypoxia.
clinical manifestation of CO poisoning
presents with varying symptoms depending on the level of Carboxy-Hb saturation:
- 10% Carboxy-Hb:
Headache,
vertigo,
eye impairment,
myalgia,
arthralgia
- 20% Carboxy-Hb:
Vomiting, dyspepsia, dizziness, dyspnea
- 30% Carboxy-Hb:
Visual disturbance, polycythemia, hypotonia, tachypnea
- 40-60% Carboxy-Hb: Cheyne-Stokes breathing, convulsions, acute pulmonary edema, toxic hepatitis, nephropathy
- >70% Carboxy-Hb: Instant death
Chronic poisoning may manifest as
neurasthenic or asthenic syndrome with disturbances in the vegetative nervous system, chronic encephalopathy leading to decreased memory, concentration, and vigilance, Parkinson-like syndrome, emotional lability, cerebral infarction, and ischemic heart disease.
long-term effect of CO poisoning
+persistent neurological deficits, including cognitive impairment, memory loss, and mood disorders.
+cardiovascular complications such as chronic ischemic heart disease and arrhythmias may also develop.
+increased risk of respiratory conditions such as chronic bronchitis and emphysema.
diagnosis of CO poisoning
Diagnosis of occupational CO intoxication involves obtaining a detailed work environmental history
and assessing the ratio of Carboxy-Hb to Oxy-Hb, which is typically elevated in affected individuals. Elevated troponin I levels may indicate ischemic cardiomyopathy.
treatment of CO poisoning
1.Immediate cessation of CO exposure is crucial.
2.High-flow oxygen therapy facilitates the displacement of CO from hemoglobin.
3.Hyperbaric oxygen therapy accelerates the dissociation of Carboxy-Hb.
4. Intravenous administration of glucose solution with Vitamin C and
5. symptomatic therapy with glucocorticosteroids, diuretics, pyracetam, Vitamin B6, and calcium gluconate may be necessary to manage complications
medical expertise in CO poisoning
preventing occupational CO intoxication involves the 1. use of CO detectors and gas masks equipped with hopcalite filters (containing copper) to oxidize CO to CO2, minimizing exposure risks in the workplace.
2. Regular monitoring and education of workers are essential for early detection and prevention of CO poisoning.
3. Ongoing medical follow-up is crucial for individuals with chronic CO exposure to monitor for delayed or progressive symptoms and to manage long-term complications effectively
