الفهرس 
ANATOMY AND PHYSIOLOGY OF THE RESPIRATORY SYSTEMOnly 14 pages are availabe for public view
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Abstract
Carbon dioxide is colorless gas with physical properties that provide continuous gas exchange between inspired air and the blood in the pulmonary circulation, supplying oxygen and removing carbon dioxide which is then cleared from the lungs by subsequent expiration.
Breathing control in healthy people is by CO2 concentrations in the brain and arterial blood. The breathing centre regulates our breathing movements through special chemoreceptors to measure CO2 concentrations in the brain and arterial blood. The central chemoreceptors detect changes in the pH of the cerebro-spinal fluid and they are responsible for long term or slow changes in breathing. Since CO2 dissolves in the blood and can penetrate through the blood-brain barrier, the main reason for pH variations in the brain are changes in CO2 concentrations.
Peripheral chemoreceptors including the carotid and aortic bodies monitor immediate changes in CO2, O2 and pH concentrations of the blood and control our breathing in the short run.
carbon dioxide used in insufflation into fallopian tubes and abdominal cavities and in laparoscopic surgery.
Laparoscopy results in intra-operative cardio-respiratory changes during pneumoperitoneum. PaCO2 increases due to CO2 absorption form peritoneal cavity. Therefore pathophysiologic changes and complication of laparoscopy are first reviewed in compromised patients, cardio respiratory disturbance aggravate this increase in PaCO2. Hemodynamic changes are accentuated in high risk cardiac patient.
Monitoring devices potentially increase the specificity and precision of clinical judgments. Our understanding of the physiologic effects of anesthesia and its inherent risks can be enhanced by the appropriate use of intra-operative physiologic monitoring. Capnometry is the measurement and numeric representation of the CO2 concentration during inspiration and expiration. Carbon dioxide monitoring the partial pressure of expiratory CO2 has evolved as an important physiologic and safety monitor. CO2 is usually sampled near the endotracheal–gas delivery interface. Alterations in ventilation, cardiac output (CO), distribution of pulmonary blood flow and metabolic activity influence end tidal CO2 concentration and the capnograph display obtained during quantitative expired gas analysis.
Hypercapnia is generally defined as a blood gas carbon dioxide level over 45 mmHg. Since carbon dioxide is in equilibrium with bicarbonate in the blood hypercapnia can also result in high serum bicarbonate (HCO3-) concentration. Normal bicarbonate concentrations vary from 22 to 28 milligrams per deciliter. Hypercapnia is generally caused by hypoventilation, lung disease or diminished consciousness. It may also be caused by exposure to environments containing abnormally high concentrations of carbon dioxide (usually due to volcanic or geothermal causes) or by rebreathing exhaled carbon dioxide. It can also be an initial effect of administering supplemental oxygen on a patient with sleep apnea. In this situation the hypercapnia can also be accompanied by respiratory acidosis.
Symptoms of early hypercapnia where arterial carbon dioxide pressure PaCO 2 is elevated but not extremely include flushed skin, full pulse, extra-systoles, muscle twitches, hand flaps, reduced neural activity and possibly a raised blood pressure. In severe hypercapnia (generally PaCO 2 greater than 100 kPa or 75 mmHg) symptomatology progresses to disorientation, panic, hyperventilation, convulsions, unconsciousness, and eventually death.
In the initial stages hypercapnia stimulates the respiratory centre and the resultant hyperventilation helps to lower the PaCO2 to normal levels. In established hypercapnia the respiratory centre becomes insensitive to raised PaCO2. In such cases the stimulus for the respiratory centre is hypoxia. Injudicious administration of oxygen may abolish this hypoxic stimulus and give rise to depression of respiration and carbon-dioxide narcosis results.
Hypocapnia is a deficiency of carbon dioxide in the arterial blood less than 35 mm Hg for partial CO2 pressure in the arterial blood. Hypocapnia is caused by chronic hyperventilation leading to alveolar hypocapnia (lack of CO2).The pathological effect of both alveolar and arterial hypocapnia is reduced levels of oxygen in body cells (tissue hypoxia) that promotes virtually all chronic diseases.
The decision to institute hypocapnia for therapeutic purposes should be undertaken only after careful consideration of the risks and benefits and should in general be limited to emergency management of life-threatening increases in intracranial pressure or pulmonary-vascular resistance. The risk of accidental hypocapnia should be recognized and measures taken to prevent it. Prophylactic induction of hypocapnia currently has no clinical role.