FAQ - Hypercapnia
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what is the blood gas values to determine hypercapnia & hypoxia?


I need the blood gas values of a patient with htpoxia and hypercapnia
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Permissive hypercapnia is hypercapnia, (i.e. high concentration of carbon dioxide in blood), in respiratory insufficient patients in which oxygenation has become so difficult that the optimal mode of mechanical ventilation (with oxygenation in mind) is not capable of exchanging enough carbon dioxide. Carbon dioxide is a gaseous product of the body's metabolism and is normally expelled through the lungs.

In acute respiratory distress syndrome (ARDS), permissive hypercapnia (allowing increased CO2 retention) by decreasing the tidal volume on the ventilator (usually 10-15 mL/kg/min) to 8 mL/kg/min may decrease barotrauma by decreasing ventilatory peak airway pressures and leads to improved respiratory recovery. The permissive hypercapnia leads to respiratory acidosis which has negative side effects, but given that the patient is in ARDS, improving ventilatory function is more important.

Since hypoxemia is a major life threatening condition and hypercapnia is not, one might choose to accept the latter. Hence the term, "permissive hypercapnia."

Symptoms of early hypercapnia (i.e. where PaCO2 is elevated but not extremely so) include flushed skin, full pulse, extrasystoles, muscle twitches, hand flaps, and possibly a raised blood pressure. In severe hypercapnia (generally PaCO2 greater than 10kPa or 75mmHg), symptomatology progresses to disorientation, panic, hyperventilation, convulsions, unconsciousness, and eventually death.

Hypoxia is a pathological condition in which the body as a whole (generalised hypoxia) or region of the body (tissue hypoxia) is deprived of adequate oxygen supply. Low oxygen content in the blood is referred to as hypoxaemia. Hypoxia in which there is complete deprivation of oxygen supply is referred to as anoxia.

Generalised hypoxia occurs in healthy people when they ascend to high altitude, where it causes altitude sickness, and the potentially fatal complications of altitude sickness, high altitude pulmonary oedema (HAPE) and high altitude cerebral oedema (HACE). Hypoxia also occurs in healthy individuals when breathing mixtures of gases with a low oxygen content, for example while diving underwater, especially with closed-circuit rebreather systems that control the amount of oxygen in the air breathed in. Altitude training uses mild hypoxia to increase the concentration of red blood cells in the body for increased athletic performance.

Symptoms of generalized hypoxia depend on its severity and speed of onset. In the case of altitude sickness, where hypoxia develops gradually, the symptoms include headaches, fatigue, shortness of breath, and nausea. In severe hypoxia, or hypoxia of very rapid onset, changes in levels of consciousness, seizures, coma and death occur. Severe hypoxia induces a blue discolouration of the skin, called cyanosis (haemoglobin is blue when it is not bound to oxygen (deoxyhaemoglobin), as opposed to the rich red colour that it has when bound to oxygen (oxyhaemoglobin)). In cases where the oxygen is displaced by another molecule, such as carbon monoxide, the skin may be 'cherry red' instead of cyanotic.


[edit] Causes of tissue hypoxia
Hypoxic hypoxia, when there is an inadequate supply of oxygen. The term "hypoxic hypoxia" refers to the fact that hypoxia occurs as a consequence of low partial pressure of oxygen in arterial blood, in contrast to the other causes of hypoxia listed below, in which the partial pressure of oxygen in arterial blood is normal. Hypoxic hypoxia may be due to:
Low partial pressure of atmospheric oxygen (e.g. at high altitude).[1]
Either Sleep apnea or Hypopnea causing a decrease in oxygen saturation of the blood.
Inadequate pulmonary ventilation (e.g. in chronic obstructive pulmonary disease or respiratory arrest).
Shunts in the pulmonary circulation or a right-to-left shunt in the heart. Shunts can be caused by collapsed alveoli that are still perfused or a block in ventilation to an area of the lung. Whatever the mechanism, blood meant for the pulmonary system is not ventilated and so no gas exchange occurs (the ventilation/perfusion ratio is zero). Normal anatomical shunt occurs in everyone, because of the Thebesian vessels which empty into the left ventricle and the bronchial circulation which supplies the bronchi with oxygen.
Anemic hypoxia in which arterial oxygen pressure is normal, but total oxygen content of the blood is reduced.[2]
Hypemic Hypoxia when there is an inability of the blood to deliver oxygen to target tissues.
Carbon monoxide poisoning which inhibits the ability of haemoglobin to release the oxygen bound to it.
Methaemoglobinaemia in which an abnormal version of haemoglobin accumulates in the blood
Histotoxic hypoxia in which quantity of oxygen reaching the cells is normal, but the cells are unable to effectively use the oxygen due to disabled oxidative phosphorylation enzymes.
Ischemic, or stagnant hypoxia in which there is a local restriction in the flow of otherwise well-oxygenated blood. The oxygen supplied to the region of the body is then insufficient for its needs. Examples are cerebral ischemia, ischemic heart disease and Intrauterine hypoxia, which is an unchallenged cause of perinatal death.

[edit] Pathophysiology
After mixing with water vapour and expired CO2 in the lungs, oxygen diffuses down a pressure gradient to enter arterial blood around where its partial pressure is 100mmHg (13.3kPa).[1] Arterial blood flow delivers oxygen to the peripheral tissues, where it again diffuses down a pressure gradient into the cells and into their mitochondria. These bacterial like cytoplasmic structures strip hydrogen from fuels (glucose, fats and some amino acids) to burn with oxygen to form water. Released energy (originally from the sun and photosynthesis) is stored as ATP, to be later used for energy requiring metabolism. The fuel's carbon is oxidized to CO2, which diffuses down its partial pressure gradient out of the cells into venous blood to finally be exhaled by the lungs. Experimentally, oxygen diffusion becomes rate limiting (and lethal) when arterial oxygen partial pressure falls to 40mmHg or below.

If oxygen delivery to cells is insufficient for the demand (hypoxia), hydrogen will be shifted to pyruvic acid converting it to lactic acid. This temporary measure (anaerobic metabolism) allows small amounts of energy to be produced. Lactic acid build up in tissues and blood is a sign of inadequate mitochondrial oxygenation, which may be due to hypoxemia, poor blood flow (e.g. shock) or a combination of both.[3] If severe or prolonged it could lead to cell death.


[edit] Vasoconstriction and vasodilation
In most tissues of the body, the response to hypoxia is vasodilation. By widening the blood vessels, the tissue allows greater perfusion.

By contrast, in the lungs, the response to hypoxia is vasoconstriction. This is known as "Hypoxic pulmonary vasoconstriction", or "HPV".  (+ info)

describe the ventilatory responses to hypoxia and hypercapnia?


  (+ info)

why does airway obstruction in chronic lung disease cause hypercapnia?


a. airway obstruction causes pulmonary edema
b. airway obstruction causes alveolar destruction
c. airway obstruction causes prolonged inspiration and rapid expiration
d. airway obstruction causes air trapping
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D.

a. pulmonary edema is generally cardiac related
b. the airway obstruction did not cause the alveolar destruction
c. prolonged expiration is caused by airway obstruction  (+ info)

What is HYPERCAPNIA? The sentence reads '...chronic pulmonary disease related to acute HYPERCAPNIA...'.


When you breathe you take in oxygen and also breathe out carbondioxide whcih is a waste product. In diseases of the lung the ability of the lung to excrete carbondioxide becomes impaired. As a consequence more of carbondioxide remains in the body. You can measure this in the blood and fing increased levels of carbondioxide. This condition is called hypercapnia. It may occur in any chronic disease of the lung.  (+ info)

Can hypercapnia cause brain damage?


Hypercapnia or hypercapnea, also known as hypercarbia, is a condition where there is too much carbon dioxide (CO2) in the blood. HYpercapnea is a condition marked by an unusually high concentration of carbon dioxide in the blood as a result of hypoventilation.

The normal level of CO2 in the blood is 40mmHg; but when it reaches above 45mmHg; hypercapnea can occur.

If severe hypercapnia is reached (levels of CO2 in the blood at 75 mm Hg or higher), a person will exhibit disorientation, convulsions, panic and unconsciousness, leading to death.

Death will occur because of a lack of oxygen in the blood, leading to complete organ failure as the oxygen has been overtaken by the CO2. In some cases, victims who have been exposed to very high levels of CO2 in the atmosphere have been known to almost immediately die of asphyxiation, as the CO2 serves to displace, or push out, the oxygen in the air.

The best way to treat hypercapnia is to remove a person from exposure to CO2 and give him oxygen. If the exposure was at mild to moderate levels (45 mm Hg to 65-70 mm Hg), the patient should recover fully. If the exposure was at levels higher than 75 mm Hg, the patient may suffer from permanent damage of the central nervous system.  (+ info)

Can you interpret a arterial blood gas test?


Arterial Blood Gas test results held 5 minutes.
Ph=7.43 Pco2=43 Po2=82 O2=97.0 HCO3=27.9
CTCO2=29.2 Base Ex. mmo/L=3.4 and FCOHB Carboxy HGB=1.0
There is also a graph accompaning the abg results it states-
Arterial Ph and the graph shows arterial Ph between 7.0 and 7.1 and the explosion on the graph says "metabolic acidosis" Then there is another part of the graph that shoots off sideways and it is between 7.2 and 7.3 it states "chronic hypercapnia" then there is another offshoot that exits at 7.0 and is inelgible to read looks like A gles or Agyles hyperc- no longer elgible. Can you interpret this please???
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The ABG that you posted. The 7.43 is normal as long as it is within the 7.35-7.45 range. The CO2 level is also considered normal between 35-45. The PO2 is also considered normal between 80 - 100. The HCO3 or Bicarb is slightly higher than the 22 - 26 that is considered normal. The graph I have never seen so I wouldn't be able to interpret that for you. Hope this helps.  (+ info)

Otology: Complexing question for any medical practicioners and/or medical researchers.?


Is it possible for this string of reactions to occur in the human body over a long period of time (3 years) :

Eustachian tube dysfunction -> Middle ear Inflammation -> Hypoventilation -> Hypercapnia -> Acidosis
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middle ear infllammation doesnt lead to hypoventilation,unless severe septicaemia and another complication arises  (+ info)

The major sign of hypoventilation is?


a. cyanosis
b. increased airway resistance
c. hypercapnia
d. dyspnea
e. hypoxia
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I may be looking to far into this question. The best indication of ventilation (with out a doubt) is PaCO2 or carbon dioxide in the arterial blood. To much is hypercapnia or low ventilation. This is a blood test result.

Signs are what someone can SEE and symptoms are what someone can FEEL.

If you consider a blood test as a sign, then C is your answer.

If you do not consider a blood test a sign then A, cyanosis is your answer.

I hope I didn't confuse you.  (+ info)


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