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<title>Anesthesia General</title>
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<link>http://anesthesiageneral.com</link>
<description>All About General Anesthesia, Regional Anesthesia and Critical care</description>
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<title>Acute Lung Injury and ARDS</title>
<link>http://anesthesiageneral.com/acute-lung-injury-and-ards/</link>
<comments>http://anesthesiageneral.com/acute-lung-injury-and-ards/#comments</comments>
<pubDate>Fri, 09 Sep 2011 17:35:16 +0000</pubDate>
<dc:creator>Dr Akif</dc:creator>
<category>
<![CDATA[Critical Care]]>
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<category>
<![CDATA[Acute Lung Injury and ARDS]]>
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<![CDATA[The European—American Consensus Conference in 1993 provided working definitions of Acute Lung Injury and ARDS to improve diagnostic consistency and interpretation of the results of clinical and epidemiological studies. 4 Both Acute Lung Injury and ARDS are characterized by the presence of hypoxaemia and pulmonary infiltrates without elevated left atrial pressure. The two conditions are distinguished by severity of pulmonary gas exchange impairment: A Pao2—Fio, ratio of 300 or less defines acute lung injury, and a ratio of 200 or less defines ARDS regardless of the amount of positive end-expiratory pressure (PEEP) needed to support oxygenation.
The lung in Acute Lung Injury and ARDS is characterized by a major change in the elastic property of the alveoli. Surface tension plays an important role in determining the lung elasticity. The forces created as a result of surface tension tend to collapse the alveoli. These collapsing forces are defined by the Laplace law: ...]]>
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<item>
<title>Most common causes of acute respiratory distress syndrome ARDS</title>
<link>http://anesthesiageneral.com/most-common-causes-of-acute-respiratory-distress-syndrome-ards/</link>
<comments>http://anesthesiageneral.com/most-common-causes-of-acute-respiratory-distress-syndrome-ards/#comments</comments>
<pubDate>Tue, 06 Sep 2011 17:48:40 +0000</pubDate>
<dc:creator>Dr Akif</dc:creator>
<category>
<![CDATA[Critical Care]]>
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<category>
<![CDATA[Most common causes of acute respiratory distress syndrome ARDS]]>
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<guid isPermaLink="false">http://anesthesiageneral.com/?p=1353</guid>
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<![CDATA[Most common causes of acute respiratory distress syndrome ARDS are the clinical condition first described by Ashbaugh in 1967, to describe a group of patients with acute inflammation of the lungs resulting in severe hypoxia that is not amenable for correction by oxygen therapy.
The reported incidence of ARDS is about 1.5—13.5% per 100,000 population with a mortality of 2760%.2 A variety of aetiological factors — pneumonia, aspiration, mechanical trauma, pulmonary embolism, and systemic sepsis — are the most common causes of acute respiratory distress syndrome ARDS
Histologically, the most common causes of acute respiratory distress syndrome ARDS is characterized by diffuse damage to both the endothelial and epithelial surfaces of the alveoli that disrupts the lung’s barrier function, flooding alveolar spaces with fluid, inactivating surfactant, causing inflammation, and producing severe gas exchange abnormalities and loss of lung compliance.
Computed tomography of the chest demonstrates heterogeneous areas of consolidation and atelectasis, predominantly in ...]]>
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<item>
<title>Oxygenation Capacity</title>
<link>http://anesthesiageneral.com/oxygenation-capacity/</link>
<comments>http://anesthesiageneral.com/oxygenation-capacity/#comments</comments>
<pubDate>Tue, 23 Aug 2011 10:41:10 +0000</pubDate>
<dc:creator>mubashir</dc:creator>
<category>
<![CDATA[Drugs]]>
</category>
<category>
<![CDATA[Oxygenation Capacity]]>
</category>
<guid isPermaLink="false">http://anesthesiageneral.com/?p=608</guid>
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<![CDATA[Oxygenation capacity is the volume of oxygen at standard pressure and temperature carried by 100 mL of blood after saturation with room air.
Oxygenation capacity includes the oxygen in combination with haemoglobin (1.39 mL/g) and oxygen in solution in plasma (0.3 mL).
It should also be mentioned that most of the oxygen that dissolves in plasma diffuses into the red cell and binds to hemoglobin.
One gram of hemoglobin can bind 1.36 mL O2 (numbers between 1.34 and 1.39 are used). This means that 1 L of blood with a hemoglobin content of 150 g/L can bind 204 mL of O2 if fully saturated.
The Oxygenation capacity with a saturation of 98%, which is normally achieved in arterial blood, the hemoglobin-bound oxygen amounts to 200 mL/L of blood. This should be compared with the mere 3 mL of O2 that is physically dissolved in 1 L of blood at a Pao2 of 100 mm ...]]>
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<item>
<title>Excess Oxygen</title>
<link>http://anesthesiageneral.com/excess-oxygen/</link>
<comments>http://anesthesiageneral.com/excess-oxygen/#comments</comments>
<pubDate>Mon, 22 Aug 2011 10:50:58 +0000</pubDate>
<dc:creator>Dr Akif</dc:creator>
<category>
<![CDATA[General Anesthesia]]>
</category>
<category>
<![CDATA[Excess Oxygen]]>
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<guid isPermaLink="false">http://anesthesiageneral.com/?p=833</guid>
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<![CDATA[Excess Oxygen can cause pulmonary oxygen toxicity which results in a lot of damage to the body tissues. To summarize briefly, the excess oxygen can cause, pulmonary toxicity, Acute respiratory distress syndrome, rertolental fibroplasia, convulsions and Paul burt effect.
Here we will be dicussing the mechanisms of these tissue injuries that occur with use of excess oxygen.
The following the changes at the tissue level that can happen with excess oxygen usage:
• Mitochondrial damage due to enzyme malfunction. This is the main reason for the different problems occuring with excess oxygen.
• Surfactant production is impaired, and the lung tends to collapse.
• Histological changes such as atelectasis, pulmonary capillary congestion, interstitial and alveolar oedema, capillary degeneration and haemorrhage, etc.
• There is fall in heart rate and cardiac output, causing mild to severe haemodynamic derangements.
• Generalized increase in the peripheral vascular resistance and systemic pressure resulting in hypertension.
These were a few important changes occurung in the body with excess oxygen use.
You can read further about Oxygen toxicity, ...]]>
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<item>
<title>Oxygen Partial Pressure</title>
<link>http://anesthesiageneral.com/oxygen-partial-pressure/</link>
<comments>http://anesthesiageneral.com/oxygen-partial-pressure/#comments</comments>
<pubDate>Mon, 22 Aug 2011 10:38:42 +0000</pubDate>
<dc:creator>mubashir</dc:creator>
<category>
<![CDATA[Critical Care]]>
</category>
<category>
<![CDATA[Oxygen Partial Pressure]]>
</category>
<guid isPermaLink="false">http://anesthesiageneral.com/?p=606</guid>
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<![CDATA[About one-fifth (20.9%) of air contains oxygen. In the inspired air, oxygen has partial pressure at 1/5 of the atmospheric pressure, i.e., 159 mm Hg.
Oxygen partial pressure decreases to 100 mm Hg up to alveoli. Oxygen tension in venous blood is 40 mm Hg. 
The larger the O2 or CO2 tension difference between the gas phase in the alveolus and plasma in the capillary, the greater the diffusion.
The mixed venous blood entering the pulmonary capillary has a Oxygen Partial Pressure of 40 mm Hg (5.3 kPa), and alveolar Oxygen Partial Pressure is approximately 100 mm Hg (13.3 kPa), thus creating a driving pressure of 60 mm Hg (8 kPa).
When blood flows through the capillary, it takes up oxygen (and delivers CO2), but because oxygen pressure builds up in capillary blood, the diffusion rate slows down and becomes zero when pressure is equilibrated over the alveolar-capillary wall.
In a normal lung at ...]]>
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<item>
<title>Alveolar partial pressure of oxygen</title>
<link>http://anesthesiageneral.com/alveolar-partial-pressure-of-oxygen/</link>
<comments>http://anesthesiageneral.com/alveolar-partial-pressure-of-oxygen/#comments</comments>
<pubDate>Mon, 22 Aug 2011 10:32:27 +0000</pubDate>
<dc:creator>Dr Akif</dc:creator>
<category>
<![CDATA[Drugs]]>
</category>
<category>
<![CDATA[Alveolar partial pressure of oxygen]]>
</category>
<guid isPermaLink="false">http://anesthesiageneral.com/?p=1025</guid>
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<![CDATA[For the Alveolar partial pressure of oxygen we see, Increasing the inspired concentration (F1) of an anaesthetic agent increases the alveolar concentration (FA). A 75% nitrous oxide (N20) in oxygen mixture increases the FI/FA ratio of N20.
The amount of nitrous oxide absorbed will be greater than the nitrogen given out in the alveoli, hence the alveoli shrink and thereby increase the concentration of the gases (N20) present in the alveoli.This is how the mechanism of alveolar partial pressure of oxygen can be studied.
Oxygen cascade describes the changes in the oxygen content of the air as it moves from the atmosphere till it ultimately reaches the alveoli. The alveolar partial pressure of oxygen  is less compared to the atmosphereic oxygen partial pressure because as the air enters the airway passages it gets mixed with the expired air, which contains carbondioxide and water vapor.
This water vapor and carbondioxide ultimately decrease the partial pressure of the oxygen thus ...]]>
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<item>
<title>Pharmacological management of pain</title>
<link>http://anesthesiageneral.com/pharmacological-management-of-pain/</link>
<comments>http://anesthesiageneral.com/pharmacological-management-of-pain/#comments</comments>
<pubDate>Mon, 22 Aug 2011 10:16:11 +0000</pubDate>
<dc:creator>nabeel</dc:creator>
<category>
<![CDATA[Drugs]]>
</category>
<category>
<![CDATA[pharmacological management of pain]]>
</category>
<guid isPermaLink="false">http://anesthesiageneral.com/?p=705</guid>
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<![CDATA[The drugs remain the main modality to achieve pharmacological management of pain . Various routes of administration for various drugs have been employed.
The quest for an ideal, suitable analgesic continues. Conventionally three classes of drugs are employed to achieve various degrees of analgesia in pharmacological management of pain : 
1. Opioids:
For a long time opiods are have remained  the standard for the pharmacological management of pain . Opioids have the characteristic for intense analgesia due to their effects on the opioid receptors.
Pain control by opioids needs to be considered in the context of brain circuits modulating analgesia and the functions of the various types of receptors in these circuits.
The analgesic effects of opioids arise from their ability to directly inhibit ascending transmission of nociceptive information from the spinal cord dorsal horn and to activate pain control circuits that descend from the midbrain, via the rostral ventromedial medulla (RVM), to the spinal cord dorsal horn.
2. Non-opioids
The most commonly used ...]]>
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<item>
<title>Chronic oxygen deficiency</title>
<link>http://anesthesiageneral.com/chronic-oxygen-deficiency/</link>
<comments>http://anesthesiageneral.com/chronic-oxygen-deficiency/#comments</comments>
<pubDate>Mon, 22 Aug 2011 10:03:27 +0000</pubDate>
<dc:creator>Dr Akif</dc:creator>
<category>
<![CDATA[Critical Care]]>
</category>
<category>
<![CDATA[Chronic oxygen deficiency]]>
</category>
<guid isPermaLink="false">http://anesthesiageneral.com/?p=830</guid>
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<![CDATA[&#160;
&#160;
&#160;
Chronic oxygen deficiency is defined as a prolonged lack of oxygen to the body as that occurs in living in high altitudes or by having severe chronic lung disease.
Chronic oxygen deficiency have the following effects :

There is decreased mental efficiency due the prolonged deficiency of oxygen
Sleepiness, headache, lassitude and fatigubility are also common
Euphoria is also sometimes seen.
Increased ventilation or hyperventilation is occurs as a compensatory mechanism in Chronic oxygen deficiency to maintain the oxygen saturation and normal bodily functions.
Persistent increased ventilation results in reduction in the alveolar ventilation and carbon dioxide tension.
Respiratory alkalosis, is the end result of prolonged hyperventilation as that occurs in Chronic oxygen deficiency.
Metabolic acidosis, is a compensatory phenomenon to maintain the acid base balance.
Interference with oxygen transport mechanism also occurs in the long run, as a final attempt to proper oxygenation inspite of the apparent lack of it due to various reasons.

Some important causes of Chronic oxygen deficiency are the following:

Living at high altitutes. ...]]>
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<item>
<title>Benzodiazepine equivalence</title>
<link>http://anesthesiageneral.com/benzodiazepine-equivalence/</link>
<comments>http://anesthesiageneral.com/benzodiazepine-equivalence/#comments</comments>
<pubDate>Mon, 22 Aug 2011 09:52:07 +0000</pubDate>
<dc:creator>Dr Akif</dc:creator>
<category>
<![CDATA[Drugs]]>
</category>
<category>
<![CDATA[Benzodiazepine equivalence]]>
</category>
<guid isPermaLink="false">http://anesthesiageneral.com/?p=874</guid>
<description>
<![CDATA[Among benzodiazepine equivalence , differences in the onset and duration of action are due to their potency, lipid solubility and pharmacokinetics.
Benzodiazepine equivalence is used to understand the relative differences in the action and effects of the different types of benzodiazepines.
All benzodiazepines are highly lipid soluble and are highly bound to plasma proteins, especially albumin. Following oral administration, benzodiazepines are highly absorbed from the gastrointestinal tract and after IV injection they rapidly enter the CNS and other highly perfused organs.
Therefore, any condition producing hypoalbuminaemia may result in increase of the unbound fraction of benzodiazepine equivalence , resulting in enhanced clinical effects produced by these drugs.
Miller&#8217;s anesthesia says the following about benzodiazepine equivalence -
The binding of benzodiazepines to their respective receptors is of high affinity and is stereospecific and saturable; the order of receptor affinity (potency) of the three agonists is lorazepam &#62; midazolam &#62; diazepam. Midazolam is approximately 3 to 6 times, ...]]>
</description>
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<slash:comments>0</slash:comments>
</item>
<item>
<title>4 Types of Hypoxia</title>
<link>http://anesthesiageneral.com/4-types-of-hypoxia/</link>
<comments>http://anesthesiageneral.com/4-types-of-hypoxia/#comments</comments>
<pubDate>Mon, 22 Aug 2011 09:47:16 +0000</pubDate>
<dc:creator>mubashir</dc:creator>
<category>
<![CDATA[Critical Care]]>
</category>
<category>
<![CDATA[4 Types of Hypoxia]]>
</category>
<guid isPermaLink="false">http://anesthesiageneral.com/?p=611</guid>
<description>
<![CDATA[There are 4 types of Hypoxia . 
The 4 types of Hypoxia are as follows:
1. Anoxic hypoxia or Diffusion hypoxia
Anoxic hypoxia also called as diffusion hypoxia is essentially due to the deficency of oxygen being absorbed by the lungs. This is either due to a decrease in the inspired concentration of oxygen in the air which can result in suffocation.
Another reason is due to a defect in the absorption of oxygen by the lungs due to some pathology or defect at the alveolo cappilary membrane of the lungs, where the real gas exchange takes place.
2. Anaemic hypoxia
Another among the 4 Types of Hypoxia is the Anemic hypoxia. This is due to decreases oxygen binding capacity of the lungs, most commonly due to a decrease in the hemoglobin concentration. Hemoglobin is the main carrier of oxygen in the circulation throughout the body. Hence, if hemoglobin is less, the supply of oxygen to the tissues is decreased.
3. Stagnant hypoxia
The next among the 4 Types of ...]]>
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