YouTube video lecture on Metabolic Acidosis
Comments from students:
This is a best and most simplified explanation of metabolic acidosis!
Very good Video. Tons of good info.
I see metabolic acidosis all the time in septic patients in respiratory failure.
I applaud your brilliance and zeal most of all!
Every blessing!
AWESOME video! You really break it down and make it easy to understand. I would like to know just what the signs and symptoms of metabolic acidosis/alkalosis and respiratory acidosis/alkalosis would be. My instructor just gives us vital signs and expects us to figure it out and she did not explain how.
Showing posts with label metabolic acidosis. Show all posts
Showing posts with label metabolic acidosis. Show all posts
Sunday, 24 June 2012
Thursday, 22 March 2012
SGD: Compensation in Metabolic Acidosis
Questions asked by a student at SGD:
In Metabolic Acidosis, there is a marked drop in bicarbonate concentration, and pH falls considerably. The compensation is a steady (smooth hyperbolic) increase in PCO2. In the acute phase response or compensation, the blood buffers try to correct the change first and breathing slows down (becomes slower, hypoventilate). The slowed breathing continues past the 10-minute critical timeline and for up to 12 to 24 hours (approx. 1 day) whereby the body is able to retain sufficient CO2 to increase the PCO2 and the pH steadies to a higher level but never reaching 7.40. A rising pH and PCO2 are sufficient to tell us that compensation is taking place. When the PCO2 is high and pH near normal, then that is considered as complete compensation, and the patient should be breathing normally by 24 hours (one day observation).
- Why in Metabolic Acidosis, the compensation has no acute phase?
- Why is Respiratory Alkalosis single phase?
- Is the compensation acute or chronic?
- How long is the compensation in Metabolic Acidosis?
In Metabolic Acidosis, there is a marked drop in bicarbonate concentration, and pH falls considerably. The compensation is a steady (smooth hyperbolic) increase in PCO2. In the acute phase response or compensation, the blood buffers try to correct the change first and breathing slows down (becomes slower, hypoventilate). The slowed breathing continues past the 10-minute critical timeline and for up to 12 to 24 hours (approx. 1 day) whereby the body is able to retain sufficient CO2 to increase the PCO2 and the pH steadies to a higher level but never reaching 7.40. A rising pH and PCO2 are sufficient to tell us that compensation is taking place. When the PCO2 is high and pH near normal, then that is considered as complete compensation, and the patient should be breathing normally by 24 hours (one day observation).
Wednesday, 5 October 2011
Hyperchloremic acidosis
Introduction
Hyperchloremic acidosis is a form of metabolic acidosis associated with a normal anion gap, a decrease in plasma bicarbonate concentration, and in an increase in plasma chloride concentration (see anion gap for a fuller explanation).
Source:
Hyperchloremic acidosis in Wikipedia
Hyperchloremic acidosis is a form of metabolic acidosis associated with a normal anion gap, a decrease in plasma bicarbonate concentration, and in an increase in plasma chloride concentration (see anion gap for a fuller explanation).
Causes
- Renal tubular acidosis failure of HCO3- resorption (i.e., proximal renal tubular acidosis) or failure of H+ secretion (i.e., in distal renal tubular acidosis)
- Renal failure
- Gastrointestinal loss of HCO3- with diarrhoea (vomiting will tend to cause hypochloraemic alkalosis).
- Ingestions
- Ammonium chloride, Hydrochloric acid
- Hyperalimentation fluids (i.e., total parenteral nutrition, TPN)
- Alcohol (such as ethanol) can affect anion gap by inducing alcohol dehydrogenase enzyme.
Source:
Hyperchloremic acidosis in Wikipedia
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