FAQ - acidosis
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alkalosis and acidosis--is there and easy way to see how they work?

I need to have a grasp of the normal values of metabolic/respiratory acidosis and alkalosis and how they all work. How do you discern is someone has alk/acidosis metabolically or via respiration and how do you tell if it is compensated?
Can anyone tell me what patients with any of these problems would look like when you see them?
Thanks VERY much in advance!

Hope you're sitting down. This is going to take a while.
Carbon Dioxide and Bicarbonate form the basis of the PH in the blood. When co2 is released by the cells as waste it combines with h2o to form carbonic acid, H2CO3. This is a weak acid. To buffer this there is bicarbonate, HCO3. The H2CO3 loses a hydrogen ion in the lungs becoming H2O and CO2. The CO2 is released into the alveoli and exhaled. That hydrogen ion that was lost is picked up by the bicarbonate to form H2CO3 which again goes to the lungs etc. If there are too many hydrogen ions around the blood becomes acidotic and the body tries to compensate for this by making more bicarbonate to combine with the hydrogen ion.
I assume you are a student in a Respiratory Therapy program is you're asking this question.
The PH, PCO2 and HCO3 in the blood gases are your guide to compensation.
Respiratory acidosis results from hypoventilation and not enough Co2 being blown off. The Ph goes down. There is a direct relationship between Ph and Pco2. For every milimeter increase in Co2 the Ph will drop 0.01. example: Pco2 goes up to 50 mmhg the ph would become 7.30. The opposite is also true. Compensation occurs when the ph increases (alkalosis) or decreases (acidosis). If a patient is in respiratory failure his co2 will go up making the ph go down.If this is an acute thing there is very little if any compensation. That takes time. If the pco2 is chronically elevated than the hco3 increases to compensate so both numbers will be elevated. As in COPD pts. The ph in this circumstance wil be just slightly acidotic as the compensation stops when the ph approches normal. The patient is said to be in a compensated respiratory acidosis.Get it?
Ok let's move on. If a patient presents with diabetic ketoacidosis his HCO3 will be low because it's root cause is a metabolic problem. They will be breathing to beat the band to blow off enough Co2 to bring his PH back to normal levels. It's called Kussmal breathing after the doctor who described it. The doctors in the Er wil give the pt. HCO3 to bring his ph back up to normal. That is an example of a metabolic acidosis.The doctors are trying to compensate for the increased hydrogen ion levels.
Respiratory alkalosis results from hyperventilation. It could be from anxiety, fear or whatever. Sometimes we do this when we have the pt on mechanical ventilation and are overdoing it a bit. That's why we monitor blood gases to make sure we are not over or under ventilating a pt. In the ER with an anxiety pt they usually make the pt breth into a paper sack so they can rebreath their own co2.
Metabolic alkalosis results from a chemical imbalance in the blood usually the electrolytes. This has to treated by a doctor
The best transfer of oxygen to the cells takes place at a PH of 7.40
Deviation from that will effect how well the hemoglobin can take up or release the O2. But that is a topic for another timw.
God bless and keep you healthy..  (+ info)

How would you expect this to affect blood ph and respiratory rate and is this a state of acidosis or alkalosis?

Patient ingested E Coli and was diagnosed with food poisoning and has had chronic diarrhea for the past 24 hours. The patient has a medical history of Chron's Disease. The diarrhea has been going on nonstop for 24 hours. How would you expect this to affect the blood ph and respiratory rate? Is the patient suffering from a state of acidosis or alkalosis and would you expect this to be related to metabolic or respiratory disorder and why?

To answer this, you need more information. Renal function and pulmonary function will influence the end result. Also the activity of the Crohn's needs to be established, and whether an enteroenteric fistula is present.

However: Assuming he has non-secretory diarrhea (ie not bicarbonate wasting as in a villous adenoma of the colon), then the primary event will be a metabolic alkalosis due to volume contraction. If his kidney function is normal, he will attempt to retain sodium (along with bicarbonate) and lose potassium in the urine. Due to some fairly complex actions in the proximal and distal tubule, he will effectively retain bicarbonate, leading to the alkalosis.

If he has normal pulmonary function, he will probably not have a respiratory compensation (it would have to be hypoventilation, which is hard to do unless other things are going on (such as sedatives, altered level of conciousness etc).

As time goes by, and if the diarrhea persists, in the absence of volume replacement, he will ultimately develop pre-renal azotemia, which will affect the metabolic component (he will develop a metabolic acidosis that is distinct from the metabolic alkalosis he already has).

If he goes on to develop hypeovolemic shock, other things come into play - etc etc etc.

Its not always straighforward. I hope this helps.  (+ info)

What is metabolic acidosis in chronic renal failure due to?

Hi, is the metabolic acidosis in chronic renal failure is due by pH level ?

It is due to increased production of H+ by the body or the inability of the body to form bicarbonate (HCO3-) in the kidney, thus, leading to acidemia. Blood pH is low (less than 7.35)

Arterial blood gas (ABG) sampling is essential for the diagnosis.

Med study...  (+ info)

An elderly, semiconscious patient is tentatively diagnosed as having acidosis. What components of the?

arterial blood will be most valuable to quantify in determining if the acidosis is of respiratory origin?

An easy way to determine if it is respiratory is the ph and co2 will be going in opposite directions of each other.For respiratory acidosis, the ph goes down and the co2 up.To tell if it is acute or chronic...look at the bicarb...acute the bicarb will be normal...chronic the bicarb will go up trying to bring the ph back to normal range.  (+ info)

Why hypochloremic acidosis and bicarbonate administration? Why do we do this? ?

Why hypochloremic acidosis and bicarbonate administration? Why do we do this?

  (+ info)

A patient arrives in the ER in severe metabolic acidosis. What does this mean, and what could be the cause?

A patient arrives in the ER in severe metabolic acidosis. What does this mean, and what could be the cause?

Metabolic acidosis is a clinical disturbance characterized by an increase in plasma acidity.
Can be caused by Lactic acidosis - Numerous causes, including circulatory failure, drugs and toxins, and hereditary causes. Ketoacidosis - Diabetes, alcoholism, and starvation
Or Ingestions -Salicylates, methanol, ethylene glycol, isoniazid,3 iron, paraldehyde, sulfur, toluene, ammonium chloride, phenformin/metformin,4 and hyperalimentation fluids  (+ info)

Why does acidosis shift the oxyhemoglobin dissociation curve to the right?

I was looking this up, but why would an acidotic state inhibit the saturation of oxygen to hemoglobin? Is there an interaction between hydrogen and hemoglobin that inhibits the saturation? Thanks to all!

Your question goes right to the heart of why the oxyhemoglobin dissociation curve is so important.
As the blood is arterializing in the pulmonary capillary bed oxygen diffuses across the a-c membrane and into the plasma first. If the plasma is relatively acidotic the heme groups in the erythrocytes takes it up very slowly or, in other words, has a weak attraction. This is due to the presence of CO2 in the heme molecule.. It does not compete with oxygen binding sites as does CO but rather changes the configuration of the molecule to make it less attractive to O2. The reverse is also true. Less CO2 means the heme group is more attractive to O2 and binds more securely. Thus you have the shifts in the oxyhemeglobin dissociation curve. So it's not the increased H+ concentration that effects the absorption of O2 it's the CO2 itself. Although, of course, the increased CO2 level directly effects the pH it's not the pH that directly effects the curve. It could be mentioned here that CO poisoning and methhemoglobin are competitive for hemeglobin binding sites and therefore will render a patient hypoxemic even in the presence of adequate O2 levels. CO causes the hemeglobin to change color to a cherry red while methemoglobin will turn it brown, If you run into a case like that you might want to draw both a venous and an arterial sample to look at the difference of PaO2 and PvO2. The less the difference the more influence CO and methemeglobin is having.
This can be demonstrated in the case of a patient in diabetic ketoacidosis. Although they might be profoundly acidotic their CO2 levels are very low in an attempt to compensate. But O2 levels are normal or above, barring other concomittent conditions.
Of course, in school you're taught a simplified version of the effect of pH, temperature and CO2 on the curve but just a little research will show you it's good as a rule of thumb only.
And btw, there are four heme groups per RBC. When one is fully saturated the blood is then said to be 25% saturated, two is 50% and so on. The last heme group cannot be not be fully saturated because of the presence of CO and methemeglobin which both bind more tightly within the heme group. Thus a patient can, or at least, never should be said to be 100% saturated unless they are in a hyperbaric chamber. No matter what your oximeter reads. Remember it takes a PaO2 of >350mmhg to approach 100%.
God bless and I hope this helps rather than confuse you further.  (+ info)

How does your body adjust to acidosis?

Does it try neutralize the acids, or something?

It does compensate for acidosis through either a metabloic or respiratory pathway (depending on why it was caused). However, you are not able to compensate for a long period of time and you will quickly feel the effects. Acidosis is NOT a good thing. It means your blood pH is too acidic, which can cause a variety of problems. Chances are if you have acidosis you know and are in the hospital due to the symptoms.  (+ info)

What is the significance of a normal –high bicarbonate in respiratory acidosis?

normal high means it is still within normal range, but on the high side

This means that the body is compensating for the acidosis.
Respiratory acidosis is caused when carbon dioxide is not removed from the blood due to hypoventilation, (slow breathing) or obstructions in the exchange of gases. Such conditions are caused by emphysema, asthma, bronchitis, pneumonia and pulmonary edema. Carbon dioxide increases in the blood since it cannot effectively diffuse out of the lungs.
The body has its own methods to correct abnormalities in pH.
These are referred to as "compensation" methods. In a case of respiratory acidosis, the kidneys attempt to compensate for the low pH.
The compensation is to increase excretion of H+ ion and therefore increase the retention or reabsorption of HCO3- (bicarbonate) into the blood. An increase in HCO3- ions in the blood causes the buffer equation to shift left, thus H+ ions decrease and pH increases.

Hope that answers your question. You can have compensated and uncompensated respiratory acidosis :)  (+ info)

How does rhabdomyolysis cause hyperkalemia and metabolic acidosis?

Be specific.
Thanks. :]

This sounds suspiciously like a Homework question but I'll give you the benefit of a doubt.

First, you must understand what rhabdomyolysis is and how it affects the body. Hyperkalemia is RARELY caused by rhabdo but rhabdo can be caused by hyperkalemia. When hyperkalemia is caused by rhabdo, it often goes unnoticed becaue of the counteracting effect of rhabdo on serum potassium.

Rhabdo is a disease of the skeletal muscle that involves the breakdown & destruction (lysis) of muscle tissue and thus muscle cells. As a result of cell lysis, electrolytes such as potassium and phosphate and myoglobin & creatine kinase (CK) are leaked from ruptured muscle tissue cells into the plasma of circulating blood. If tissue destruction is significant enough, the amount of K+ will reach hyperkalemic levels. Because K+ is leaking from an intracellular area of high concentration to a plasma area normally of low concentration, hyperkalemia is develop quickly. That's the key -- it's because plasma is normally an area of low K+ concentration. The normal range of serum K+ is quite narrow, 3.5-5.5 mEq/dL. You can easily see that it doesn't take much to go outside the range either direction.

Rhabdo is a rare cause of met acidosis. Myocyte is another word for muscle cell and you should be as familiar with this as you are with your own name. Recall that rhabdo is a lysis of muscle tissue and that tissue is made up of cells. The lysis action injures myocytes so that other substances besides myoglobin, CK, K+ and P+ are leaked. Lactic acid and other organic acids are also leaked from ruptured myocytes, promoting lactic acidosis which is one type of metabolic acidosis.  (+ info)

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