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Acid-base map and compensatory mechanisms
Buffering and Henderson-Hasselbalch equation
Physiologic pH and buffers
The role of the kidney in acid-base balance
Plasma anion gap
Renal system anatomy and physiology
Body fluid compartments
Movement of water between body compartments
Measuring renal plasma flow and renal blood flow
Regulation of renal blood flow
TF/Px ratio and TF/Pinulin
Phosphate, calcium and magnesium homeostasis
Free water clearance
Kidney countercurrent multiplication
Distal convoluted tubule
Loop of Henle
Proximal convoluted tubule
Tubular reabsorption and secretion
Tubular reabsorption and secretion of weak acids and bases
Tubular reabsorption of glucose
Tubular secretion of PAH
0 / 7 complete
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Respiratory Alkalosis Interventions
respiratory alkalosis and p. 612
respiratory alkalosis from p. 612
respiratory alkalosis p. 612
causes of p. 612
in delirium tremens p. 589
high altitude p. 688
pulmonary embolism p. 693
With respiratory alkalosis, “alkalosis” refers to a process that causes alkali accumulation or acid loss, and “respiratory” refers to the fact that it’s a failure of the respiratory system carrying out its normal pH- balancing job.
Normally, during an inhalation, the diaphragm and chest wall muscles contract to pull open the chest and that sucks in air like a vacuum cleaner. Then, during an exhalation, the muscles relax, allowing the elastin in the lungs to recoil, pulling the lungs back to their normal size and pushing that air out. Ultimately, the lungs need to pull oxygen into the body and get rid of carbon dioxide CO2. CO2 binds to water H2O in the blood and forms H2CO3 carbonic acid, which then dissociates into hydrogen H+ and bicarbonate ions HCO3-. So, in order to prevent pH fluctuations, the CO2 concentration, or the partial pressure of CO2, called PCO2, needs to be kept within a fairly narrow range. For this reason, lungs maintain the ventilation rate they need to get rid of CO2 at the same rate that it’s created by the tissues. If PCO2 levels start to fall and pH starts to rise, peripheral chemoreceptors that are located in the walls of the carotid arteries and in the wall of the aortic arch start to fire less, and that notifies the respiratory centers in the brainstem that they need to decrease the respiratory rate and depth of breathing. As the respiratory rate decreases and breaths become more shallow, the minute ventilation decreases - that’s the volume of air that moves in and out of the lungs in a minute. The decreased ventilation, means less carbon dioxide CO2 moves out of the body, increasing the PCO2 in the body, which lowers the pH.
In respiratory alkalosis, the normal mechanism of ventilation gets disturbed, and the minute ventilation goes higher than what’s needed to balance the pH. For ventilation to increase, the respiratory centers have to start firing more than usual. This increased firing may be a normal compensatory response, or an abnormal response to a situation that doesn’t really call for increased ventilation. Increased ventilation is a normal response to things like hypoxia, a low oxygen level, which can happen with diseases like pneumonia or a pulmonary embolism, or even when a person climbs a high mountain like Mount Everest. But, increased ventilation can be an abnormal response that sometimes happens in situations like anxiety and panic attacks, in sepsis, or in overdoses with salicylates.
Respiratory alkalosis is a type of acid-base imbalance that occurs when there is a decrease in the amount of carbon dioxide (CO2) in the body, leading to an increase in the pH of the blood above 7.45. Respiratory alkalosis can occur due to a variety of causes, including hyperventilation, which is rapid and deep breathing leading to excessive removal of CO2 from the body. Hyperventilation can be seen in conditions like hypoxia, pulmonary embolism, panic attacks, sepsis, or in overdoses with salicylate drugs.
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