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Respiratory Acidosis And Metabolic Alkalosis At The Same Time

Acid-base Physiology I And Ii

Acid-base Physiology I And Ii

Sort Overview of pH Regulation On a mixed diet, pH is threatened by the production of STRONG acids (sulfuric, hydrochloric, and phosphoric) mainly as a result of protein metabolism. -These strong acids are buffered in the body by chemical buffer bases, such as extracellular fluid (ECF) HCO3-. -The kidneys ELIMINATE hydrogen ions (combined with urinary buffers) and anions in the urine. -At the same time, they add NEW HCO3- to the ECF to replace the HCO3- CONSUMED in buffering strong acids. -The respiratory system REMOVES of CO2. pH Terms Acidosis: a PROCESS by which acid accumulate Alkalosis: a PROCESS by which alkali (base) accumulates Acidosis and Alkalosis DO NOT imply that any ABNORMALITY in pH has necessarily occurred Acidemia: pH below 7.35 -H+ concentration above 44 nEq/L Alkalemia: pH above 7.45 -H+ concentration below 36 nEq/L With the suffix -emia we are referring to the pH of the BLOOD Buffer A substance which can ABSORB or DONATE H+ ions -This activity may mitigate-but not entirely prevent-changes in pH -The most effective buffers have pK values (-log of K = ionization constant) close to PHYSIOLOGIC pH values HB<->H+ + B- A blood sample has a measured pH of 7.23. This measurement would be best described as reflecting: 1. Acidosis 2. Acidemia 3. Alkalosis 4. Alkalemia ---- 2. (pH is under 7.4) Following a short burst of strenuous exercise the most rapid system available to correct pH is the: 1. Buffers 2. Kidneys 3. Lungs -- Buffer: Rapid and in cell and produce acid that is circulating bicarb/hydrogen ions to the lungs (MOST IMMEDIATE) -Order of speed: Buffers (Fast)>Lungs>>>Kidneys (slowest) The isohydric principle A number of buffers are available to STABILIZE the blood pH, including: -The carbonic acid / bicarbonate pair (H2CO3 / HCO3-): pK = 6.1 -Phosphat Continue reading >>

Metabolic Alkalosis: Practice Essentials, Pathophysiology, Etiology

Metabolic Alkalosis: Practice Essentials, Pathophysiology, Etiology

Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FASN more... Metabolic alkalosis is a primary increase in serum bicarbonate (HCO3-) concentration. This occurs as a consequence of a loss of H+ from the body or a gain in HCO3-. In its pure form, it manifests as alkalemia (pH >7.40). As a compensatory mechanism, metabolic alkalosis leads to alveolar hypoventilation with a rise in arterial carbon dioxide tension (PaCO2), which diminishes the change in pH that would otherwise occur. Normally, arterial PaCO2 increases by 0.5-0.7 mm Hg for every 1 mEq/L increase in plasma bicarbonate concentration, a compensatory response that is very quick. If the change in PaCO2 is not within this range, then a mixed acid-base disturbance occurs. For example, if the increase in PaCO2 is more than 0.7 times the increase in bicarbonate, then metabolic alkalosis coexists with primary respiratory acidosis. Likewise, if the increase in PaCO2 is less than the expected change, then a primary respiratory alkalosis is also present. The first clue to metabolic alkalosis is often an elevated bicarbonate concentration that is observed when serum electrolyte measurements are obtained. Remember that an elevated serum bicarbonate concentration may also be observed as a compensatory response to primary respiratory acidosis. However, a bicarbonate concentration greater than 35 mEq/L is almost always caused by metabolic alkalosis. Metabolic alkalosis is diagnosed by measuring serum electrolytes and arterial blood gases . If the etiology of metabolic alkalosis is not clear from the clinical history and physical examination, including drug use and the presence of hypertension, then a urine chloride ion concentration can be obtained. Calculation of the serum anion gap may al Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Respiratory acidosis is an acid-base balance disturbance due to alveolar hypoventilation. Production of carbon dioxide occurs rapidly and failure of ventilation promptly increases the partial pressure of arterial carbon dioxide (PaCO2). [ 1 ] The normal reference range for PaCO2 is 35-45 mm Hg. Alveolar hypoventilation leads to an increased PaCO2 (ie, hypercapnia). The increase in PaCO2, in turn, decreases the bicarbonate (HCO3)/PaCO2 ratio, thereby decreasing the pH. Hypercapnia and respiratory acidosis ensue when impairment in ventilation occurs and the removal of carbon dioxide by the respiratory system is less than the production of carbon dioxide in the tissues. Lung diseases that cause abnormalities in alveolar gas exchange do not typically result in alveolar hypoventilation. Often these diseases stimulate ventilation and hypocapnia due to reflex receptors and hypoxia. Hypercapnia typically occurs late in the disease process with severe pulmonary disease or when respiratory muscles fatigue. (See also Pediatric Respiratory Acidosis , Metabolic Acidosis , and Pediatric Metabolic Acidosis .) Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (ie, >45 mm Hg) with an accompanying acidemia (ie, pH < 7.35). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal or near-normal pH secondary to renal compensation and an elevated serum bicarbonate levels (ie, >30 mEq/L). Acute respiratory acidosis is present when an abrupt failure of ventilation occurs. This failure in ventilation may result from depression of the central respiratory center by one or another of the following: Central nervous system disease or drug-induced r Continue reading >>

Abg’s—it’s All In The Family

Abg’s—it’s All In The Family

By Cyndi Cramer, BA, RN, OCN, PCRN RealNurseEd.com 3.0 Contact Hour Self Learning Module Objectives: Identify the components of the ABG and their normal ranges Interpret ABG values and determine the acid base abnormality given Identify the major causes of acid base abnormalities Describe symptoms associated with acid base abnormalities Describe interventions to correct acid base abnormalities Identify the acceptable O2 level per ABG and Pulse Oximetry Identify four causes of low PaO2 The Respiratory System (Acid); CO2 is a volatile acid If you increase your respiratory rate (hyperventilation) you "blow off" CO2 (acid) therefore decreasing your CO2 acid—giving you ALKLAOSIS If you decrease your respiratory rate (hypoventilation) you retain CO2 (acid) therefore increasing your CO2 (acid)—giving you ACIDOSIS The Renal System (Base); the kidneys rid the body of the nonvolatile acids H+ (hydrogen ions) and maintain a constant bicarb (HCO3). Bicarbonate is the body’s base You have Acidosis when you have excess H+ and decreased HCO3- causing a decrease in pH. The Kidneys try to adjust for this by excreting H+ and retaining HCO3- base. The Respiratory System will try to compensate by increasing ventilation to blow off CO2 (acid) and therefore decrease the Acidosis. You have Alkalosis when H+ decreases and you have excess (or increased) HCO3- base. The kidneys excrete HCO3- (base) and retain H+ to compensate. The respiratory system tries to compensate with hypoventilation to retain CO2 (acid) To decrease the alkalosis Compensation The respiratory system can effect a change in 15-30 minutes The renal system takes several hours to days to have an effect. RESPIRATORY ACIDOSIS: pH < 7.35 (Normal: 7.35 - 7.45) CO2 > 45 (Normal: 35 – 45) 1. Causes: Hypoventilation a. Depressio Continue reading >>

Acid-base Disorders - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition

Acid-base Disorders - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition

(Video) Overview of Acid-Base Maps and Compensatory Mechanisms By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincents Ascension Health, Birmingham Acid-base disorders are pathologic changes in carbon dioxide partial pressure (Pco2) or serum bicarbonate (HCO3) that typically produce abnormal arterial pH values. Acidosis refers to physiologic processes that cause acid accumulation or alkali loss. Alkalosis refers to physiologic processes that cause alkali accumulation or acid loss. Actual changes in pH depend on the degree of physiologic compensation and whether multiple processes are present. Primary acid-base disturbances are defined as metabolic or respiratory based on clinical context and whether the primary change in pH is due to an alteration in serum HCO3 or in Pco2. Metabolic acidosis is serum HCO3< 24 mEq/L. Causes are Metabolic alkalosis is serum HCO3> 24 mEq/L. Causes are Respiratory acidosis is Pco2> 40 mm Hg (hypercapnia). Cause is Decrease in minute ventilation (hypoventilation) Respiratory alkalosis is Pco2< 40 mm Hg (hypocapnia). Cause is Increase in minute ventilation (hyperventilation) Compensatory mechanisms begin to correct the pH (see Table: Primary Changes and Compensations in Simple Acid-Base Disorders ) whenever an acid-base disorder is present. Compensation cannot return pH completely to normal and never overshoots. A simple acid-base disorder is a single acid-base disturbance with its accompanying compensatory response. Mixed acid-base disorders comprise 2 primary disturbances. Compensatory mechanisms for acid-base disturbances cannot return pH completely to normal and never overshoot. Primary Changes and Compensations in Simple Acid-Base Disorders 1.2 mm Hg decrease in Pco2 for every 1 mmol/L decrease in HC Continue reading >>

Acute Acid-base Disorders. 2. Specific Disturbances.

Acute Acid-base Disorders. 2. Specific Disturbances.

Acute acid-base disorders. 2. Specific disturbances. Evaluation of the acid-base status of the body requires measurement of bicarbonate (total carbon dioxide) concentration, pH, and partial pressure of CO2 in arterial blood. Calculation of standard bicarbonate and base excess or deficit is not necessary. The normal concentration of free hydrogen ions (H+) is approximately 40 millimoles/liter, which is equivalent to a pH of 7.4. The normal load of fixed acids is 50 to 80 millimoles in 24 hours. A steady state is maintained by excretion of an equal amount of H+ by the kidneys, which at the same time regenerate bicarbonate to replenish buffer stores. Renal excretion of H+ is in the form of titratable acid and ammonium. Synthesis of ammonia can increase severalfold under the stimulus of acidosis. This is the chief mechanism of long-term compensation. Metabolic acidosis can be due to an excessive acid load (endogenous or exogenous), impaired renal excretion of H+, or bicarbonate loss. Determination of the "anion gap" (unmeasured anions) helps to establish the mechanism of acidosis. Acidosis with a normal anion gap is due to either bicarbonate loss or ingestion of certain chloride salts. A gap larger than normal indicates the presence in the body of acids other than acidfying chloride salts. Management of metabolic acidosis requires accurate diagnosis, clear understanding of the mechansim, and individualized treatment. Metabloic alkalosis is due to loss of H+ (usually from stomach or kidneys) or ingestion of alkali. Measurement of urinary chloride helps establish the mechanism of alkalosis. In saline-responsive alkalosis, the urinary chloride level is very low. This is usually due to gastric loss of H+, and the condition responds to administration of saline solution. When th Continue reading >>

Metabolic/ Respiratory Acidosis And Alkalosis

Metabolic/ Respiratory Acidosis And Alkalosis

Metabolic/ respiratory acidosis and alkalosis Call me stupid--but I'm having such a time with determining whether a person is in respiratory or metabolic acidosis/alkalosis based on the ABG levels. I know how to determine the acidosis/ alkalosis part---its the difference between metabolic and respiratory that screws me up. If anyone has any suggestions on how to tell the two apart--please share!!!! Ummm, I can't help you without "refreshing." That was last semester for me, and I've already forgotten. You don't use it, you will lose it. Ugggg. I was able to figure it out back then (like, 4 months ago), but I never understood the dynamics between the 2. So, if someone is in Resp Acidosis, what does it mean, what will I objectively see, what will they report, what will I do to help them??? Metabolic Alkalosis Vs. Resp Acidosis - I have no idea how the sx differ. Ya me. Call me stupid--but I'm having such a time with determining whether a person is in respiratory or metabolic acidosis/alkalosis based on the ABG levels. I know how to determine the acidosis/ alkalosis part---its the difference between metabolic and respiratory that screws me up. If anyone has any suggestions on how to tell the two apart--please share!!!! It is hard sometimes, and one can forget easily with out looking at ABGS frequently. co2 might be hco3 in some labs and the 18 or 22 might be 1-2 numbers different. Just write down this down and then circle which ones apply to your ABG results. Then what it is called is the one that caused the acidosis or alkalosis. pco is resp and co2 is metabolic ex your pt abgs are Ph 7.30, pco2, 40 co2 10 This is metabolic acidosis. Call me stupid--but I'm having such a time with determining whether a person is in respiratory or metabolic acidosis/alkalosis based on the Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. See also separate Lactic Acidosis and Arterial Blood Gases - Indications and Interpretations articles. Description Metabolic acidosis is defined as an arterial blood pH <7.35 with plasma bicarbonate <22 mmol/L. Respiratory compensation occurs normally immediately, unless there is respiratory pathology. Pure metabolic acidosis is a term used to describe when there is not another primary acid-base derangement - ie there is not a mixed acid-base disorder. Compensation may be partial (very early in time course, limited by other acid-base derangements, or the acidosis exceeds the maximum compensation possible) or full. The Winter formula can be helpful here - the formula allows calculation of the expected compensating pCO2: If the measured pCO2 is >expected pCO2 then additional respiratory acidosis may also be present. It is important to remember that metabolic acidosis is not a diagnosis; rather, it is a metabolic derangement that indicates underlying disease(s) as a cause. Determination of the underlying cause is the key to correcting the acidosis and administering appropriate therapy[1]. Epidemiology It is relatively common, particularly among acutely unwell/critical care patients. There are no reliable figures for its overall incidence or prevalence in the population at large. Causes of metabolic acidosis There are many causes. They can be classified according to their pathophysiological origin, as below. The table is not exhaustive but lists those that are most common or clinically important to detect. Increased acid Continue reading >>

Metabolic Alkalosis - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition

Metabolic Alkalosis - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition

(Video) Overview of Buffering and the Henderson-Hasselbalch Equation By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincents Ascension Health, Birmingham Metabolic alkalosis is primary increase in bicarbonate (HCO3) with or without compensatory increase in carbon dioxide partial pressure (Pco2); pH may be high or nearly normal. Common causes include prolonged vomiting, hypovolemia, diuretic use, and hypokalemia. Renal impairment of HCO3 excretion must be present to sustain alkalosis. Symptoms and signs in severe cases include headache, lethargy, and tetany. Diagnosis is clinical and with arterial blood gas and serum electrolyte measurement. The underlying condition is treated; oral or IV acetazolamide or hydrochloric acid is sometimes indicated. Metabolic alkalosis is bicarbonate (HCO3) accumulation due to Intracellular shift of hydrogen ion (H+as occurs in hypokalemia ) Regardless of initial cause, persistence of metabolic alkalosis indicates that the kidneys have increased their HCO3 reabsorption, because HCO3 is normally freely filtered by the kidneys and hence excreted. Volume depletion and hypokalemia are the most common stimuli for increased HCO3 reabsorption, but any condition that elevates aldosterone or mineralocorticoids (which enhance sodium [Na] reabsorption and potassium [K] and hydrogen ion [H+] excretion) can elevate HCO3. Thus, hypokalemia is both a cause and a frequent consequence of metabolic alkalosis. The most common causes of metabolic alkalosis are Volume depletion (particularly when involving loss of gastric acid and chloride [Cl] due to recurrent vomiting or nasogastric suction) Among other causes (see Table: Causes of Metabolic Alkalosis ) are disorders that cause Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3−) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. Terminology : Acidosis refers to a process that causes a low pH in blood and tissues. Acidemia refers specifically to a low pH in the blood. In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed. Signs and symptoms[edit] Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur. Extreme acidemia leads to neurological and cardia Continue reading >>

Alkalosis

Alkalosis

Your blood is made up of acids and bases. The amount of acids and bases in your blood can be measured on a pH scale. It’s important to maintain the correct balance between acids and bases. Even a slight change can cause health problems. Normally, your blood should have a slightly higher amount of bases than acids. Alkalosis occurs when your body has too many bases. It can occur due to decreased blood levels of carbon dioxide, which is an acid. It can also occur due to increased blood levels of bicarbonate, which is a base. This condition may also be related to other underlying health issues such as low potassium, or hypokalemia. The earlier it’s detected and treated, the better the outcome is. Acid-base balance » There are five main types of alkalosis. Respiratory alkalosis Respiratory alkalosis occurs when there isn’t enough carbon dioxide in your bloodstream. It’s often caused by: hyperventilation, which commonly occurs with anxiety high fever lack of oxygen salicylate poisoning being in high altitudes Metabolic alkalosis Metabolic alkalosis develops when your body loses too much acid or gains too much base. This can be attributed to: excess vomiting, which causes electrolyte loss overuse of diuretics a large loss of potassium or sodium in a short amount of time antacids accidental ingestion of bicarbonate, which can be found in baking soda laxatives alcohol abuse Hypochloremic alkalosis Hypochloremic alkalosis occurs when there’s a significant decline of chloride in your body. This can be due to prolonged vomiting or sweating. Chloride is an important chemical needed to maintain balance in bodily fluids, and it’s an essential part of your body’s digestive fluids. Hypokalemic alkalosis Hypokalemic alkalosis occurs when your body lacks the normal amount Continue reading >>

Types Of Disturbances

Types Of Disturbances

The different types of acid-base disturbances are differentiated based on: Origin: Respiratory or metabolic Primary or secondary (compensatory) Uncomplicated or mixed: A simple or uncomplicated disturbance is a single or primary acid-base disturbance with or without compensation. A mixed disturbance is more than one primary disturbance (not a primary with an expected compensatory response). Acid-base disturbances have profound effects on the body. Acidemia results in arrythmias, decreased cardiac output, depression, and bone demineralization. Alkalemia results in tetany and convulsions, weakness, polydipsia and polyuria. Thus, the body will immediately respond to changes in pH or H+, which must be kept within strict defined limits. As soon as there is a metabolic or respiratory acid-base disturbance, body buffers immediately soak up the proton (in acidosis) or release protons (alkalosis) to offset the changes in H+ (i.e. the body compensates for the changes in H+). This is very effective so minimal changes in pH occur if the body is keeping up or the acid-base abnormality is mild. However, once buffers are overwhelmed, the pH will change and kick in stronger responses. Remember that the goal of the body is to keep hydrogen (which dictates pH) within strict defined limits. The kidney and lungs are the main organs responsible for maintaining normal acid-base balance. The lungs compensate for a primary metabolic condition and will correct for a primary respiratory disturbance if the disease or condition causing the disturbance is resolved. The kidney is responsible for compensating for a primary respiratory disturbance or correcting for a primary metabolic disturbance. Thus, normal renal function is essential for the body to be able to adequately neutralize acid-base abnor Continue reading >>

A Primer On Arterial Blood Gas Analysis By Andrew M. Luks, Md(cont.)

A Primer On Arterial Blood Gas Analysis By Andrew M. Luks, Md(cont.)

Step 4: Identify the compensatory process (if one is present) In general, the primary process is followed by a compensatory process, as the body attempts to bring the pH back towards the normal range. If the patient has a primary respiratory acidosis (high PCO2 ) leading to acidemia: the compensatory process is a metabolic alkalosis (rise in the serum bicarbonate). If the patient has a primary respiratory alkalosis (low PCO2 ) leading to alkalemia: the compensatory process is a metabolic acidosis (decrease in the serum bicarbonate) If the patient has a primary metabolic acidosis (low bicarbonate) leading acidemia, the compensatory process is a respiratory alkalosis (low PCO2 ). If the patient has a primary metabolic alkalosis (high bicarbonate) leading to alkalemia, the compensatory process is a respiratory acidosis (high PCO2 ) The compensatory processes are summarized in Figure 2. (opens in a new window) Important Points Regarding Compensatory Processes There are several important points to be aware of regarding these compensatory processes: The body never overcompensates for the primary process. For example, if the patient develops acidemia due to a respiratory acidosis and then subsequently develops a compensatory metabolic alkalosis (a good example of this is the COPD patient with chronic carbon dioxide retention), the pH will move back towards the normal value of 7.4 but will not go to the alkalemic side of normal This might result in a pH of 7.36, for example but should not result in a pH such as 7.44 or another value on the alkalemic side of normal. If the pH appears to "over-compensate" then an additional process is at work and you will have to try and identify it. This can happen with mixed acid-base disorders, which are described further below. The pace of co Continue reading >>

Acid-base Imbalance - An Overview | Sciencedirect Topics

Acid-base Imbalance - An Overview | Sciencedirect Topics

Gary P. Carlson, Michael Bruss, in Clinical Biochemistry of Domestic Animals (Sixth Edition) , 2008 Mixed acid-base disorders occur when several primary acid-base imbalances coexist (de Morais, 1992a). Metabolic acidosis and alkalosis can coexist and either or sometimes both of these metabolic abnormalities may occur with either respiratory acidosis or alkalosis (Nairns and Emmett, 1980; Wilson and Green, 1985). Evaluation of mixed acid-base abnormalities requires an understanding of the anion gap, the relationship between the change in serum sodium and chloride concentration, and the limits of compensation for the primary acid-base imbalances (Saxton and Seldin, 1986; Wilson and Green, 1985). Clinical findings and history are also necessary to define the factors that may contribute to the development of mixed acid-base disorders. The following are important considerations in evaluating possible mixed acid-base disorders: Compensating responses to primary acid-base disturbances do not result in overcompensation. With the possible exception of chronic respiratory acidosis, compensating responses for primary acid-base disturbances rarely correct pH to normal. In patients with acid-base imbalances, a normal pH indicates a mixed acid-base disturbance. A change in pH in the opposite direction to that predicted for a known primary disorder indicates a mixed disturbance. With primary acid-base disturbances, bicarbonate and pCO2 always deviate in the same direction. If these parameters deviate in opposite directions, a mixed abnormality exists. Although mixed acid-base abnormalities undoubtedly occur in animals and have been documented in the veterinary literature, they are often overlooked (Wilson and Green, 1985). An appreciation of the potential for the development of mixed Continue reading >>

Abg: Respiratory Acidosis/metabolic Alkalosis

Abg: Respiratory Acidosis/metabolic Alkalosis

Home / ABA Keyword Categories / A / ABG: Respiratory acidosis/metabolic alkalosis ABG: Respiratory acidosis/metabolic alkalosis A combined respiratory acidosis / metabolic alkalosis will result in elevated PaCO2 and serum bicarbonate. Which process is the primary disorder (e.g. primary respiratory acidosis with metabolic compensation versus primary metabolic alkalosis with respiratory compensation) is dependent on the pH in an acidotic patient, the acidosis is primary (and the alkalosis is compensatory) and vice versa. Compensation behaves in accordance with the following rules: Metabolic Acidosis: As bicarbonate goes from 10 to 5, pCO2 will bottom out at 15. pCO2 = 1.5 x [HCO3-] + 8 (or pCO2 = 1.25 x [HCO3-]) Metabolic Alkalosis: compensation here is less because CO2 is driving force for respiration. pCO2 = 0.7 x [HCO3-] + 21 (or pCO2 = 0.75 x [HCO3-]) Acutely: [HCO3-] = 0.1 x pCO2 or pH = 0.008 x pCO2 Chronically: [HCO3-] = 0.4 x pCO2 or pH = 0.003 x pCO2 Respiratory Alkalosis: Metabolic compensation will automatically be retention of chloride (i.e., hyperchloremic, usually referred to as loss of bicarb although it is the strong ion difference that matters). If you have an anion gap, then youve automatically got a little bit of an acidosis on top of the compensation (because the compensation should be a NON-gap acidotic process. Acutely: [HCO3-] = 0.2 x pCO2 (or pH = 0.008 x pCO2) Chronically: [HCO3-] = 0.4 x pCO2 (or pH = 0.017 x pCO2) Continue reading >>

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