Disorders of Acid Base Balance

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Acid-Base Balance Ahmed Abughaban 2021040088 Acid-Base abnormalities  Metabolic Acidosis  Metabolic Alkalosis  Respiratory Acidosis  Respiratory Alkalosis Mechanisms of acid-base balance Respiratory system Kidneys Buffers HCO3 reabsorption Excretion of organic acids Titrable acids (HPO4) Ammonium (NH4) Ca, Hb, PP bones Metabolic Acidosis  Definition:  Primary decrease in serum HCO3  Decreased pH  Accumulation of acids Anion Gap Represents the unmeasured anions in plasma. AG=Na - (Cl + HCO3) Normal AG= 10-12 mEq/L Causes of ↑AG metabolic acidosis: “Accumulation of acids” 1. lactic acidosis 2. Ketoacidosis - diabetic, alcoholic, starvation 3. Toxins - ethylene glycol, methanol, salicylates 4. RF - acute & chronic Causes of normal AG metabolic acidosis: 1- Renal • RTA • Fanconi’s synd 2- GIT • Severe diarrhea • GIT fistula 3- Drugs (+ renal insuff.) • K sparing diuretics • Heavy metals • ACEIs • NSAIDs “Loss of alkali” POG unmeasured NON-IONIZED AG unmeasured IONIZED Plasma Osmolal Gap POG= measured - calculated plasma osm Steps in Acid-Base Diagnosis  Obtain ABG & electrolytes  Check pH & compare HCO3 on ABG & measured for accuracy  Calculate AG  Try to identify the cause according to the AG  Estimate compensatory response (PaCo2 ↓ 1.25 mmHg per mmol/L ↓ in HCO3) Disorders of Acid-Base Balance Disorders of Acid-Base Balance Bởi: OpenStaxCollege Normal arterial blood pH is restricted to a very narrow range of 7.35 to 7.45 A person who has a blood pH below 7.35 is considered to be in acidosis (actually, “physiological acidosis,” because blood is not truly acidic until its pH drops below 7), and a continuous blood pH below 7.0 can be fatal Acidosis has several symptoms, including headache and confusion, and the individual can become lethargic and easily fatigued ([link]) A person who has a blood pH above 7.45 is considered to be in alkalosis, and a pH above 7.8 is fatal Some symptoms of alkalosis include cognitive impairment (which can progress to unconsciousness), tingling or numbness in the extremities, muscle twitching and spasm, and nausea and vomiting Both acidosis and alkalosis can be caused by either metabolic or respiratory disorders As discussed earlier in this chapter, the concentration of carbonic acid in the blood is dependent on the level of CO2 in the body and the amount of CO2 gas exhaled through the lungs Thus, the respiratory contribution to acid-base balance is usually discussed in terms of CO2 (rather than of carbonic acid) Remember that a molecule of carbonic acid is lost for every molecule of CO2 exhaled, and a molecule of carbonic acid is formed for every molecule of CO2 retained 1/8 Disorders of Acid-Base Balance Symptoms of Acidosis and Alkalosis Symptoms of acidosis affect several organ systems Both acidosis and alkalosis can be diagnosed using a blood test Metabolic Acidosis: Primary Bicarbonate Deficiency Metabolic acidosis occurs when the blood is too acidic (pH below 7.35) due to too little bicarbonate, a condition called primary bicarbonate deficiency At the normal pH of 7.40, the ratio of bicarbonate to carbonic acid buffer is 20:1 If a person’s blood pH drops below 7.35, then he or she is in metabolic acidosis The most common cause of metabolic acidosis is the presence of organic acids or excessive ketones in the blood [link] lists some other causes of metabolic acidosis *Acid metabolites from ingested chemical Common Causes of Metabolic Acidosis and Blood Metabolites Cause Metabolite Diarrhea Bicarbonate Uremia Phosphoric, sulfuric, and lactic acids Diabetic ketoacidosis Increased ketones Strenuous exercise Lactic acid Methanol Formic acid* Paraldehyde β-Hydroxybutyric acid* 2/8 Disorders of Acid-Base Balance Common Causes of Metabolic Acidosis and Blood Metabolites Cause Metabolite Isopropanol Propionic acid* Ethylene glycol Glycolic acid, and some oxalic and formic acids* Salicylate/aspirin Sulfasalicylic acid (SSA)* The first three of the eight causes of metabolic acidosis listed are medical (or unusual physiological) conditions Strenuous exercise can cause temporary metabolic acidosis due to the production of lactic acid The last five causes result from the ingestion of specific substances The active form of aspirin is its metabolite, sulfasalicylic acid An overdose of aspirin causes acidosis due to the acidity of this metabolite Metabolic acidosis can also result from uremia, which is the retention of urea and uric acid Metabolic acidosis can also arise from diabetic ketoacidosis, wherein an excess of ketones is present in the blood Other causes of metabolic acidosis are a decrease in the excretion of hydrogen ions, which inhibits the conservation of bicarbonate ions, and excessive loss of bicarbonate ions through the gastrointestinal tract due to diarrhea Metabolic Alkalosis: Primary Bicarbonate Excess Metabolic alkalosis is the opposite of metabolic acidosis It occurs when the blood is too alkaline (pH above 7.45) due to too much bicarbonate (called primary bicarbonate excess) A transient excess of bicarbonate in the blood can follow ingestion of excessive amounts of bicarbonate, citrate, or antacids for conditions such as stomach acid reflux—known as heartburn Cushing’s disease, which is the chronic hypersecretion of adrenocorticotrophic hormone (ACTH) by the anterior pituitary gland, can cause chronic metabolic alkalosis The oversecretion of ACTH results in elevated aldosterone levels and an increased loss of potassium by urinary excretion Other causes of metabolic alkalosis include the loss of hydrochloric acid from the stomach through vomiting, potassium depletion due to the use of diuretics for hypertension, and the excessive use of laxatives Respiratory Acidosis: Primary Carbonic Acid/CO2 Excess Respiratory acidosis occurs when the blood is overly acidic due to an excess of carbonic acid, resulting from too much CO2 in the blood Respiratory acidosis can result from 3/8 Disorders of Acid-Base Balance anything that interferes with respiration, such as pneumonia, emphysema, or congestive heart failure Respiratory Alkalosis: Primary Carbonic Acid/CO2 Deficiency Respiratory alkalosis occurs when the blood is overly alkaline due to a deficiency in carbonic acid and CO2 levels in the blood This condition usually occurs when too ...RESEARC H ARTIC LE Open Access Acid-base balance and hydration status following consumption of mineral-based alkaline bottled water Daniel P Heil Abstract Background: The present study sought to determine whether the consum ption of a mineral-rich alkalizing (AK) bottled water could improve both acid-base balance and hydration status in young healthy adults under free-living conditions. The AK water contains a naturally high mineral content along with Alka-PlexLiquid, a dissolved supplement that increases the mineral content and gives the water an alkalizing pH of 10.0. Methods: Thirty-eight subjects were matched by gender and self-reported physical activity (SRPA, hrs/week) and then split into Control (12 women, 7 men; Mean +/- SD: 23 +/- 2 yrs; 7.2 +/- 3.6 hrs/week SRPA) and Experimental (13 women, 6 men; 22 +/- 2 yrs; 6.4 +/ - 4.0 hrs/week SRPA) groups. The Control group consumed non-mineralized placebo bottled water over a 4-week period while the Experimental group consumed the placebo water during the 1st and 4th weeks and the AK water during the middle 2-week treatment period. Fingertip blood and 24-hour urine samples were collected three times each week for subsequent measures of blood and urine osmolality and pH, as well as total urine volume. Dependent variables were analyzed using multivariate repeated meas ures ANOVA with post-hoc focused on evaluating changes over time within Control and Experimental groups (alpha = 0.05). Results: There were no significant changes in any of the dependent variables for the Control group. The Experimental group, however, showed significant increases in both the blood and urine pH (6.23 to 7.07 and 7.52 to 7.69, respectively), a decreased blood and increased urine osmolality, and a decreased urine output (2.51 to 2.05 L/day), all during the second wee k of the treatment period (P < 0.05). Further, these changes reversed for the Experimental group once subjects switched to the placebo water during the 4th week. Conclusions: Consumption of AK water was associated with improved acid-base balance (i.e., an alkalization of the blood and urine) and hydration status when consumed under free-living conditions. In contrast, subjects who consumed the placebo bottled water showed no changes over the same period of time. These results indicate that the habitual consumption of AK water may be a valuable nutritional vector for influencing both acid-base balance and hydration status in healthy adults. Background Acid-base equilibrium within the body is tightly main- tained through the interaction of three complementary mechanisms: Blood and tissue buffering systems (e.g., bicarbonate), the diffusion of carbon dioxide from the blood to the lungs via respiration, and the excretion of hydrogen ions from the blood to the u rine by the kid- neys. At any given time, acid-ba se balance is collectively influenced by cellular metabolism (e.g., ex ercise), dietary intake, as well as disease states known to influence either acid production (e.g., diabetic ketoacidosis) or excretion (e.g., renal failure). Chronic low-grade meta- bolic acidosis, a condition associated with “the Western diet” (i.e., high dietary intake of cheese, meats, and pro- cessed grains with relativel y low intake of fruits and vegetables) has been linked with indicators of poor health or health risk such as an increased association with cardiometabolic risk factors [1], increased risk for the development of osteoporosis [2], loss of lean body Correspondence: dheil@montana.edu Movement Science/Human Performance Laboratory, Department of Health & Human Development, H&PE Complex, Hoseaus Rm 121, Montana State University, Bozeman, MT USA Heil Journal of the International Society of Sports Nutrition 2010, 7:29 http://www.jissn.com/content/7/1/29 © 2010 Heil; licen see BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://c reativecommons.org/licenses/by/2.0 SHOR T REPOR T Open Access The effects of Energised Greens™ upon blood acid-base balance during resting conditions Mark Turner 1 , Richard Page 1 , Nigel Mitchell 2 and Jason Siegler 3* Abstract Background: The consumption of fresh fruit & vegetable in concentrate form (FVC) have recently become an alternative approach to combating excessive renal acid loads often associate d with Western Diets. Additionally, these FVC ’ s have been purported to induce metabolic alkalosis, which perhaps may enhance the blood buffer ing capacity of an individual. Therefo re, the aim of this pre liminary study was to profile the acid-base response after ingestion of an acute dose of fruit and vegetable extract (Energised Greens™ (EG), Nottingham, UK) and compare it to a standard, low dose (0.1 g·kg -1 ) of sodium bicarbonate (NaHCO 3 ). Findings: As part of a randomized, cross over design participants consumed 750 mL of water with either 9 g of EG (manufacturer recommendations), 0.1 g·kg -1 of NaHCO 3 or a placebo (plain flour) in opaque encapsulated pills following an overnight fast. Capillary samples were obtained and analyzed every 15 min for a period of 120 min following ingestion. Significant interactions (p < 0.01), main effects for condition (p < 0.001) and time (p < 0.001) were evident for all acid-base variables (pH, HCO 3 - , BE). Interactions indicated significant elevation in blood alkalosis for only the NaHCO 3 condition when compared to both placebo and EG from 15 to 120 minutes. Conclusions: Despite previous findings of elevated blood pH following acute mineral supplementation, manufacturer recommended doses of EG do not induce any significant changes in acid-base regulation in resting males. Background The practice of mani pulating acid-base balance for pur- poses of improving performance has been on goin g for nearly a century [1]. However, enhancing blood buffer- ing c apacity generally requires high acute loads of alka- line substances (e.g. sodium bicarbonate (NaHCO 3 ), sodium citrate (C 6 H 5 Na 3 O 7 )orsodiumlactate (C 3 H 5 NaO 3 )) that generally place a great deal of stress on the gastrointestinal (GI) system [2]. The prospective negative implications of such a response often push ath- letes away from using these supplements. The potential for manipulating acid-base balance acutely using alterna- tive strategies, such as through the high alkali-forming nature of certain food extracts(fruitandvegetables)in replace of such buffers is warranted, particularly if the claims of improving alkalinity are indeed true [3]. Tradi- tionally, fruit and vegetable extracts have been used to provide the body with additional (or supplemental) vita- mins and minerals to combat excessive renal acid loads often associated with Western Diets. By alkalizing the internal milieu, proponents have claimed this approach improves gastric motility, digestion and vitamin and mineral absorption when compared to the acidic wes- tern diet [3-5]. With specific reference to inducing metabolic alkalosis, these ex tracts generally contain high levels of ions recognized for their alkalinizing proper ties (e.g. citrate which is ultimately metabolized to bicarbo- nate) [5]. However, the extent to which acute or chronic consumption of these extracts influences blood alkali- nity, and ultimately whether or not the relative shift towards metabolic alkalosis substantially alters blood buffering capacity, has not been investigated. Although the acute effects of fruit and vegetable extracts upon blood buffering capacity have not been researched per se, recently König et al. has investigate d the effect of acute multi-mineral supplementation upon both blood and urine pH [3]. These authors indicated a pronounced increase in blood pH three to four hours * Correspondence: J.Siegler@uws.edu.au 3 School of Biomedical and Health Sciences, University of Western Sydney, Penrith, Australia Full list of author information is available at the end of the article 204 A TOT = total concentration of weak acid; CO 2TOT = total concentration of CO 2 ; PaCO 2 = arterial CO 2 tension; PCO 2 = partial CO 2 tension; SBE = standard base excess; SID = strong ion difference. Critical Care April 2005 Vol 9 No 2 Morgan Abstract Stewart’s quantitative physical chemical approach enables us to understand the acid–base properties of intravenous fluids. In Stewart’s analysis, the three independent acid–base variables are partial CO 2 tension, the total concentration of nonvolatile weak acid (A TOT ), and the strong ion difference (SID). Raising and lowering A TOT while holding SID constant cause metabolic acidosis and alkalosis, respectively. Lowering and raising plasma SID while clamping A TOT cause metabolic acidosis and alkalosis, respectively. Fluid infusion causes acid–base effects by forcing extracellular SID and A TOT toward the SID and A TOT of the administered fluid. Thus, fluids with vastly differing pH can have the same acid–base effects. The stimulus is strongest when large volumes are administered, as in correction of hypovolaemia, acute normovolaemic haemodilution, and cardiopulmonary bypass. Zero SID crystalloids such as saline cause a ‘dilutional’ acidosis by lowering extracellular SID enough to overwhelm the metabolic alkalosis of A TOT dilution. A balanced crystalloid must reduce extracellular SID at a rate that precisely counteracts the A TOT dilutional alkalosis. Experimentally, the crystalloid SID required is 24 mEq/l. When organic anions such as L-lactate are added to fluids they can be regarded as weak ions that do not contribute to fluid SID, provided they are metabolized on infusion. With colloids the presence of A TOT is an additional consideration. Albumin and gelatin preparations contain A TOT , whereas starch preparations do not. Hextend is a hetastarch preparation balanced with L-lactate. It reduces or eliminates infusion related metabolic acidosis, may improve gastric mucosal blood flow, and increases survival in experimental endotoxaemia. Stored whole blood has a very high effective SID because of the added preservative. Large volume transfusion thus causes metabolic alkalosis after metabolism of contained citrate, a tendency that is reduced but not eliminated with packed red cells. Thus, Stewart’s approach not only explains fluid induced acid–base phenomena but also provides a framework for the design of fluids for specific acid–base effects. Introduction There is a persistent misconception among critical care personnel that the systemic acid–base properties of a fluid are dictated by its pH. Some even advocate ‘pH-balanced’ fluids, particularly when priming cardiopulmonary bypass pumps [1]. This is not to deny the merit of avoiding very high or very low pH in fluids intended for rapid administration. Extremes of pH can cause thrombophlebitis, and on extravasation tissue necrosis, and rapid administration is a hemolysis risk (specific data on this topic are sparse). However, these effects occur before equilibration. What must be understood is that fluids with widely disparate pH values can have exactly the same systemic acid–base effects. To illustrate, the acid–base properties of ‘pure’ 0.9% saline (pH 7.0 at 25°C) are identical to those of 0.9% saline equilibrated with atmospheric CO 2 (pH 5.6 at 25°C). Until recently, the challenge was to find a logical basis for predicting the acid–base properties of intravenous fluids. In this review important concepts of quantitative physical chemistry are presented, concepts originally set out by the late Peter Stewart [2–5]. They provide the key to understanding fluid induced acid–base phenomena and allow a more informed approach to fluid design. On this background we consider the effects of intravenous fluids on acid–base balance. The Stewart approach in brief There are just three independent variables that, when imposed on the physical chemical milieu of body fluids, dictate their acid–base status. They are strong ion 184 AG = anion gap; [A TOT ] = total concentration of weak acids; BE = base excess; PCO 2 = partial CO 2 difference; SCO 2 = CO 2 solubility; SID + = strong ion difference; SIG = strong ion gap. Critical Care April 2005 Vol 9 No 2 Corey Abstract Complex acid–base disorders arise frequently in critically ill patients, especially in those with multiorgan failure. In order to diagnose and treat these disorders better, some intensivists have abandoned traditional theories in favor of revisionist models of acid–base balance. With claimed superiority over the traditional approach, the new methods have rekindled debate over the fundmental principles of acid–base physiology. In order to shed light on this controversy, we review the derivation and application of new models of acid–base balance. Introduction: Master equations All modern theories of acid–base balance in plasma are predicated upon thermodynamic equilibrium equations. In an equilibrium theory, one enumerates some property of a system (such as electrical charge, proton number, or proton acceptor sites) and then distributes that property among the various species of the system according to the energetics of that particular system. For example, human plasma consists of fully dissociated ions (‘strong ions’ such as Na + , K + , Cl – and lactate), partially dissociated ‘weak’ acids (such as albumin and phosphate), and volatile buffers (carbonate species). C B , the total concentration of proton acceptor sites in solution, is given by C B = C + Σ i C i e – i – D (1) Where C is the total concentration of carbonate species proton acceptor sites (in mmol/l), C i is the concentration of noncarbonate buffer species i (in mmol/l), e – i is the average number of proton acceptor sites per molecule of species i, and D is Ricci’s difference function (D = [H + ] – [OH – ]). Equation 1 may be regarded as a master equation from which all other acid–base formulae may be derived [1]. Assuming that [CO 3 2– ] is small, Eqn 1 may be re-expressed: C B = [HCO 3 – ] + Σ i C i e – i (2) Similarly, the distribution of electrical charge may be expressed as follows: SID + = C – Σ i C i Z – i (3) Where SID + is the ‘strong ion difference’ and Z – i is the average charge per molecule of species i. The solution(s) to these master equations require rigorous mathematical modeling of complex protein structures. Traditionally, the mathematical complexity of master Eqn 2 has been avoided by setting ∆C i = 0, so that ∆C B = ∆[HCO 3 – ]. The study of acid–base balance now becomes appreciably easier, simplifying essentially to the study of volatile buffer equilibria. Stewart equations Stewart, a Canadian physiologist, held that this simplification is not only unnecessary but also potentially misleading [2,3]. In 1981, he proposed a novel theory of acid–base balance based principally on an explicit restatement of master Eqn 3: Bicarbonate ion formation equilibrium: [H + ] × [HCO 3 – ] = K′ 1 × S × PCO 2 (4) Where K′ 1 is the apparent equilibrium constant for the Henderson–Hasselbalch equation and S is the solubility of CO 2 in plasma. Review Bench-to-bedside review: Fundamental principles of acid-base physiology Howard E Corey Director, The Children’s Kidney Center of New Jersey, Atlantic Health System, Morristown, New Jersey, USA Corresponding author: Howard E Corey, howard.corey@ahsys.org Published online: 29 November 2004 Critical Care 2005, 9:184-192 (DOI 10.1186/cc2985) This article is online at http://ccforum.com/content/9/2/184 © 2004 BioMed Central Ltd 185 Available online http://ccforum.com/content/9/2/184 Carbonate ion formation equilibrium: [H + ] × [CO 3 –2 ] = K 3 × [HCO 3 – ] (5) Where K 3 is the apparent equilibrium dissociation constant for bicarbonate. Water dissociation equilibrium: [H + ] × [OH – ] = K′ w (6) Where K′ w is the autoionization constant for water. Electrical charge equation: [SID + ] = [HCO 3 – ] + [A – ] + [CO 3 –2 ] + [OH – ] – [H + ] (7) Where [SID + ] is the difference .. .Disorders of Acid- Base Balance Symptoms of Acidosis and Alkalosis Symptoms of acidosis affect several organ systems Both acidosis and alkalosis can be diagnosed using a blood test Metabolic Acidosis:... lactic acids Diabetic ketoacidosis Increased ketones Strenuous exercise Lactic acid Methanol Formic acid* Paraldehyde β-Hydroxybutyric acid* 2/8 Disorders of Acid- Base Balance Common Causes of Metabolic... Questions Which of the following is a cause of metabolic acidosis? excessive HCl loss increased aldosterone 6/8 Disorders of Acid- Base Balance diarrhea prolonged use of diuretics C Which of the following