emphysema can lead to which acid/base disturbance? what would be the compensation?

• Journal List
• J Biomed Biotechnol
• v.2012; 2012
• PMC3303884

J Biomed Biotechnol. 2012; 2012: 915150.

Acrid-Base Disorders in Patients with Chronic Obstructive Pulmonary Disease: A Pathophysiological Review

Cosimo Marcello Bruno

Section of Internal Medicine and Systemic Diseases, University of Catania, 95100 Catania, Italy

Maria Valenti

Department of Internal Medicine and Systemic Diseases, Academy of Catania, 95100 Catania, Italy

Received 2011 Sep 29; Accepted 2011 Oct 26.

Abstract

The authors describe the pathophysiological mechanisms leading to evolution of acidosis in patients with chronic obstructive pulmonary disease and its deleterious effects on effect and mortality rate. Renal compensatory adjustments consequent to acidosis are also described in detail with accent on differences between acute and chronic respiratory acidosis. Mixed acid-base disturbances due to comorbidity and side effects of some drugs in these patients are likewise examined, and practical considerations for a correct diagnosis are provided.

1. Introduction

Chronic obstructive pulmonary disease (COPD) is a major public wellness trouble. Its prevalence varies co-ordinate to land, age, and sexual activity. On the basis of epidemiologic data, the projection for 2020 indicates that COPD volition be the third leading crusade of death worldwide and the fifth leading cause of disability [ane]. Nearly 15% of COPD patients need admission to full general hospital or intensive respiratory intendance unit for astute exacerbation, leading to greater use of medical resources and increased costs [2–5]. Fifty-fifty though the overall prognosis of COPD patients is lately improved, the bloodshed rate remains high, and, amid others, acid-base disorders occurring in these subjects can impact the issue.

The aim of this paper is to focus on the principal pathogenic mechanisms leading to acid-base of operations disorders and their clinical consequences in COPD patients.

2. Hypercapnia and Respiratory Acidosis

A major complicance in COPD patients is the evolution of stable hypercapnia [6, vii].

In the healthy subject, about 16,000–20,000 mmol/24-hour interval of carbon dioxide (CO_two), derived from oxidation of nutrients containing carbon, are produced. Nether normal weather condition, the production of CO₂ is removed by pulmonary ventilation. However, an alteration in respiratory exchanges, as occurs in advanced stage of COPD, results in retention of CO_two. Carbon dioxide is then hydrated with the formation of carbonic acrid that subsequently dissociates with release of hydrogen ions (H⁺) in the body fluids according to the post-obit equation:

CO₂ + H₂O ⇒ H₂CO₃ ⇒ HCO₃ + H⁺.−

(1)

Thus, the result of hypercapnia due to amending of gas exchange in COPD patients mainly consists in increase of H⁺ concentration and development of respiratory acidosis, also called hypercapnic acidosis [8]. According to the traditional method to assess acid-base status, the Henderson-Hasselbach equation expresses the relationship between pH (logarithm of inverse concentration of H⁺), bicarbonate ion concentration (⁻HCO₃), and fractional force per unit area of CO_ii (pCO₂):

pH = vi.1 + log⁡⁡HCO₃−/0.03pCO₂.

(2)

Information technology is axiomatic that the pH and the concentration of hydrogen ions are strictly adamant by the bicarbonate/pCO₂ ratio, rather than their individual values. A modify in pH can thus be adamant by a primitive alteration of numerator of this equation, that is, bicarbonate (metabolic disorders) or of denominator, that is, pCO_ii (respiratory disorders). In either example, compensatory mechanisms are activated to determine a consensual variation of the other factor to keep this ratio every bit constant as possible and minimize changes in pH. The extent of these compensatory changes are largely dependent on that of the primary amending and can exist to some extent predicted (expected compensatory response) [9].

Consequently, the compensation to respiratory acidosis consists in a secondary increase in bicarbonate concentration, and the arterial blood gas analysis is characterized past a reduced pH, increased pCO₂ (initial variation), and increased bicarbonate levels (compensatory response).

iii. Compensatory Mechanisms in Astute and Chronic Respiratory Acidosis

The response to respiratory acidosis occurs in a dissimilar extent either in acute or chronic phase. When hypercapnia occurs acutely, the buffering of H⁺ takes place by proteins, mainly hemoglobin, and other intracellular nonbicarbonate buffers equally follows:

H₂CO₃   + Hb− ⇒ HHb   + HCO₃.−

(three)

The effectiveness of this machinery is express. In such condition, for every increase of 10 mmHg pCO₂ we wait only 1 mEq increase in bicarbonate concentration [10].

Subsequently, renal adaptive changes occur mainly in the proximal tubular cells than in distal tubules leading to increased bicarbonate reabsorption and increased excretion of titratable acid and ammonium [xi, 12].

H⁺ excretion across apical membrane occurs past a Na⁺/H⁺ antiporter (NHE3) and to a lesser extent past a proton pump (Figure 1). The secreted H⁺ into the tubular fluid combines with filtered bicarbonate ions leading to carbonic acrid formation. The carbonic anhydrase is so split into CO₂ and H₂O. CO₂ diffuses into the prison cell where CO₂ is rehydrated to carbonic acid. This gives ascension to bicarbonate ion that exits from the cell through the basolateral membrane into the interstitium via a 3HCO₃/Na (NBCe1) symporter, while H⁺ is secreted again into the lumen. The basolateral membrane Na⁺/Thou⁺ ATPase antiporter, maintaining a depression intracellular sodium concentration, further enhances the NHE3 activity.

H⁺ secretion and ⁻HCO₃ reabsorption in the tubular cells.

In summary, reabsorption of bicarbonate requires carbonic anhydrase and is strictly associated to natrium reabsorption.

Experimental studies show that total NHE3 and NBCe1 protein abundance are upregulated past chronic respiratory acidosis [13]. Still, the main mechanism responsible for the tiptop in serum bicarbonate is the increased excretion of titratable acid and ammonium [12], which are stimulated past persistently elevated pCO₂.

Ammonia (NH₃), in the proximal cell, is formed by deamination of glutamine to glutamic acrid and then to alpha-ketoglutarate. Therefore, for each molecule of glutamine, two molecules of ammonia are formed (Figure two). Ammonia binds H⁺ resulting in ammonium ion (NH₄⁺) which is afterward secreted into the renal tubular lumen by NHE3, with NH₄⁺ substituting for H⁺ on the transporter, and excreted into the urine as ammonium chloride (NH₄Cl). For alternative, some NH₄⁺ can be secreted into the tubular fluid as NH₃, where information technology is and so protonated. Thus, ammonia replaces bicarbonate ion acting as urinary buffer and binding hydrogen ion. Consequently, for each H⁺ excreted every bit ammonium ion, a "new ⁻HCO₃" is returned to the claret. Nevertheless, a significant reabsorption of NH₄⁺ occurs in the ascending limb of the loop of Henle. In the distal tubule, NH_iv⁺ reabsorbed is subsequently excreted by a NH₄⁺-transporter belonging to Rh glycoproteins family, localized on both apical and basolateral membranes of collecting duct cells [14].

Cellular mechanism for ammoniagenesis and NH₄⁺ secretion. NH₃ tin can exist secreted into the tubular fluid, where it is and so protoned, or it can bind H⁺ within the prison cell, and be secreted equally ammonium ion.

Thus, collecting duct cells plays a pivotal role in maintaining acid-base balance and net acid excretion. If ammonium reabsorbed was not excreted in the urine, information technology would be metabolized by the liver generating H⁺, and a "new ⁻HCO₃" product would exist negated.

Inorganic phosphates, especially in the distal nephron, as well play a function.

H⁺ derived from the breakdown of carbonic acrid are excreted into the tubular lumen where they are buffered past phosphates (ⁱⁱ⁻HPO₄ + H⁺⇒⁻H_twoPO₄), while ⁻HCO_iii crosses the basolateral membrane via an anion exchange (AE) Cl⁻/⁻HCO_three antiporter (Figure 3).

Titration of nonvolatile acids. H⁺ secreted into the tubular fluid combines with phosphate (urinary buffer), and a new ⁻HCO₃ is generated within the cell.

Phosphates so bind hydrogen ions replacing "regenerated" bicarbonate ions. Interestingly, acidemia and hypercapnia reduce the threshold for reabsorption of phosphate, thus making available a larger amount of urinary buffer in the distal tubule [15, xvi].

Pendrin is a bicarbonate/chloride exchanger located in the upmost domain of the type B and non-A, non-B intercalated jail cell of collecting ducts (Figure iv). Hypercapnia determines a reduction of pendrin expression by up to fifty%, contributing to the increased plasma bicarbonate and decreased plasma chloride observed in chronic respiratory acidosis [11, 17].

Pendrin, localized in the cellular apical membrane of cortical collecting ducts and connecting tubules, acts as a Cl⁻/⁻HCO_three exchanger regulating the acid-base status and chloride homeostasis.

The renal response is completed in its total extent after 3–5 days, resulting in a new steady state in which increment of three.v mEq in bicarbonate concentration is expected for every increase of 10 mmHg pCO₂ [xviii, 19]. Then, in the setting of chronic respiratory acidosis, renal compensation offers more significant pH protection in contrast to intracellular buffering in the astute state of affairs.

For instance, if nosotros consider an astute pCO_two increment to eighty mmHg, bicarbonate concentration compensatory increases past 4 mEq.

In understanding to Henderson-Hasselbach equation,

p H = half-dozen.1 +log⁡(28/0.03 × 80) = 7.17.

(4)

Conversely, if we consider a chronic increase of pCO₂ to lxxx mmHg, we could notice a compensatory increase of almost 14 mEq in bicarbonate concentration. Thus,

p H = 6.1 +log⁡(38/0.03 × 80) = 7.29.

(v)

In the last case, the variation in pH value is significantly smaller than in the previous one (0.11 versus 0.23 units). This explains why chronic respiratory acidosis is mostly less severe and better tolerated than acute with like hypercapnia. Effigy 5 shows the different slope of the relationship between pCO_ii and bicarbonate in acute and chronic respiratory acidosis.

Relationship between pCO_two and bicarbonate in acute and chronic respiratory acidosis.

4. Clinical Consequences of Acidosis

Acidosis is an adverse prognostic indicator and is responsible for several deleterious effects on hemodynamics and metabolism [xx–22]. Acidosis causes myocardial depression, arrhythmias, subtract of peripheral vascular resistances, and hypotension. In addition, hypercapnic acidosis is responsible for weakness of respiratory muscles, increment of proinflammatory cytokines and apoptosis, and cachexia. Moreover, in hypercapnic COPD patients a decrease of renal blood flow, an activation of the renin-angiotensin organization, and increase of circulating values of antidiuretic hormone, atrial natriuretic peptide, and endothelin-1 accept been reported [23]. It has been supposed that these hormonal abnormalities tin play a function in retentiveness of salt and water and development of pulmonary hypertension, independently from the presence of myocardial dysfunction.

Clinical and epidemiological information clearly demonstrate that severity of acidosis is associate with poor prognosis.

In the written report of 139 patients with COPD and respiratory failure, Jeffrey et al. [24] concluded that arterial H⁺ concentration is an important prognostic factor for survival.

In a retrospective written report on 295 episodes of COPD exacerbation, Guy et al. [25] reported that intubation and bloodshed rate was highest at the everyman pH grouping. Similarly, Kettel et al. [26] and Warren et al. [27] reported an higher mortality rate in patients with a pH value at access below 7.23 and 7.26, respectively. Plant et al. [28] reported that the more acidemic patients had an higher mortality rate both in group with conventional therapy and in grouping undergone to noninvasive ventilation. Like findings were reported by more than contempo papers [29–31] confirming that a more astringent acidosis worsens the outcome of COPD patients.

Prognosis of COPD patients is also adversely afflicted past comorbidity. Chronic renal failure was found associated with COPD in 22–44% of cases, depending on the study series and diagnostic criteria [32–34]. Renal failure tin contribute to evolution of hypertension, peripheral arterial vascular disease, and onset of ischemic heart disease.

In addition, when renal failure occurs in COPD patients, the compensatory office of kidney in respiratory acidosis may exist less effective, resulting in a reduced ammoniagenesis and titratable acidity product with consequent smaller increase of serum bicarbonate and more astringent acidosis. Clinical reports demonstrated that bicarbonate levels in these patients are inversely related to survival and that concomitant renal failure is predictive of expiry and risk of exacerbation [31, 35, 36].

These previous clinical studies indirectly confirm the role and the importance of kidney part as compensatory organ in acrid-base of operations disorders.

5. Mixed Acid-Base Disorders

Respiratory acidosis is non the only acid-base disturbance observed in patients with COPD. The presence of comorbidity and side effects of some drugs used to care for COPD patients cause different disorders. These conditions are defined as mixed acid-base disorders.

The master clinical conditions leading to a mixed acrid-base disorder are summarized in Tabular array one. Heart failure, acute pulmonary edema, renal failure, and the onset of sepsis or severe hypoxia are, for example, the most mutual causes of metabolic acidosis associated with hypercapnia. An abuse of diuretics with volume depletion, hypokalaemia, and use of steroids are the most normally associated factors with simultaneous presence of metabolic alkalosis.

Table ane

Mixed acid-base of operations disturbances in COPD.

Astute on chronic respiratory acidosis	Respiratory acidosis and metabolic alkalosis
Reexacerbation of COPD	Volume depletion
	Diuretics
	Airsickness
	Severe hypokalemia
	Steroids
	Posthypercapnic alkalosis
Respiratory acidosis and metabolic acidosis	Resp. acidosis, met. acidosis, and met. alkalosis
Astringent hypoxemia
Acute pulmonary edema	Renal failure and vomiting Severe hypoxemia and volume depletion Sepsis and hypokalemia
Renal failure
Sepsis
Daze
Diabetes mellitus
Acute alcoholism
Exogenous poisoning

Metabolic alkalosis may as well be the consequence of a too rapid removal of CO_ii in patients undergoing mechanical ventilation. In these subjects, the kidney is non able to speedily remove the bicarbonate excess after the normalization of CO₂ tension, even though some authors hypothesized that cellular transport processes might have a "memory" of preexisting conditions, and increased bicarbonate reabsorption might persist for some time [13, 37].

Both metabolic acidosis and metabolic alkalosis tin coexist with respiratory acidosis. This clinical setting may occur, for example, in patients with COPD who develop heart failure and are treated with loftier doses of diuretics or who have renal failure and vomiting or astringent hypoxia and extracellular book depletion.

In these cases, fifty-fifty if the final shift of the pH depends on the prevalence of acidogenic or alkalogenic factors, the production and/or removal of both metabolic bases and inorganic acids are altered.

Systematically investigated studies on acid-base of operations disorders in patients with COPD are few, but at that place are evidences that about one-third of these patients have multiple disorders in which the associated respiratory acidosis-metabolic alkalosis is the most oft found disorder [38, 39].

The presence of a mixed acid-base of operations disturbance complicates the clinical pathophysiology and poses difficulties in diagnosis and treatment.

A limitation of the Henderson-Hasselbach method in this clinical setting is the dependence of serum bicarbonate on pCO_two. A variation in the bicarbonate level can be due to a metabolic disorder or tin exist the consequence of an initial variation in pCO₂. In the mixed disorders, the bicarbonate level tin event in a confounding factor considering the contradistinct bicarbonate value, alone, suggests an acid-base imbalance, merely information technology does non distinguish the metabolic component from respiratory component.

Therefore, alternative methods have been proposed to improve quantify the metabolic component in mixed disorders.

Amongst these, standard base of operations excess (SBE), corrected anion gap (cAG), and the Stewart approach are the most frequently utilized [40–43].

SBE can be defined as the amount of potent acid or strong base of operations that must exist added to each liter of fully oxygenated claret to restore the pH to 7.40 at a temperature of 37°C and pCO₂ kept at 40 mmHg and hemoglobin concentration standardized to 5 g/dL. The cAG is the difference betwixt the sum of the main cations and the main anions, corrected for albumin concentration and serum phosphate. Nevertheless, SBE and cAG do non entirely solve the trouble and are been criticized.

SBE is an approach that extrapolates results "in vitro" to the more complex multicompartimental real-life situation of body fluids because, in vivo, acrid or base loads are non only titrated in the claret compartment, and total buffering capacity can exist different from in vitro.

Furthermore, SBE does not resolve the interdependence of pCO₂ and bicarbonate because, in respiratory disorders, the renal compensatory adjustments upshot in changes in SBE.

The cAG should reveal the presence of unmeasured anions in the blood, and it is useful to decide the cause of metabolic acidosis (hyperchloremic rather than normochloremic) once information technology has been diagnosed.

The Stewart approach [43] is based on the principals of conservation of mass, electrical neutrality, and dissociation constant of electrolytes and identified three independent variables determining hydrogen ion concentration in solution: stiff ion departure (SID), pCO₂, and total weak acid (A_tot). Although Stewart method proposes a dissimilar approach, its reliability compared to the traditional method is still a debated question. Some authors [39, 44, 45] consider the diagnostic performance of the Stewart method better than the conventional arroyo to appraise acid-base condition, peculiarly to quantify the metabolic component, only others [46–49] concluded that it does non improve the diagnostic accuracy and does non provide any tool to better manage these disorders because the traditional approach, with just minor adjustments, tin provide the aforementioned applied data.

So when and how to suspect a mixed disorder according to the traditional method?

For this purpose, a stepwise approach has been proposed by several authors [50–53], and some uncomplicated concepts could help in supposing the presence of a mixed disorder.

(ane) Discordant Variation of Bicarbonates and pCO₂ . Compensatory mechanisms are aimed to keep constant bicarbonate/pCO₂ ratio, and a primitive variation of ane of the terms is followed past a consensual variation of the other. Therefore, increase of bicarbonates and decrease of pCO₂ or decrease of bicarbonates and increase of pCO₂ suggest a mixed disorder.

(2) The Presence of Normal pH Value and Significant Alteration in Bicarbonates and pCO₂ Levels As well Suggest a Mixed Disorder. The adaptive mechanisms practice non restore the pH to a normal value. Normal pH, in this instance, argues for the coexistence of two opposing problems rather than a perfectly compensated elementary disorder.

(iii) Compensatory Response Is Significantly Different than Expected Response. Observed bicarbonate levels or pCO₂ significantly unlike than "expected" proves the existence of a mixed disorder. In fact, the amount of compensatory variation depends on the extension of primitive change, and it tin can be reasonably provided. When expected response does not occur, at that place is an condiment disorder responsible for variation of bicarbonate or pCO₂.

(4) Delta Ratio, That Is, Δanion gap/ΔHCO₃ > ii. When a metabolic acid (HA) is added to extracellular fluid, it dissociates in H⁺ and organic anion (⁻A). H⁺ react with a molecule of bicarbonate while unmeasured organic anion (⁻A) volition increment anion gap (positive less negative charges). Theoretically, the variation in the anion gap should exist equal to the decrease in bicarbonate and so that the ratio between these two changes should be equal to one. Still, a significant corporeality of organic acid is buffered past intracellular proteins, not by ⁻HCO₃, while nigh of excess anions remain in the extracellular fluids considering they exercise non freely cantankerous the cellular membrane. Consequently, in a pure metabolic acidosis, the change in bicarbonate concentration is lesser than anion gap, and delta ratio is between i and 2. A delta ratio value higher up 2 indicates a lesser fall in bicarbonate than expected on basis of the alter in anion gap. This finding suggests a concurrent metabolic alkalosis or preexisting high HCO_iii levels due to chronic respiratory acidosis.

In any case, the interpretation of arterial blood gas analysis cannot ignore the findings of clinical history and concrete examination that tin support a correct diagnosis.

Clinicians should also consider the preexisting atmospheric condition, drugs usually taken, symptoms presented in the final days and hours besides equally hydration status of patients, the presence of heart and renal failure, diabetes, hypokalemia, or signs of sepsis.

Therapy of mixed disorders is often difficult. The attempt to correct the pH at all costs with the use of alkaline or acidifying drugs could be harmful, and the clinician'south attention should be paid to place underlying pathophysiological changes.

6. Conclusions

Respiratory acidosis due to hypercapnia is a common and severe complication observed in patients with chronic obstructive pulmonary illness in advanced phase. Evolution of acidosis worsens the prognosis and is associated with college mortality rate. Mechanisms of bounty consist of an increased renal reabsorption of bicarbonate and increased excretion of H⁺. These adjustments of renal function are more than constructive in chronic form and explain why the latter is less severe and better tolerated than acute. Mixed acid-base disorders are as well frequently observed in COPD patients. Clinical history, physical examination, and a careful evaluation of arterial blood gas analysis may assistance in proper diagnosis and targeted therapy.

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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3303884/

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