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Acid-Base DisordersPCCSU Article | 10.01.11

By Deepa Bangalore, MD; and Janice L. Zimmerman, MD, FCCP

Dr. Bangalore is Intensivist and Dr. Zimmerman is Professor of Clinical Medicine and Head, Critical Care Division,Department of Medicine, The Methodist Hospital, Weill Cornell Medical College, Houston, Texas.

Dr. Bangalore and Dr. Zimmerman have disclosed no significant relationships with the companies/organizations whoseproducts or services may be discussed within this chapter.

Objectives

1. Describe different approaches to acid-base analysis and their limitations.

2. Review the diagnosis, manifestations, and management of metabolic acidosis.

3. Discuss less common causes of metabolic acidosis and their management.

4. Review the diagnosis, manifestations and management of metabolic alkalosis and respiratory acid-base disorders.

Key words: anion gap; base deficit; lactic acidosis; metabolic acidosis; metabolic alkalosis; respiratory acidosis;respiratory alkalosis; strong ion difference; strong ion gap

Abbreviations: AG = anion gap; Atot = Total weak acid concentration; BE = base excess; SBE = standard baseexcess; SID = strong ion difference; SIDapp = apparent strong ion difference; SIDeff = effective strong iondifference; SIG = strong ion gap

Acid-base disturbances are common in critically ill and chronically ill patients and result from a variety of underlyingclinical disorders. Although the contribution of acid-base disturbances to morbidity and mortality is not always clear,the appropriate analysis of the abnormalities can offer insight into underlying etiologies and potentially influencetherapeutic interventions.

Acid-Base Analysis

Three methods of analysis have been used to describe the acid-base status of patients: the traditional approach, baseexcess (BE) approach, and the physicochemical approach. All of these methods describe the respiratory component ofacid-base changes based on change in PCO2 but differ in how the metabolic component of acid-base disorders isanalyzed (Table 1).

Table 1—Comparison of Components of Acid-Base Analysis Methods

Acid-Base Disorder Traditional Base Excess Physicochemical

Respiratory acidosis ↑PCO2 ↑PCO2 ↑PCO2

Respiratory alkalosis ↓PCO2 ↓PCO2 ↓PCO2

Metabolic acidosis ↓HCO3-, anion gap ↓Base excess ↓SID, ↑Atot

Metabolic alkalosis ↑HCO3- ↑Base excess ↑SID

The traditional method relies on analysis of changes in bicarbonate concentration and the anion gap to assess themetabolic component. In general, an increased bicarbonate concentration indicates a metabolic alkalosis and adecreased bicarbonate concentration indicates a metabolic acidosis. The relation of pH and bicarbonate concentrationis described by the Henderson-Hasselbalch equation: pH = pK + log HCO3

-/H2CO3 = 6.1 + log HCO3-/0.03 × PCO2.

The Henderson equation shows the interrelation between pH, HCO3- and pCO2: H+ = 24 × PCO2/HCO3

-. The anion gap(AG) is used to classify metabolic acidoses into high AG or normal AG type.

Siggaard and Anderson developed nomograms and algorithms that form the methodology for analyzing acid-basestatus based on BE. Base excess quantifies the degree of metabolic acidosis or alkalosis as the amount of acid or basethat must be added to a sample of whole blood in vitro to restore the pH of the sample to 7.40 while the PCO2 is heldconstant at 40 mm Hg. To correct for inaccuracies when applied in vivo, BE has been modified to standardize theeffect of hemoglobin and PCO2.The standard base excess (SBE) formula is written as follows:

SBE = 0.9287 × (HCO3- – 24.4 + 14.83 × [pH – 7.4]),

where SBE is given in mEq/L.

The SBE changes with any change in weak acid concentrations. A change in base excess describes a change in themetabolic component of acid-base status, with positive BE indicating metabolic alkalosis and negative BE indicatingmetabolic acidosis.

The physicochemical approach, sometimes referred to as Stewart’s approach, identifies three independent variablesthat determine acid-base status: PCO2, strong ion difference (SID), and total nonvolatile weak acids (Atot).1,2 Thesevariables also determine changes in dependent variables, such as pH, HCO3

-, CO32-, OH- and H+. The SID is the



difference between the sum of all strong cation concentrations and the sum of all strong anion concentrations. Allconcentrations must be expressed in mEq/L. The formula for calculating SID (in mEq/L) is as follows:

SID = [Na+ + K+ + Ca2 + Mg2+] – [Cl- + Lactate].

This calculation is also referred to as the apparent SID (SIDapp), taking into account that there are other unmeasuredions in the plasma. Under normal circumstances, the cationic concentration exceeds the anionic concentration so thatplasma SIDapp is approximately +40 to 42 mEq/L. In pathologic conditions, strong anions, such as lactate, formate,sulfates, ketoacids, and fatty acids, may be present in higher concentrations. Plasma proteins, such as albumin (whichcarries a negative charge at physiologic pH), and inorganic phosphates are the main components of Atot, but alsocontribute to SID. According to the physicochemical approach, metabolic acid-base changes result only from changesin SID and/or Atot. SID changes with deficits or excess of water in plasma (associated with changes in Na+

concentrations) and changes in the concentrations of strong anions (such as Cl-). Changes in Atot are primarilyattributable to changes in the concentration of phosphates and albumin.

Effective SID (SIDeff) is an estimate of the anions that balance the excess cations in order to maintainelectroneutrality. SIDeff is derived from PCO2 (from which HCO3

- and CO32- can be estimated) and the concentration

of weak acids (albumin and phosphate), with the following formula, in which albumin is measured in g/L and PO4 inmmol/L:

SIDeff = (12.2 × PCO2/10-pH) + 10 × [Albumin × (0.123 × pH – 0.631)] + [PO4 × (0.309 × pH – 0.469)].

A simplified formula for bedside use has been suggested to approximate SIDeff,1 again with albumin in g/L and PO4 inmmol/L:

SIDeff = HCO3- + 0.28 × Albumin + 1.8 × PO4.

Strong ion gap (SIG) is the difference between the apparent and effective SID (SIG = SIDapp – SIDeff).3 It is ameasure of the balance of anions and cations, similar to the AG. SIG is positive in situations where unmeasuredanions are in excess (acidosis) and negative when unmeasured cations are in excess (alkalosis). “Strong ion gap” is amisnomer as both strong and weak ions may produce a gap. In healthy people, the SIG has a mean value ofapproximately 0 mEq/L.

Attempts to identify which method of acid-base analysis is most correct or most clinically useful have resulted innumerous debates and studies.4-6 Support for each of these methods can be found in the literature. Studies have alsofound that the traditional approach using the AG corrected for albumin concentration was equivalent to thephysicochemical approach for diagnosis of acid-base disorders in ICU patients. In a retrospective study, the SIG wasfound to correlate with the anion gap corrected for all known anions, such as albumin and phosphates.3 Severalstudies have also found high correlations between the SID, BE, and AG. Although the physicochemical approach iscomprehensive in identifying acid-base imbalances, it is cumbersome to use at the bedside. It does allow identificationof the components contributing to metabolic disorders (strong ions, weak acids, or changes in albumin). However, it isnot clear whether identification of subtle acid-base abnormalities by the physiochemical method is of clinicalsignificance. The traditional approach, in which AG corrected for albumin concentration is used, is easy to apply at thebedside but fails to account for the influence of other nonbicarbonate buffers and electrolytes on acid-base status. Thetraditional approach allows diagnosis of the acid-base disorder but does not always identify the mechanism. The BEapproach has the advantage of readily available results from arterial blood gas analysis. However, it cannot be used toidentify coexisting metabolic acidoses and alkaloses, nor does it aid in identifying the etiology of an acid-baseabnormality.

The clinician must be aware of the limitations and advantages of each acid-base approach. The clinician shouldintegrate the analysis of the acid-base status with the patient’s clinical history and additional testing results whendetermining the most appropriate interventions. Analysis of acid-base status in a critically ill patient at a single pointin time provides only a snapshot of a complex and rapidly changing environment.

Metabolic Acidosis

Metabolic acidosis is a common acid-base disorder in critically ill patients that may contribute to acute ventilatory andcirculatory deterioration. Comorbid conditions and therapeutic interventions (eg, fluid resuscitation, diuretics,mechanical ventilation) may both lead to mixed acid-base disorders in these patients. Although metabolic acidosis issuggested by a low bicarbonate level, diagnosis requires a careful analysis of additional factors, such as albuminconcentration, unmeasured anions, and coexisting acid-base disorders.

The traditional method of analysis focuses on the AG to suggest etiologies of metabolic acidoses (see Tables 2 and 3).The AG is usually calculated as [Na+ – (Cl- + HCO3

-)], although calculation including potassium—[(Na+ + K+) – (Cl- +HCO3

-)]—is also used. The normal AG is usually 8 to 12 ± 4 to 6 mEq/L, but the normal range varies with thelaboratory and whether potassium is included in the calculation. The majority of unmeasured anions contributing tothe AG in normal individuals are albumin and phosphate. Decreases in either of these components will decrease theAG and could mask an increase in organic acids, such as lactate. Correcting the AG for changes in albuminconcentration increases the utility of the traditional method in detecting metabolic acidoses.7,8 For every decrease of 1g/dL in albumin, a decrease of 2.5 to 3 mEq in AG occurs. The corrected AG can be calculated as follows, with albumingiven in g/dL:

Corrected AG = Observed AG + 2.5 × (Normal Albumin – Measured Albumin).

Table 2—Causes of Normal Anion Gap (Hyperchloremic) Metabolic Acidosis

GI Loss of HCO3-

Diarrhea

Ileostomy

Ureterosigmoidostomy

Renal Loss of HCO3-

Proximal renal tubular acidosis

Isolated



Fanconi syndrome Familial

Cystinosis

Tyrosinemia

Multiple myeloma

Wilson disease

Ifosfamide

Osteopetrosis

Carbonic anhydrase inhibitors

Ileal bladder

Reduced Renal H+ Secretion

Distal renal tubular acidosis (classic type I)

Familial

Hypercalcemic/hypercalciuric states

Sjögren syndrome

Autoimmune disease

Amphotericin

Renal transplant

Type 4 renal tubular acidosis

Hyporeninemic hypoaldosteronism

Tubulointerstitial disease

Nonsteroidal antiinflammatory drugs

Defective mineralocorticoid synthesis/secretion

Addison disease

Acquired adrenal enzymatic defects (chronic heparin therapy)

Congenital adrenal enzymatic defects

Inadequate renal response to mineralocorticoid

Sickle cell disease

Systemic lupus

Potassium-sparing diuretic

Pseudohypoaldosteronism (type 1 and 2)

Early uremia

HCl/HCl Precursor Ingestion/Infusion

HCl

NH4Cl

Arginine Cl

Other

Recovery from sustained hypocapnia

Treatment of diabetic ketoacidosis

Toluene inhalation with good renal function

Table 3—Causes of an Increased Anion Gap and Strong Ion Gap

Renal failure

Ketoacidoses

Diabetic ketoacidosis

Alcoholic ketoacidosis

Starvation

Metabolic errors

Lactic acidoses

L-lactic acidosis

D-lactic acidosis

Toxins

Acetaminophen

Cyanide

Ethylene glycol



Iron Isoniazid

Metformin

Methanol

Paraldehyde

Propofol

Propylene glycol

Salicylates

Toluene

Valproic acid

Dehydration

Sodium salts

Sodium lactate*

Sodium citrate

Sodium acetate

Sodium penicillin ( >50 mU/d)

Decreased unmeasured cations

Hypomagnesemia*

Hypocalcemia*

Alkalemia

*Already accounted for in SIG.

Corrections for changes in phosphate concentration have less impact on the AG. Every decrease of 1 mg/dL inphosphate leads to a decrease of 0.5 mEq in AG. Pathologic paraproteinemias also decrease the AG becauseimmunoglobulins (IgG) are largely cationic. Conversely, an elevated AG does not always reflect an underlyingacidosis. In patients with significant alkalemia (usually pH >7.5), albumin is more negatively charged, which increasesunmeasured anions in the absence of an acidosis. The respiratory compensation for metabolic acidosis (an increase inminute ventilation) can be estimated by either of the following formulas, both with PCO2 expressed in mm Hg: PCO2 =1.5 × HCO3

- + 8 ± 2 or PCO2 = 1.2 × ΔHCO3-.

The delta gap (Δgap) is a concept used to identify additional acid-base disorders when a metabolic acidosis is present.It is based on the assumption that every increase of 1 mEq/L in the AG will result in a similar decrease in the HCO3

-

concentration. The calculation is expressed as follows: Δgap = (deviation of the AG from normal) – (deviation ofHCO3

- concentration from normal). Although the expected normal value is zero, small deviations may not besignificant and must always be interpreted along with clinical information. A positive Δgap suggests the concomitantpresence of a metabolic alkalosis and a negative value suggests the presence of a hyperchloremic normal AG acidosis.

The physicochemical approach suggests a different approach to classifying metabolic acidoses (Table 4): free waterexcess, increase in strong anions (hyperchloremia), and increase in weak acids. When a change in extracellular fluidvolume is accompanied by an alteration in the proportional water content of the plasma, there is a reduction in SIDthat leads to acidosis. Hyperchloremia leads to a reduction in the SID and a consequent decrease in pH. Thephysicochemical approach to acid-base analysis suggests that the acidosis seen in fluid-resuscitated patients is aresult of the chloride concentration changes rather than dilution of the bicarbonate concentration. Following normalsaline infusion, the plasma Cl- concentration increases to a greater extent than Na+ concentration. Aggressive fluidinfusion can also result in dilution of total weak acids (Atot), and this could give rise to a concomitant metabolicalkalosis.

Table 4—Primary Metabolic Acid-Base Disturbances Described by the Physicochemical Approach

Acidosis Alkalosis

Water deficit/excess ↓Na+,↓SID (dilution acidosis) ↑Na+, ↑SID (concentration alkalosis)

Change in strong anions ↑Cl-, ↓SID ↓Cl-, ↑SID

↑Unmeasured acid, ↓SID —

Change in weak acids ↑Albumin, ↑phosphate, ↑Atot, ↓SID ↓Albumin, ↓phosphate, ↓Atot, ↑SID

Crystalloids with a SID of zero, such as saline solution, cause an acidosis by lowering extracellular SID enough tooverwhelm the metabolic alkalosis of Atot dilution.

When infusions containing organic anions such as L-lactate are administered, L-lactate can be regarded as a weak ionthat does not contribute to fluid SID, provided it is readily metabolized. The presence of weak acids contributing toAtot must be considered with administration of colloids. Albumin and gelatin preparations contain weak acids, whereasstarch preparations do not. The SID and presence of weak acids in fluid options may affect the choice of fluidreplacement therapy for specific acid-base effects.

Specific AcidosesLactic Acidosis: Two types of lactic acidosis exist: type A and type B. Type A lactic acidosis is usually present incritically ill patients and results from overproduction of L-lactate through anaerobic glucose metabolism as a result ofinadequate tissue oxygen delivery.9 L-lactate often accounts for the unmeasured anion detected by an increased aniongap. Type B lactic acidosis is associated with adequate oxygen delivery and is being recognized more frequently. Type



B lactic acidosis results from altered cell metabolism (usually mitochondrial function), increased aerobic metabolism orglucose production with enhanced pyruvate production, or inhibition of cytochrome oxidase. β-Agonists, includingepinephrine and dobutamine, stimulate glycolysis with production of excess pyruvic acid that may not be clearedowing to inhibition of pyruvate dehydrogenase. Excess pyruvic acid is converted to lactate. Several drugs can alsoresult in elevated lactate levels without evidence of hypoperfusion (Table 5). In addition, type B lactic acidosis can beassociated with certain malignancies, such as lymphomas and leukemias. It is important to recognize the presenceand etiology of type B lactic acidoses in order to distinguish them from the more clinically ominous type A lacticacidosis. In some cases, specific medications may need to be discontinued because the lactate level suggests toxicity.

Table 5—Drugs and Conditions Associated With Type B Lactic Acidosis

Dobutamine

Epinephrine

Etomidate

Linezolid

Lorazepam

Metformin

Nucleoside reverse transcriptase inhibitors

Pentobarbital

Propofol

Tetracyclines

Thiamine deficiency

Valproic acid

D-lactic Acidosis: D-lactic acidosis can result from overgrowth of D-lactate-producing bacteria, such as Lactobacillusspecies, Streptococcus bovis, Bifidobacterium species, and Eubacterium species in patients with anatomic(ileojejunal bypass) or functional short bowel syndrome (malabsorption).10 D-lactate is not measured by laboratoryassays but does contribute to the AG as an unmeasured anion. Symptoms can be precipitated after ingestion ofcarbohydrates with absorption of D-lactate from the affected intestinal segment, but can also occur after consumptionof dairy products or lactobacillus tablets. Symptoms of D-lactic acidosis include transient neurologic findings, such asheadache, weakness, delirium, visual disturbances, dysarthria, ataxia, cranial nerve palsies, and changes in affect.

Pyroglutamic Acidosis: Pyroglutamic acid is recognized as another etiology of anion gap metabolic acidosis, especiallyin association with acetaminophen use.11,12 Pyroglutamic acid (5-oxoproline) can be overproduced when glutathioneis depleted (associated with acetaminophen use, sepsis, liver dysfunction, and malnutrition) through effects on the γ-glutamyl cycle, resulting in increased production of γ-glutamylcysteine, which is converted to pyroglutamic acid.Additionally, inhibition of 5-oxoprolinase (associated with penicillins and vigabatrin) can lead to pyroglutamic acidosis.The dose of acetaminophen associated with pyroglutamic acidosis has been variable but acidosis resolves withdiscontinuation of acetaminophen. Repletion of glutathione stores with N -acetylcysteine has been suggested despitethe lack of evidence.

Hospital-Acquired Acidoses: Some drugs used in critically ill patients can lead to anion gap metabolic acidoses thatare important to recognize. Propylene glycol is a solvent found in IV formulations of lorazepam, diazepam, etomidate,phenytoin, nitroglycerin, esmolol, phenobarbital, pentobarbital, and other drugs. The greatest risk for causing acidosisoccurs with the use of high-dose lorazepam for more than 3 days.13 However, toxicity has also been reported withshort-term high-dose use. Lorazepam contains 830 mg/mL of propylene glycol and accumulation occurs with doses>0.1 mg/kg/h or in the presence of hepatic or renal dysfunction. Signs and symptoms correlate with an increasedosmolar gap. The clinical manifestations of propylene glycol toxicity can mimic sepsis and other inflammatorydisorders. These manifestations include CNS depression or agitation, renal dysfunction, seizures, arrhythmias, andhemolysis. Management includes discontinuation of lorazepam and substitution of another sedating drug.

Propofol infusion syndrome is typically seen in pediatric patients but is being reported more frequently in the adultpopulation.14 Acidosis results from lactate production. The exact etiology is unknown but may be related tomitochondrial utilization of free fatty acids or a genetic predisposition. Reported risk factors include dose, duration ofuse, age, sepsis, head injury, steroid use and catecholamine infusion. Experience is variable but the syndrome isusually associated with doses >4 µg/kg/h and durations longer than 48 h. Manifestations can include arrhythmias,heart failure, rhabdomyolysis, hyperkalemia, acute renal failure, bradycardia, and hyperlipemia. An increased need forinotropic support in a patient receiving propofol with no other clear etiology can be a clue to propofol infusionsyndrome.

Clinical Manifestations and Management of Metabolic AcidosisThe predominant clinical manifestations of metabolic acidosis may be difficult to distinguish from manifestations of theunderlying disorder. Metabolic acidosis results in increased cerebral blood flow but mental status is often decreased.Pulmonary effects include an increase in minute ventilation, respiratory failure, pulmonary edema, and increasedpulmonary vascular resistance. Cardiovascular effects may include arrhythmias and a decrease in myocardial functionor response to catecholamines. Acute acidemia enhances oxygen unloading from hemoglobin by shifting theoxyhemoglobin dissociation curve to the right. However, if acidosis persists, it causes the red blood cell concentrationof 2,3-diphosphoglycerate to fall and restores the oxyhemoglobin dissociation curve to baseline. Other metaboliceffects of metabolic acidosis include hyperkalemia, hypercalcemia, insulin resistance, and increased proteincatabolism. Chronic metabolic acidosis can lead to development of osteoporosis, osteomalacia, renal osteodystrophy,renal hypertrophy, nephrocalcinosis, and nephrolithiasis.

Treatment of metabolic acidosis requires identification of the underlying etiology. Treatment of normal AG metabolicacidoses (hyperchloremic) involves replacing volume with a low-chloride, bicarbonate-containing fluid. Otherinterventions may include insulin for diabetic ketoacidosis, antidote for poisonings, renal replacement therapy foracute kidney injury, and restoration of oxygen delivery in hypoperfusion states. Administration of bicarbonate doesnot improve outcome in metabolic acidosis. Some studies suggest that bicarbonate may improve myocardialresponsiveness when the pH is <7.1 and the patient has severe hemodynamic instability. However, myocardialperformance is often normal in metabolic acidosis.



Metabolic Alkalosis

Metabolic alkalosis is diagnosed by findings of increased pH with an increased bicarbonate concentration using thetraditional method. In the physicochemical approach, the bicarbonate change is seen as the effect rather than thecause. An increase in the SID resulting from a decrease in Cl- or water deficit with increase in Na+ can result in ametabolic alkalosis (Table 4). Hypoalbuminemia is another cause of metabolic alkalosis detected by physicochemicalanalysis that may be missed by other approaches. Hypophosphatemia alone does not cause enough change in Atot toresult in metabolic alkalosis because the normal value of phosphate is only about 1 mmol/L.

Etiologies of metabolic alkalosis can be characterized as chloride depleted (hypovolemic) or chloride expanded(hypervolemic; Table 6). Urine chloride <20 mEq/L can be used to distinguish chloride-depleted causes of metabolicalkalosis. Hypokalemia is common to all causes of metabolic alkalosis.

Table 6—Etiologies of Metabolic Alkalosis

Hypovolemic, chloride depleted

GI loss of H+

Vomiting

Gastric suction

Cl− rich diarrhea

Villous adenoma

Renal loss of H+

Diuretics

Posthypercapnia

Hypervolemic, chloride expanded

Renal loss of H+

Primary hyperaldosteronism

Primary hypercortisolism

Adrenocorticotropic hormone excess

Pharmacologic hydrocortisone/mineralocorticoid excess

Renal artery stenosis with right ventricular hypertension

Renin-secreting tumor

Hypokalemia

Bicarbonate overdose

Pharmacologic overdose of NaHCO3

Milk-alkali syndrome

Massive blood transfusion

Reprinted with permission from Zimmerman.15

Clinical Manifestations and Management of Metabolic AlkalosisClinical manifestations of metabolic alkalosis include tachycardia, arteriolar constriction including the coronaryarteries, supraventricular and ventricular arrhythmias, hypoventilation, decreased cerebral blood flow, altered mentalstatus, and seizures. Metabolic effects include stimulation of anaerobic glycolysis, hypokalemia, hypomagnesemia,hypophosphatemia, and decreased ionized calcium concentrations. Oxygen release at the tissue level may be impairedin metabolic alkalosis because a leftward shift in the oxyhemoglobin dissociation curve decreases hemoglobin’s oxygenaffinity.

Treatment involves identifying the cause and correcting it, if possible. Volume replacement with chloride-containingfluid is indicated for etiologies associated with chloride depletion. It is important to correct metabolic alkalosis beforeventilator weaning in an intubated patient as this acid-base disorder causes compensatory hypoventilation. Potassiumdeficiencies should be corrected. It is rarely necessary to administer hydrochloric acid to correct severe metabolicalkalosis. Deliberate hypoventilation with sedation in intubated patients may be an option for severe conditions.Although acetazolamide will increase excretion of bicarbonate, efficacy is limited and administration can result inmetabolic acidosis and exacerbate potassium losses.

Respiratory Disorders

Increases and decreases of PaCO2 indicate respiratory acidosis and respiratory alkalosis, respectively. The clinicalmanifestations of respiratory disorders depend on the absolute change and the rate of change in PaCO2, the underlyingetiology (Tables 7 and 8), and the presence of hypoxemia. Evaluation of the respiratory component of acid-baseabnormalities is the same for all three methods of acid-base analysis. Formulas for changes in PaCO2 arising fromacute and chronic respiratory disorders allow prediction of pH and bicarbonate concentration. These formulas are lesshelpful when chronic and acute respiratory conditions are present simultaneously.

Table 7—Etiologies of Respiratory Acidosis

Airway obstruction

Foreign body

Tongue displacement

Laryngospasm

Obstructed endotracheal tube



Severe bronchospasm Obstructive sleep apnea

Respiratory center depression

General anesthesia

Sedative or narcotic drugs

Cerebral injury, ischemia

Increased CO2 production

Malignant hyperthermia

Shivering

Hypermetabolism

High-carbohydrate diet

Neuromuscular disorders

Drugs or toxins

Electrolyte disorders

Spinal cord injury

Guillain-Barré syndrome

Myasthenia gravis

Polymyositis

Lung conditions

Restrictive disease

Obstructive disease

Hemothorax or pneumothorax

Flail chest

Acute lung injury

Obesity-hypoventilation syndrome

Inappropriate ventilator settings


Table 8—Etiologies of Respiratory Alkalosis

Hypoxemic drive

Pulmonary disease with arterial-alveolar gradient

Cardiac disease with right-to-left shunt

Cardiac disease with pulmonary edema

High altitude

Acute and chronic pulmonary disease

Emphysema

Pulmonary embolism

Pulmonary edema

Mechanical overventilation

Stimulation of respiratory center

Neurologic disorders

Pain

Psychogenic

Liver failure with encephalopathy

Sepsis/infection

Salicylates

Progesterone

Pregnancy

Fever


In acute respiratory acidosis, the following formulas apply:

Decrease in pH = 0.08 × (PaCO2 – 40)/10, andIncrease in [HCO3

-] = ΔPaCO2/10 ± 3.



The formulas for chronic respiratory acidosis are as follows:

Decrease in pH = 0.03 × (PaCO2 – 40)/10, andIncrease in [HCO3

-] = 3.5 × ΔPaCO2/10.

For acute respiratory alkalosis, use the following formulas:

Increase in pH = 0.08 × (40 – PaCO2)/10, andDecrease in [HCO3

-] = 2 × ΔPaCO2/10.

For chronic respiratory alkalosis, these are the formulas:

Increase in pH = 0.03 × (40 – PaCO2)/10, andDecrease in [HCO3

-] = (5 to 7) × ΔPaCO2/10.

Clinical Manifestations and Management of Respiratory AcidosisRespiratory acidosis can result in somnolence, confusion, combativeness, delusions, stupor, and coma. Cerebralvasodilation can also increase cerebral blood flow and intracranial pressures. Cardiovascular manifestations includetachycardia, hypertension, depressed myocardial contractility, peripheral vasodilation, and arrhythmias. Severehypercapnia causes renovascular constriction and hypoperfusion via the renin-angiotensin axis. Hypercapnia alsostimulates antidiuretic hormone secretion, resulting in increased salt and water retention. There is a complex interplayof PaCO2 and pH on the oxyhemoglobin dissociation curve as CO2 shifts it to the right (Bohr effect) and acidemia shiftsthe curve to the left. This effect is further complicated by increased 2,3-diphosphoglycerate concentrations in chronicrespiratory acidosis.

The treatment of respiratory acidosis is to provide ventilation, which may necessitate intubation and mechanicalventilation in some patients. Bicarbonate administration offers no benefit and generates additional CO2 for elimination.

Clinical Manifestations and Management of Respiratory AlkalosisAcute respiratory alkalosis (hyperventilation) can cause circumoral numbness, paresthesias, muscle cramps,carpopedal spasms, and seizures. Low PaCO2 causes cerebral vasoconstriction with the potential for hypoperfusion, anincrease in plasma catecholamines, tachycardia, and arrhythmias (especially with pH >7.6). Metabolic changes includehypokalemia, hypophosphatemia, and ionized hypocalcemia.

Management of significant respiratory alkalosis involves treating the underlying condition (ie, supplying oxygen,analgesic administration, adjusting ventilator settings). In some circumstances, sedation may be needed to controlsevere respiratory alkalosis.

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