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of the diaphragm crosses the psoas muscles medially, forming the medial arcuate ligaments, and the quadratus lumborum muscles laterally, forming the lateral arcuate ligaments. The skeletal attachments of the lateral arcuate ligaments are the first lumbar transverse process and the midpoint of the 12th rib. The costal origins include the lower six ribs and costal cartilages, the fibres of the diaphragm interdigitating with those of transversus abdominis. The small sternal attachment comprises two muscle slips running from the back of the xiphoid process. The superior epigastric vessels run between the sternal and costal attachments; congenital herniation may occur here. The superior surface of the diaphragm is covered by pleura overlying endothoracic fascia, except where the central tendon is fused to the pericardium. The inferior surface is covered by peritoneum overlying transversalis fascia, except over the bare area of the liver and over the posterosuperior surfaces of the kidneys and suprarenal glands. In these areas the viscera lie in direct contact with the diaphragm. Structures that pass through or behind the diaphragm cross three major openings and a number of minor ones. The aortic opening, between the vertebral column and the median arcuate ligament at the level of T12, conveys the aorta, azygos vein and thoracic duct. The cisterna chyli lies behind the right crus. The oesophageal opening at the level of T10, to the left of the midline but within a loop of right crural fibres, conveys the oesophagus, branches of the left gastric vessels, and the two vagal trunks, together with a conical extension of the transversalis fascia attached to the oesophagus above the diaphragm (the phrenooesophageal ligament). Here, in the lower oesophagus, venous tributaries of the left gastric (portal) vein communicate with those of the azygos (caval). The vena caval opening is in the central tendon to the right of the midline at the level of T8, and conveys the inferior vena cava (attached to the margins of the opening) and the right phrenic nerve. The crura are pierced by the greater and lesser splanchnic nerves and by the hemiazygos vein, while the sympathetic trunks pass behind the medial and the subcostal nerves behind the lateral arcuate ligaments. The left phrenic nerve pierces the diaphragm just anterior to the central tendon. The motor nerve supply to the diaphragm is exclusively from the phrenic nerves (C3, 4, 5), which branch as they pass through the diaphragm. The line of rightleft demarcation passes through the oesophageal opening. Sensory supply to the central part of the diaphragm comes from the phrenic nerves, while the peri-phery is supplied by the lower six intercostal nerves. Blood supply comes from the intercostal, superior and inferior phrenic branches of the aorta, and anteriorly from branches of the internal thoracic artery. Hernia of abdominal contents through the diaphragm may occasionally be congenital, through defects mentioned above, but is much more commonly acquired and usually occurs through the oesophageal opening (hiatus). Traumatic hernia may also occur, where the diaphragm is torn in closed crush injuries of the trunk. u

AcidBase Balance and Arterial Blood Gas Analysis


Simon Fletcher A Dhrampal

An understanding of normal acidbase physiology, and accurate interpretation of arterial blood gas (ABG) measurements, is important for diagnosis and guiding appropriate therapy of acidbase disorders. Background Soren (1909) introduced the pH scale (pH = log10 1/[H+]), as a measure of hydrogen ion activity. A change of one pH unit represents a 10-fold change in hydrogen ion concentration. Henderson (1909) applied the Law of Mass Action to the equilibrium reaction for carbonic acid (CO2 + H2O H2CO3 H+ + HCO3 ), giving the Henderson equation: [H+] = K1 x [H2CO3]/[HCO3 ] where K1 = dissociation constant By substituting [CO2] for [H2CO3], a further equation reads: [H+] = K2 x [CO2]/[HCO3 ] Hasselbach (1916) logarithmically rearranged the above equation and introduced the partial pressure of carbon dioxide (PCO2) for [CO2] to yield the HendersonHasselbach (HH) equation. pH = pK + log10 [HCO3 ]/PCO2 x 0.23 (where 0.23 is the CO2 solubility coefficient) pH is easier to understand in this context, as the concentration of hydrogen ions is very small (normal [H+] = 40 nanomol/l). The poliomyelitis epidemic in continental Europe in the early 1950s heralded the practice of intensive care. For the first time large numbers of patients required artificial ventilation for extended periods. It was apparent that the partial pressure of CO2 in arterial blood (PaCO2) should inform this therapy. HCO3 and pH were measured, and PaCO2 derived using the HH equation, a protracted and inaccurate process. Astrup (1960) demonstrated a linear relationship between pH and log10PCO2. By measuring the pH of a blood sample, and remeasuring pH after equilibration with two different CO2 mixtures, the PCO2of the patient could be interpolated.

Simon Fletcher is a Consultant in Anaesthesia and Intensive Care at the Norfolk and Norwich Hospital, Norwich, UK. A Dhrampal is Specialist Registrar in Anaesthetics at the Norfolk and Norwich Hospital, Norwich, UK.

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Stewart model The HH concept of acid/base balance is an oversimplification. The calculation assumes that PCO2 and HCO3 are independent variables, but they are in dynamic equilibrium. In biological solutions, many chemical equilibria interact to determine the pH of the solution, governed by basic physicochemical laws, such as that of mass action and electrical neutrality. Stewart developed a modelling tool for predicting pH, and demonstrated that it is determined by 3 independent variables: PCO2, weak acid concentration and strong ion difference. The weak acids are principally phosphates and plasma proteins (mainly albumin). Strong ions are those fully dissociated in biological solution. The relevant cations are Na+, K+, Mg2+ and Ca2+, the anions Cl and lactate. Bicarbonate is not a strong ion and therefore not an independent variable. Fundamental concepts Acidosis is the accumulation of excess acid, whether arising from metabolic (and pathological) processes or through respiration insufficiency. If this accumulation is unopposed by compensatory changes, the pH will fall and lead to acidaemia (pH <7.35). An acid is a substance which dissociates to produce H+. A strong acid will dissociate completely, and a weak acid will dissociate partially. A base is a substance that will accept H+ ions. An alkali dissociates to produce hydroxyl (OH ) ions. A buffering system consists of acid or alkali which, at physiological pH, is present in both its associated and ionized form. Thus, considering the carbonic acid/bicarbonate system: H2CO3 Weak acid HCO3 Conjugate base + H+

Other important extracellular buffers include proteins (albumin) and phosphate: H-protein protein + H+ H2PO4 HPO42 + H+ The important intracellular systems are proteins and phosphate. Haemoglobin (Hb), which is abundant, is pivotal, especially in the transport of the volatile acid load. A synopsis of the elimination of CO2 is given in Figure 1. Figure 2 summarizes the interdependent roles of the kidney and liver in the regulation of acidbase balance. Measurement and analysis of ABGs Many modern devices also automatically measure single ion concentrations (Na+, K+, Cl , Ca2+) as well as lactate, glucose and Hb concentration. While the measurements are now routine, the information obtained should never be interpreted in isolation, since it constitutes just one part of the assessment process, and is not a substitute for history-taking and physical examination. Measured and derived variables Figure 3 depicts a typical reading from a ABG analyser. The parameters displayed are often customized to local requirements: many others are omitted, e.g. only standard bicarbonate and base excess (see below) are shown in Figure 3. When interpreting an ABG result, consider the following: The analyser must be calibrated regularly. Use lightly heparinized blood samples to prevent costly blockage of the microcapillary tubes in an analyser. Excess heparin may give an erroneously low pH. Individuals should be trained on ABG analyser usage. Avoid undue delay before analysis, as RBCs continue to metabolize in the interim. Avoid excessive exposure of the sample to air. Note the fractional concentration of O2 in inspired gas (FIO2) and temperature of the patient, and enter into the analyser. Excluding the add onsthose parameters not strictly part of the analyzeronly 4 parameters (glucose, lactate, H+, Na+ etc) are directly measured. These are described below. Electrodes pO2, pH and pCO2 have specific electrodes, the principles of which have changed little since first description. The Clark electrode measures pO2 and is polarographic. A voltage is applied across the 2 electrodes, the induced current being directly related to the pO2. The pH electrode consists of two half-cells. A stable reference

Buffering systems act within seconds to minimize changes in pH. Thus, if a strong acid (one that is completely dissociated at physiological pH) is added, the system moves to the left, removing H+ ions. A strong alkali has the opposite effect. A buffering system works most effectively if the pH is near its pK value. Normal metabolic processes release about 100 mmol H+/day from cells and both organic and inorganic acids are generated. CO2 is also produced in these metabolic processes, which combines with H2O (when catalysed by carbonic anhydrase) to form carbonic acid. The potential daily H+ load from this source is >12,000 mmol. Enzymatic (and therefore, cellular) function depends on a closely regulated pH between 7.35 and 7.45 in the extracellular fluid, and 7.0 to 7.3 intracellularly. Normal homeostatic mechanisms (which include buffering and excretion) respond to the continuously fluctuating H+ output to maintain pH within these limits. The lungs, red blood cells (RBCs), kidney, liver and gastrointestinal tract are all active in this respect. However, many pathological processes can lead to a deranged acidbase status. Physiological buffers The bicarbonate system has a pK of 6.1 and is quantitatively the most important extracellular buffer, accounting for 60% of body total.

CO2 elimination
Carried in blood and evolved in lungs Present in 3 forms in the blood: bicarbonate (90%), dissolved (5%), complexed with protein (carbamino compounds) (5%) Haemoglobin main buffer for carbonic acid, deoxygenated Hb (venous blood) also has higher affinity for CO2 (carbamino group). Known as Haldane effect Ventilation responds to increased CO2 production (exercise) and metabolic changes in pH 1

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The role of the kidney and liver in the regulation of acidbase balance
The role of the kidney Recycles filtered bicarbonate load (massive) Regenerates lost bicarbonate (main buffer for non-volatile acids) Recycling depends on complex, adenosine triphosphate (ATP)-driven, Na+/H+ exchange Secreted H+ reacts with HCO3 CO2 produced diffuses into luminal cells where HCO3 is regenerated NaHCO3 reabsorbed into blood H+ elimination depends on urinary buffers Phosphate and bicarbonate have a small contribution Ammonia is crucial: Glutamine metabolized in tubular cells to yield NH4+ and HCO3 HCO3 reabsorbed, therefore regenerating that lost in buffering non-volatile acid NH4+ (balanced with Cl ) is ultimately excreted The role of the liver Converts ammonium bicarbonate to urea (no positive bicarbonate balance) This process both up- and down-regulates, depending on acidbase status 2

Specimen blood gas report


PATIENT REPORT Identifications Patient ID Operator Sample type Inspired O2 fraction as percentage (FIO2 ) Temperature Arterial blood gas values pH Concentration of H+ in blood (cH+) Partial pressure of CO2 (PaCO2) Partial pressure of O2 (PaO2) Oximetry values Concentration of haemoglobin (ctHb) Oxygen saturation (sO2) Electrolyte values Concentration of K+ (cK+) Concentration of Na+ (cNa+) Metabolite values Concentration of glucose (cGlu) Concentration of lactate (cLac) Temperature-corrected values pH (T)c cH+(T) c pCO2(T) c pO2(T) c Oxygen status Oxygen content (ctO2) Partial pressure O2 when 50% saturated (p50c) Acidbase status Standard base excess (cBase(Ecf)) Standard bicarbonate (cHCO3-(P,st)) 3

Arterial 21.0% 37.1C

7.364 43.3 nmol/l 5.70 kPa 12.9 kPa 9.4 g/dl 99.2% 5.0 mmol/l 137 mmol/l 7.6 mmol/l 0.8 mmol/l 7.362 43.4 nmol/l 5.72 kPa 13.0 kPa 13.0 vol % 3.62 kPa -0.9 mmol/l 23.6 mmol/l

electrode is connected to the pH electrode, the induced voltage being proportional to the [H+]. The pH electrode separates a buffered solution and the sample with a pH-sensitive glass membrane. The potential difference across this membrane is measured. The Severinghaus electrode measures pCO2 directly. CO2 diffuses across a membrane and thence a chemical reaction releases H+ ions. [H+] is measured by a modified pH electrode. Most devices also contain a co-oximeter, which measures the proportion of each of four Hb moieties present in the sample: oxygenated, reduced, carboxy- and methaemaglobin. Derived measurements Much of the data produced by these analysers is mathematically derived from the directly measured parameters using equations integrated within their microprocessors. Only those relating to acidbase changes will be considered. Serum bicarbonate is normally 24 mmol/l and is derived from the HH equation, and is the actual concentration in the sample. As this is a variable of both the pCO2 and non-volatile acid production, various methods are described to attempt to clarify their relative contributions. Standard bicarbonate is the [HCO3 ] of the sample when in equilibrium with a gas mixture containing pCO2 5.3kPa (38.7 mmHg) and pO2 13.3 kPa (97.2 mmHg) at 37C. The normal value is around 24 mmol/l. A value <24 mmol/l indicates metabolic acidosis and vice versa. The same concept can be applied to pH.

Base excess is the concentration (mmol/l) of strong acid or base required to return a sample of whole blood, at 37C and with pCO2 5.3 kPa (38.7 mmHg) to a pH of 7.4. Base excess was originally calculated using nomograms derived from volunteer studies, but this has been replaced by the Van Slyke equation, derived from theoretical concepts, but validated for in vitro calculations, over a wide range of actual pCO2. Base excess is a positive figure, indicating metabolic alkalosis, while base deficit is negative and indicative of acidosis (normal range -2 to +2). Standard base excess is a calculation attempting to convert the in vitro to an in vivo measurement and may be more representative. Interpretation of acidbase status While not perfect (for reasons discussed earlier), the use of indices derived from the HH approach to the carbon dioxidecarbonic acidbicarbonate relationship to analyse acidbase disturbances works relatively well in most clinical circumstances. Other helpful indices include the anion gap, serum lactate, ketones, blood sugar and assessment of renal function. The Stewart approach

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is useful in interpretation of more complex derangements, particularly in the presence of a metabolic acidosis. One should tackle the problem in a systematic way, starting with the blood gases. These should be checked for: date and time of analysis patient identification a user-entered FIO2 a user-entered patient temperature. It is relatively common practice to correct the meaured blood gases for patient temperature and use these corrected values in any assessment. There is no evidence to support this practice. We recommend ignoring temperature-corrected variables. Whatever the underlying causes, there are only 4 basic acid base disturbances. These are respiratory acidosis and alkalosis, and metabolic acidosis and alkalosis (see later). The actual picture may conceal an acute or chronic problem, a combination of two pathological processes or frequently a primary derangement partially or completely compensated for by the other system. For instance, a metabolic acidosis may be compensated by respiratory alkalosis although, as this compensation is not a pathological process, it should not be termed an alkalosis. Continuing the systematic approach to analysis, the blood gases should then be reviewed and certain questions answered: What is the pH? Is it outside the normal range? Is it low (acidaemia) or high (alkalaemia)? The pH will, by definition, be within the normal range if the primary abnormality is fully compensated. What is the base excess or standard bicarbonate? Is a metabolic acidosis or alkalosis present? What is the PaCO2? Is there a respiratory component to the derangement? Various nomograms have been developed which help to identify the type of acidbase derangement present when the above variables are plotted. This is shown in Figure 4 as a modified version of the Siggaard-Anderson plot. Respiratory disorders A primary respiratory disorder exists when the PaCO2 is abnormal, but not as compensation for another abnormality. Respiratory acidosis pH is low while PaCO2 is elevated, as is bicarbonate. Base excess and standard bicarbonate are within the normal range (by definition). Respiratory acidosis, when seen in acute respiratory failure indicates a serious, potentially lifethreatening condition. In contrast, patients who are in a chronic state of CO2 retention (e.g. in severe chronic obstructive pulmonary disorder) often have a fully compensated blood gas picture. PaCO2 is elevated but pH is normal. Renal compensation further elevates [HCO3 ] and induces positive base excess and high standard bicarbonate. Respiratory alkalosis is seen in conditions which induce hyperventilation, either acute (hypoxia or acute anxiety) or chronic (usually due to hypoxia). If uncompensated, pH is elevated, PaCO2 is low, as is bicarbonate. Base excess and standard bicarbonate are normal. The kidneys do not usually fully compensate for chronic respiratory alkalosis. Thus pH remains high or high-normal, PaCO2 remains low, as does bicarbonate. A moderate base deficit and slightly reduced standard bicarbonate completes the

picture. Since only partial compensation is the norm, the primary pathology is the respiratory alkalosis. Metabolic alkalosis is usually secondary to excessive gastrointestinal losses (vomiting), diuretic therapy or over-administration of bicarbonate. In acute metabolic alkalosis, the pH, standard bicarbonate and base excess are all elevated. PaCO2 will be in the normal range until significant respiratory compensation has occurred. As compensation involves hypoventilation, PaCO2 will be elevated and bicarbonate rises further. The base excess and standard bicarbonate will remain largely unchanged. A sustained metabolic alkalosis may seem contradictory, given the ability of the kidneys to rapidly lose bicarbonate. Thus, the condition will be present only if this ability is lost or inhibited. Acute renal failure will inhibit compensation, particularly if the precipitating cause has resulted in significant volume depletion. More often, the pathological process leading to the metabolic alkalosis will also induce significant electrolyte loss, particularly of Cl and K+ ions. Cl ions are exchanged for HCO3 ions in the kidney, and this process is inhibited in hypochloraemic states (e.g. profound vomiting). Thus, these patients typically present with a hypochloraemic hypokalaemic metabolic alkalosis. Prevention and management as many of the causes of metabolic alkalosis can be anticipated, prevention is frequently possible. This may involve the administration of H2 antagonists to patients with high gastric losses, reducing diuretic therapy, or providing adequate amounts of electrolyte replacements to patients at risk.

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Management, in the first instance, is adequate volume replacement and correction of electrolyte disturbances. This usually involves the administration of NaCl and KCl solutions. Attention to the precipitating cause should proceed simultaneously. Metabolic acidosis whatever the aetiology, this is a process leading to a fall in serum [HCO3 ]. It is frequently seen in the critically ill and, if unopposed, will lead to an acidaemia. The blood gas picture also reveals a significant base deficit and low standard bicarbonate. Some respiratory compensation is to be expected unless the patient is severely compromised. Hyperventilation lowers the PaCO2 and, with the consequent shift in equilibrium, further lowers [HCO3 ]. The cause of acidosis may be clinically obvious (shock or renal failure, etc) but cannot be reliably inferred from the blood gas analysis alone. For further insight into the underlying aetiology other indices must be examined. A helpful and widely used classification depends on the status of the anion gap. The anion gap Electrical neutrality in plasma is a fundamental principle and thus the total number of cations and anions must be equal. The major extracellular (measurable) cations are Na+, K+, Ca2+ and Mg2+, and anions are Cl and HCO3 . Anions such as albumin, phosphates, sulphates and other organic compounds would account for about 12 mmol/l, but are not usually measured, thus producing the anion gap. If a normal anion gap is present, then HCO3 loss must have been replaced by Cl . If the anion gap has increased, then bicarbonate must have been replaced (at least in part) by another compound, usually an organic acid (e.g. lactate). There are a number of factors that may confound this approach in the critically ill. Patients frequently have a low serum albumin (which reduces the anion gap) and thus may mask the presence of an organic acid. Absolute values of the major serum electrolytes may also be low due to water overload. Stewarts model is most helpful with respect to this problem. Consider again the three independent variables that determine pH. PaCO2 levels are more relevant to respiratory abnormalities. The other variables are weak acids and strong ion difference, largely Na+ and Cl . As the strong ion difference falls, so pH falls, i.e. Cl is an acidifying ion. This explains why normal saline is acidic and why excess administration of the same actually worsens a metabolic acidosis. A fall in the concentration of albumin increases pH, also explained by Stewarts model. A simplified application of the Stewart model has been proposed that helps to eliminate some of the problems associated with the anion gap by looking at the Na+/Cl ratio. Thus, in a patient with a metabolic acidosis, a ratio <0.75 is highly predictive of the presence of abnormal tissue acids. Conversely, a ratio >0.79 (a normal anion gap) suggests their absence. Between these variables, a mixed picture is present. The causes and management of metabolic acidosis Normal anion gap and high Na+/Cl ratio is relatively uncommon but, in the acute setting, may be due to excessive HCO3 losses that occur, for instance, in the presence of gastrointestinal fistula or diarrhoea. Excessive administration of 0.9% (normal)

saline solution, as discussed above, may be the primary cause. Other causes include a number of congenital or aquired metabolic disorders, including the renal tubular acidoses. Specific management should be directed at the cause. If due to excess HCO3 loss, this can be replaced; if due to excess chloride administration, fluid management should be changed. Increased anion gap and low sodium chloride ratio abnormal acid or acids will be present. The most common precipitating conditions are discussed below. Lactic acidosis lactate is produced in tissue metabolism of glucose in the presence of inadequate oxygen: anaerobic metabolism. This is usually due to reduced tissue perfusion and is thus a feature of shock. In septic shock, lactic acidosis may be a function of abnormal cellular oxygen utilization and not due to hypoxia per se. Lactate concentration can be measured within minutes, (normal value <1.0 mmol/l). Management includes attention to the underlying cause and active resuscitation of the patient with fluids and inotropes. The use of alkalizing agents is controversial. As lactate is largely eliminated within the liver, lactic acidosis may also occur with liver dysfunction. This is seen in the critically ill as part of global organ dysfunction. Diabetic ketoacidosis a degree of ketosis is normal in the fasting subject. Ketoacidosis occurs when low insulin levels result in excess, uninhibited production of ketones by the liver. These patients are also often severely dehydrated and may thus have an associated lactic acidosis. The main ketone produced in the presence of shock is -hydroxy butyrate, which is not detected by conventional analytical techniques, and thus ketosis may be missed unless glucose is measured. Management involves fluid and electrolyte administration, with insulin therapy to stop ketone production and reduce blood sugar. Excessive administration of normal saline may replace one acidosis with another. Renal failure acidosis results from progressive accumulation of acidic metabolic waste, normally excreted by this organ. The rate of progression depends on the severity of the renal failure and the catabolic state of the patient. Early intervention with renal replacement therapy may be life-saving in the septic patient. Salicylate poisoning causes a complex metabolic derangement, with acidosis being due to the presence of salicylic acid, lactic acid, ketoacids and other organic compounds. Measurement of serum salicylate levels is usually diagnostic. Management includes basic resuscitation measures, and volume expansion with normal saline. Glucose should also be given and any other electrolyte abnormality corrected. A forced alkaline diuresis using sodium bicarbonate is indicated in this condition. Methanol and ethylene glycol poisoning these inert compounds become toxic when metabolized to organic acids. These intermediary metabolites may cause irreversible organ damage and death. Diagnosis relies on suspicion (patient may appear drunk), the presence of a metabolic acidosis and increased serum osmolality, but with normal electrolyte (increased osmolar gap). Laboratory measurement of these alcohols is possible, but treatment should not await this confirmation. These patients should be given ethanol (the preferred substrate for alcohol dehydrogenase) which will reduce toxic metabolite production. Early initiation of haemofiltration or dialysis may be life-saving. u

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