- Blood Gases in Coronary Care UnitAnunay Gupta, SS Kothari
- Electrolyte AbnormalitiesJacob Jose
- Hyponatremia in Heart FailureHarikrishnan S
- Ventilator Settings in Cardiac ICUChitra Mehta, Yatin Mehta
- Noninvasive VentilationAnant Mohan, Saurabh Mittal
- Weaning in Patients with Cardiac DiseasesMayank Singhal, Rohit MK, Parag Barwad
- Ventilator Associated PneumoniaRandeep Guleria, Saurabh Mittal
- Hemodynamic Monitoring in Cardiac Critical Care UnitsAnunay Gupta, Saurabh Kumar Gupta
INTRODUCTION
Analysis of arterial blood gases (ABG) plays a significant role in management of critically ill patients. ABG provides rapid and accurate information about acid-base status, oxygenation, CO2 elimination and electrolytes status. In this review, we address the role of blood gases in the patient management in coronary care unit (CCU) from a practical point of view.
IS THIS BLOOD GAS MEASUREMENT RELIABLE?
One of the critical things in analysis of any blood gas report is to know the validity of the report. If calculated value of H+ (nmol/L) from the reported value match the H+ provided in report (which is usually provided by the machine), there is internal validity of the values and the report can be analyzed further. H+ can be calculated as H+ = 24 × PCO2/HCO3–1. Normal value of H+ is 36–44 nmol/L which corresponds to pH of 7.36–7.44. Another simpler method to calculate H+ is just subtracting the last two digits of the pH (e.g. 20 in pH 7.20) from 80; this value is approximately equal to the H+ concentration as provided by machine described as rule of thumb.2 Every laboratory should have internal validity program which should monitor instrument performance. There are other conditions which might change the blood gas values and those should be kept in mind while interpreting ABG results:
Delayed analysis: As the consumption of O2 and production of CO2 continues after blood drawn into syringe, readings may change with time.3 It leads to falsely low PaO2 and high PaCO2. Routinely, delay should not be more than 10 minutes to minimize the clinically significant error. It has been shown that samples should be preferably cooled with icepacks even, if analysis is done as soon as possible for oxygen test done in cardiac catheterization lab to assess reversibility in severe pulmonary artery hypertension.4
4Excessive heparin: Excessive heparin has two problems, heparin is acidic and hence modify pH results and dilution al effect can lead to falsely low PaCO2 values.5 Only 0.05 mL is required to anticoagulate 1 mL of blood. Dead space volume of a standard 5 mL syringe with 1 inch 22 guage needle is 0.2 mL, filling the syringe dead space with heparin provides sufficient volume to anticoagulate a 4 mL blood sample.
Presence of air bubbles: Mixing with air bubbles can lead to erroneous results, increase in PaO2 and decrease in PaCO2. Hence, any air bubble which is present should be gently removed without agitation and sample should be analyzed as soon as possible.6
Patient’s body temperature: In blood gas analyzers samples are reported temperature at normal body temperature. If severe hyper- or hypothermia is present, values of pH and PCO2 at 37°C can be significantly different from patients actual value. When blood is cooled, CO2 becomes more soluble reducing its PCO2 by about 4.5% per °C fall in temperature and the pH rises by about 0.015 per °C fall in temperature. However as discussed by Shapiro,7 available data suggest that in most circumstances, there is no advantage of temperature correction in most of the clinical circumstances.
Type of syringe: With use of normal plastic syringes pH and PCO2 remain unaffected, however pO2 falls with time.8 O2 seems to have a greater chance to diffuse across plastic than glass, why a glass syringe can better preserve oxygen in a blood sample for blood gas analysis.9 So glass syringes can be used, if there is delay in transport.
Leukocytosis: In patients with normal leukocyte count 0.1 mL of O2/ dL is consumed in ten minutes. Hence, can cause falsely low PaO2 in patients with significant leukocytosis.10
IS VENOUS BLOOD COMPARABLE TO ARTERIAL BLOOD FOR ANALYSIS?
For arterial blood gas samples, normal pH is 7.35–7.45, the normal PCO2 is 35–45 mm Hg, and normal HCO3 concentration is 21–27 mEq/L. Normal value of PaO2 is equal to more than 80 mm Hg and saturation >95%. Hypoxemia is usually defined as PaO2 <80 mm Hg. These values are for adult populations. (a normal newborn infant breathing room air has PaO2 between 40–70 mm Hg.) Also normal PaO2 values decreases with age. Normal Base Excess is –2 to +2 mEq/L. The P50 is the oxygen tension at which hemoglobin is 50% saturated. It is important to realize that normal P50 is only 26.7 mm Hg and due to the shape of Hemoglobin dissociation curve significant ‘clinical problem’ may be present despite ‘not so poor’ saturation that might rapidly deteriorate to hypoxia. In other words, PaO2 should also be analyzed in addition to saturation.
5Venous blood gas analysis is relative easier than arterial blood gas analysis and lesser painful to the patient. Normal value for peripheral venous blood gas (PVBG) obviously differs from arterial sample but the VBG can be used for analysis with understanding of the differences. Studies have shown the venous blood can be relied for pH and HCO3 values, but not for PaO2 or PCO2.11 Saturation of venous blood is in the range of 70–75%. There is a good correlation between HCO3– levels in venous and arterial blood. HCO3 levels are usually 1.4 mEq/L higher in venous blood.12 Hence, reference values for venous blood gases are the following: pH, 7.36 to 7.38, PvCO2, 43 to 48 mm Hg, and bicarbonate, 25–26 mmol/L. The agreement between arterial and venous blood gas values is likely to be more among patients with normal blood pressure comparable to those who are hypotensive.12 As patients in CCU may be sicker and hypotensive, arterial blood gas should be preferred whenever feasible.
Oxymeter or blood gas measurement: It is not often realized that ABG machines computes saturation but not directly measure, whereas the oxymeter measures saturation although does not give PaO2 values. Thus, oxymeter is more reliable, if properly done for saturation measurement. However, there are numerous caveats for oxymeter measurements like proper waveform, no direct exposure to light, etc.
IS IT ACUTE OR CHRONIC ABNORMALITY?
Clinical history is most important in distinguishing between an acute or chronic respiratory acid-base disorders. Whenever acute changes in PaCO2 occurs, a predictable change in pH is seen which can be easily remembered as depicted in Table 1.1.
Any discrepancy in pH value outside this suggests a chronic or metabolic derangement. Similarly, a respiratory acid-base disorder is called “acute” or “chronic” depending on whether a secondary change in the bicarbonate concentration meets certain criteria described in Table 1.2. A general rule to remember is that HCO3– and CO2 moves in same direction.
IS IT ONLY RESPIRATORY OR METABOLIC (MIXED)?
If secondary change as discussed above in case of respiratory acidosis differs from that what is expected, associated metabolic disorder or mixed disorder is diagnosed.
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In case of metabolic acidosis or alkalosis, there are multiple formulas for calculation of compensation for change in PaCO2 as discussed in Table 1.2.13 However, although the bedside rule is convenient, only bicarbonate levels of approximately 12–16 mEq/L result in reliable expected arterial PaCO2 values. Similarly, in case of metabolic alkalosis only bicarbonate levels of approximately 28–32 mEq will give reliable expected value. Therefore, it is not reliable at all HCO3– concentrations. Hence, should not be used.13 If PaCO2 < expected PaCO2 then there is concomitant respiratory alkalosis. However if PaCO2 > expected PaCO2, then there is concomitant respiratory acidosis. Secondary responses should not be called as compensatory response, a general rule to appreciate is that compensation can not correct the primary abnormality. Hence, there is a limit to the maximum respiratory compensation that can be attained. With severe metabolic acidosis (e.g. serum HCO3 concentration less than 6 mEq/L), the PCO2 can fall no lower than 8 to 12 mm Hg. Similarly, even in severe metabolic alkalosis, PaCO2 usually do not increase by more than 55 mm Hg. Hence PaCO2 more than 55 with metabolic alkalosis is usually mixed disorder with associated respiratory acidosis. Chronic respiratory alkalosis and mild chronic respiratory acidosis (pCO2 60 mm Hg) are only simple acid-base disorder that can fully compensate and bring pH value to normal. However, this occur only if disease causing process has been present for 7–14 days.
Alveolar–arterial gradient: Alveolar-arterial gradient (A-a gradient) can help us in differentiating between pulmonary or extrapulmonary causes of respiratory acid-base disturbances. A-a gradient measures difference between partial pressure of oxygen between the alveolar and arterial side of alveolar-capillary membrane. Its normal value is 5–10 mm Hg in young and increases to 10–20 mm Hg in elderly. It is calculated as 7FIO2 × (barometric pressure–water-vapor pressure) – PaO2 – (PaCO2 ÷ gas-exchange ratio). The fraction of inspired oxygen (FIO2) is 0.21 in room air, the barometric pressure is 760 mm Hg at sea level, and the water-vapor pressure is 47 mm Hg and the gas-exchange ratio, which is approximately 0.8 at steady state levels. Keeping above values in formula leads to simpler version, i.e. 150 – PaO2 − 1.25 × PaCO2. A higher value than normal is suggestive of pulmonary cause of hypoxia. But it is important to realize that this is while breathing room air. The value of 150 pertains to a FiO2 of 21% as discussed above and for 100% oxygen this amounts to 500 mm Hg. A useful rule of thumb is that this value will be 5 × FiO2 concentration.
Example: A 54-year-old patient presented to CCU with anterior wall MI. He is diaphoretic, having intermittent premature complexes was shifted to CCU. His ABG values were:
Interpretation: As pH is high and PaCO2 is low, is the primary disorder is respiratory alkalosis. Being and acute condition the changes in pH and PCO2 are as expected (Table 1.1); expected HCO3 is as for acute compensated respiratory alkalosis. PO2 – 55 is suggestive of hypoxemia. Hence, patient is having acute alveolar hyperventilation leading to respiratory alkalosis and hypoxemia. Alveolar arterial gradient was 57.2 mm Hg suggestive of pulmonary cause of hypoxemia due to V/Q mismatch likely due to pulmonary edema.
The patient is managed with IV morphine, oxygen with mask (FIO2 - 40%) diuretics, nitroglycerine and stabilized in CCU. His blood gases were repeated few minutes later and revealed:
Interpretation: Acute respiratory acidosis with mild hypoxemia and high alveolar arterial gradient of 147 mm Hg.
The possible cause of above blood gas picture is excessive dose of morphine which has causes hypoventilation. There is pulmonary edema as reflected by pO2 of 80 mm Hg on FiO2 of 40%. Since A-a gradient is high, the hypoxemia is not due to hypoventilation, but from pulmonary edema.
Anion gap: Calculation of anion gap is useful in evaluation of metabolic acidosis. Measure of excess of “unmeasured anions” in metabolic acidosis, calculated as [Na+] − [Cl−] − [HCO3−]. Normal anion gap is 8–12 mEq/L. Increased anion gap acidosis is seen in the conditions when concentration of bicarbonate decreases relative to levels of sodium and chloride because of overproduction of acid (in ketoacidosis, lactic acidosis), under excretion of acid (renal failure), excessive cell lysis (rhabdomyolysis). Normal anion gap acidosis is seen when bicarbonate loss is replaced with chloride ion. Important causes are diarrhea, renal tubular acidosis and Addison’s disease.
Deciding about intubation and extubation: Blood gas analysis helps in deciding the need of mechanical ventilation. Primary indication is acute ventilatory failure defined as sudden increase in PaCO2 > 50 mm Hg with accompanying respiratory acidosis, other indication being severe hypoxemia with cyanosis defined as PaO2 < 40 mm Hg, SaO2 < 75 %. While making a decision to extubate the patient, maintenance of adequate PaO2 (80 – 100 mm Hg) with a PEEP less than or equal to 10 cm H2O and a FIO2 less than or equal to 0.40 are suggested. Similarly, other blood gas parameters should be in near normal range. Of course, the clinical status and the disorder that needed ventilation will be important in this decision.
Pulmonary edema: A 24-year-old adult presented to casualty with history of rheumatic heart disease and severe mitral stenosis and demonstrated rales half way up in each lung field. Following blood gases were obtained:
pH 7.20, pO2 47, pCO2 25, HCO3 10, BE 18.
Interpretation: Compensated severe metabolic acidosis as expected pCO2 should be 21–25 with severe hypoxemia.
Tissue hypoxemia should be assumed whenever acidemia and hypoxemia coexists. Acidemia is feature of severe acute pulmonary edema and can be of metabolic or respiratory origin or both. In above-discussed case, metabolic acidosis is predominantly due to lactic acidosis,14 lactate accumulation occurs secondary to hypoxia in poorly perfused tissue due to low cardiac output and improves with treatment of pulmonary edema.
Chronic heart failure: A 50-year-old man with CHF on both loop and thiazide diuretics presented to casualty with excessive weakness and cramps. Blood gases revealed:
pH 7.56, PaCO2 50, HCO3 42, PaO2 78, SaO2 97%, Na+ 130, K+ 2.8.
Interpretation: ABG is suggestive of mild hypoxemia, hyponatermia, hypokalemia and compensated metabolic alkalosis.
This finding is typically seen in patients who are on diuretics which interfere with NaCl reabsorption such as thiazide type diuretics and loop diuretics. These effects are related to activation of renal angiotensinogen system and secondary hypoaldesteronism due to renal hypoper fusion and loss of Na+. In patients of chronic heart failure presenting in emergency with worsening of symptoms, blood gas analysis may help in clinical decision whether symptoms worsening is due to excessive diuresis. These patients benefit with the use of potassium sparing agents such as spironolactone.
9Pulmonary embolism: For patients who are suspected to be having pulmonary embolism, an abnormal ABG is common, but it is neither sensitive nor specific for diagnosis since abnormal gas exchange are often due to and worsened by underlying cardiopulmonary disease in these patients.15 Common abnormalities seen in these patients in ABG include: Hypoxemia 74%, Increased alveolar-arterial gradient for oxygen (62–86%), Respiratory alkalosis and hypocapnia 41%.16 Normal ABGs can be seen in eighteen percent of patients.17 A subtle clue to the presence of pulmonary embolism can come from the fact that the work of breathing in these patients is increased far more than the ABG would suggest, since they have an increased in physiological dead space. Massive PE-associated, associated with obstructive shock and respiratory arrest can show respiratory or lactic acidosis or both. ABGs may be of prognostic value. Patients with hypoxemia or SpO2 <95% at time of diagnosis are at higher risk of in-hospital complications of pulmonary embolism, including respiratory failure, obstructive shock, and death.18 Hence, all patients with hypoxemia should be admitted.
Sepsis: Sepsis is a systemic response to infection. Blood gases reveal metabolic acidosis due to result of hypoper fusion and impaired oxygen delivery leading to increased lactic acid levels.Tissue oxygenation is adequate in sepsis. Hence, hypoxemia is usually not seen in sepsis. Increase in lactic acid levels seen is due to cytopathic hypoxia, i.e. inhibition of pyruvate dehydrogenase enzyme by bacterial endotoxins which converts pyruvate to acetyl CoA in mitochondria. Modern blood gas analyzers provide serum lactate values. A lactate level above 2 mEq/L is abnormal, but in patients with sepsis, a blood lactate level above 4 mEq/L have poor prognostic value.19,20 Hypoxemia can be seen depending when respiratory infection is cause of sepsis.
Cyanotic spells: Cyanotic spells also called as paroxysmal hyperpnea, hypoxic or hypercyanotic spells, are dramatic and alarming features of Fallot’s tetralogy. Infant becomes acutely cyanotic, hypercapnic, diaphoretic in later stage may become limp and unconscious. There is increased right to left shunt across VSD as pathophysiologic mechanism. Blood gas analysis during the episode will reveal hypoxemia (low pO2), acidosis and hypercapnea will be seen despite hyperventilation. In fact, the presence of raised PaCO2 in these patients suggests severe derangement. It is not at once apparent to clinicians not used to seeing cyanotic CHDs that in this group of patients PaCO2 is not equal to ventilation, since the effective pulmonary blood flow is the limiting issue, one might see a patient obviously hyperventilating but still retaining CO2. Acidosis will have both metabolic and respiratory component. Sodium bicarbonate is used to treat metabolic acidosis in spell and reverses the 10respiratory centre stimulating effect of acidosis. No time should be wasted to do blood gas analysis during spell and patient should be treated with morphine, beta-blockers and bicarbonate even in the absence of blood gas determination as acidosis is integral part of pathophysiological mechanism of spell.
CONDITIONS IN WHICH BLOOD GAS HELPS IN MANAGEMENT
MI with Ketoacidosis: Myocardial infarction is a well-known precipitating cause of diabetic ketoacidosis. Blood gas analysis in myocardial infarction demonstrates acute alveolar hyperventilation and mild hypoxemia. With associated-DKA blood has will reveal significant metabolic acidosis and respiratory alkalosis, hypoxemia is usually not a feature of DKA.
Pulmonary embolism and chronic obstructive pulmonary disease (COPD): A COPD patient recently discharged from hospital presents to casualty with worsening of respiratory distress. ABG done revealed-
pH 7.40, pCO2 51, HCO3 28, SaO2 88% , PaO2 53 , BE 3
Interpretation: Acute compensated respiratory acidosis with hypoxemia.
However, patients pre-discharge PaCO2 was 65 mm Hg. As there was hypocapnia, a possibility of pulmonary embolism was kept and patient underwent CT angiography which revealed thrombus in right pulmonary artery. In a meta-analysis21 it was seen that one out of four patient who require hospitalization may have pulmonary embolism. Hence it should be considered in differential diagnosis in patients of COPD presenting with acute exacerbation. Many a time, it is difficult to differentiate between acute exacerbation of COPD and pulmonary embolism. Authors22 have reported a drop in PaCO2 5 mm Hg or more as statistically indicative of concomitant PE. Hypoxemia is seen in both pulmonary embolism and acute exacerbation of COPD, however improvement in hypoxemia with oxygen point towards diagnosis of COPD, while major pulmonary embolism may be resistant to correction due to intrapulmonary or possible intracardiac shunting.
Stokes-Adam syndrome: In a patient admitted with recurrent cardiogenic syncope. His blood gases were:
pH 7.2, HCO3 15 , PaCO2 29, SaO2 94%, Na 134, K 6.8, Cl 100
Interpretation: High anion gap metabolic acidosis with hyperkalemia.
Blood gas analysis may play a role in etiologic diagnosis in addition to a 12–lead ECG. One of the important secondary cause of complete heart block causing syncope is hyperkalemia secondary to acute or chronic renal failure.
11A 64-year-old Type 2 diabetic patient was brought to casualty with altered sensorium and chest pain. His ECG showed wide complex (sine wave) regular tachyarrhythmia of 110 beats/minute with blood pressure of 106/66 mm Hg. Results of arterial blood gases on 30% inspired oxygen were:
pH 7.25, pCO2 32, PO2 143, SaO2 98%, HCO3 17, BE 8, Na+ 111, K+ 6.6, Cl–76
Interpretation: Primary metabolic acidosis with increased anion gap, hyperkalemia with respiratory compensation.
His blood sugar revealed “high” on glucometer. Urine showed 1 + ketones. A diagnosis of hyperosmolar diabetic non-ketotic coma was made. Diabetic ketoacidosis differs from non-ketotic coma with the presence of significant metabolic acidosis pH < 7.2. It is important to realize that presentation of diabetic non-ketotic coma can mimic as cerebrovascular accident.
Methemoglobinemia: A 25-day-old male child was referred with cyanosis noticed few days after birth and was suspected to have cyanotic congenital heart disease. However, clinical examination was normal. His basal oxygen saturation was 81%.Following blood gases were obtained.
pH 7.42, PO2 148 , pCO2 32 , SaO2 82%, HCO3 23, with elevated methemoglobin levels (32%).
Interpretation: Normal Blood gas except desaturation with normal PaO2 and high methemoglobin levels.
In a child presenting with cyanosis but without any structural heart disease, methemoglobinemia should always kept as a differential diagnosis. Possible cause being use of or exposure to oxidant drugs such as chloroquine,23 chemicals, local anesthetic agents, and nitroglycerin. Presence of high pO2 with low saturation in arterial blood is an indicator of methemoglobinemia. Modern day blood gas analyzers usually give value of methemoglobin, so it should be a routine to have a look at methemoglobin levels, if provided, otherwise diagnosis of methemoglobinemia is likely to be missed. Normal value of methemoglobin in blood is less than 2% of total hemoglobin.24
Less well looked after blood gases assets—chloride and sodium: Serum chlorides levels are important to calculate anion gap as discussed here. Normal serum chloride concentrations range from 96–106 mEq/L. In cases of normal anion gap acidosis, loss of HCO3 is compensated by excessive reabsorption of chlorides from renal tubules, hence it is also known as hyperchloremic metabolic acidosis. However in case of normal anion gap metabolic acidosis serum chloride levels are normal as remaining anions from dissociated acids balance the loss of bicarbonate. Urinary chloride levels help us in differentiating chloride responsive and chloride resistant 12metabolic alkalosis. Whenever effective circulatory volume is reduced, kidney absorbs more chloride and bicarbonate leading to diminish urinary chloride levels. Urinary chloride levels less than 25 mmol/L is suggestive of chloride responsive metabolic alkalosis and usually improves with administration of fluids containing sodium chloride. Urinary chloride levels more than 40 mmol/L is suggestive of chloride resistant metabolic alkalosis usually occurs due to excessive loss of sodium chloride from kidney, common causes being mineralocorticoid excess and severe hypokalemia.
Example: A 15-year-old girl came to out patient department with a diagnosis of dilated cardiomyopathy and worsening dyspnea and generalized body swelling. She was on 20 mg twice daily dose of furosemide. His furosemide dose was increased to oral 60 mg twice daily. But there was worsening of edema and symptoms. Hence was admitted in CCU. Her RFT are deranged with urea of 73 and creatinine 1.4. Following blood gases were obtained:
pH 7.46, PaCO2 42, HCO3 27, Na+ 116 mEq/L, K+ 5.1, Cl– 98.
Interpretation: Chronic metabolic alkalosis with respiratory compensation with extremely low sodium levels.
As patient has developed worsening of edema on diuretics and very low sodium levels, hyponatremia in this setting is multifactorial. congestive heart failure causing fluid retention and dilutional hyponatremia, drug use and other factors may be important. Presence of hyponatremia is associated with poor prognosis.25 Most of the ABG analyzer provides serum electrolytes, however, serum sodium does not correlates well with laboratory values as compared to serum potassium levels.25 Hence, appropriate clinical evaluation with blood gas values can help in the correct management of hyponatremia in CHF patients with heart failure. The electrolyte management is discussed separately.
CONCLUSION
The analysis of blood gases in CCU provides very valuable information for the diagnosis and management of cardiac patients. Interpreted in the right clinical context, this understanding provides vital clues for the management. Physicians must familiarize themselves with the basic understanding of these changes as discussed.
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