Dr.

Nitin Bhalla

Aims of ABG analysis

y Arterial Blood Gases are vital for investigating: 1) Gas exchange a) Elucidating mechanism of Hypoxemia b) Diagnosing and monitoring gas exchange in patients with impending or established respiratory failure and those undergoing mechanical ventilation. 2) Acid base Balance. 3) Monitor patients during cardiopulmonary surgery

and intraoperative monitoring.

Normal values
Parameter pH PaO2 PaCO2 HCO3Standard HCO3Base excess Anion Gap Normal value 7.35 - 7.45 70 - 104 mm Hg 36 - 44 mm Hg 22 - 26 mmol/l 22 - 26 mmol/l -2 to +2 mmol/l 9 - 13 mEq/l

Response to an Acid-Base Perturbation

y The body s response to a change in acid-base status has

three components: First defence: Second defence: Third defence: Buffering Respiratory Renal

Analytic tools for Acid base Analysis

1) Boston School "Henderson-Hasselbalch 2) Copenhagen School "Base Excess 3) Anion Gap Approach 4) Stewart

Fencl approach

Boston approach
y HENDERSON-HASSELBALCH EQUATION

y HENDERSON'S EQUATION FOR CONCENTRATION

OF H+ -

Copenhagen School "Base Excess

Base deficit/excess - This is defined as the amount of strong acid or base required to return pH to 7.4, assuming a Pco2 of 40 mm Hg and temperature of 38C.

Anion Gap Approach

y Anion gap = [Na+ + K+ ]

[Cl- + HCO3-]

Stewart Fencl Approach

y Gives more accurate reflection of true acid base status y Based on concept of electrical neutrality y It states

There exists in Plasma a SID of 40 44 mEql/l balnced by the negative charge on bicarbonates and the buffer base (Atot)

y Independent variables: SID, [ATOT], and Pco2 y Dependent variables determined by them: [HA], [A-],

[HCO3-], [CO32-], [OH-], and [H+].

Blood is analysed by three separate electodes

y pH electrode y O2 electrode y CO2 electrode

The Sanz electrode The Clark electrode The Severinghaus electrodes

A Stepwise, Conventional Approach for acid base disorder

In Metabolic acidosis, calculate Anion Gap; In metabolic alkalosis, check chloride in urine.

Clinical conditions associated with specific acid base disorders

Clinical Condition Vomiting Diarrhea Severe diarrhea Diuretic therapy Sepsis Hypotension, low cardiac output states, severe anemia. Cirrhosis Renal failure Suspected Acid base disorder Metabolic alkalosis Metabolic alkalosis; Metabolic acidosis (normal anion gap) Metabolic acidosis Metabolic alkalosis Respiratory alkalosis Metabolic acidosis Metabolic (lactic) acidosis

Respiratory alkalosis Metabolic acidosis

Clinical Condition Diabetic ketoacidosis

Suspected Acid base disorder Metabolic acidosis (wide anion gap) at presentation. A normal anion gap metabolic acidosis often develops during therapy. Respiratory acidosis Respiratory alkalosis Respiratory alkalosis or acidosis depending on whether there is type 1 or type 2 respiratory failure respectively. Metabolic (lactic) acidosis if hypoxemia severe Respiratory alkalosis Respiratory alkalosis Respiratory alkalosis (respiratory acidosis when respiratory muscle fatigue occurs)

Severe COPD Pregnancy Hypoxemia

Pneumonia (reflex hyperventilation) ALI/ARDS (reflex hyperventilation) Asthma exacerbation

Clinical Condition Pulmonary thromboembolism Biguanide, INH therapy Renal tubular acidosis

Suspected Acid base disorder Respiratory alkalosis Metabolic acidosis (lactic acidosis) Metabolic acidosis (normal anion Gap)

General approach to acid-base disorders

Compensations for acid-base

Metabolic acidosis
y

Metabolic alkalosis Respiratory acidosis

espiratory alkalosis

For every 1 mmol/L decrease in HCO3 1 mm Hg decrease in PCO2 Expected PCO2 = 1.5 (HCO3) + 8 2 For every 1 mmol/L increase in HCO3 0.7 mm Hg increase in PCO2 Acute: For i crease i ol/ i crease i Chronic: For i crease i 4 ol/ i crease i Ac te: For every 10 mm Hg decrease in PCO2 2 mmol/L decrease in HCO3 Chr ic: For every 10 mm Hg decrease in PCO2 mmol/L decrease in HCO3

Anion Gap
y The term anion gap (AG) represents the concentration

of all the unmeasured anions in the plasma.

y ANION GAP = [Na+]

[ [Cl-] + [HCO3-] ]

y Normal values: 9 - 13 mEq/L y Help differentiate between causes of a metabolic

acidosis: high anion gap versus normal anion gap.

Diagnostic approach to metabolic acidosis

Another aproach
Metabolic Acidosis Anion Gap High AG Lactate LA (A/B) Negative Normal AG Urinary AG Positive

Blood Sugar & (raised BG & UK DKA) Urinary Ketones (normoglyc. & raised UK - Alcoholic / Starvation) Intoxication

GI Loses

Impair. Of renal function

Urinary anion gap

y Urinary Anion Gap = ( UA - UC ) = [Na+]+ [K+] - [Cl-] y Key Fact: The urinary anion gap can help to

differentiate between GIT and renal causes of a hyperchloraemic metabolic acidosis.

Osmolar gap
Osmolar gap = Osmolality Osmolarity
y The osmolar gap is the difference between the 2 values: y y y y y

the osmolality (which is measured) and the osmolarity(which is calculated from measured solute concentrations). Osmolality of a solution is the number of osmoles of solute per kilogram of solvent. Osmolarity of a solution is the number of osmoles of solute per litre of solution. An elevated osmolar gap provides indirect evidence for the presence of an abnormal solute which is present in significant amounts. An osmolar gap > 10 mOsm/l is often stated to be abnormal. Main Use of Osmolar gap: Screening test for detecting abnormal low MW solutes (esp ethanol, methanol & ethylene glyco

Delta ratio
y This Delta Ratio is sometimes useful in the assessment of metabolic acidosis.

Delta ratio = (Increase in Anion Gap / Decrease in bicarbonate)

y Delta Ratio Assessment Guideline

< 0.4 0.4 - 0.8 1 to 2 -

>2-

Hyperchloraemic normal anion gap acidosis Consider combined high AG & normal AG acidosis BUT note that the ratio is often <1 in acidosis associated with renal failure Usual for uncomplicated high-AG acidosis Lactic acidosis: average value 1.6 DKA more likely to have a ratio closer to 1 due to urine ketone loss (esp if patient not dehydrated) Suggests a pre-existing elevated HCO3 level so consider: a concurrent metabolic alkalosis, or a pre-existing compensated respiratory acidosis

Metabolic alkalosis
y Metabolic alkalosis occurs when there is an excess of

buffers present, raising the systemic pH. y In general, metabolic alkaloses are generated by either bicarbonate intake in excess of loss or by the primary loss of H+ y The most common reason for impairment of renal excretion of bicarbonate is chloride deficiency and renal failure. y In the setting of chloride depletion, the kidney is unable to excrete the excess bicarbonate, and therefore the alkalosis is maintained.

Classification of metabolic alkalosis by chloride handling

Chloride sensitive (urine Cl less than 20 mEq/L) Gastrointestinal acid losses Nasogastric suction, vomiting Congenital Cl losses in stool? Rectal adenoma Chloride resistant (urine Cl greater than 40 mEq/L) Hypertensive Renovascular hypertension Hyperaldosteronism Liddle syndrome Glycyrrhizic acid

Renal acid losses Penicillins, citrate Postdiuretic Posthypercapnic

Normotensive Diuretics (contraction alkalosis) Bartter and Gitelman syndromes Administration of alkali

Alveolar-Arterial PO2 Gradient and PaO2/FIO2 Ratio

PaO2 and Age

y The normal level of PaO2 declines with advancing age. y PaO2= 109 0.43 age in years y PaO2 in healthy young adults (at sea level) Average PaO2: 95 mm Hg (range 85 100 mmHg) y In a healthy 60 year old (at sea level) Average PaO2: 83 mmHg

A-a DO2
y The value of PaO2 (the partial pressure ofO2 in the

arterial blood) cannot be interpreted in isolation. y The difference between the PAO2 (which is a calculated value) and the PaO2 (which is measured in the laboratory) helps quantify the pulmonary pathology that is causing hypoxemia. y Alveolar Gas Equation PAO2 = [FiO2 (Pb Pw)] [1.2 x PaCO2]

A-a DO2 = PAO2 PaO2

A-aDO2
y It allows separation of extrapulmonary from pulmonary causes of respiratory failure . y With extrapulmonary failure, the A-a gradient remains normal. With shunt or V / Q mismatch, the gradient is usually elevated. y The second value is that it can be a measure of the severity of gas exchange impairment. y At any age, an A-a gradient exceeding 20 mm Hg on room air should be considered abnormal and indicative of pulmonary dysfunction. y A-aDO2 = 2.5 + (0.25 X Age in years). y Room Air - A-aDO2 = 7 14 mm Hg 100% O2 - A-aDO2 < 70 mm Hg

A-aDO2

Increased

Normal

V/Q mismatch Right to Left Shunt Diffusion Defect

Disorders causing hypoventilation

The Respiratory Quotient (RQ) in the Alveolar Air Equation

FiO2

< 0.6
PAO2 = FiO2 (Pb Pw) 1.2 (PaCO2)

> 0.6

PAO2 = FiO2 (Pb Pw) 1.0(PaCO2)

FiO2

PB

PW

PaCO2

PAO2 PaO2 SpO2 CaO2 DO2 Hb CO

Limitations of A-aDO2
y The respiratory quotient is not always 0.8 y When the Fio2 is above 0.21, the A-a gradient becomes

a less accurate measure of the efficiency of gas exchange and therefore a less valuable tool for the measurement of shunt. y Variable and unreliable FiO2 esp. patients on nasal prongs and V/M y PW Changes with Body temperature. y Irregular breathing pattern of patient.

PaO2 / FiO2 ratio

y The Pao2 divided by the Fio2 (Pao2/Fio2 ratio) can be used to assess the severity of the gas exchange defect. y The normal value for the ratio of the partial pressure of oxygen in arterial blood to Fio2 (Pao2/Fio2, where Fio2 is expressed as a decimal ranging from 0.21 to 1.00) is 300 to 500. y A value of less than 300 is indicative of gas exchange derangement and a value below 200 is indicative of severe impairment. y Although the Pao2/Fio2 is felt to be a more reliable measure of degree of gas exchange impairment at higher Fio2s, it too has the potential to be unreliable, particularly in the presence of a large shunt or a low Fio2

Hypoxemia

Low PaO2 and Low /Normal PaCO2

Low / Normal PaO2 and High PaCO2

Normal PaO2 and Low PaCO2

Hypoventilation

A-a DO2 increased

A-a DO2 increased

Respiratory alkalosis Compenasation for meatbolic acidosis

No

Yes

Yes

No

Yes

Consider a Shunt ( with Hypoventilation if PaCO2 is high)

Is

O 2 c rr c t

    
l

Low i 2 Hi altit low i 2

ith O2?

Hypoventilation Low respiratory Drive Neuromuscular

No

Consider V/Q mismatch (with Hypoventilation if PaCO2 is High)

The Difference Between V/Q Mismatch and Shunt

Timing of ABG

Source of errors in ABG analysis

Source 1. Plastic syringe

Error falsely low Pao2 values (when PaO2 > 221 mm Hg) plastic syringes with high surface area to volume ratios (e.g., 1mL tuberculin syringes) worsen gas permeability errors as compared to standard 3-mL syringes. pH if normal or alkaline acidemia increases if very acidic - acidemia decreases dilutes dissolved gasses, shifting their concentration to that of heparin (Po2 approximately 150 mm Hg, Pco2 less than 0.3 mm Hg at sea level and room temperature). The dilution error is no greater than 4% if a glass syringe and 22-gauge needle are only wetted with approximately 0.2 mL heparin and 3 to 5 mL blood collected. If an ABG specimen is not analyzed within 1 minute of being drawn or not immediately cooled to 2C, the Po2 and pH fall and Pco2 rises because of cellular respiration and consumption of oxygen.

2. Heparin

3. Delay or temperature effect

Source

Error

4. Leucocytosis and thrombocytosis 5. Air Bubble

Leucocytosis and thrombocystosis leads to increased O2 comsumption and therefore, falsely low PaO2. Variable effect on PaO2, and predictable effect on pH and PaCo2. The PaCO2 of Blood will trend towards zero i.e. decrease and effect on pH is related to or secondary to its effect on PaCO2. Pyrexia (> 39C) Overestimation of Hypoxia and pH ; under estimation of acidosis. Hypothermia ( reverse)

6. Pyrexia and Hypothermia

Peri-operative acid base disturbances

Acid-Base Disturbances Commonly Seen Perioperatively

Hypoventilation narcosis, incomplete reversal of neuromuscular blockade Hyperventilation anxiety, pain

Respiratory acidosis Respiratory alkalosis Metabolic acidosis secondary to unmeasured anions (widened gap acidosis)

Hypoperfusion lactic acidosis; diabetic ketoacidosis; renal failure Hyperchloremia normal saline, hetastarch, or albumin infusions; renal tubular acidosis; bladder reconstructions

Metabolic acidosis secondary to measured anions (non-gap hyperchloremic acidosis)

Hypotonic fluid administration; sodium loss Metabolic acidosis secondary to free water excess diarrhea; administration of hyperosmolar (hyponatremia, dilution acidosis) fluids mannitol, alcohol, hyperproteinemia

Metabolic alkalosis

Hyperventilation of patient with history of carbon dioxide retention (COPD); sodium gain (sodium bicarbonate, massive blood transfusion); chloride loss nasogastric suctioning

Peri-operative period
y Metabolic acid-base disturbances are common perioperatively and often are iatrogenic. y y

y y y

In particular, these disturbances reflect manipulation of SID by administration of electrolyte or osmotically imbalanced solutions. Hyperchloremic acidosis is seen frequently in the operating suite. In maintaining perioperative patients, hypotonic and dextrose-containing fluids should be avoided. Excessive administration of hypotonic fluids, such as dextrose 5% or 0.45% sodium chloride, leads to an expansion in free water, hyponatremia, and acidosis. If larger volumes of crystalloid are administered, it is important to use balanced buffered solutions that mirror the electrolyte content of ECF, such as lactated Ringer solution, Normosol, or Plasma-Lyte. Normal saline should be administered to pt. with continuous nasogastric suctioning. Care must be taken to avoid hypokalemia, hypocalcemia, hypomagnesemia, and hypophosphatemia. Human albumin solution, some hetastarches, and gelatins (available in Europe) are formulated in sodium chloride; large volumes cause hyperchloremic acidosis.

Case # 1
y Mr. Karl is a 80 year-old nursing home resident admitted with urosepsis. Over the last two hours he has developed shortness of breath and is becoming confused. His ABG shows the following results:

pH PaCO2 PaO2 HCO3 SaO2

7.02 55 77 14 89%

y What is your interpretation? y What interventions would be appropriate for Mr. Karl?

Case # 2
A 24 year-old woman is found down at street by some bystanders. The medics are called and, upon arrival, find her with an oxygen saturation of 88% on room air and pinpoint pupils on exam. She is brought into the ER where a room air arterial blood gas is performed and reveals: pH 7.25, PCO2 60, PO2 65, 26, HCO3Base Excess 1. On his chemistry panel, her Sodium 137, chloride 100, bicarbonate 27.

Case # 3
A 45 year-old woman with a history of inhalant abuse presents to the emergency room complaining of dyspnea. She has an SpO2 of 99% on room air and is obviously tachypneic on exam with what appears to be Kussmaul s respirations. A room air arterial blood gas is performed and reveals: pH 6.95, PCO2 9, PO2 128, 2. HCO3A chemistry panel revealed Sodium 130, chloride 98, 2. HCO3-

Case # 4
y Mr. Frank is a 60 year-old with pneumonia. He is admitted with dyspnea, fever, and chills. His blood gas is below:

pH PaCO2 PaO2 HCO3 SaO2

7.28 56 70 25 89%

y What is your interpretation? y What interventions would be appropriate for Mr. Frank?

Case # 5
y A 48-year-old morbidly obese patient is admitted to the hospital with shortness y

of breath and fever. In the emergency room, he is started on intravenous antibiotics. Over the next 3 hours, he becomes severely short of breath and develops a diminished level of consciousness. He is intubated and placed on mechanical ventilation. His past medical history is significant for diabetes mellitus and hypertension. Social history is significant for one pack per day tobacco abuse for 20 years. Current medications include amlodipine 5 mg PO daily, enalapril 5 mg PO bid, and hydrochlorothiazide 12.5 mg PO bid. Physical exam shows blood pressure of 156/88 mm Hg, pulse 76 beats/minute, and temperature 96F. The patient is morbidly obese. Cardiovascular exam is normal. Lung exam reveals bilateral breath sounds with diffuse crackles on the right and egophony. The initial ventilator settings are synchronous intermittent mandatory ventilation (SIMV) with a rate of 20, tidal volume of 800 mL, and positive endexpiratory pressure (PEEP) of 5 cm H2O, with an FiO2 of 1.0. Thirty minutes after mechanical ventilation is initiated, the following labs are drawn.

y y y y

pH PO2 (mm Hg) PCO2 (mm Hg) Bicarbonate (mEq/L)

7.65 340 32 34 141 4.2 100

y Serum Sodium (mEq/L) y Potassium (mEq/L) y Chloride (mEq/L)

y Blood urea nitrogen (BUN) (mg/dL) 13 y Phosphorus (mg/dL) 3.8 y Creatinine (mg/dL) 0.8 y Albumin (g/dL) y Glucose (mg/dL)

3.8 152

Q. What acid-base disorder is present in this patient?

Case # 6
y A 44-year-old female with cirrhosis secondary to autoimmune hepatitis is admitted

to the hospital for fever and abdominal pain. The patient is listed for an orthotopic liver transplantation and has been clinically stable for the past month. She noted abdominal pain and fever that have gotten progressively worse over the last 2 days. Her past medical history is otherwise nonsignificant. y Current medications include spironolactone 100 mg PO bid, furosemide 80 mg PO bid, and lactulose 30 mL PO bid. Previous surgeries include the placement of a transjugular intrahepatic portosystemic shunt (TIPS) and a cholecystectomy. y Physical exam is significant for blood pressure of 74/55 mm Hg, pulse of 72 beats/minute, temperature 100.8F, and respiratory rate of 24 breaths/minute. She appears cachectic. Cardiovascular and chest exams are normal. Her abdomen is distended and there is diffuse tenderness. She has 1+ pitting edema in the lower extremities. Spontaneous bacterial peritonitis is suspected, and the patient is admitted to the hospital. Admission labs are given below:

y y y y

pH PO2 (mm Hg) PCO2 (mm Hg) Bicarbonate (mEq/L)

7.23 78 28 11

y Serum Sodium (mEq/L) 128 y Potassium (mEq/L) 5.1 y Chloride (mEq/L) 106 y BUN (mg/dL) y Creatinine (mg/dL) y Phosphorus (mg/dL) y Albumin (g/dL) y Glucose (mg/dL)

20 1.3 2.1 1.4 84

Case # 7
y 66-year-old man is seen in the emergency room. He has had 8 days of

severe diarrhea, abdominal pain, and decreased food intake, but adequate intake of liquids. He believes that he became sick after babysitting his grandson who had similar symptoms. y His medical history is significant for diabetes and hypertension. Surgical history only consists of coronary artery bypass grafting 3 years ago. His medications include enalapril 20 mg PO bid, aspirin 81 mg PO daily, atenolol 50 mg PO daily, hydrochlorothiazide 25 mg PO daily, and metformin 1 g PO bid. He has a family history of diabetes and premature coronary artery disease. He does not smoke or use drugs, and drinks alcohol occasionally. y Physical exam is significant for blood pressure of 105/70 mm Hg and a pulse of 72 beats/minute; blood pressure drops to 90/50 mm Hg when the patient stands. Temperature is 98.8F, and respiratory rate is 32 breaths/minute. There is a small amount of occult blood in the stool. Labs are given below:

y y y y y y y y y y y y

pH 7.27 PO2 90 PCO2 30 Bicarbonate (mEq/L) 13 Serum Sodium (mEq/L) 136 Potassium (mEq/L) 3.9 Chloride (mEq/L) 114 BUN (mg/dL) 21 Creatinine (mg/dL) 1.2 Albumin (g/dL) 4.0 Glucose (mg/dL) 128 Urine pH Sodium (mEq/L) Potassium (mEq/L) Chloride (mEq/L)

6 32 21 80

Case # 8
y A 21-year-old male presents to the emergency room with severely diminished

mental status. He states that he has felt nauseated for the last few days and has been unable to eat well. This morning, he vomited several times and was brought to the emergency room by his girlfriend. a tonsillectomy as a child but no other surgeries.

y His past medical history is negative for any chronic medical problems. He had y Physical exam is significant for blood pressure of 122/57 mm Hg, pulse of 105

beats/minute, respiratory rate of 28 breaths/minute, and temperature of 99.3F. He is thin and in moderate distress. Chest exam is normal. His abdomen is soft and nontender. Stool is negative for occult blood.

y In the emergency room, the patient begins to vomit large amounts, and he

aspirates a significant amount of stomach contents and develops respiratory failure. He is intubated and started on mechanical ventilation. After 1 hour of mechanical ventilation, the following laboratory values are received:

y y y y y y y y y y y y

pH 7.41 pO2 67 PCO2 27 Bicarbonate (mEq/L) 16 Serum Sodium (mEq/L) Potassium (mEq/L) 3.7 Chloride (mEq/L) 91 BUN (mg/dL) 11 Phosphorus (mg/dL) 2.2 Albumin (g/dL) 3.6 Creatinine (mg/dL) 1.7 Glucose (mg/dL) 84

138

Case # 9
y A 64-year-old is admitted to the intensive care unit with

pneumonia and septic shock. The patient states that he has had increasing shortness of breath and fever over the past 4 days. y His past medical history is significant for hypertension. Surgical history is significant for a previous cholecystectomy. Medications include amlodipine and hydrochlorothiazide. y Physical exam shows a blood pressure of 85/50 mm Hg, pulse of 110 beats/minute, respiratory rate of 22 breaths/minute, and temperature of 101.8F. The cardiovascular examination is significant for a 2/6 systolic murmur and there are crackles over his entire right lung field. There is trace pedal edema. y Chemistry values on admission are given below:

y y y y y y y y y y y y

pH 6.95 PO2 (mm Hg) 51 PCO2 (mm Hg) 48 Bicarbonate (mEq/L) 10 Serum Sodium (mEq/L) Potassium (mEq/L) 4.8 Chloride (mEq/L) 103 BUN (mg/dL) 22 Creatinine (mg/dL) 1.4 Phosphorus (mg/dL) 2.8 Albumin (g/dL) 3.8 Glucose (mg/dL) 115

135