Dr. T.R.Chandrashekar Intensivist, Liver transplantation. BMC & RI super-specialty Hospital. Bangalore.

Arterial Blood Gas Analysis

Why Order an ABG?

Aids in establishing a diagnosis Helps guide treatment plan Aids in ventilator management Improvement in acid/base management allows

for optimal function of medications Acid/base status may alter electrolyte levels

critical to patient status/care

Blood Gas Interpretation-means analyzing the data to determine patient’s state of:

Ventilation

Oxygenation

Acid-Base

Approach to ABG Interpretation

Assessment of Acid-Base Status

Assessment of Oxygenation & Ventilation Status

There is an interrelationship, but less confusing if considered separately…..

Volume –Osmolality Electrolytes

-----XXXX Diagnostics----Blood Gas Report

Measured 37.0 0CpH 7.452 pCO2 45.1 mm HgpO2 112.3 mm Hg

Calculated Data

HCO3 act 31.2 mmol / LO2 Sat 98.4 %O2 ct 15.8pO2 (A -a) 30.2 mm Hg pO2 (a/A) 0.78

Entered Data

FiO2 %Ct Hb gm/dl

-----XXXX Diagnostics-----

Blood Gas Report328 03:44 Feb 5 2006Pt ID 3245 / 00

Measured 37.0 0CpH 7.452 pCO2 45.1 mm HgpO2 112.3 mm Hg

Corrected 38.6 0CpH 7.436pCO2 47.6 mm HgpO2 122.4 mm Hg

Calculated Data

HCO3 act 31.2 mmol / LHCO3 std 30.5 mmol / LB E 6.6 mmol / LO2 ct 15.8 mL / dlO2 Sat 98.4 %ct CO2 32.5 mmol / LpO2 (A -a) 30.2 mm Hg pO2 (a/A) 0.78 Entered DataTemp 38.6 0CFiO2 30.0 %ct Hb 10.5 gm/dl

Calculated parameters

Measured parameters

FIO2 X 5=PaO2

Why would I require a ABG ?

Oxygenation status?- Pulse oximeter SPO2✔ Ventilation status ? – ETCO2✔ Acid base status?

Stable patient Normal hemodynamics Good UO Surgical stress + Sick patient

Hepatic/ Renal dysfunction Massive blood/ fluid usageSpecific surgeries- liver transplantation/ Hypotensive anaesthesia/ aortic surgeriesIHD/COPD/ Asthma ……

Assessment of Oxygenation

PaO2=Not informative

CaO2= DO2- Better

DO2~VO2=ScVO2 and Lactate- IdealO2 delivery is a Cardio-Respiratory function

TIME =TISSUE

Oxygen DonOxygen Don’t Go’t Go

Where the Blood Won’t FlowWhere the Blood Won’t Flow

Oxygen delivery DO2

Oxygen requirement VO2

Oxygen Cascade

Atmospheric Air- 150 mmHg ( 21%)

PAO2-Alveolar Oxygen-100 mmHg ( CO2 / Water Vapour)

PaO2- 90mm Hg ( A-a difference)

SaO2 ( can be measured if Co-oximeter / calculated ODC)- Limitations

CaO2- Oxygen content (1.34 x Hb x Sao2)

DaO2 = Oxygen delivery = (CaO2 x Cardiac output)

If A-a difference is more -does it tell us

anything ?

OO22

COCO22

AlveoliPAO2

Atmospheric air /FIO2

Water vapour is added- Nose/ upper airway

Alveolar Oxygen

PaO2 (2% dissolved O2)

Measured in ABG

SaO2

O.

D.

C.

98% of O2 is Hb bound-

1.34 x Hb% x Sao2

CaO2-oxygen content +PaO2 x 0.003ml

Oxygen Delivery=CaO2 x Cardiac output

Cardiac output - SV x HR Preload / Afterload/ Contractility

Oxygen delivery DO2 is a Cardio- Respiratory Function

=

Intra-operative bleeding HbAspiration/ collapseCardiac depressants drugs/ MIStress response- Afterload

Causes for DO2

The power of hemoglobin

Normal Hypoxemia Anemia

PaO2 90 mm Hg 45 mm Hg 90 mm Hg

SaO2 98% 80% 98%

Hb 15 g/dL 15 g/dL 7.5 g/dL

CaO2 200 ml/L 163 ml/L 101 ml/L

% change - 18.6% - 49.5%

Restrictive transfusion strategy is the order of the day

PaCO2=60 mmHg

PAO2 = FIO2 (BP-47) – 1.2 (PaCO2) =.21 (760- 47) – 1.2 (60)

= 150 – 72 = 78

An elevated PaCO2 will lower the PAO2

and as a result will lower the PaO2

We always correlate PaO2 with FiO2

BUT…………………………. never forget to correlate with

PaCO2

PAO2=FIO2(Barometric Pressure-H2O)-1.2(PCO2)

PAO2 = FIO2 (760– 47 mm Hg)- 1.2 (PaCO2)

PAO2 = 0.21(713)-1.2(40)=100 mmHg

“1.2” is dropped when FIO2 is above 60%.

PAO2 is affected by PCO2

A-aDo2 A-aDo2 = PAO2-PaO2(from ABG)= 10-15 mmHg / Increases with age

Increased P(A-a)O2 -lungs are not transferring oxygen properly from alveoli into the pulmonary capillaries.

OO2 2

COCO22

PaO2

AlveoliPAO2

P(A-a)O2

Diffusion defect Interstitial edema ILD/ARDS

V/Q Mismatch-Dead SpaceAmendable to increased FIO2

Shunt ( >30%) not amendable to increased FIO2 / May require PEEP

P(A-a)O2 signifies some sort of problem within the lungs

If DO2 is normal is everything OK?

Next question is

Is DO2~VO2 ? Lactate levels

ScVO2/SVO2

A central venous ABG may

be more informative than

arterial ABG

ScVO2

DO2

Consumption O2

75%

Factors that influence mixed and central venous Factors that influence mixed and central venous SOSO22

↑VO2 ↓DO2 ↑ DO2 ↓VO2 Stress Pain Hyperthermia Shivering

↓ PaO2

↓ Hb

↓ Cardiac output

↑ PaO2

↑ Hb

↑ Cardiac output

HypothermiaAnesthesia

_ + DO2 Oxygen delivery VO2 Oxygen requirement

Summary –Oxygenation assessment CaO2 x CO =Delivery

ScVO2 & Lactate levels = Surrogates for DO2~VO2

Lacti-Time- prognostic indicator Is lactate bad? May not due to anaerobic metabolism Body’s response to stress Alternate energy shuttle ScVO2 Range

60-80% Normal

60-50% More extraction warning sign

50-30% Lactic acidosis Demand > Supply

30-20% Severe lactic acidosisCell death

ScVO2

SVO2

> 5-7

65 yr old male with DM IHD –in septic shock on ventilatorABG-PaO2-90 PH 7.42, PCO2 43Hb-12 gm%, Spo2 98%CaO2-17 Vol%BP 90/40 mmHg ,Temp 103FWhat is the problem ?

ScVO2 58%, Lactate 8 mMoles/L

Fluid resuscitation

Noradrenaline / DobutamineFever control

After 2hrs ScVO2 68%, Lactate 2 mMoles/L

Case …. PaO2 and DO2 are normal

65 yr old male with DM IHD –in septic shock on ventilatorABG-PaO2-90 PH 7.42, PCO2 43Hb-12 gm%, Spo2 98%CaO2-17 Vol%BP 70/40 mmHg ,Temp 102FWhat is the problem ?ScVO2 45% Lactate 10 mMoles/L

Microcirculatory Mitochondrial Dysfunction (MMDS)

Fluid resuscitation

Noradrenaline / DobutamineFever control

After 2hrs ScVO2 38%, Lactate 14 mMoles/L

PaO2 and DO2 are normal

Assessment of Ventilatory Status….

Oxygenation Acid-Base

HCO3

PAO2 = FIO2 (BP-47) – 1.2 (PCO2) pH ~ ------------

PaCO2

PaO2

» VCO2 x .863

» PaCO2 = --------------------

» VA

» VA=Minute ventilation-Dead space volume

» f(VT) – f(VD)

PaCO2 is key to the blood gas universe; without understanding PaCO2 you can’t understand oxygenation or acid-base.

The ONLY clinical parameter in PaCO2 equation is RR

VCO2=CO2 production

Difficulties in sampling and accurate measurement limits the usefulnessOf dead space in clinical practice =2ml/kg

Breathing pattern’s effect on PaCO2

Patient Vt f MV Description A (400)(20) = 8.0L/min (slow/deep) B (200)(40) = 8.0L/min (fast/shallow)

Patient Vt-Vd f Alveolar ventilation A (400-150) (20) = 5.0L/min B (200-150) (40) = 2.0L/min

PaCO2 = alveolar ventilation

Not on Minute ventilation which is measured

Condition State ofPaCO2 in blood alveolar ventilation

> 45 mm Hg Hypercapnia Hypoventilation

35 - 45 mm Hg Eucapnia Normal ventilation

< 35 mm Hg Hypocapnia Hyperventilation

PaCO2 abnormalities…

PCO2 / RR- 65 / 7 in Drug overdosageTrue hypoventilation

PCO2 / RR - 65 / 37 in bilateral consolidation Reduced alveolar ventilation/ dead space ventilation

PCO2 / RR - 22 / 37 in post operative patient with pain and fever-Increased alveolar ventilation

Acid-Base DisturbancesAcid-Base Disturbances

Perioperative acid base disturbances

Sick patients + Stress of surgery

Decreased organ perfusionReduced immunityActivity of coagulation factors and complement system impaired

Cardiac depressionVasoplegiaArrhythmias Inotropes or vasopressors do not workReduced O2 deliveryO2 delivery is a Cardio-Respiratory function

Hypo perfusion— Anaerobic metabolism-Lactic acidosis- More Cardiac depression and vasoplegia-Viscous cycle

There is always a underlying cause- treatment of which is the most important step in acid base problems

Deodorant

Flush

Problem

.Patient has Peritonitis/ SepsisBP 80/60 mmHgpH of 7.12, HCO3 14, Lactate of 6 PCO2 23Metabolic acidosis

NAHCO3

Infusion to correct pH

Fluid resuscitationInotropes/ vasopressorsSurviving Sepsis bundle

•Fever , pain, shivering-Increased metabolic demands

Limited cardio pulmonary reserves -more problems

•Narcotics , Sedatives, NMB –hypoventilation

•Nasogastric suctioning-Chloride loss- Metabolic alkalosis

•Hypotension may lead to lactic acidosis, renal dysfunction

Septic patients / Elderly / diabetic HT Nephropathy / IHD

Commonly encountered acid base disturbances seen in Perioperative period

Basics •[H+]= 40 nEq/L at pH-7.4•For every 0.3 pH change = [H+] double

160nEq/L40 nEq/L

16nEq/L

[ H+] in nEq/L = 10 (9-pH)

CO2 + H2O H2CO3 H+ + HCO3-

CO2H+

HCO3-

Acid-Base physiology

Respiratory

Metabolic

Bicarbonate is the transport from of CO2 hence both should move in the same direction

Ventilation controls PCO2

Kidney losses H+ and reabsorbs bicarbonate (HCO3-)

PCO2-Respiratory acidosis

(Hypoventilation)

PCO2-Respiratory alkalosis(Hyperventilation)

HCO3- - Metabolic acidosis

HCO3- - Metabolic Alkalosis

Very fast 80% in ECF

Starts within minutes good response by 2hrs, complete by 12-24 hrs

Starts after few hrs complete by 5-7 days

Acid-base Balance Henderson-Hasselbalch Equation

[HCO3-]

pH = pK + log ------------- .03 [PaCO2]

For teaching purposes, the H-H equation can be shortened to its basic relationships:

HCO3- ( KIDNEY)

pH ~ --------------------

PaCO2 (LUNG)

Maximum compensationHCO3-= 40/10

CO2=60/10

Stewart approach

• Stewart (physical chemistry principles) suggested that the traditional Henderson-Hasselbalch explanation of the underlying physiology and pathophysiology is wrong.

• “Traditional” approach merely looks at a mirror image of that proposed by Stewart. In fact HH equation is a component of Stewart approach

• The ‘‘modern’’ approach is clinically difficult, more CPU based

• Requires knowledge of protein and phosphate concentrations and more electrolytes than may be routinely measured

Characteristics of 1° acid-base disorders

DISORDER PRIMARY RESPONSES

COMPENSATORY RESPONSE

Metabolic acidosis

↓ PH ↓ HCO3- ↓ pCO2

Metabolic alkalosis

↑ PH ↑ HCO3- ↑ pCO2

Respiratory acidosis

↓ PH ↑ pCO2 ↑ HCO3-

Respiratory alkalosis

↑ PH ↓ pCO2 ↓ HCO3-

pH HCO3 CO2

7.20 15 40

7.25 15 30

7.38 15 20

Un Compensated

Partially Compensated

Fully Compensated

(pH abnormal)

(pH in normal range)

This amount of compensation rarely occurs in Acute situations

Metabolic acidosis with compensatory Respiratory alkalosis

Body’s physiologic response to Primary disorder in order to bring pH towards NORMAL limit

Full/Partial compensation/uncompensated

BUT never overshoots, If overshoot pH is present -Take it for granted it is a MIXED disorder

Normal functioning

• Clinical history

• pH normal, abnormal PCO2 and HCO3

• PCO2 and HCO3 moving in opposite directions

• Degree of anticipated compensation for primary disorder is inappropriate??

Primary Respiratory disorders Metabolic compensations

RESPIRATORY disorders CO2 Change lead to change in HCO3

Acidosis-expected change in HCO3 = 1

Alkalosis-expected change in HCO3 = 2 x

Acidosis-expected change in HCO3 =3 x

Alkalosis-expected change in HCO3 = 4 x

Acute respiratory

Chronic respiratory

For every 10 mmHg CO2 change Expected HCO3 Change is given below

Step 5 continued…CompensationStep 5 continued…Compensation

Primary Metabolic disorders Respiratory compensations

Metabolic disorders compensation by changing CO2

Metabolic Acidosis: Compensation CO2

Winters’ formula

pCO2 = 1.5 x [HCO3-] + 8 ± 2

Last two digits of pH = PaCO2

pH being 7.23 = PaCO2should fall to 23mmHg

Metabolic Alkalosis: Compensation CO2

pCO2 = 0.7x [HCO3-] + 20 ± 5

Unpredictable because increasing CO2 causes increased RR

More anions are unmeasured than are cations

Major unmeasured anions• albumin• phosphates• sulfates• organic anions- ketones and

lactate

Anion gap-AG = [Na+] - [Cl- +HCO3-]

Anion gap is thus an artifact of measurement, and not a physiologic reality

1 gm/dl decrease in serum albumin causes a 2.5 drop in the AG.

• Elevated anion gap represents metabolic acidosis• Normal value: 12 ± 4mmol/L (More than 20 is usually significant)

chandrakavi@gmail.com

• Practice gentle mechanical ventilation and do not try to bring ABG to perfect normal.

• Treat the patient not the ABG report

2. Look at pH? (Acidosis /Alkalosis)

3. HCO3- // PCO2 (respiratory or metabolic or mixed )

4. Match either pCO2 at the HCO3with pH

(which is primary & which is compensation)

5. Fix the level of compensation.

6.If metabolic acidosis, calculate-Anion gap

7. Treat the Patient not the ABG

1. Consider the clinical settings! Anticipate the disorder

7 steps to analyze ABG

1st Step-Clinical History

COPD- Chronic Respiratory Acidosis-Compensatory Met alkalosis

Post O.P patient -residual NMB, drowsy Respiratory Acidosis not well compensated

Cardiac arrest Metabolic/Respiratory acidosis

Septic shock Metabolic acidosis

2nd stepLook at the pH - Label it.

70 yr old man operated for # neck femur under GA/ extubated drowsy shallow breathing on 2l of O2 Spo2 88%ABG shows

pH of 7.28- ACIDOSISPaCO2 of 80 mm Hg, HCO3- of 25 mEq/L. Na+ 143, CL-104

Label it. (Respiratory or metabolic) pH of 7.28, PaCO2 of 80 mm Hg-Respiratory acidosis HCO3- of 25 mEq/L- Alkalosis

Normal pCONormal pCO22 levels are 35-45mmHg. levels are 35-45mmHg.

Below 35 is alkalosis, Below 35 is alkalosis,

Above 45 is acidosis.Above 45 is acidosis.

3RD step-Look at -pCO2/ HCO3 which has moved in acidotic direction

Next match either -pCO2 or HCO3 with the pH pH of 7.28-Acidosis

PaCO2 of 80 mm Hg-Respiratory acidosis

HCO3- of 25 mEq/L- Compensatory alkalosis

pH and PCO2have moved in same direction

So it is Primary respiratory acidosis

4TH Step- Find the primary problem and what is compensatory

HCO3- of 25 mEq/L is going in opposite direction of pH.Metabolic compensation Is it full/partial/uncompensated ???Another disorder- mixed disorder ????

RESPIRATORY disorders- CO2 Change lead to change in HCO3

Acidosis-expected change in HCO3 = 1

Alkalosis-expected change in HCO3 = 2 x

Acidosis-expected change in HCO3 =3 x

Alkalosis-expected change in HCO3 = 4 x

Acute respiratory

Chronic respiratory

For every 10 mmHg CO2 change expected HCO3 Change is given below

Step 5 continued…CompensationStep 5 continued…Compensation

5TH fix compensation- full or partial??

Do the calculations…. pH of 7.28, PaCO2 of 80 mm Hg, (80-40=40 mmHg increased) HCO3- of 25 mEq/L

PCO2 is increased by =40 (for every 10 rise in CO2 /HCO3 should increase by 1)

HCO3=should be increased by 4

i.e. 24+4=28( for full compensation)

Respiratory acidosis with partially compensated metabolic alkalosis

• Calculate the anion gap if it is more there is Metabolic acidosis

AG = [Na+] - [Cl- +HCO3-AG = [Na+] - [Cl- +HCO3-]]

Sixth Step- AG in case of metabolic acidosis

pH of 7.30, PaCO2 of 80 mm Hg, and HCO3- of 27 mEq/L. Na+ 143, CL-104

AG+143- (104+27)=140-131=12

7Th Step Treat the Patient not the ABG

PCO2-60mmHg,

PO2-54mmHg

RR-40/min,

55 yr old patient with

chronic neurological

weakness conscious, comfortable

PCO2-60mmHg,

PO2-54mmHg

RR-40/min, Spinal surgery post OP

extubated with residual NMB effect and drowsy

Severe respiratory distress

Reversal /vent support

chandrakavi@gmail.com

• Practice gentle mechanical ventilation and do not try to bring ABG to perfect normal.

• Treat the patient not the ABG report

Too much normal saline hyperchloremic acidosis Can we explain why increased Cl- causes Acidosis??

Normal saline infusion leads to hyperchloremic acidosis

Dilution of HCO3

-

CO2

CO2 increasesHCO3

- unchanged

pH falls

Metabolic CO2 production

pH falls

Water H2O dissociates and adds H+

Explanation of acidosis by HH method Explanation of acidosis by Stewart

In NS- Na/Cl is 150 mEq/LIn ECF -Na 145/ Cl 102

Two approaches used in Acid base evaluation

HCO3- ( KIDNEY) 20

PaCO2 (LUNG) 1

pH ~

Metabolic’ component of acid-base physiology is bicarbonate

Stewart approachTraditional approachHenderson-Hasselbalch Water is an important source of H +

Ionic Strength: weak and strong

Electrical Neutrality is maintained at all timesMetabolic’ component of acid-base physiology is Strong Ion Difference (SID)

SID=(Na+ +K+ +Ca2++Mg2+)-(Cl-+Lactate) is 40 to 42 mEq/L

Two commonly used approaches

pH rely on three independent Factors

1. SID- Strong ion difference

2. (ATOT)- total concentration of weak acids (albumin and phosphate)

3. PCO2

‘Metabolic’ component of acid-base physiology is not dependent on bicarbonate but instead, predominately on SID

Henderson-Hasselbalch Stewart approach

HCO3- ( KIDNEY)

PaCO2 (LUNG)

pH --------- ------~

Modified Stewart approach

= ([Na+] – [Cl-]) – 38 (1)

= 0.25x [4.2–albumin] (2)

Thus true BE = BE – [1 + 2]

At bedside- it works well!

{where 38 is normal average difference in strong ions – Na and Cl}

NaCl effect

Albumin effect

Story, Belmo, Balasubramanyam

where 4.2 is normal serum albumin

Base excess

The base excess is a calculated value that quantifies metabolic derangements.

It hypothetically ‘‘corrects’’ pH to 7.4 by ‘‘adjusting’’ measured PaCO2 to 40 mmHg, allowing a comparison of the ‘‘corrected’’ HCO3

with the normal HCO3.(i.e.,24mEq/L)at pH 7.4. A negative value means that HCO3 stores are depleted.

Base excess=HCO3+10(pH-7.4)-24

Uncompensated Respiratory Acidosis

pH = 7.4PaCO2 = 40 HCO3 = 24

Post op pt –drowsy

Uncompensated Respiratory Alkalosis

pH = 7.4PaCO2 = 40 HCO3 = 24

Pt on vent pressure support has pain

Acute asthmatic

Normal A.B.G.

pH = 7.4PaCO2 = 40 HCO3 = 24

Partially compensated Metabolic Acidosis

pH = 7.4PaCO2 = 40 HCO3 = 24 20 yr old male with Acute Gastroenteritis…..

Case

A 46-year-old man has been in the hospital for two days with pneumonia. He was recovering but has just become diaphoretic, dyspneic, and hypotensive. He is breathing oxygen through a nasal cannula at 3 l/min.

pH 7.41PaCO2 20 mm Hg HCO3- 12 mEq/LCaO2 17.2 ml O2/dl

PaO2 80 mm Hg

SaO2 95%

Hb 13.3 gm%

How would you characterize his state of oxygenation,ventilation, and acid-base balance?

Normal pH Respiratory alkalosis and Metabolic acidosis.

Winters formulapCo2=1.5 x 12 +8=26

Case

Mrs. H is found pulseless and not breathing this morning. After a couple minutes of CPR she responds with a pulse and starts breathing on her own. A blood gas is obtained:pH----------- 6.89 pCO2 -------70 pO2 ---------42 HCO3------- 13 SaO2-------- 50%

What is your interpretation? What interventions would be appropriate for

Mrs. H?

Mrs. H has a severe metabolic and respiratory acidosis with hypoxemia

Case …..

A 44 year old moderately dehydrated man was admitted with a two day history of acute severe diarrhea. Electrolyte results: BP 90/60 mmHg

Na+ 134, K+ 2.9, Cl- 108, BUN 31, Cr 1.5.

ABG: pH 7.31 PCO2 33 mmHg

HCO3 16 PaO2 93 mmHg What is the acid base disorder?

HistoryAcidosis from diarrhea or lactic acidosis as a result of hypovolemia and poor perfusion.

Normal anion gap acidosis with adequate compensation

Look at the pH- acidemic. What is the process? Look at the PCO2, HCO3- .

PCO2 and HCO3- are abnormal in the same direction, therefore less likely a mixed acid base disorder.

Calculate the anion gap

The anion gap is Na - (Cl + HCO3-) = 134 -(108 + 16) = 10

Is compensation adequate? Calculate the estimated PCO2.

Winter's formula;

PCO2 = 1.5 × [HCO3-]) + 8 ± 2 = 1.5 ×16 + 8 ± 2 = 30-34.

Case....

A 50 year old insulin dependent diabetic woman was brought to the ED by ambulance. She was semi-comatose and had been ill for several days. Current medication was digoxin and a thiazide diuretic for CHF.Lab results Serum chemistry:

Na 132, K 2.7, Cl 79, Glu 815, Lactate 0.9 urine ketones 3+ ABG: pH 7.41 PCO2 32

HCO3- 19 pO2 82

History:Elevated anion gap acidosis secondary to DKA Metabolic alkalosis in the setting of thiazide diuretics use.

Case...... 2. Look at the pH. - Note that the pH is normal which would suggest no

acid base disorder. But remember, pH may be normal in the presence of a mixed acid base disorder.

3. What is the process? Look at the PCO2, HCO3- . PCO2 is low indicating a possible respiratory alkalosis. The HCO3- is also low indicating a possible metabolic acidosis. Because the pH is normal, we are unable to distinguish the initial, primary change from the compensatory response.

We suspect however that the patient has DKA, and therefore should have a metabolic acidosis with an anion gap that should be elevated. We can confirm this by calculating the anion gap.

4. Calculate the anion gap The anion gap is Na - (Cl + HCO3-) = 132 -(79 + 19) = 34 Since gap is greater than 16, it is therefore abnormal and confirms the presence of metabolic acidosis.

Why is the pH normal? If the patient has metabolic acidosis, we suspect a low ph unless there is another process acting to counteract the acidosis, i.e alkalosis.

Delta Gap 34-12=22 + 19=41 Met alk Since the delta ratio is greater than 2, we can

deduce that there is a concurrent metabolic alkalosis. This is likely due to to the use of thiazide diuretic. Note that DKA is often associated with vomiting, but in this case;vomiting was not mentioned.

Another possibility is a pre-existent high HCO3- level due to compensated chonic respiratory acidosis. But we have no reason to suspect chronic respiratory acidosis based on the history.

Assessment: Mixed elevated anion gap metabolic acidosis and metabolic alkalosis likely due to DKA and thiazide diuretics.

Anion gap issues

A 1 gm/dl decrease in serum albumin causes a 2.5 mEq/L drop in the AG.

One problem with the anion gap is deciding what value is truly abnormal.

In the majority of patients with anion gap between 16 and 20 mEq/L, no specific anion gap acidosis can be diagnosed.

Above 20 mEq/L the probability of a true anion gap acidosis increases markedly (and is 100% if the AG is above 29 mEq/L)

As a practical matter, you should consider an AG 20 mEq/L as reflecting an anion gap metabolic acidosis and search for the cause should be instituted

Delta gap = HCO3 + ∆ AG

Delta Gap = 24….Pure AG acidosis

< 24 = non AG acidosis

> 24 = metabolic alkalosis

∆ AG =Measured Anion gap-12

Delta Gap = 24 …… AG Met Acidosis < 24 ….. Non AG Met acidosis > 24 ….. Non AG Met acidosis + Meta. Alkalosis

CaO2 = (1.34 x Hb x SaO2) +dissolved O2

DO2 = CO X CaO2

Cardiac outputMitochondria in end organs

7 g % ALI/ARDS

PE

Sepsis induced myocardial depression

Drugs

Inotropes

Pericardial effusion

vv

MMDS-cannot extract O2O2

lactateCO2

vvaa

DO2/VO2

Patients have to be kept well above the Critical Point so that

Does not plateau- Consumption remains supply dependent even with supraphysiological levels

VO2 is supply dependent

VO2 is supply independent

Oxygenation to the tissue is not compromised

MMDS and O2 extraction failureShunting due to micro-emboli