Arterial Blood Gas Analysis
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Transcript of Arterial Blood Gas Analysis
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)
• 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
• 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