Indications for Mechanical Ventilation&

Dr. T.R.ChandrashekarChief -Department of Critical Care

K.R.Hospital, BangaloreKarnataka, India

Arterial Blood Gas Analysis

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

2

Ventilation

Oxygenation

Acid-Base

Discuss Indications for Mechanical Ventilation along with ABG interpretation and clinical examples

Approach to ABG Interpretation

Assessment of Acid-Base Status

Assessment of Oxygenation & ventilatory Status

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

Volume –Osmolality Electrolytes

Always mention and see… FiO2 / ct Hb

-----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

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

Matching delivery

= Requirement

Assessment of Oxygenation

O2 delivery is a Cardio-Respiratory function

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

P(A-a)O2

SaO2

O.

D.

C.

Temp H+2,3-DPG

98% of O2 is Hb bound-1.34 x Hb% x Sao2CaO2-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

=

DO2-Oxygen delivery- CaO2 x Cardiac output

Did oxygen delivery meet the demand?

Patient with sepsis on ventilator has fever 103F ,BP 80/60 mmHg, HR 140/mt, PaO2 100 mmHg, PcO2 42 mmHg, PH 7.23, HCO3 20, SaO2 98%Hb 12 gm%, Not responding to Fluids/ inotropesDelivery (DO2 )looks OKHow to assess the consumption?

Lactate-Anaerobic meatabolismLacti-timeScVo2- oxygen saturation in Superior vena Cava

ScVO2

DO2

Consumption O2

CO2

O2

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

FIO2

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%.

5 X FIO2=PaO2

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

V/Q Mismatch-Dead Space

Shunt

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

Oxygenation Physiology

PAO2

Diffusion defect

Pao2

Shunt

Does not respond to FIO2

Responds to FIO2

Diffusion defect is a rare cause1µm

Oxygenation over within 1/3 timeIf HR >240 it affects

CO2 has over 20 times moreDiffusion coefficientSevere ARDS/ILD

CO2

Atmospheric air

Nitrogen

FIO2- O2

PaO2

V/Q Mismatch

Alveolar-arterial Difference

OO22

COCO22

Alveolar – arterial G.

100 - 45 = 55 ……………….Wide A-a

Oxygenation Failure Wide Gap

PCO2 = 40PaO2 = 45

PAO2 = 150 – 1.2 (40)

= 150 - 50 = 100

Ventilation FailureNormal Gap

PCO2 = 80PaO2 = 45

PAO2 = 150-

1.2(80) = 150-100 = 50 Alveolar arterial G.

50 – 45 = 5…………….Normal A-a

Interpretation of shunt fractions

<10%<10% NormalNormal

10-20%10-20% Mild shuntMild shunt

20-30%20-30% Significant shuntSignificant shunt

>30%>30% Critical shunt, even Critical shunt, even 100% O2 cannot 100% O2 cannot restore Pao2restore Pao2

arterial-Alveolar O2 tension ratio

a/A ratio

>0.75 normal

0.40-0.75 acceptable

0.29-0.39 poor

<0.20 very poor

a/A ratioNomogram

Oxygen Dissociation Curve: SaO2 vs. PaO2

CaO2A B

Which patient is more hypoxemic, and why?

Patient A: pH 7.48, PaCO2 34 mm Hg, PaO2 85 mm Hg, SaO2 95%, Hemoglobin 7 gm%-

Patient B: pH 7.32, PaCO2 74 mm Hg, PaO2 59 mm Hg, SaO2 85%, Hemoglobin 15 gm%-

Patient A: Arterial oxygen content = .95 x 7 x 1.34 = 8.9 ml O2/dl Patient B: Arterial oxygen content = .85 x 15 x 1.34 = 17.1 ml

O2/dl

Hypoxic/Hypercarbic

Anemic

98% of O2 is Hb bound-1.34 x Hb% x Sao2

+ ( 2% )PaO2 x 0.003mlCaO2 =

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%

20 v

ol% 15 vol %

O2 Transport; Normal

= C.O X arterial O2 content5 L blood x150 /L blood x 1.39 ml O2/g Hb(= 20 ml O2/dl blood, or 20 vol %

= 1000 ml O2/min= 250 ml( oxygen consumption)

750 ml = Venous O2 return( = 15 vol%)

DO2

ScVO2-60%-80% normal range

Is the central venous oxygen saturation measured from a CVP cannula

Reflects the global balance between oxygen Delivery and consumption

ScVO2 SVO2ScVO2 Range

60-80% Normal

60-50% More extraction warning sign

50-30% Lactic acidosis Demand > Supply

30-20% Severe lactic acidosisCell death

> 5-7

Factors which alter ScVo2

Decreased DeliveryDO2

Increased Consumption VO2

Fever, ShiveringTraumaPain / anxiety

DysarhythmiaCCF/ MISepsis

Hypoxia/hypoxemiaSuctioning, ARDS/ COPD

HemorrhageOccult bleedingRBC disordersAnemia

65 yr old male with DM IHD –in septic shock on ventilatorABG-PaO2-90 PH 7.42, PCO2 43Hb-12 gm%, Spo2 98%CaCo2-17 Vol%BP 90/40 mmHg ,Temp 103FWhat is the problem ?

ScVO2 48%, Lactate 8 mMoles/L

Fluids Nor adrenaline / Dobutamine

Fever control

Case ….

65 yr old male with DM IHD –in septic shock on ventilatorABG-PaO2-90 PH 7.42, PCO2 43Hb-12 gm%, Spo2 98%CaCo2-17 Vol%BP 90/40 mmHg ,Temp 103FWhat is the problem ? ScVO2 68%, Lactate 2 mMoles/L

Microcirculatory Mitochondrial Dysfunction (MMDS)

ScVo2

Lactate metabolism

Glucose

Pyruvate Lactate

Oxidative phosphorylation

2 ATP

36 ATP NAD+CO2+H2O

O2 + NADH

GlycolysisADP

Cell Cytoplasm

Mitochondria

Oxygen

cc

Energy Failure and Lacti-Time

Aerobic

metabolism

36 ATP

Lack of O

2 delivery

Anaerobic

metabolism

2 ATP +

Lactic a

cid

The time before lactate becomes less than 2 is important prognostic indicator-LACTI- TIME

Septic patient admitted to ICU BP 90/50, HR 150/mtScVO2-45%, Lactate 6 mmoles/L ,PH 7.16, PaO2/PCO2- 68/39 mmHg

After 2hrs- fluid resuscitation/Noradrenaline

BP140/80 mmHgScVo2-65% Lactate

3 mmoles/L

After 2hrs- fluid resuscitation/Noradrenaline

BP 70/40 mmHgScVo2-45% Lactate

7mmoles/L Microcirculatory mitochondrial

dysfunction (MMDS)

Summary –Oxygenation assessment

CaO2 x CO =Delivery ScVO2=consumption Lactate=Delivery not meeting demand

Anaerobic metabolism- decreased ATP production -cell death

Lacti-Time- prognostic indicator

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

Breathing pattern’s effect on PaCO2

Patient Vt f Ve Description A (400)(20) = 8.0L/min (slow/deep) B (200)(40) = 8.0L/min (fast/shallow) Patient Vt-Vd f Va A (400-150)(20) =5.0L/min (slow/deep) B (200-150)(40) =2.0L/min (fast/shallow)

PaCO2 = alveolar ventilation

Not on Minute ventilation which is measured Dead space quantification at bed side not possible

Condition State of

PaCO2 in blood alveolar ventilation

> 45 mm Hg Hypercapnia Hypoventilation

35 - 45 mm Hg Eucapnia Normal ventilation

< 35 mm Hg Hypocapnia Hyperventilation

PaCO2 abnormalities…

PCO2-65 mmHg with rate 7/mt in Drug overdosage 65/7-true hypoventilation

PCO2-65 mmHg with rate 37/mt in bilateral consolidation 65/37- Reduced alveolar ventilation/ dead space ventilation

PCO2-22 mmHg with rate of 37/mt in post operative patient with pain and fever-Increased alveolar ventilation

Quantification of Dead space

VD

VVTT=

25-40% NORMAL (2ml/Kg)

In MV pts till 55% is normal

More than 60% is abnormal

dead space

Quantification of Dead spaceQuantification of Dead space

VD/VT=(PaCO2-PETCO2)/PaCO2

Minute volume in liters Ҳ PaCO2(mmHg)

Body weight in kg

Normal index<5

More than 8 indicates an increase dead space

Limitation-need to measure minute volume accurately

Difficulties in sampling and accurate measurement limits the usefulnessOf dead space in clinical practice

Case Scenarios ….

20 year old male with OP poisoning with fasciculation's, neck muscle weakness with RR 35/mt, increased WOB, SPO2 on 4l/mt on RBM

84%, pooling secretions, HR 150/mt on atropine drip, BP 140/60

ABG PH 7.37 Pao2-52 Pco2-32 Do we intubate this guy?

YES

Intubated minimal settings ABG stabilisedHas Pulse oximeter/ ETCO2Do we require to repeat ABG’s NO

If pt develops hypotensionOn inotrope /not synchronising Yes

Treat the Patient not the ABG

ABG-PCO2-60mmHg, PO2-58mmHg

with HR-80/min, BP- 130/80mmHg, RR-14/min,

A 45 yr old patient with chronic neurological weakness conscious, comfortable

ABG-PCO2-60mmHg, PO2-58mmHg

and with HR-120/min,BP-100/70 mmHg,RR-40/min,

A 24yr old asthmatic severe respiratory

distress, drowsy

Intubate

Case Scenario….

40 yr old diabetic male pt with urinary sepsis Has BP 90/60 mmHg after fluid resuscitation,

high dose noradrenaline,has tready pulse, is tachypenic 35/mt with increased WOB-is restless. On 6L of O2 RBM

ABG PH-7.38

PaCO2-36 mmHg

PCO2-100 mmHg

Sao2-98%, ScVo2-50%, Lactate 6 mmoles/L

Do we intubate this patient

Normal respiratory effort-5% CONearly 20-30% CORest respiratory muscle and so CO is utilised by essential organs

55 year old chronic smoker, Diabetic male admitted with Lower limb cellulitis has Sepsis and Rt mid and lower zone pneumonia on 6L of O2 on RBM

HR 140/mt BP 100/60 mmHg RR- 35 with increased WOB ABG PH-7.28

PaCO2-56 mmHg

PCO2 - 58 mmHg

FIO2 70%Pao2-58 hypoxemicPco2-56/35- decreased Alveolar ventilationIntubation

IF the same guy is already on 5L/O2 / on noradrenaline fluid resuscitation- we probably intubate

40 yr old male Diabetic in ketosis with pylonephritis

Drowsy received in casualty- BP 70/50 mmHg, RR 28/mt,

Fever-103F, HR 150/mt, WOB normal

SC-1.6 WBC 20,000, LFT normal

ABG done on room air PH-7.28

PCO2-36 mmHg

PaO2 - 58 mmHg

HCO3 18 mmoles/L

O2 4L RBM Fluids 2l Noradrenaline Imipenem +cilastin 1g IV,

Paracetamol BP 140/80, HR 100/mt, UO 100ml/hr

ABG PH-7.38

PaCO2-36 mmHg

PCO2 - 78 mmHg

HCO3 20 mmoles/L Mentation better

A 29-year-old woman has excessive bleeding normal delivery has Hb of 5 g%, fluids-3L/mt given

Bp 100/60mmHg HR 114/mt PH-7.38

PaCO2-33 mmHg

PCO2 - 78 mmHg

HCO3 22 mmoles/L

Cao2- 7 vol % ScVO2 55 % Lactate 5 mMoles/L What do we do? Packed cells FFP Platelet 1:1:1 (FFP to PRBC

to platelets)

Causes of Respiratory failure

Respiratory Center in Brain

Neuromuscular Connections

Thoracic Bellows

Airways (upper & lower)

Lung parenchyma (alveoli)

Head injuryDrug overdose

Spinal cord injury

MyopathiesMyasthenia

C

COPD

ARDS

Brain

Nerves

Bellows

Airways

Alveoli

It only requires one disrupted “link” to cause respiratory failure !

Some points which help us to decide when to ventilate patients?

Primary cause for Respiratory failure-time for the disease to resolve

Hypoxemia on high FIO2 Increased PCO2 Increased WOB Airway protection ?

+ABG values

Do not treat the ABG, treat the patient If you’re not sure whether or not the patient needs a

ventilator, the patient needs a ventilator

Shibu lijack

Acid Base Acid Base analysisanalysis

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)

Acid-Base Physiology

CO2 + H2O H2CO3 H+ + HCO3-

CO2H+

HCO3-

Acid-Base physiology

Respiratory

Metabolic

Ventilation controls PCO2

Kidney losses H+ and reabsorbs bicarbonate (HCO3-)

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

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

24/4036/60

24/4018/30

Characteristics of 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

7.37 15 20

Un Compensated

Partially Compensated

Fully Compensated

(pH abnormal)

(pH in normal range)

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

Full compensationPartial compensationNo compensation…. (uncompensated)

BUT never overshoots, If a overshoot pH is there, Take it granted it is a MIXED disorder

Normal functioning

RESPIRATORY disorders…Expected HCO3 for a Change in CO2 ......... 1 2 3 4

Acidosis…. (expected) HCO3 = 0.1 x ∆ CO2

Alkalosis…. (expected) HCO3 = 0.2 x ∆ CO2

Acidosis…. (expected) HCO3 = 0.35 x ∆ CO2

Alkaosis…. (expected) HCO3 = 0.4 x ∆ CO2

Acute respiratory

Chronic respiratory

HCO3- ( KIDNEY)

pCO2 (LUNG)pH=

what has changed ? CO2

Compensation

Metabolic Acidosis: Compensation

Winters’ formula

pCO2 = 1.5 x [HCO3-] + 8 ± 2

Metabolic Alkalosis: Compensation pCO2 = 0.7x [HCO3-] + 20 ± 5

Na+

Unmeasured cations Unmeasure

d anions

Cl-

HCO3-

‘Mind the gap’

cations = Anions

Anion gap = metabolic acidosis

Anion Gap

AG = [Na+] - [Cl- +HCO3-]• Elevated anion gap represents

metabolic acidosis• Normal value: 12 ± 4mmol/L• Major unmeasured anions

– albumin– phosphates– sulfates– organic anions

-- Clinical history

-- pH normal, abnormal PCO2 and HCO3

-- PCO2 and HCO3 moving opposite directions

-- Degree of compensation for primary - disorder is inappropriate

2. Look at pH?

3. Look up HcO3-// PCo2

4. Match either pCO2ot the HCO3with pH

5. Fix the level of compensation.

6.If metabolic acidosis, calculate-Anion gap

7.Correlate clinically

1. Consider the clinical settings! Anticipate the disorder

7 steps to analyze ABG

First Step-Clinical History

COPD- Chronic Respiratory Acidosis-Met alkalosis

Asthma-Acute Respiratory Acidosis not well compensated

Cardiac arrest-Acute Metabolic/Respiratory acidosis

Septic shock-Acute Metabolic acidosis

The second step

Look at the pH - Label it.

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

ACIDOSIS

Look at -pCO2. Label it. pH of 7.30, PaCO2 of 80 mm Hg, and

HCO3- of 27 mEq/L. Increased

Normal pCO2 levels Normal pCO2 levels are 35-45mmHg. are 35-45mmHg. Below 35 is Below 35 is alkalotic, above 45 alkalotic, above 45 is acidic.is acidic.

The third step

• look at the HCO3- Label it. pH of 7.30, PaCO2 of 80 mm Hg, and HCO3- of 27 mEq/L

• INCREASEDA normal HCO3 level is 22-26 A normal HCO3 level is 22-26 mEq/L. If the HCO3 is below mEq/L. If the HCO3 is below 22, the patient is acidotic. If 22, the patient is acidotic. If the HCO3 is above 26, the the HCO3 is above 26, the patient is alkaloticpatient is alkalotic

Next match either the pCO2 or the HCO3 with the pH to determine the acid-base disorder.

• pH of 7.30, PaCO2 of 80 mm Hg, and HCO3- of 27 mEq/L• pH is on acidotic side & PCO2 is

increased. So it is respiratory acidosis

The Fourth Step

• Does either the CO2 or HCO3 go in the opposite direction of the pH?

• pH of 7.30, PaCO2 of 80 mm Hg, and HCO3- of 27 mEq/L

• To find the primary and what is compensatory

• HCO3 is going in opposite direction of pH. So it is metabolic compensation

Fifth Step

RESPIRATORY disorders…Expected HCO3 for a Change in CO2 ......... 1 2 3 4

Acidosis…. (expected) HCO3 = 0.1 x ∆ CO2

Alkalosis…. (expected) HCO3 = 0.2 x ∆ CO2

Acidosis…. (expected) HCO3 = 0.35 x ∆ CO2

Alkaosis…. (expected) HCO3 = 0.4 x ∆ CO2

Acute respiratory

Chronic respiratory

HCO3- ( KIDNEY)

pCO2 (LUNG)pH=

what has changed ? CO2

Is the compensation full or partial??

Do the calculations…. pH of 7.30, PaCO2 of 80 mm Hg, and HCO3-

of 27 mEq/L

PCO2 is increased by =40 HCO3-=should be increased by 4 i.e. 24+4=28( for full compensation)

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

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

Sixth Step

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

Pathogenesis of Metabolic Acidosiswith AG

Fixed acid accumulation and low serum bicarbonate

Renal failure Renal,GI Lactic Salicylate

Ketones Methanol

Phosphate Ethylene glycol

HCl

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

Equivalent rise of AG and Fall of HCO3……

….Pure Anion Gap Metabolic Acidosis

Discrepancy…….. in rise & fall

+ Non AG M acidosis, + M Alkalosis

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

Finally

RESPIRATORY disorders…Expected HCO3 for a Change in CO2 ......... 1 2 3 4

Acidosis…. (expected) HCO3 = 0.1 x ∆ CO2

Alkalosis…. (expected) HCO3 = 0.2 x ∆ CO2

Acidosis…. (expected) HCO3 = 0.35 x ∆ CO2

Alkaosis…. (expected) HCO3 = 0.4 x ∆ CO2

Acute respiratory

Chronic respiratory

HCO3- ( KIDNEY)

pCO2 (LUNG)pH=

what has changed ? CO2

Compensation

Metabolic Acidosis: Compensation

Winters’ formula

pCO2 = 1.5 x [HCO3-] + 8 ± 2

Metabolic Alkalosis: Compensation pCO2 = 0.7x [HCO3-] + 20 ± 5

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.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 7.41

PaCO2 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.

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• I shall practice gentle mechanical ventilation and not try to bring ABG to perfect normal.

• I shall treat the patient not the ABG report

• I shall always correlate ABG report clinically

PaO2

O2 CASCADE

AIR

ALVEOLAR

POST PULMONARY

ARTERIAL

Hb

MICRO-

CIRCULATION

MIXED VENOUS