sravan abg ppt modified

Seminar on ABG

Presentor : Dr.

Sravan

Chair Person : Dr.

Vinathi

Extraction

Blood is most commonly drawn from the radial

artery because it is

◦ easily accessible

◦ easily compressed to control bleeding

◦ less risk for occlusion.

The femoral artery (or less often, the brachial

artery) is also used, especially during emergency

situations or with children.

Blood can also be taken from an arterial catheter

already placed in one of these arteries.

Precautions

Samples drawn in plastic syringes should not be iced

and should always be analyzed within 30 minutes.

Parameters Of ABG

pH

PaO2

PCo2

Hco3-

Sao2

Lactate

Anion Gap

Electrolytes

Glucose

The Key to Blood Gas Interpretation:

Four Equations, Three Physiologic

Processes

Equation Physiologic

Process

1) PaCO2 equation Alveolar ventilation

2) Alveolar gas equation Oxygenation

3) Oxygen content equation Oxygenation

4) Henderson-Hasselbalch equation Acid-base balance

These four equations, crucial to understanding and

interpreting arterial blood gas data, will provide the structure

for this slide presentation.

PaCO2 Equation: PaCO2 reflects ratio of metabolic

CO2 production to alveolar ventilation

VCO2 x 0.863 VCO2 = CO2 production

PaCO2 = ------------------- VA = VE – VD

VA VE = minute (total) ventilation (= resp. rate x

tidal volume)

VD = dead space ventilation (= resp. rate x dead space volume

0.863 converts VCO2 and VA units to mm Hg

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

VCO2 x 0.863

PaCO2 = ------------------

VA VA = VE – VD

Inadequate VE leading to decreased VA and increased

PaCO2: sedative drug overdose; respiratory muscle

paralysis; central hypoventilation

Increased VD leading to decreased VA and increased

PaCO2: chronic obstructive pulmonary disease; severe

restrictive lung disease (with shallow, rapid breathing)

Hypercapnia (cont)

Dangers of Hypercapnia

Elevated PaCO2 poses a threat for three reasons:

1) An elevated PaCO2 will lower the PAO2 and as a

result will lower the PaO2.

(Alveolar gas equation)

2) An elevated PaCO2 will lower the pH

( Henderson-Hasselbalch equation).

3) The higher the baseline PaCO2, the greater it will

rise for a given fall in alveolar ventilation, e.g., a 1

L/min decrease in VA will raise PaCO2 a greater

amount when the baseline PaCO2 is 50 mm Hg than

when it is40 mmHg.

A-a Gradient

FIO2 = 713 x O2%

A-a gradient = PA O2 - PaO2

◦ Normal is 0-10 mm Hg

◦ 2.5 + 0.21 x age in years

With higher inspired O2 concentrations, the A-a

gradient will also increase

Alveolar Gas Equation

PAO2 = PIO2 - 1.2 (PaCO2)*

Where PAO2 is the average alveolar PO2, and PIO2 is the

partial pressure of inspired oxygen in the trachea

PIO2 = FIO2 (PB – 47 mm Hg)

FIO2 is fraction of inspired oxygen and PB is the barometric

pressure. 47 mm Hg is the water vapor pressure at normal

body temperature.

* Note: This is the “abbreviated version” of the AG equation, suitable for most clinical purposes. In the longer

version, the multiplication factor “1.2” declines with increasing FIO2, reaching zero when 100% oxygen is inhaled. In

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

PAO2 = PIO2 - 1.2 (PaCO2)where PIO2 = FIO2 (PB – 47 mm Hg)

Except in a temporary unsteady state, alveolar PO2 (PAO2) is always

higher than arterial PO2 (PaO2). As a result, whenever PAO2

decreases, PaO2 also decreases. Thus, from the AG equation:

If FIO2 and PB are constant, then as PaCO2 increases both PAO2

and PaO2 will decrease (hypercapnia causes hypoxemia).

If FIO2 decreases and PB and PaCO2 are constant, both PAO2 and

PaO2 will decrease (suffocation causes hypoxemia).

If PB decreases (e.g., with altitude), and PaCO2 and FIO2 are

constant, both PAO2 and PaO2 will decrease (mountain climbing

leads to hypoxemia).

Alveolar Gas Equation

PaO2-FiO2 ratio

Normal PaO2/FiO2 is 300-500

<250 indicates a clinically significant gas exchange

derangement

Hypoxemia

Hypoventilation

V/Q mismatch

Right-Left shunting

Diffusion impairment

Reduced inspired oxygen tension

Right to Left Shunt

Parenchymal diseases leading to atelectasis or alveolar flooding

(lobar pneumonia or ARDS)

Pathologic vascularcommunications

(AVM or intracardiacshunts)

Reduced inspired oxygen

delivery Delivery to tissue beds determined by arterial

oxygen content and cardiac output

Oxygen content of blood is affected by level &

affinity state of hemoglobin◦ Example is CO poisoning: reduction of arterial O2 content despite

normal PaO2 and Hgb caused by reduction in available O2 binding

sites on the Hgb molecule

Tissue hypoxia may occur despite adequate

oxygen delivery◦ CN poisoning causes interference with oxygen utilization by the

cellular cytochrome system, leading to cellular hypoxia

P(A-a)O2

P(A-a)O2 is the alveolar-arterial difference in partial pressure of oxygen. It is commonly called the “A-a gradient,” it results from gravity-related blood flow changes within the lungs (normal ventilation-perfusion imbalance).

PAO2 is always calculated based on FIO2, PaCO2, and barometric pressure.

PaO2 is always measured on an arterial blood sample in a “blood gas machine.”

Normal P(A-a)O2 ranges from @ 5 to 25 mm Hg breathing room air (it increases with age).

A-a increases 5 to 7 mmHg for every 10% increase

in FiO2

Average PaO2 95mmHg (range 85– 100 mmHg)

Estimating A-a gradient:

Normal A-a gradient = (Age+10) / 4

Predicted O2 (PaO2) = 109-0.43* age in

years

Physiologic Causes of Low PaO2

NON-RESPIRATORY P(A-a)O2

Cardiac right-to-left shunt Increased

Decreased PIO2 Normal

Low mixed venous oxygen content* Increased

RESPIRATORY P(A-a)O2

Pulmonary right-to-left shunt Increased

Ventilation-perfusion imbalance Increased

Diffusion barrier Increased

Hypoventilation (increased PaCO2) Normal

Oxygen Content

Neither the PaO2 nor the SaO2 tells how much oxygen is in the blood.

CaO2 provides the oxygen content, (units = ml O2/dl) calculated as:

CaO2 = quantity O2 bound + quantity O2 dissolvedto hemoglobin in plasma

CaO2 = (Hb x 1.34 x SaO2) + (.003 x PaO2)

1.34 ml O2 bound to each gm of Hb.

0.003 is solubility coefficient of oxygen in plasma

Acid/Base Balance

• The pH is a measurement of the acidity or alkalinity of

the blood.

• It is inversely proportional to the no. of (H+) in the

blood.

• The normal pH range is 7.35-7.45.

Calculation of pH

203.0log10.6 3

PaCO

HCOpH

3

2

24HCO

PaCOH

Henderson-

Hesselbach

equation

Validation of ABG

The first part in ABG validation is:

Determination of Hydrogen Ion Concentration by

using

3

2

24HCO

PaCOH

The second part of ABG validation is

• To confirm that for given hydrogen ions the pH is

correct.

Hydrogen ion concentration can be calculated

at a given pH by using this method

At pH of 7.4 hydrogen ion concentration is 40 nmol/L

If pH < 7.4

For every 0.1 decrease in pH multiply hydrogen ion concentration by 1.2 for example

For pH 7.3 = 40 * 1.2

For pH 7.2 = 40 * 1.2*1.2 and so on

If pH > 7.4

For every 0.1 increase in pH multiply hydrogen ion concentration by 0.8 for example

For pH 7.5 = 40 * 0.8 For pH 7.6 = 40 * 0.8*0.8

pH in the Physiologic range

Relationship

between the pH

and H+

concentration (in

nanomol/L) in the

physiologic range

Acids and Bases

Acid : A substance that can “donate” H+ ion or when added

to solution raises H+ ion (i.e., lowers pH).

Base : A substance that can “accept” H+ ion or when added

to solution lowers H+ ion (i.e., raises pH).

(Definitions proposed by Bronsted)

H2CO3 <-> H+ + HCO3–

HCl <-> H+ + Cl-

NH4+ <-> H+ + NH3

H2PO4- <-> H+ + HPO42-

ACID BASE

Acidemia is present when blood pH <7.35.

Alkalemia is present when blood pH >7.45.

Metabolic

refers to disorders that result from a primary

alteration in [H+] or [HCO3-].

Respiratory

refers to disorders that result from a primary

alteration in PCO2 due to altered CO2 elimination.

Terminology

Daily Acid Production

Metabolism of

carbohydrates and fats → 15,000 mmol of CO2

CO2 + water → H2CO3 (weak acid)

CO2 removed via respiration.

Noncarbonic acids derived from the metabolism of proteins.

Eg. Oxidation of sulfur-containing amino acids → H2SO4

1 meq/kg of non-volatile acid produced daily.

These H+ ions are excreted in the urine.

Vo

lati

le A

cid

sN

on

-Vo

lati

le A

cid

s

15,070 mmoles = 15,070 million nanomoles.

The ultimate pH of the body will

depend on ……..

The amount of acid produced.

The buffering capacity of the body.

The rate of acid excretion by the lungs and kidneys.

At the end of the day, what would pH be if all

acid produced is retained in the body ?

pH

Initial H+

concentration

40 nanomoles/L

7.40

Daily H+

addition

15,070 ×106 nanomoles

Final H+

concentration

40 + {(15,070/42) ×106}

= 358 ×106 nanomoles/L 0.45

*Nanomole = one billionth of a mole.

Normal acid base homeostasis

Acid base balance

Acid base homeostasis is essential for normal cellular

enzyme function.

Arterial pH is maintained within a very narrow range

(7.35 and 7.45) by the interteraction of

Adjustment occurs within ….

1. Blood buffers ….seconds to minutes.

2. Lungs ….1 to 15 minutes.

3. Kidneys ….hours to days.

Buffering

Buffers are chemical systems that either accept or release H+, so that changes in the free H+ concentration are minimized.

Buffer, by themselves, do not remove acid/alkali from the body.

Production of “new” bicarbonate linked to excretion of ammonium ions

Buffering

Say 10 millimoles/L of H+ are produced

(= 10 × 106 nanomoles/L).

If unchecked, pH would decrease to <2.0 which is

fatal.

But, this acid load is bufferred by 10 mmoles/L

(=10 meq/L) of HCO3–, producing CO2 and water.

Therefore, HCO3– concentration decreases from 24

to 14.

Consequently pH decreases from 7.40 to 7.32,

which is within physiological range.

Illustration

Buffering

Extracelular buffers (40 – 45%)

1.Bicarbonate/Carbon Dioxide buffer

system

2.Inorganic phosphates

3.Plasma proteins

Intracellular and Bone buffers (55 – 60%)

1.Proteins

2.Organic and inorganic phosphates

3.Hemoglobin

4.Bone

Why learn/analyze ABG?

Provides information on the physiological processes

that maintain pH homeostasis.

Plays a pivotal role in diagnosis and management

of critically ill patients.

◦ Proper evaluation of ABG guides appropriate

diagnosis and, therefore, treatment.

An ABG Report

Parameters of importance Measured

pH

pCO2

Calculated

HCO3

Metabolic Acidosis

Metabolic Acidosis

Accumulation of metabolic acids (non-carbonic) caused by:

◦ Excess acid production which overwhelms renal capacity for excretion. e.g. Diabetic ketoacidosis.

◦ Loss of alkali:Leaves un-neutralized acid behind. e.g. Diarrhea.

◦ Renal excretory failure: Normal total acid production in face of poor renal function. e.g. Chronic renal failure.

Primary Defect: Decrease in HCO3

Causes of Metabolic Acidosis

Acid Gain

1. L-lactic acid (= tissue hypoxia)

2. Ketoacids (= DKA, starvation)

3. D-lactic acid (= Low GI motility or altered GI flora, eg. blind loop syndromes)

4. Intoxicants which are acids or become acids Methanol to formic acid

Ethylene glycol to glyoxalic acid

Paraldehyde to acetic acid

Acetylsalicylic acid

Toluene to hippuric acid

5. Renal Failure

Anion Gap =

Na – [Cl + HCO3]

Type A

-Shock

- Acute severe hypoxia

- Acute severe anemia

Type B

- Metformin

- Malignancy

- Thiamine deficiency

- Cyanide

- NRTI

Causes of Lactic Acidosis

Causes of Metabolic Acidosis

Loss of NaHCO3

1. Loss via GI tract (diarrhea, ileus, fistula)

2. Loss in Urine (proximal RTA, acetazolamide)

3. Failure of kidneys to make new bicarbonate

(distal RTA)

4. Acid production and the excretion of its anion in

the urine without [H+] or [NH4+] (Eg. Defective

renal reabsorption of betahydroxybutarate)

Metabolic acidosisCo

mp

en

sato

ry C

han

ge

Sequential response to a H+ load, culminating in the restoration of

acid-base balance by the renal excretion of the excess H+

H+ Load

2 – 4 HoursMinutes to

Hours

Intracellular

and bone

buffering

Respiratory

buffering by

lowering

PCO2

Extracellular

buffering by

HCO3

Increased

Renal H+

excretion

Hours to

daysImmediate

Anion Gap

Unmeasured

Cation

Unmeasured

Anion

High Anion Gap Metabolic Acidosis

Example: 15 millimoles of organic acid added.

15 mEq of bicarbonate will be used up while buffering.

Normal Anion Gap Metabolic Acidosis

Example: 15 mEq of bicarbonate is lost.

Kidneys reclaim extra chloride to maintain electroneutrality.

High Anion Gap Met. Acidosis

Ketoacidosis

Lactic Acidosis

Uremia

Toxicity

◦ Salicylate

◦ Ethylene Glycol

◦ Methanol

◦ Paraldehyde

Massive rhabdomyolysis

Anion Gap =

(Na – HCO3 – Cl)

Anion Gap

AG = [Na – (Cl + HCO3)]

Increased unmeasured cation:

◦ Normally present cationsK+, Ca2+ , Mg2+

◦ Abnormal cations:Lithium, IgG

Decreased unmeasured anion:

◦ Hypoalbuminemia

Lab Error:

◦ Hyponatremia due to viscous serum

◦ Hyperchloremia in Bromide toxicity

◦ Random lab errors

Decreased unmeasured cation:

◦ Decreased K, Ca, Mg

Increased unmeasured anion:

◦ Organic:lactate, ketones

◦ Inorganic: PO42-, sulfates

◦ Hyperalbuminemia

◦ Exogenous anions: salicylates, formate, penicillin, nitrate, etc.

◦ Incompletely idenitified: uremia, paraldehyde, ehtylene glycol, HHS, etc

Lab Error:

◦ Falsely increased Na

◦ Falsely decreased Cl or HCO3

Pattern of Changes in Acid-Base Disorders

Primary

disorder

Initial

change

Compensatory

change

Metabolic

acidosis↓ HCO3 ↓ PCO2

Metabolic Alkalosis

Metabolic Alkalosis

from renal or extra-renal sources.

Compensatory change:

◦ Tissues and RBC exchange intracellular H+

for extra-cellular Na+ and K+

◦ Hypoventilation and elevation of PaCO2

(Maximal PaCO2 rarely exceeds 55 mmHg)

Primary Defect: Rise in HCO3

Pattern of Changes in Acid-Base

Disorders

Primary

disorder

Initial

change

Compensatory

change

Metabolic


Metabolic

alkalosis↑ HCO3 ↑ PCO2

Metabolic Alkalosis – Pathogenesis

Loss of hydrogen ion from upper GI tract

(vomiting) or urine (diuretics)

Addition of alkali – administration of bicarbonate

or its precursors (citrate, lactate, etc.)

Generation

Maintenance

• Volume/chloride depletion

• Hypokalemia

• Aldosterone excess

Metabolic Alkalosis – Causes

Saline Responsive Urine Chloride (<10 mEq/L)

Saline ResistantUrine Chloride (>20 mEq/L)

ECF Volume Depletion

Vomiting/Gastric Suction

Diuretics

Hypercapnia correction

Hypertensive (Normal

or increased ECF)

Hyperaldosteronism

Cushing syndrome

No ECF Vol. Depletion

NaHCO3 infusion

Multiple transfusions

Normo/Hypotensive

Bartter’s syndrome

Severe K depletion

Metabolic Alkalosis – Clinical Features

Metabolic Alkalosis – Clinical Features

CNS:

◦ Increased neuromuscular excitability leading to paresthesia, light headache, and carpopedal spasm

CVS:

◦ Hypotension, cardiac arrhythmias

Other:

◦ Weakness, muscle cramps, postural dizziness

◦ Muscle weakness and polyuria due to hypokalemia

Respiratory:

◦ Compensatory hypoventilation may lead to hypoxia symptoms in patients with pre-existing lung disease

D/D of Metabolic Alkalosis

Urine

Electrolyte

Saline

Sensitive

Saline

Resistant

Cl < 10 mEq/L(unless on diuretics)

> 20 mEq/L

Na < 20 mEq/L (unless recent

vomiting)

> 20 mEq/L

K May be high

if high distal

Na(diuretics or recent

vomiting)

Usually high

as

aldosterone

is acting

Metabolic Alkalosis – Treatment

Treat underlying cause

Saline reponsive

◦ Normal saline with KCl or Isolyte-G

◦ H2 inhibitors or PPI

◦ In diuretic induced, dose reduction, KClsuplementation, spironolactone

◦ Discontinue exogenous sources of alkali (bicarbonate, RL, acetate, citrate)

◦ When pH > 7.65, may administer 0.1 N HCl via central veins

◦ Dialysis

Saline Resistant – Treat the cause. Spironolactone, K correction and Na restriction.

Respiratory Acidosis


Decrease in pulmonary clearance of CO2

Compensatory Change:

◦ Acute (<24 hrs): Buffering by tissue and RBC to

increase HCO3. Rarely more than 4 mEq

◦ Chronic (>72 hrs): Stimulation of renal tubular

secretion of H+ thus synthesizing more HCO3. Chloride

is lost along with NH4+

Primary Defect: Rise in PCO2

Respiratory Acidosis – Causes

CNS Depression

◦ Drugs (anaesthesia, sedatives), infection, stroke

Neuromuscular impairment

◦ Myopathy, Myasthenia gravis, polymyositis, hypokalemia

Ventilation restriction

◦ Rib fracture, pneumothorax, hemothorax

Airway

◦ Asthma, obstruction

Alveolar diseases

◦ COPD, pulmonary edema, ARDS, pneumonitis

Miscellaneous

◦ Obesity, Hypoventilation

Response to an increase in PCO2

Increased PCO2

Hours to Days10 to 30

minutes

Increased

Renal H+

Excretion

Intracellular

Buffering

Respiratory Acidosis – Treatment

Acute

◦ Treat the cause.

◦ Bronchodilators.

◦ Mechanical ventilation.

◦ Antibiotics

Chronic

◦ Oxygen -long term supplemental.

◦ Nasal continuous positive airway pressure.

◦ Improving respiratory muscle function.

◦ Drugs- Progesterone, Doxapram, Almitrine,

Acetazolamide, Methyphenidate and Caffeine.

Respiratory Alkalosis


Compensatory Change:◦ Acute (<24 hrs): Buffering by tissue and RBC

to lower HCO3. Rarely to less than 18 mEq/L

◦ Chronic (>72 hrs): Impairs kidney's ability to excrete acid thus lowering HCO3. If more than 2 weeks, pH may return to normal.

Primary Defect: Decrease in PCO2

Respiratory Alkalosis – Causes

Hypoxemia◦ Pneumonia, interstitial diseases, pulm emboli, edema, etc.

◦ CHF

◦ Severe anemia

◦ High altitude resisdence

Direct stimulation of the medullary respiratory center◦ Psychogenic/voluntary

◦ Pain

◦ Pregnacy

◦ Hepatic failure

◦ Gram Negative sepsis

◦ Salicylate toxicity

◦ Rapid correction of metabolic acidosis

◦ Neurological – CVA, trauma, tumors, infections, etc.

Mechanical Ventilation (overtreatment)

Respiratory Alkalosis – Treatment

Treat the cause

Does not need treatment unless pH > 7.50

Relief of hypoxia.

Rebreathing into a non compliant bag as

long as hyperventilation exists.

Treatment of anxiety.

Pattern of Changes in Acid-Base Disorders

Primary

disorder

Initial

change

Compensatory

change

Metabolic


Metabolic

alkalosis↑ HCO3 ↑ PCO2

Respiratory

acidosis↑ PCO2 ↑ HCO3

Respiratory

alkalosis↓ PCO2 ↓ HCO3

The Boston Approach

to

Acid-Base Disorders

5-Steps in the Evaluation of

Systemic Acid Base Disorders

1. Comprehensive history and physical

examination.

2. Evaluate simultaneously performed ABG &

serum electrolytes.

3. Identification of the dominant disorder.

4. Calculation of compensation.

5. Calculate the anion gap and the Δ.

1.Anion Gap

2.Δ AG

3.Δ Bicarbonate

Step 3:

Identification of the dominant disorder

Primary

disorder

pH Initial

change

Compensatory

change

Metabolic

acidosis↓ ↓ HCO3 ↓ PCO2

Metabolic

alkalosis↑ ↑ HCO3 ↑ PCO2

Step 3:

Identification of the dominant disorder

pH HCO3 PCO2Dominant

(Primary) disorder

↓ ↓ ↓ Metabolic acidosis

↑ ↑ ↑ Metabolic

alkalosis

↓ ↑ ↑ Respiratory

acidosis

↑ ↓ ↓ Respiratory

alkalosis

Dictums in ABG Analysis

pH and Primary parameter change in the

same direction suggests a metabolic

problem

pH and Primary parameter change in the

opposite direction suggests a respiratory

problem

What is the Magnitude of

Compensation?

1.2

0.7

0.1 0.3

0.2 0.5

Compensation Formula Simplified

Acute Chronic

Metabolic

Respiratory

Acidosis

Alkalosis

Acidosis

Alkalosis

Step 4. Check if the compensatory

response is appropriate or not.

If the compensation is not appropriate,

suspect a second (and perhaps a triple)

acid-base disorder.

Step 4:

Calculation of compensation

Note: The formula calculates the change in the compensatory parameter.

Disorder pH Primary change

Compensatory Response

Equation

Metabolic Acidosis

[HCO3-] PCO2 ΔPCO2 1.2 ΔHCO3

Metabolic Alkalosis

[HCO3-] PCO2 ΔPCO2 0.7 ΔHCO3


PCO2 [HCO3-] Acute:

ΔHCO3- 0.1 ΔPCO2

Chronic:ΔHCO3

- 0.3 ΔPCO2


PCO2 [HCO3-] Acute:

ΔHCO3- 0.2 ΔPCO2

Chronic:ΔHCO3

- 0.5 ΔPCO2

Step 5: Calculate the “gaps”

Anion gap = Na+ − [Cl− + HCO3−]

Δ AG = Anion gap − 12

Δ HCO3 = 24 − HCO3

Δ AG = Δ HCO3 −, then Pure high AG Met. Acidosis

Δ AG > Δ HCO3 −, then High AG Met Acidosis + Met. Alkalosis

Δ AG < Δ HCO3−, then High AG Met Acidosis + HCMA

Note:

Add Δ AG to measured HCO3− to obtain

bicarbonate level that would have existed IF the high AG metabolic acidosis were to be absent, i.e., “Pre-existing Bicarbonate.”

Bicarbexistinge

BicarbCurrent

AGDelta

__Pr

_

_

Delta AG / Delta HCO3 Ratio

Ratio 1-2 : High anion gap acidosis

Ratio > 2 : HAG acidosis and metabolic

alkalosis

Ratio < 1 : HAG acidosis and NAG acidosis

: DKA with ketone excretion

: CKD with anion excretion but H+

retention

Dictums in ABG Analysis

1. Primary change & Compensatory change alwaysoccur in the same direction.

2. pH and Primary parameter change in the samedirection suggests a metabolic problem.

pH and Primary parameter change in the oppositedirection suggests a respiratory problem.

3. Renal and pulmonary compensatory mechanisms return pH toward but rarely to normal.

Corollary:

A normal pH in the presence of changes in PCO2 or HCO3 suggets a mixed acid-base disorder.

Normal Values for Major Acid-Base variables

S Na = 135 – 145 mEq/L

S K = 3.5 – 5.5 mEq/L

S Cl = 97 – 110 mEq/L

pH H+

nanoEq/L

PaCO2

mmHg

HCO3–

mEq/L

Arterial 7.37 – 7.43 37 – 43 36 – 44 22 – 26

Venous 7.32 – 7.38 42 – 48 42 – 50 23 – 27

Common clinical states and associated acid-base disorders

Clinical state Acid-base disorder

Renal failure Metabolic acidosis

Vomiting Metabolic alkalosis

Severe diarrhea Metabolic acidosis

Cirrhosis Respiratory alkalosis

Hypotension Metabolic acidosis

COPD Respiratory acidosis

Sepsis Respiratory alkalosis, metabolic acidosis

Pulmonary embolus Respiratory alkalosis

Pregnancy Respiratory alkalosis

Diuretic use Metabolic alkalosis

Clues to Mixed Acid-Base Disorders

Normal pH (with the exception of chronic respiratory alkalosis)

PCO2 and HCO3 deviating in opposite directions

pH change in the opposite direction of a known primary (dominant) acid-base disorder

Is a VBG just as good as an

ABG?

Risk with ABG

◦ Significant pain

◦ Hematoma

◦ Aneurysm formation

◦ Thrombosis or

embolization

◦ Needlestick injuries .

Advantages with ABG

◦ PaO2

◦ Arterial

Oxyhemoglobin

saturation (SaO2)

Brandenburg and Dire investigated 66 patients (DKA) .

An ABG and VBG were subsequently drawn. 44 pts

had acidosis with arterial pH less than 7.35.

Among these cases, the mean difference between

arterial and venous pH values was 0.02 (range 0.0 to

0.11) with a Pearson’s correlation coefficient (r) of

0.9689

This study concludes that venous blood gas

measurements accurately demonstrated the degree of

acidosis in patients with DKA.

Lactate

In 2000, Lavary et al studied 375 patients and

compared arterial and venous lactates and showed

that there was no significant difference between

the two

Recent study in 2002 investigated whether venous

pCO2 and pH could be used to screen for

significant hypercarbia ,

the authors stated that a venous pCO2 of

44mmHg had a sensitivity for detection of

hypercarbia of 100% and a specificity of 57%, thus

making it an effective screening test for hypercarbia

Comparing Electrolytes

In ABG & Biochem Lab Analyser

Case Scenarios in

Acid-Base Disorders

Case 1

A 15 yr old juvenile diabetic presents with abdominal pain, vomiting, fever & tiredness for 1 day. He had stopped taking insulin 3 days ago. Examination revealed tachycardia, BP- 100/60, signs of dehydration. Abdominal examination was normal.

ABG:pH 7.31PaCO2 26 mmHgHCO3 12 mEq/LPaO2 92 mm Hg

Evaluate the acid-base disturbance(s)?

Serum Electrolytes:

Na 140 mEq/L

K 5.0 mEq/L

Cl 100 mEq/L

Case 1: Solution

Dominant disorder is Metabolic Acidosis

Compensation formula:

Δ PaCO2 = 1.2 × Δ HCO3

= 1.2 × 12

= 14.4

PaCO2 = 40 – 14 = 26

Compensation is appropriate.

Anion Gap = 140 – (100 + 12)

= 28

AG is high.

pH 7.31

PaCO2 26

HCO3 12

PaO2 92

Na 140

K 5.0

Cl 100

Case 1: Solution

Δ AG = 28 – 12= 16

Δ HCO3 = 24 – 12= 12

Δ AG > Δ HCO3-

Final Diagnosis:

High AG Met. Acidosis + Met. Alkalosis

pH 7.31

PaCO2 26

HCO3 12

PaO2 92

Na 140

K 5.0

Cl 100

Case 2

A 24 yr old boy presents with continuous vomiting of 3 days duration, mental confusion, giddiness, and tiredness for 1 day.

Examination revealed tachycardia, hypotension and dehydration.

ABGpH 7.50PaCO2 48HCO3 32PaO2 90


Serum Electrolytes:Na 139K 3.9Cl 85

Case 2: Solution

Dominant disorder is Metabolic Alkalosis

Compensation formula:Δ PaCO2 = 0.7 × Δ HCO3

= 0.7 × 8

= 5.6

PaCO2 = 40 + 6 = 46


Anion Gap = 139 – (85 + 32)

= 22

AG is high.

pH 7.50

PaCO2 48

HCO3 32

PaO2 90

Na 139

K 3.9

Cl 85

Case 2: Solution

Δ AG = 22 – 12

= 10

High AG metabolic acidosis

Final Diagnosis:

Metabolic Alkalosis + High AG Met. Acidosis

pH 7.50

PaCO2 48

HCO3 32

PaO2 90

Na 139

K 3.9

Cl 85

Case 3: Varieties of Metabolic Acidosis

Patient A B C

ECF volume Low Low Normal

Glucose 600 120 120

pH 7.20 7.20 7.20

Na 140 140 140

Cl 103 118 118

HCO3-

10 10 10

AG 27 12 12

Ketones 4+ 0 0

High-AG

Met.

Acidosis

Non-AG

Met.

Acidosis

Non-AG

Met.

Acidosis

Renal handling of Hydrogen in

Metabolic Acidosis

In the setting of metabolic acidosis, normal kidneys try to increase H+ excretion by increasing titratable acidity and ammonia. The latter is excreted as NH4

+.

When NH4+ is excreted, it also causes increased

chloride loss, to maintain electrical neutrality.

Chloride loss, therefore, will be in excess of Na and K.

Urine Anion-Gap = Na + K – Cl

In metabolic acidosis, if Urine anion gap is negative, it suggests that the kidneys are excreting H+ effectively.

Urine Electrolytes in Metabolic

Acidosis

Patient A B C

U. Na 10 50

U. K 14 47

U. Cl 74 28

Urine AG –50 +69

Dx: Diarrhea RTA

In Normal anion gap Metabolic Acidosis, Positive Urine AG suggests distal Renal Tubular Acidosis

Negative Urine AG suggests non-renal cause for Metabolic Acidosis.

Urine Anion Gap = (U. Na + U. K – U. Cl)

Case 4

A 50 yr old man presented with history of progressive dyspnoea with wheezing for 4 days.

He also had fever, cough with yellowish expectoration.

He had increased sleepiness for 1 day.

On examination, he was tachypnoeic, pulse-100/min bounding, BP-160/96, central cyanosis +, drowsy, asterixis +, RS – B/L extensive wheezing +.

CXR- hyperinflated lung fields with tubular heart.

Case 4: Laboratory data

ABG:pH 7.30PaCO2 60 mmHg

HCO3 28 mEq/L

PaO2 68 mm Hg

Serum Electrolytes:Na 136 mEq/L

K 4.5 mEq/L

Cl 98 mEq/L


Case 4: Solution

Dominant disorder is Respiratory Acidosis

Compensation formula:Δ HCO3 = 0.3 × Δ PaCO2

= 0.3 × 20

= 6

HCO3 = 24 + 6 = 30


Anion Gap = 138 – (98 + 28)

= 10

AG is normal.

pH 7.30

PaCO2 60

HCO3 28

PaO2 68

Na 136

K 4.5

Cl 98

Case 5

20 year old girl presented with complaints of

difficulty in breathing and upper abdominal

discomfort for the past 1 hr.

On examination, vitals normal, patient

hyperventilating, RS – normal, Abdomen – normal.

Case 5: Laboratory data

ABG:pH 7.50PaCO2 25 mmHg

HCO3 21 mEq/L

PaO2 100 mm Hg

Serum Electrolytes:Na 137 mEq/L

K 3.9 mEq/L

Cl 99 mEq/L

Calcium 9.0 mEq/L


Case 5: Solution

Dominant disorder is Respiratory Alkalosis


= 0.2 × 15= 3

HCO3 = 24 – 3 = 21


Anion Gap = 137 – (99 + 21)= 17

AG is slightly high which can be seen in respiratory alkalosis.

pH 7.50

PaCO2 25

HCO3 21

PaO2 100

Na 137

K 3.9

Cl 99

Calcium 9.0

Case 6

pH PaCO2 HCO3 Acid-Base status

7.28 50 23 respiratory acidosis and

metabolic acidosis

7.50 33 25 respiratory alkalosis

and metabolic alkalosis

7.23 34 14 metabolic acidosis and

respiratory acidosis

For each of the following sets of arterial blood gas

values, what is (are) the likely acid-base disorder(s)?

Case 7

Explain the acid-base status of a 35-year-old man with

history of chronic renal failure treated with high dose

diuretics admitted to hospital with pneumonia and the

following lab values:

ABG Serum Electrolytes

pH 7.52 Na+ 145 mEq/L

PaCO2 30 mm Hg K+ 2.9 mEq/L

PaO2 62 mm Hg Cl-98 mEq/L

HCO3

-21 mEq/L

Case 7: Solution

Dominant disorder is Respiratory Alkalosis


= 0.2 × 10= 2

HCO3 = 24 – 2 = 22


Anion Gap = 145 – (98 + 21)= 26

AG is very high suggestive of metabolic acidosis.

pH 7.52

PaCO2 30

HCO3 21

PaO2 62

Na 145

K 2.9

Cl 98

Case 7: Solution

Δ AG = 26 – 12= 14

Δ HCO3 = 24 – 21= 3

Δ AG > Δ HCO3-

High AG Met Acidosis + Met. Alkalosis

Final Diagnosis:

Respiratory Alkalosis +

High AG Metabolic Acidosis +

Metabolic Alkalosis

pH 7.52

PaCO2 30

HCO3 21

PaO2 62

Na 145

K 2.9

Cl 98

Case 8

The following values are found in a 65-year-old patient.

Evaluate this patient's acid-base status?

ABG Serum Chemistry

pH 7.51 Na + 155 mEq/L


HCO3- 39 mEq/L Cl- 90 mEq/L

CO2 40 mEq/L

BUN 121 mg/dl

Glucose 77 mg/dl

Case 8: Solution

Dominant disorder is Metabolic Alkalosis


= 0.7 × 16= 11.2

PaCO2 = 40 + 11 = 51


Anion Gap = 155 – (90 + 40)= 25

AG is high.

pH 7.51

PaCO2 50

HCO3 40

PaO2 62

Na 155

K 5.5

Cl 90

BUN 121

Case 8: Solution

Δ AG = 25 – 12

= 13

High AG metabolic acidosis

Final Diagnosis:

Metabolic Alkalosis +

High AG Metabolic Acidosis

pH 7.51

PaCO2 50

HCO3 40

PaO2 62

Na 155

K 5.5

Cl 90

BUN 121

Case 9

A 52-year-old woman has been mechanically ventilated

for two days following a drug overdose. Her arterial blood

gas values and electrolytes, stable for the past 12 hours,

show:

ABG Serum Chemistry

pH 7.45 Na + 142 mEq/L


Cl- 100 mEq/L

HCO3- 18 mEq/L

Case 9: Solution

Dominant disorder is Chronic Respiratory Alkalosis


= 0.5 × 15= 7.5

HCO3 = 24 – 8 = 16


Anion Gap = 142 – (100 + 18)= 24

AG is very high suggestive of metabolic acidosis.

pH 7.45

PaCO2 25

HCO3 18

Na 142

K 4.0

Cl 100

Case 9: Solution

Δ AG = 24 – 12= 12

Δ HCO3 = 24 –18= 6

Δ AG > Δ HCO3-

High AG Met Acidosis + Met. Alkalosis

Final Diagnosis:

Chronic Respiratory Alkalosis +

High AG Metabolic Acidosis +

? Metabolic Alkalosis

Case 10

An 18-year-old college student is admitted to the ICU for an acute asthma attack, after not responding to treatment received in the Casualty department. ABG values (on room air) show: pH 7.46, PaCO2 25 mm Hg, HCO3- 17 mEq/L, PaO2

55 mm Hg, SaO2 87%. Her peak expiratory flow rate is 95 L/min (25% of predicted value).

Asthma medication is continued. Two hours later she becomes more tired and peak flow is < 60 L/minute. Blood gas values (on 40% oxygen) now show: pH 7.20, PaCO2 52 mm Hg, HCO3- 20 mEq/L, PaO2 65 mm Hg. At this point intubation and mechanical ventilation are considered. What is her acid-base status?

Case 10 Solution

Initial status:

◦ chronic respiratory alkalosis, resulting from

several days of hyperventilation (pH almost

normal)

When her asthamatic condition has

worsened, she has acutely hypoventilated.

The second set of blood gas values reflects

acute respiratory acidosis on top of a

chronic respiratory alkalosis.

Case 11

A 21 year old male with progressive renal insufficiency is

admitted with abdominal cramping. He had congenital

obstructive uropathy with creation of ileal loop for

diversion. On admission,

ABG Serum Chemistry

pH 7.20 Na + 140 mEq/L


Cl- 110 mEq/L

HCO3- 10 mEq/L

Case 11: Solution

Dominant disorder is Metabolic Acidosis


= 1.2 × 14= 16.8

PaCO2 = 40 – 17 = 23


Anion Gap = 140 – (110 + 10)= 20

High anion-gap metabolic acidosis.

pH 7.20

PaCO2 24

HCO3 10

Na 140

K 5.6

Cl 110

Case 11: Solution

Δ AG = 20 – 12= 8

Δ HCO3 = 24 –10= 14

Δ AG < Δ HCO3-

High AG Met Acidosis + Normal-AG Met. Acidosis

Final Diagnosis:

Mixed Metabolic Acidosis

pH 7.20

PaCO2 24

HCO3 10

Na 140

K 5.6

Cl 110

Case 12

A 45 year old female with hypertension was treated with low salt diet and diuretics. BP 135/85.Otherwise normal.See initial lab values.

She developed profound water diarrhea, nausea and weakness.

On exam, HR = 96, T=100.6 F, BP 115/70. Abdominal tenderness with guarding on palpation.

Paramete

rInitial

Subse

quent

Na 137 138

K+ 3.1 2.8

Cl- 90 102

HCO3 35 25

pH 7.51 7.42

PaCO2 47 39

Case 12: Solution

Initally, dominant disorder is Metabolic Alkalosis


= 0.7 × 11= 7.7

PaCO2 = 40 + 8 = 48


Anion Gap = 137 – (90 + 35)= 12

AG is normal.

pH 7.51

PaCO2 47

HCO3 35

Na 137

K 3.1

Cl 90

Case 12: Solution

Subsequently, she has developed

pH HCO3 PaCO2

↓ ↓ ↓

pH 7.51 7.42

PaCO2 47 39

HCO3 35 25

Na 137 138

K 3.1 2.8

Cl 90 102

Case 12: Solution

Subsequently, she has developed

The decrease in bicarbonate is almost same as the rise in chloride.

Final Diagnosis:

pH HCO3 PaCO2

↓ ↓ ↓ Metabolic acidosis

Metabolic Alkalosis +

Hyperchloremic (non-AG) Metabolic Acidosis

Case 13

A patient with salicylate overdose.pH = 7.45PCO2 = 20 mmHgHCO3 = 13 mEq/L

Dominant disorder: Respiratory alkalosis

Appropriate Compensation would have been HCO3 of 20 (24 – 4)

Lower than expected HCO3 suggests presence of metabolic acidosis as well.

Case 14

A 55 year old female with DM Nephropathy was admitted with acute LV failure and hyperkalemia. ST-T changes and increased troponin noted.

Hemodialysis was initiated.

CAG revealed near normal coronaries.

She was about to be discharged home when she developed sudden cardiorespiratory arrest.

CPR and ACLS begun and after about 8 mins cardiac rhythm returned.

She was transferred to ICU and placed on ventilator at about 1 PM.

Case 14 (continued): ABG & Ventilator settings

Parameter 1 PM 2 PM 6 PM 8 PM

pH 6.99 7.24 7.52 7.54

PO2 162 73 274 131

PaCO2 49 33 17 20

HCO3 12 14 13 16

Base Excess –20 –12 –6 –3

Ventilator settings

Mode CMV CMV CMV CMV

Rate 20 20 20 16

Tidal volume 400 400 500 500

FIO2 100% 80% 80% 60%

Action TakenSod. Bicarb

3 amps.

Increase

Tidal vol.

Decrease

Rate

Decr. Rate &

Ch. To SIMV

“Life is a struggle,not against sin, not against the Money Power,not against malicious animal magnetism ,

but against hydrogen ions."H.L. MENCKEN

sravan abg ppt modified

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