Blood Gas Abnormalities

6

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Blood Gas Abnormalities HARRY F. WEISBERG Division of Biochemistry, Department of Pathology, Mount Sinai Medical Center, Milwaukee, Wis. 53201

The term "blood gases" has different meanings; the most accurate refers to the gases in the blood -- carbon dioxide, oxygen, and nitrogen -- whereas the most expedient refers to the data obtained from present-day laboratory instruments -pH, Pco , and Ρo . Some confusion results since the data over lap two major areas of diagnosis. Diagnosis of "acid-base imbalance" i s accomplished using values for pH and P c o (though a r t e r i a l blood samples are touted as the best, venous blood can also be used). The diagnosis of "hypoxia" requires a r t e r i a l blood P o values; however, three types of hypoxia have normal a r t e r i a l values (vida i n f r a ) . Acid-base imbalance can easily be diagnosed by use of a diagram (Figure 1) or a flowchart (Figure 2) in which 13 diag nostic areas are identified. Knowledge of the pH and P c o values can distinguish areas or diagnoses 1-7. The CO content or actual bicarbonate value i s used to distinguish a "mixed" metabolic and respiratory abnormality from a "pure respiratory" abnormality -- area 8 from 9 or 10 and area 11 from 12 or 13. Base excess/deficit (previous base excess ±) or the ∆CT (delta CO content) is necessary only to distinguish between an "acute" or "chronic" respiratory condition -- 9 vs 10 and 12 vs 13 (Figures 1 and 2). Figure 2 has many sets of data i n parentheses; these are not necessary for the d i f f e r e n t i a l diagnosis of an acid-base imbalance. I n similar fashion, the P02 values are not needed i n the diagnosis of an abnormal condition of acidbase. Table 1 summarizes the data of Figures 1 and 2 and, i n addition, gives the physio-pathological basis for the alterations of the ( a r t e r i a l ) P02. A c l a s s i f i c a t i o n of the causes of hypoxia i s presented i n Table I I . Only anoxic anoxia (due to decreased ambient oxygen or to respiratory disease) has a r t e r i a l P02 values decreased (with accompanying decreased venous P02 values). However, hemic, ischemic, and histoxic hypoxia may be present (termed non-ventilatory hypoxia) with normal a r t e r i a l P02 values. Thus the best evaluation of hypoxia i s an analysis of both a r t e r i a l and venous 2

2

2

2

2

2

2

153

Forman and Mattoon; Clinical Chemistry ACS Symposium Series; American Chemical Society: Washington, DC, 1976.


154

CLINICAL CHEMISTRY

Interpretation of Electrolyte, Acid-Base, and Oxygen Imbalance

Figure 1. Acid-base balance evaluation diagram with 13 diagnostic areas (1)



2

W

ACUTE VS CHRONIC RESPIRATORY

*CT OR "BE/D"

MIXED VS RESPIRATORY

tC0 CT] OR CHCO,-]

V

; N

\

F %

•f

·

:'

ν( t >

i

if

"

Ν

·

ι

SU ï

φ

1'I

ν

t *

! + 5 5

*

!

φ

t

g*

Τ

*

NORMAL ACID-BASE

NET ACID, ACUTE As 4A • NVH

4A 4B

NET ALK, PARTIAL COMP MIXED RESP ACIDftMET ACID

7 8

}

13A

13B

RESP ALK, ACUTE RESP ALK, CHRONIC, PARTIAL COMP AS 13A • INAPPROPRIATE VENTILATION

ά13B

t

!3 •

MIXED RESP ALK & NET ALK

PARTIAL COMP

RESP ACID, CHRONIC,

^

T

12 13A

+

:

II

12 12 OR 13

11

10

iι η

·; -) ·Φ ,- £Ν (•

; ;

Interpretation of Electrolyte, Acid-Base, and Oxygen Imbalance

RESP ACID, ACUTE

NET ALK, ACUTE As 6A + NVH

6A 6B

9

MET ACID, PARTIAL COMP As 5A + SHOCK

5A 5B

v

b

(

J

Figure 2. Flow-chart for differential diagnoses of acid-base imbalance (1)

RESP ALK, COMP (NET ACID, COMP)

3

As 1A + NVH**

a

NYH (NON-VENTιLATORY HYPOXIA); P 02 NORHAL BUT P 02 ABNORMAL.

L

!

yΦ

t. · . · —,

Τ

b

yl i • +

}

_J ; (

I

10 *γ 99OROR10

I

NOT NEEDED FOR DIFFERENTIAL DIAGNOSIS OF ACID-BASE IMBALANCE.

1

I

RESP ACID. COMP (MET ALK, COMP)

lA lB

# f

()

!

Φ

(•> (•>

Φ

φ

+

3 ?

1

Î2

j

fl

!

ψ

(Ν)

I I

ι

2 2

t

!

ι I

•

Ν

Î1

I


156

CLINICAL CHEMISTRY

TABLE I D i f f e r e n t i a l Diagnosis of Acid-Base Equilibrium. Ρ(>2 values are a r t e r i a l * From Weisberg (1). Pco or PH [ H C 0 ]


2

#

2

3

[C0

2

or

CT]

[HCO3-]

ACT or BE/D

Ρο **

COMMENTS

2

Eupffe»n1a la

Ν

Ν

Ν

Ν

Ν

Normal blood "gases'* (Hemic hypoxia) (Ischemic hypoxia) (Histotoxic hypoxia)

lb

Ν

Ν

Ν

Ν

Ψ

Î/0 inequality Shunts

2

Ν

t

+

4-

Respiratory Acidosis, Compensated; see #8, #9, and #10 Hypoventilation* (ShuntsΓ (¥/Q Inequality) » (Metabolic Alkalosis, Compensated)"; see #6, #7, and #11 11

4·

4-

4a

Ν

Ψ

4b

Ν

4-

3

Ν

4·

+Ν

Respiratory Alkalosis, Compensated; see #11, #12, and #13 Hyperventilation (Metabolic Acidosis, Compensated); see #4, #5, and #8

Ν

Metabolic Acidosis, Uncompensated (Hemic hypoxia) (Ischemic hypoxia) (Histotoxic hypoxia)

Ψ

tf/Q inequality Shunts

*Ν

Metabolic Acidosis, Partial compensation (by Hyperventilation)

ΝΨ

Metabolic Acidosis & Shock; see #13b

Ν4-

Mixed Respiratory Acidosis & Metabolic Acidosis

HypopfflBm1a

5a

Ψ

4-

4-

5b 8

4-

10

4·

4-

Ν +

9

4-

t

ΨΝ

4-

'Respiratory Acidosis, Acute

t

t

Ψ

Respiratory Acidosis, Chronic (Partial compensation)


6.

WEISBERG

Blood Gas Abnormalities

157

TABLE I (CONTINUED) D i f f e r e n t i a l Diagnosis of Acid-Base Equilibrium. PO? values are a r t e r i a l . From Weisberg (1).


Hyperptfemia t

6a

Ν

Metabolic Alkalosis, Uncompensated (Hemic hypoxia) (Ischemic hypoxia) (Histotoxic hypoxia)

4-

V/Q Inequality Shunts

6b

i

7

+

t

4·

Metabolic Alkalosis, Partial compensation (by Hypoventilation)

11

Ν

t

Nt

Mixed Respiratory Alkalosis & Metabolic A1kalosis

12

Ν

tN

Respiratory Alkalosis, Acute

13a

+

t

Respiratory Alkalosis, Chronic (Partial compensation) Impaired diffusion

13b

4-

0

Decreased ambient 0* (Impaired diffusion) (Shunt) (tf/0 inequality) "Inappropriate pulmonary ventilation in acutely i l l patient" eg, Myocardial infarct Pulmonary embolus Shock Later ρΗΨ; see #5b

* Arrows show direction and not extent of change; Ν = normal. ** A "low" Po may become "normal" or "increased" due to: Hyperventilation C Therapy Increased Concentration (100% should produce P o >600) Increased pressure [hyperbaric chamber, respiratory ventilators (eg, PEEP or CPPB)] Po polarographic electrode "error" due to halogenated hydrocarbons (eg, llalothane) t Po usually 50 ° Also transient hyperventilation in response to arterial puncture. 2

2

a

2

2

2

2

2


CLINICAL CHEMISTRY

158

TABLE I I


C l a s s i f i c a t i o n of Hypoxia. Modified from Weisberg (1). I.

ANOXIC: A. AMBIENT ( F j 0 ) 1. Altitude 2. 0 D i l u t i o n ("Fire damp", "Black Damp") 3. Anesthetic or 0 Therapy mishaps 2

T

2

2

B. RESPIRATORY: 1. ALVEOLAR HYPOVENTILATION ("Ventilatory insufficiency") 2. DIFFUSION DEFECT ("Alveolar-capillary block") 3. VENTILATION/CIRCULATION (V/Q) INEQUALITY ("Physiologic" shunt) 4. VENOUS-ARTERIAL SHUNT ("Anatomic" shunt) II.

HEMIC: A. ANEMIC 1. Hemorrhage 2. Depressed marrow, etc. a. X-ray b. PhenyIhydrazine B. TOXIC 1. "Abnormal" Hemoglobin a. C0b. Metc. Sulf-


6.

WEISBERG


TABLE I I (CONTINUED)


C l a s s i f i c a t i o n of Hypoxia. Modified from Weisberg ( 1 ) . III.

ISCHEMIC ("Stagnant", "Circulatory", "Hypokinetic"): A. ISCHEMIA 1. Hypovolemia 2. Congenital defects 3. Peripheral stasis B. MINUTE-FLOW DISCREPANCY 1. Decreased cardiac output 2. Increased tissue demand for 0^

IV.

HISTOTOXIC: A. ENZYMATIC 1. Cyanide 2. Narcotics 3. Alcohol B. OXYGEN C.

"WATER & ELECTROLYTES" e.g., Na+


CLINICAL CHEMISTRY


160

blood specimens (Table I I I ) . A footnote i n Table I (and Table VI) states that P02 values may be erroneously elevated due to the effect of halogenated hydrocarbons on the polarographic electrode. Severinghaus et a l (2) reported that Halοthane, a brominehydrocarbon anesthetic, can be polarographically reduced by the Clark-type oxygen elec trode at polarizing voltages greater than 0.4 v o l t and also i n creases the s e n s i t i v i t y of the electrode to oxygen, resulting i n as much as 10-fold spuriously elevated P02 values. This was confirmed for a different type of oxygen electrode which uses a polarizing voltage of 0.7 v o l t (3). However, the consensus of conversations with various anesthesiologists does not agree with these reports (4). Halothane does not affect the a f f i n i t y of hemoglobin for oxygen (5). A more common cause for "altered" P02 values i s the age of the individual. Normal P02 values decrease with age; i n addition, surgical procedures cause a temporary (post-operative period) decrease of the individual's P02 values. Various r e gression formulas have been presented describing the decrease of P02 with increasing age under normal conditions (6-12), after surgery (10, 13-17), and with oxygen therapy (10, 16). I have used the following "rule-of-thumb" formulas to pre d i c t the expected P02 values under room a i r conditions i n normal (equation 1) and post-operative (equation 2) patients; the "vari ation" of the prediction formulas i s ί 5. P o

p-o P o P

a

- ψ

2

=

1

2

=

100 - ψ

a

0

5

(1)

( 2 )

Equations 3 and 4 are used when 100% oxygen i s given to normal and post-operative patients, respectively; i n this case the "vari ation" i s ±25.

P

a°2

p-op P o a

2

*

»

5 7 5

"

a g e

500 - I

( 3 )

a g e

(4)

Dry a i r at sea l e v e l and 20° has p a r t i a l pressures of 159, 0.3, and 601 mmHg, respectively, for the three gases, oxygen, carbon dioxide, and nitrogen. In ambient a i r (contains water vapor of 17 mmHg at 20°), the p a r t i a l pressures of the gases



I I

DIFFUSION DEFECT

AS "ARTERIAL" AS "ARTERIAL"

YES NO

tN

0

THERAPY

t(N)

(•N+)

I

AS "ARTERIAL"

AS "ARTERIAL"

Ν

HISTOTOXIC

• (N)

t

Ν

Ν

ISCHEMIC 4(N)

Ν

Ν

HYPERVENTILATION

2

AS "ARTERIAL"

AS "ARTERIAL"

t

C 0

v 2

46 (42-55)M 43 (39-52)F

P

AS "ARTERIAL"

40 (30-50)

o

Ρ 0 ν 2

YES

YES

YES

o

Ν

N(H)

TN(T)

+ (N)

t(N)

40 (35-45)M 37 (32-42)F

o

2

on 100% 0

HEMIC

NON-VENTILATORY HYPOXIA:

SHUNTS

V/Q INEQUALITY

ν

95 (75-100)

PaO„

HYPOVENTILATION

HYPOXIA:

2

AMBIENT 0 ί

NORMAL VALUES

CONDITION

PaC0

Pa0 >600

Blood Gas Values Under Various Conditions

TABLE I I I


162

CLINICAL CHEMISTRY

are 156, 0.3, and 587, respectively; upon humidification at 37° (47 mmHg water vapor), the p a r t i a l pressures are 150, 0.3, and 563. Alveolar a i r (end-pulmonary c a p i l l a r i e s ) has the same water vapor of 47 mmHg but the p a r t i a l pressures of the gases are 104, 40, and 569 mmHg whereas the values for a r t e r i a l blood (same 47 mmHg for water vapor) are 100, 40, and 573 mmHg. Note that because of differences i n gas characteristics the carbon dioxide p a r t i a l pressure i s the "same" for a r t e r i a l blood and alveolar a i r whereas alveolar P02 i s higher but alveolar Pfl * lower than i n a r t e r i a l blood. Expired a i r (at 37° with 47 mmHg water vapor) i s a mixture of alveolar and humidified ambient a i r so that the p a r t i a l pressures are 120, 27, and 566 mmHg for oxy gen, carbon dioxide, and nitrogen. Venous blood values are 47, 40, 46, and 573 mmHg for the p a r t i a l pressures of water, oxygen, carbon dioxide, and nitrogen. In order to evaluate the ventilatory status of a patient the alveolar oxygen tension (PA°2^ « determined from the "alveolar gas equation" (equation 5), s


2

P

A°2

"

F

( P

47

P

C

m u s t b

e k n o w n

(F

+

I°2 B " > " A °2 I°2

I f cc

a

n D

e

V^">

(

5

)

i n which P i s the p a r t i a l pressure of a gas i n the a l v e o l i , Fx i s the fraction of the gas i n the inspired a i r , Pg i s the barometric pressure, 47 i s the water vapor pressure at 37° at sea l e v e l , and R i s the respiratory quotient (normal of 0.8, which may drop to below 0.5 i n asphyxia). Substituting room a i r conditions at sea l e v e l results i n A

P o A

»

2

0.209 (760 - 47) - 40

(0.209 +

1

" j}^

09

>

149 - 48 101 For most c l i n i c a l purposes, using room a i r and considering a r t e r i a l Pco (P co2) the "same" as alveolar Pco2 (PA 2)» equa t i o n 5 can be " s i m p l i f i e d " to equation 6. co

2

P

A°2

a

β

1 5

P

°-! a

c o

2

( 6 )

150 - 50 100



WEISBERG

6.

163

I t may not be well known that the weather bureau reports of barometric pressure are corrected to sea l e v e l even though describing conditions i n the mountains, etc. Table IV gives the barometric pressure at various altitudes; these should be used when applicable i n equations 5 and 6. Representative c i t i e s and the variations i n their respective altitudes are given i n Table V. The difference between alveolar and a r t e r i a l P02 values i s called the oxygen Α-a gradient (also P(A-a)°2 (A-a)°2 AaDo ) and i s normally about 10 mmHg. I t i s used to evaluate ven tilation/perfusion (V/Q) inequalities. With increasing age, the gradient rises so that "normal" values for 70-80 year old i n d i viduals are 20-25 mmHg. Upon breathing 100% oxygen for 20 min utes the gradient i s increased ("normal") up to 100 mmHg. Breathing room a i r , a s i m p l i f i c a t i o n i s given i n equation 7; however, for patients on oxygen therapy, the P 02 should be subtracted from equation 5.


o r D

o r

2

a

P

(A-a)°2

1 5 0

"

P

c o

P

( 7 )

" f a 2 " a°2

In early pulmonary disease, a patient may be hyperventila ting while breathing room a i r so that the P co2 i s decreased, yet the P 02 may be r e l a t i v e l y normal; with such pulmonary path ology the P(A-a)°2 increased. With frank pulmonary disease, oxygen therapy may mask the expected hypoxia so that the P o2 i s normal or elevated; again the P(A-a)°2 *** ^e * "" creased. On the other hand, i n a patient with an elevated P co2 (hypoventilation), i f the P(A-a)°2 * elevated then the hypoventilation i s probably due to extra-pulmonary factors such as narcosis, muscle weakness, paralysis, etc. For room a i r conditions, an increase of the V/Q r a t i o w i l l show low Pc©2 and elevated P02 values with the "ultimate" being a point equal to the inspired room a i r , P 02 150 and P co2 0 mmHg. A decrease of the V/Q r a t i o w i l l show a f a l l of the P02 but a rather constant PC02; again the "ultimate" would be a point equal to mixed venous blood, P 02 40 and P co2 46 mmHg. The oxygen gradient, AaDo2, with the patient breathing 100% oxygen for 20 minutes, i s used as a c r i t e r i o n for weaning a patient from a mechanical v e n t i l a t o r (19). An abnormally high AaDo2 gradient (above 350 mmHg) i s an Indication that the patient w i l l need continued ventilatory support with high inspired fractions of oxygen. The P(A-a)°2 *- i used i n calculating the amount of shunt present (equation 8) a

a

w

a

sn o t

a

a

a

sa

a

so

03

% shunt

Β

a

P

°- * (A-a)°2 Λ ΛΟ η °· (A-a)°2 0 3

χ

P

+

a v


n


757

730 704

678

654

630

760

733 706

681

656

632

609

586

0

1000

2000

3000

4000

5000

6000

7000

8000 9000

560 539 499 479

562

541

521

501

481

564 543

522

502

483

10000

11000

12000

519

582

604

628

684 659 634 611 589 567 545 524 504 485 466

661 637 613 591 569 547 526 506 487 468

664 639 616 594 571 550 528 508 489 470

666 642 618 596 573 552 530 510 491 472

668 644 621

554 533 512 493 474

671 646 623

556

558

477

497

517 475

495

514

535

576

578

580 537

598

600

696

•686

709

712

714 688

717

720

736

738

741

691

744

746

900

800

700

694

600

500

602

626

649

674

676 651

699

722

749

752 725

400

300

701

728

754

200

584

607

100

0

ALTITUDE

Conversions for Barometric Pressure and Altitude i n Terms of mmHg per each 100 f t . Modified from Consolazio et a l . (18).

TABLE IV


6.

WEISBERG


165

i n which av i s the difference i n oxygen content of a r t e r i a l and mixed venous blood or the oxygen uptake related to cardiac output. An approximation useful c l i n i c a l l y i s given i n equation 9.


% shunt

*

25

^

Normally the shunt i s 2-6%; for room a i r conditions equation 9 becomes

25 To properly calculate the extent of a shunt, however, requires the patient to breathe 100% oxygen for 15-20 minutes. Table I I I i l l u s t r a t e s that the low P 02 i n hypoventilation, diffusion defect, and V/Q inequality i s corrected by breathing 100% oxygen whereas i n a true veno-arterial shunt i t i s not. Table VI summarizes the material presented i n the previous discussion. I t correlates the changes i n oxygen and carbon diox ide p a r t i a l pressures, showing the pathological causes for the imbalances. In addition, i t contains the various diagnoses of acid-base abnormality (using same numbers as i n Figures 1 and 2 and Table I ) . Considering the format of Table VI as a t i c - t a c toe set-up, we can label the nine portions by the letters A-I for i d e n t i f i c a t i o n i n Table VII which gives examples of various conditions associated with such blood gas abnormalities (20-30). a

Po

2

Ν

Î

Î

A

Β

C

Ν

D

ε

F

i

G

Η

I

•


166

CLINICAL CHEMISTRY

TABLE V


ALTITUDE VARIATIONS OF REPRESENTATIVE CITIES CITY

ALTITUDE

COMMENTS

Buffalo

572-i>650

Lake Erie

Chicago

580-t>600

Lake Michigan

Cleveland

572-O800

Lake Erie

Dead Sea

-1300

Lowest Spot; 23-25% Salt (vs 4-6% for Ocean)

Death Valley, C a l i f .

-282

T°>120°F; Max 134.6°F

Denver

5280

Detroit

580-t>581

Lake Huron

Duluth

602-f>1200

Lake Superior

Lake Erie

572

Huron

580

Michigan

580

Ontario

246

Superior

602


6.

WEISBERG

167


TABLE V (CONTINUED)


ALTITUDE VARIATIONS OF REPRESENTATIVE CITIES CITY Leadville, Col.

ALTITUDE

COMMENTS

10,200

Mexico City

7347->8000

Volcanoes

Milwaukee

580-* 705

Lake Michigan Mitchell F i e l d 693

Minneapolis

838Η>"1100"?

Mid-Point Equator & N. Pole at F a l l s of St. Anthony

Philadelphia Phoenix

-«> 14,000

150 1100

Pittsburgh

710->1365

Rochester, NY

500-*697

Salt Lake City

4255

San Francisco

0*938

Toronto

246*250

Tucson

2400

"Along" Lake Ontario Salt Lake 27% Salt

Lake Ontario



Pulmonary disease compensation

V7ft maldistribution

HYPOVENTILATION Shunts

poor

2

Therapy*

Local" Nonuniform" "Regional" Uneven"

General Net

"NORMA!." BLOOD GASES

[Resp Acid * Met Acid (8)]

4a, 6a)

a

2

P„o

2

Ν t

PyC0

+N ir t Histotoxic tAlso P c o ; pHf

Hemic Ischemic

(la,

NON-VENTILATORY HYPOXIA 2

ν7ή maldistribution - severe

0

Ν Pa°a

[(lb) Normal "Add-Base" (la)1 f(4b) Met Add - Acute (4a)] f(6b) Met Alk - Acute (6a)1

[Resp Acid - (9, 10, 2) Acute, Chronic, or Comp]

[Met alk - (2, 7) Comp or Partial]

HYPOXEMIA

HYPEROXEMIA

0

2

2

0

Therapy"

Therapy*

Hypothermia

Table VI. Blood Gas Imbalance. Presented in part at ASCP-CAP Annual Meeting, San Francisco, Oct. 1972 (]_) ; based on material from 20 and 2]_.



2

2

[Met A d d ft Shock (5b)]

[Met

Acid J (3, 5a) Comp or Partial]

TResp Alk - (12, 13, 3) Acute, Chronic, or Comp]

*If l a b data uncorrected to temperature of patient!

2

• B a s e d on material from R. C. Kory (1970) and on Audio-Digest Fndn "Blood Gas Analysis" (Int Med Series 19: No. 17, Sept. 1, 1972). (Numbers and letters refer to acid-base diagnosis diagram [I-187A], flowc h a r t [I-187C], and table [1-188].) °A "low" Po may become "normal" or "Increased" due to: Hyperventilation 0 Therapy: Increased Concentration Increased Pressure (hyperbaric chamber, respiratory ventilators (eg, PEEP or CPPB), etc) P o polarographlc electrode "error" due to halogenated hydrocarbons (eg, Halothane)

[Resp Alk - Chronic (13)]

TResp Alk ft Met Alk (11)]

Central Net (Impaired diffusion, Chronic) Transient (arterial puncture) Hyperventilation without pulmonary disease

HYPERVENTILATION

Pulmonary disease adequate compensation

v70 maldistribution

"Inappropriate Ventilation": Adult acute respiratory distress syndrome Nonobstructive acute respiratory failure Pulmonary fibrosis "Shock lung" "Stiff lung"

Hyperthermia

2

Ambient 0 +

^Impaired d i f f u s i o n 'Shunts


CLINICAL CHEMISTRY

TABLE VII Conditions Associated with Blood Gas Imbalance


Modified from Weisberg (1)

t

Po 4 ; Pco f 2

Ν

2

ALVEOLAR HYPOVENTILATION 1. General a. Physiological (1) Sleep (2) C0 Retention (3) Metabolic A l k a l o s i s

A

Β

C

D

Ε

F

G

Η

I

2

b.

Impaired Movement of Respiratory Cage & Diaphragm (1) Abdominal Distension (2) Ankylosing Spondylitis (3) Ascites (4) Chest Injury (5) Kyphoscoliosis (6) Myxedema (7) Obesity (8) Pleural Disease

c.

Neurological Impairment of Respiratory Drive & Cage (1) CNS Lesions of Respiratory Center (2) Muscular Dystrophy (3) Myasthenia Gravis (4) Narcotics & Drugs (5) Pickwickian Syndrome (6) Poliomyelitis

2. Net (Secondary to Pulmonary Disease) a. Obstruction to Airways (1) Asthma, Severe (2) Bronchitis, Chronic (3) Cystic Fibrosis (4) Emphysema (5) Laryngeal Spasm


6.


WEISBERG

TABLE VII (Continued) Conditions Associated with Blood Gas Imbalance Modified from Weisberg (1)


b.

Distortion of Pulmonary Parenchyma

(Β) P o N; Pco f 0 Therapy 2

2

2

(C)

Po f ; Pco f 2

0

2

Therapy

2

(A)-(D) Po + ; Pco N + Collapse of Lung Pneumonia 2

2

(D) P o ; Pco Ν "Age" Atelectasis Bronchitis, Early Cardiac Failure Congenital Heart Disease with R-L Shunt Pneumonia "Prematurity" 2 T

2

(Ε) P o N; Pco Ν Normal "Non-Ventilatory Hypoxia" Hemic Anoxia Ischemic Anoxia Histotoxic Anoxia 2

(F)

2

P o f ; Pco Ν 0 Therapy 2

2

2

(D)-(G) Po + ; Pco Ν φ Asbestosis Idiopathic Fibrosis Pulmonary Edema Sarcoidosis 2

2

(G) P0 + ; PC0 Acute Pulmonary Inflammation Alkylating Agents Busulfan Cyclophosphamide 2

2

T


CLINICAL CHEMISTRY

172

TABLE VII Conditions Associated with Blood Gas Imbalance


Modified from Weisberg (1)

Drug Overdose " I n t e r s t i a l Pulmonary F i b r o s i s " Myocardial Infarct Post-Op Pulmonary Oxygen Toxicity Radiation Pneumonitis "Shock Lung" Hemorrhage Thermal Injury Trauma (e.g., Thoracic) V i r a l Pneumonitis (G)-(H) Ρ ο Ν ; P c o Asthma, Early Pulmonary Embolus Shock, Late 2 ψ

(I)

2 v

Po t ; 2+ Anxiety Dehydration Diabetic Acidosis Hyperventilation Syndrome Neurologic Disease Shock, Early Uremia P c o

2


6.

WEISBERG

173


Literature Cited 1.


2.

3. 4. 5.

Weisberg, H. F.; Interpretation of Electrolyte, Acid-Base, and Oxygen Imbalance, Private mimeographed printing, 4th ed., 1974. Severinghaus, J. W.; Weiskopf, R. B.; Nishimura, M.; and Bradley, A. F.; Oxygen Electrode Errors Due to Polarographic Reduction of Halothane. J. Appl. Physiol. (1971), 31, 640-642. Bates, M. L.; Feingold, Α.; and Gold, M. I . ; The Effects of Anesthesia on an In-vivo Oxygen Electrode. Am. J. C l i n . Path. (1975), 64, 448 - 451. Laver, Μ. Β.; Personal Communication (1975). Weiskopf, R. B.; Nishimura, M.; and Severinghaus, J. W.; The Absence of an Effect of Halothane on Blood Hemoglobin O Equilibrium i n V i t r o . Anesthesiology (1971), 35, 579 - 581. Raine, J.; and Bishop, J. M.; Α-a Difference in O Tension and Physiological Dead Space in Normal Man. J. Appl. Physiol. (1963), 18, 284 - 288. Stephen, C. R.; and Talton, I . ; Immediate Postoperative Care, with Particular Reference to Blood-gas Studies. Can. Anesth. Soc. J. (1964), 11, 586- 597. Conway, C. M.; Payne, J. P.; and Tomlin, P. J.; A r t e r i a l Oxygen Tension of Patients Awaiting Surgery. Br. J. Anaesth. (1965), 37, 405 - 408. Sorbini, C. Α.; Grassi, V.; Solinas, E.; et al; A r t e r i a l Oxygen Tension i n Relation to Age in Healthy Subjects. Respiration (1968), 25, 3 - 13. Kitamura, H.; Sawa, T.; and Ikezono, E.; Postoperative Hypoxemia: The Contribution of Age to the Maldistribution of Ventilation. Anesthesiology (1972), 36, 244 - 252. Neufeld, O.; Smith, J. R.; and Goldman, S. L.; A r t e r i a l Oxygen Tension i n Relation to Age in Hospital Patients. J. Am. Geriatr. Soc. (1973), 21, 4 - 9. Wahba, W. M.; Body Build and Preoperative A r t e r i a l Oxygen Tension. Can. Anesth. Soc. J. (1975), 22, 653 - 658. Gordh, T.; Linderholm, H.; and Norlander, O.; Pulmonary Function i n Relation to Anaesthesia and Surgery Evaluated by Analysis of Oxygen Tension of Arterial Blood. Acta Anaesth. Scand. (1958), 2, 15 - 26. Palmer, Κ. Ν. V.; and Gardiner, A. J. S.; Effect of P a r t i a l Gastrectomy on Pulmonary Physiology. Br. Med. J. (1964), 1, 347 - 349. Nunn, J. F.; Influence of Age and Other Factors on Hypoxia i n the Postoperative Period. Lancet (1965), 2, 466 - 468. Davis, A. G.; and Spence, Α. Α.; Postoperative Hypoxemia and Age. Anesthesiology (1972), 37, 663 - 664. Marshall, Β. E.; and Wyche, M. Q.; Hypoxaemia During and After Anesthesia. Anesthesiology (1972), 37, 178 - 209. 2

6. 7. 8. 9. 10. 11. 12. 13.

14. 15. 16. 17.

2


174

18. 19.


20. 21. 22. 23. 24. 25.

26. 27. 28. 29. 30.

CLINICAL CHEMISTRY

Consolazio, C. F.; Johnson, R. E.; and Pecora, L. J.; Physiological Measurements of Metabolic Functions i n Man, McGraw-Hill, New York 1963. Sahn, S. Α.; Lakshminarayan, S.; and Petty, T. L.; Weaning from Mechanical Ventilation. J.A.M.A. (1976), 235, 2208 - 2212. Rory, R. C.; Personal Communication (1970). Audio Digest Fndn., Blood Gas Analysis, Int. Med. Series 19 (17), Sept. 1, 1972. Comroe, J. H.; Forster, R. E.; DuBois, Α. Β.; et al.; The Lung: C l i n i c a l Physiology and Pulmonary Function Tests, Year Book, Chicago, 2nd ed., 1962. Van Liere, E. J.; and Stickney, J. C.; Hypoxia, University Chicago Press, Chicago, 1963. Dejours, P.; Respiration, Oxford, New York 1966. Fishman, A. P.; Goldring, R. M.; and Turino, G. M.; General Alveolar Hypoventilation; A Syndrome of Respira tory and Cardiac Failure i n Patients with Normal Lungs. Quart. J. Med. (1966), 35, 261 - 275. Z i l v a , J. F.; and Pannall, P. R.; C l i n i c a l Chemistry i n Diagnosis and Treatment, Year Book, Chicago 1972. Snider, G. L.; Interpretation of the A r t e r i a l Oxygen and Carbon Dioxide P a r t i a l Pressures; A Simplified Approach for Bedside Use. Chest (1973), 63, 801 - 806. Mays, Ε. E.; An A r t e r i a l Blood Gas Diagram for Clinical Use. Chest (1973) 63, 793 - 800. West, J. B.; Respiratory Physiology - The Essentials, Williams & Wilkins, Baltimore, 1974. Davis, H. L.; Acute Respiratory Insufficency, i n Stollerman, G. H. (ed), Adv. Int. Med. (1974), 19, 213 - 238.


Blood Gas Abnormalities

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