Blood Gas Interpretation

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Blood Gas Interpretation 2005/8/25

Transcript of Blood Gas Interpretation

Page 1: Blood Gas Interpretation

Blood Gas Interpretation

2005/8/25

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Before beginning…

Allen’s test for radial and ulnar artery Common errors of arterial blood sampling

Air in sample: PCO2↓, pH↑, PO2↨Venous mixture: PCO2↑, pH↓, PO2↓Excess anticoagulant (dilution): PCO2↓, pH↑, P

O2↨Metabolic effects: PCO2↑, pH↓, PO2↓

Simultaneous electrolytes panel

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Acid Base Physiology

The Law of Mass Action

[A] + [B] [C] + [D]

K1/K2 = [C][D]/[A][B]

Dissociation constant for an acid Ka = [H+][A-]/[HA]

K1

K2

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Henderson-Hasselbalch Equation

CO2 + H2O H2CO3 H+ + HCO3-

[H+] = K x [CO2]/[HCO3-]

= 24 PCO2/[HCO3-]

pH = 6.1 + log ([HCO3-]/0.0301xPCO2)

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Normal Range

pH = 7.35-7.45 PCO2 = 35-45 mmHg (40 mmHg)

HCO3- = 22-26 mEq/L (24 mEq/L)

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Bicarbonate Buffering System

CO2 + H2O H2CO3 H+ + HCO3-

Oral intake

Kidney

Metabolism

Oral intake

Kidney

Stomach

Metabolism

Lung

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Acid Production and Elimination

Reaction Products Elimination

Glucose H+ + HCO3-

Fat H+ + HCO3-

Glucose H+ + lactateCysteine H+ + sulfatePhosphoproteins H+ + phosphate

Anaerobic

+O2

+O2

+O2

+O2

Lungs

24,000 mEq/day

Volatile acid

Kidneys

50-100 mEq/day

Non-volatile acid

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Determinants of CO2 in the alveolus

VA = VE – VD = VT x f (1- VD/VT)

PACO2 = k x (VCO2/VA)

Physiologic dead space = anatomic dead space + alveolar dead space

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PaCO2

PaCO2 > 40 mmHg, MV = 2x normal

PaCO2 > 80 mmHg CO2 nacrosis

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Renal Regulation of Bicarbonate

“Reabsorption“ of filtered HCO3- (4000 mmol/da

y) Formation of titratable acid (4000 mmol/day H+) Excretion of NH4+ in the urine 80-90% of HCO3

- : reabsorbed in the proximal tubule

Distal tubule: reabsorption of remained bicarbonate and secretion of hydrogen ion

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Proximal Renal Tubule

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Distal Renal Tubule

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Distal Tubule – NH4+ excretion

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Acid Base Disturbance

Metabolic acidosis: HCO3-↓

Metabolic alkalosis: HCO3- ↑

Respiratory acidosis: PCO2↑ Respiratory alkalosis: PCO2 ↓

Simple Primary Secondary mixed

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Metabolic Acidosis

Indogenous acid production (lactic acidosis, ketoacidosis)

Indogenous acid accumulation (renal failure) Loss of bicarbonate (diarrhea)

High anion gap Normal (hyperchloremic )

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Pathophysiologic Effect of Metabolic Acidosis Kussmaul respiration Intrinsic cardiac contractility↓, normal inotropic fu

nction Peripheral vasodilatation Central vasoconstriction pulmonary edema Depressed CNS function Glucose intolerance

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Anion Gap

AG = Na+ - (Cl- + HCO3-) Unmeasured anions in plasma (normally 1

0 to 12 mmol/L) Anionic proteins, phosphate, sulfate, and o

rganic anions Correction: if albumin < 4

Albumin ↓1 AG ↓ 2.5

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Anion Gap

Increase Increased unmeasured anions Decreased unmeasured cation

s (Ca++, K+, Mg++) Increase in anionic albumin

Decrease Increase in unmeasured catio

ns Addition of abnormal cations Reduction in albumin concentr

ation Decrease in the effective anio

nic charge on albumin by acidosis

Hyperviscosity and severe hyperlipidemia ( underestimation of sodium and chloride concentration)

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Causes of High-Anion-Gap Metabolic Acidosis

Lactic acidosis Toxins 

Ketoacidosis Ethylene glycol 

Diabetic Methanol 

Alcoholic Salicylates 

Starvation Renal failure (acute and chronic) 

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Metabolic Alkalosis

Net gain of [HCO3- ]

Loss of nonvolatile acid (usually HCl by vomiting) from the extracellular fluid

Kidneys fail to compensate by excreting HCO3

- (volume contraction, a low GFR, or depletion of Cl- or K+)

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Respiratory Acidosis

Severe pulmonary disease Respiratory muscle fatigue Abnormal ventilatory control Acute vs. Chronic (> 24 hrs)

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Respiratory Acidosis

Acute: anxiety, dyspnea, confusion, psychosis, and hallucinations and coma

Chronic: sleep disturbances, loss of memory, daytime somnolence, personality changes, impairment of coordination, and motor disturbances such as tremor, myoclonic jerks, and asterixis

Headache: vasocontriction

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Respiratory Alkalosis

Strong ventilatory stimulus with alveolar hyperventilation

Consuming HCO3-

> 2-6 hrs: renal compensation (decrease NH4+/acid excretion and bicarbonate re-absorption)

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Respiratory Alkalosis

Reduced cerebral blood flow dizziness, mental confusion, and seizures

Minimal cardiovascular effect in normal health Cardiac output and blood pressure may fall in

mechanically ventilated patients Bohr effect: left shift of hemoglobin-O2

dissociation curve tissue hypoxia (arrhythmia) intracellular shifts of Na+, K+, and PO4

- and reduces free [Ca2+]

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Stepwise Approach

Do comprehensive history taking and physical examination

Order simultaneous arterial blood gas measurement and chemistry profiles

Assess accuracy of data Direction of pH: always indicates the primary

disturbance Calculate the expected compensation Second or third disorders

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N

Respiratory alkalosis

Metabolic alkalsosis

Metabolic acidosis

Respiratory acidosis

7.4

7.6

7.2

pH

30 40 50

PCO2 (mmHg)

Determination of primary acid-base disorders

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Compensatory Mechanisms

Respiratory compensationComplete within 24 hrs

Metabolic compensationComplete within several days

Both the respiratory or renal compensation almost never over-compensates

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Prediction of Compensatory Responses on SimpleAcid-Base Disturbances

Disorder Prediction of Compensation  

Metabolic acidosis PaCO2 = (1.5x HCO3-) + 8 or  

PaCO2 will ↓ 1.25 mmHg per mmol/L ↓ in [HCO3-] or  

PaCO2 = [HCO3-] + 15  

Metabolic alkalosis PaCO2 will ↑ 0.75 mmHg per mmol/L ↑ in [HCO3-] or  

PaCO2 will ↑ 6 mmHg per 10-mmol/L ↑ in [HCO3-] or  

PaCO2 = [HCO3-] + 15  

Respiratory alkalosis  

Acute [HCO3-] will ↓ 2 mmol/L per 10-mmHg ↓ in PaCO2  

Chronic [HCO3-] will ↓ 4 mmol/L per 10-mmHg ↓ in PaCO2  

Respiratory acidosis  

Acute [HCO3-] will ↑ 1 mmol/L per 10-mmHg ↑ in PaCO2  

Chronic [HCO3-] will ↑ 4 mmol/L per 10-mmHg ↑ in PaCO2  

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Mixed Acid Base Disorders

Primary

Secondary

Respiratory acidosis

Respiratory alkalosis

Metabolic acidosis

Metabolic alkalosis

Respiratory acidosis

Respiratory alkalosis

Metabolic acidosis

Metabolic alkalosis

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Oxygenation

Poor diffusion across alveolar membrane Small pressure gradient between PAO2

and PaO2

Large alveolar area is required for gas transfer

Hemoglobin carries the majority of oxygen in the blood

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Oxygenation

Ventilation and alveolar disease Ventilation↓PAO2 ↓PaO2 ↓, combined

PCO2↑ Alveolar disease

Reduced alveolar area Thickened alveolar membrane V/Q mismatch Shunt

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Alveolar-arterial Oxygen Gradient

PAO2 = FiO2 (PB-PH2O) – PCO2/R = 0.21(760-47) – 40/0.8

= 100R: respiratory quotient

P(A-a)O2 = PAO2 – PaO2

(= Age x 0.4)

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Oxygen Content and Saturation

O2 content = 1.34 x Hb x Saturation + 0.0031xPO2

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Pulse Oximeters

Percentage of oxygenated hemoglobin in blood Absorption of light in the red and infra-red spectr

a Continuous monitor Accurate (3%) at high saturation, less below 8

0% Insensitive around the normal PO2

COHb and MetHb

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Clinical Example 1

72 y/o male, COPD with acute exacerbation

Under O2 2L/min

pH 7.44, PCO2 54, PO2 60, HCO3 36 Metabolic alkalosis with respiratory compe

nsation Mixed respiratory acidosis

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Clinical Example 2

30 y/o male, sudden onset dyspnea Room air 7.33/24/111/12 Metabolic acidosis Respiratory compensation Normal A-a O2 gradient O2↑: hyperventilation

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Clinical Example 3

70 y/o male, acute hemoptysis and dyspnea

Room air 7.50/31/88/24 Respiratory alkalosis Not been renal compensated yet Normal PO2, but A-a O2 gradient↑

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Clinical Example 4

18 y/o female, chest tightness and dyspnea for 4 hrs

RR 28/min, distressed, widespread wheezing O2 mask 6L/min 7.31/49/115/26 Respiratory acidosis Normal bicarbonate acute May have problems with oxygenation

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Clinical Example 5

37 y/o female, mild asthma history Wheezes for 3 weeks, increasing chest tightness and dy

spnea for 24 hrs, call for ambulance with Oxygen use RR 18/min, anxious and distressed Room air 7.37/43/97/27 Normal? r/o CO2 retention Low A-a O2: Oxygen use in the ambulance

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Clinical Example 6

19 y/o male, Duchenne muscular dystrophy on wheelchair for 7 yrs

No previous respiratory problems but frequent UTI

Room air 7.21/81/44/36 Respiratory acidosis Metabolic compensation Normal A-a O2 pure ventilatory failure

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Clinical Example 7

57 y/o male, smoker, one week URI then 36 hrs productive cough, fever and dyspnea

RR 36/min, distressed, CXR: RLL pneumonia 7.33/27/51/22, 2L/min 7.34/32/58/24, 10L/min mask Early metabolic acidosis Severe hypoxemic respiratory failure Intra-pulmonary shunting

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Thank you for your attention