Upload
dang-thanh-tuan
View
6.707
Download
2
Embed Size (px)
Citation preview
Blood Gas Interpretation
2005/8/25
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
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
Henderson-Hasselbalch Equation
CO2 + H2O H2CO3 H+ + HCO3-
[H+] = K x [CO2]/[HCO3-]
= 24 PCO2/[HCO3-]
pH = 6.1 + log ([HCO3-]/0.0301xPCO2)
Normal Range
pH = 7.35-7.45 PCO2 = 35-45 mmHg (40 mmHg)
HCO3- = 22-26 mEq/L (24 mEq/L)
Bicarbonate Buffering System
CO2 + H2O H2CO3 H+ + HCO3-
Oral intake
Kidney
Metabolism
Oral intake
Kidney
Stomach
Metabolism
Lung
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
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
PaCO2
PaCO2 > 40 mmHg, MV = 2x normal
PaCO2 > 80 mmHg CO2 nacrosis
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
Proximal Renal Tubule
Distal Renal Tubule
Distal Tubule – NH4+ excretion
Acid Base Disturbance
Metabolic acidosis: HCO3-↓
Metabolic alkalosis: HCO3- ↑
Respiratory acidosis: PCO2↑ Respiratory alkalosis: PCO2 ↓
Simple Primary Secondary mixed
Metabolic Acidosis
Indogenous acid production (lactic acidosis, ketoacidosis)
Indogenous acid accumulation (renal failure) Loss of bicarbonate (diarrhea)
High anion gap Normal (hyperchloremic )
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
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
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)
Causes of High-Anion-Gap Metabolic Acidosis
Lactic acidosis Toxins
Ketoacidosis Ethylene glycol
Diabetic Methanol
Alcoholic Salicylates
Starvation Renal failure (acute and chronic)
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+)
Respiratory Acidosis
Severe pulmonary disease Respiratory muscle fatigue Abnormal ventilatory control Acute vs. Chronic (> 24 hrs)
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
Respiratory Alkalosis
Strong ventilatory stimulus with alveolar hyperventilation
Consuming HCO3-
> 2-6 hrs: renal compensation (decrease NH4+/acid excretion and bicarbonate re-absorption)
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+]
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
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
Compensatory Mechanisms
Respiratory compensationComplete within 24 hrs
Metabolic compensationComplete within several days
Both the respiratory or renal compensation almost never over-compensates
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
Mixed Acid Base Disorders
Primary
Secondary
Respiratory acidosis
Respiratory alkalosis
Metabolic acidosis
Metabolic alkalosis
Respiratory acidosis
Respiratory alkalosis
Metabolic acidosis
Metabolic alkalosis
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
Oxygenation
Ventilation and alveolar disease Ventilation↓PAO2 ↓PaO2 ↓, combined
PCO2↑ Alveolar disease
Reduced alveolar area Thickened alveolar membrane V/Q mismatch Shunt
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)
Oxygen Content and Saturation
O2 content = 1.34 x Hb x Saturation + 0.0031xPO2
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
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
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
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↑
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
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
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
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
Thank you for your attention