Blood Gases, ph, Acid- Base Balance Blood Gases Acid-Base Physiology Clinical Acid-Base Disturbances Blood Gases Respiratory Gas Exchange Chemical Control of Respiration Dyshemoglobins Oxygen Transport Oxygen Saturation Effects of Acid on Oxygen Transport Carbon Dioxide Transport Chloride Shift 1
Respiratory Gas Exchange Respiratory Gas Exchange External respiration: exchange of O 2 & CO 2 in lungs between alveolar air & blood Internal respiration: occurring at tissue level; consumes O 2 & produces CO 2 & organic acid metabolites 2
Pulmonary Capillary Gas Exchange A. Oxygen B. Carbon Dioxide Respiratory Processes & Partial Pressures in Respiration 3
Chemical Control of Respiration Respiratory control centers In brain stem (medulla) Chemoreceptors control centers In aortic & carotid bodies Control by: Sensitive to changes in [H + ], arterial pco 2 & po 2 Alter pulmonary ventilation Increased temperatures also accelerate the respiratory rate Dyshemoglobins: malfunction; an alteration in their binding sites. Carboxyhemoglobin (COHb) - Hb binds with carbon monoxide (CO) Carbon monoxide has ~200 times the affinity for Hb than does O 2 Methemoglobin (MetHb) - ferrous ion (Fe ++ ) oxidizes to ferric state (Fe +++ ) Fetal hemoglobin (HbF) 4
Oxygen Transport reversibly bound to hemoglobin in erythrocytes (O 2 Hb) dissolved O 2 (do2) in erythrocytes & plasma Blood Oxygen Saturation Spectrophotometric methods SO 2 = Methemoglobinemia / CO Poisoning SO 2 = Hb tot = HbO 2, HHb, COHb, MetHb, SulfHb, or cyanmethemoglobin 5
Determination of Oxygen Saturation by Spectrophotometry 鮮紅的血 暗紅的血 A short light-path cuvet: 0.1-mm light-path Reference Values Oxygen content of arterial blood in normal person ~20 ml/dl Arterial Oxygen Saturation 95 to 98% saturated with Oxygen 6
Oxygen dissociation curve under normal conditions Myoglobin is more highly saturated with oxygen at lower partial pressures of oxygen than is the hemoglobin molecule 7
ph & the affinity of Hb for oxygen Oxyhemoglobin Dissociation Curve (OHDC) causing a decreased affinity (a right shift) acidosis hyperthermia (fever) hypercarbia (increased PCO 2 ) increased 2,3 DPG (an organophosphate that exists as an intermediate of glycolysis) 8
Oxyhemoglobin Dissociation Curve (OHDC) causing an increased affinity (a left shift) alkalosis hypothermia hypocarbia decreased 2,3 DPG what happens when the curve is shifted 9
Figure 3.15 Causes & Mechanisms of Hypoxaemia 缺氧 Carbon Dioxide Transport a small amount is dissolved in liquid portion of blood (plasma) a small amount binds with hemoglobin to form carboxyhemoglobin (CO2HB) majority of carbon dioxide travels as bicarbonate ion (HCO3-) 10
Transport of carbon dioxide 11
Chloride Shift: as a red cell passes through lungs, it loses Cl - to plasma HCO 3 - RBC CO 2 CO 2 plasma 12
Determination of Serum CO 2 Content (Total CO 2 ) Automated enzymatic method All forms of CO 2 are converted to HCO 3 - Addition of base Automated colorimetric method Addition of acid All forms are converted to CO 2 Dialyzed through a silicone-rubber gas-dialysis membrane Into a buffer solution of cresol red at ph 9.2 Lower ph & decrease in color intensity (430 nm) Methods for Determination of Serum or Plasma Total Carbon Dioxide Sample first alkalinized to convert all forms of CO 2 to HCO 3 - PEPC: phosphoenolpyruvate carboxylase MDH: malate dehydrogenase Decrease in A 340 nm of NADH proportional to total CO 2 content 13
Determination by pco2 electrode Reference values 22 to 30 mmol/l for health adults 14 to 26 mmol/l in premature newborns 20 to 26 mmol/l for infants Determination by pco2 electrode Increased concentration (hypercapnia) Metabolic alkalosis, compensated respiratory acidosis & frequently alkalosis accompanying a large potassium deficiency Decreased concentration (hypocapnia) Metabolic acidosis & compensated respiratory alkalosis 14
BLOOD GASES: Collection of blood Arterial Blood Whenever po 2 measurement is requested Arterialized Venous Blood Heating hand & forearm in water at 45 C for 5 min Arterialized Capillary Blood: infants Warming ear, finger, or heel at 45 C before taking sample Arterial Sampling Sites 15
Blood-gas Instrumentation ph, pco 2, & po 2 are made stimultaneously E 1 is po 2, E 2 pco 2, E 3 is ph, and E 4 is the reference for ph Normal Ranges of Laboratory Values Factor ph PaO 2 (mmhg) Mean 7.40 80 Range 7.35-7.45 85-105 PaCO 2 (mmhg) 40 33-45 HCO 3 - (meq/l) 24 22-30 16
Effects of temperature Normally assess blood gases at 37 o C Which reduces the PCO 2 by about 4.5% per o C The ph rises about 0.015 per o C Any exposure to air: po 2 and pco 2, ph Acid-Base Physiology Acids and ph Acid Buffering Acid-Base Balance Acid-Base disturbances 17
ph (puissance Hydrogen) ph= -log [H + ] Normal ph in human body is between 7.35-7.45 Blood ph Some abnormal conditions: e.g. lactic acidosis & diabetes mellitus Lactic acid, β-hydroxybutyric acid, and acetoacetic acid may accumulate Transported to excretory organs (lungs & kidneys) Minimal change in plasma ph Blood Buffer Systems 18
Buffer in the Blood A buffer is any substance that can reversibly bind hydrogen ions General form of buffering reaction is: Blood Buffer Systems Blood Urine Bicarbonate/carbonic acid buffer system Protein Buffer system Hemoglobin buffer system Plasma protein buffer (albumin) Phosphate buffer system Ammonia buffer system 19
Bicarbonate/carbonic acid Buffer System Most important buffer of plasma 95% of buffering capacity kidney Recover or not lung pulmonary ventilation Bicarbonate/carbonic acid Buffer System lung kidney 20
Henderson-Hasselbalch Equation ph = pk + log(hco 3 - / H 2 CO 3 ) or ph = pk + log(hco 3 - / 0.03 x PCO 2 ) 0.03 is solubility coefficient for carbon dioxide & pk is a constant whose value is 6.1 A normal value for bicarbonate = 24 meq/l & for carbon dioxide = 40mmHg Therefore, ph = 6.1 + log[24 /( 0.03 x 40)] or ph = 6.1 + log (24 / 1.2) = 6.1 + log 20 or ph = 6.1 + 1.3 or ph = 7.4 Proteins Buffers System - High concentration - Very important Hemoglobin buffer system Plasma protein buffer system albumin 21
Hemoglobin Buffer System Hemoglobin Buffer System Major part of buffering capacity of erythrocytes Most important buffer groups: imidazole groups 22
PLASM PROTEIN BUFFER SYSTEM Albumin account for 95% nonbicarbonate buffer value of plasma Most important buffer groups: imidazole groups of histidines + H + pk = 7.3 16 His / albumin Phosphate Buffer System H 2 PO 4 H + + HPO 4 2- In plasma (ph 7.4), 80% phosphate is in HPO 4 2- form NOT important in blood; low concentration ~5% nonbicarbonate buffer value Plays a role in buffering intracellular and tubular fluid In acid urine, it exists as H 2 PO 4 - Important; 90% 23
Buffering of hydrogen ion in urine Excreted H+ must be buffered in urine Otherwise [H+] would rise to very high levels Phosphate buffer Ammonia buffer Renal Compensatory Mechanism Na+-H+ exchange Excretion of acids Excretion of H+ as H2PO4 Production of ammonia (NH3) & excretion of ammonium ions (NH4+) Reclamation of filtered bicarbonate 24
Renal Compensatory Mechanism H + + HPO 4 2- => H 2 PO 4 - Renal Mechanisms 25
Bicarbonate Reabsorption New Bicarbonate 26
Recovery & regeneration of bicarbonate by excretion of H+ in the renal tubular cell H+ is actively secreted into urine while CO2 diffuses along its concentration gradient Recovery of bicarbonate Regeneration of bicarbonate - excretion of hydrogen ion Clinical Acid-Base Disturbances Approach to the Abnormal Blood Gas Metabolic Acidosis Metabolic Alkalosis Respiratory Acidosis Respiratory Alkalosis Therapy of Respiratory Acidosis Therapy of Metabolic Acidosis 27
Nomenclature Physiologic condition Acidosis Alkalosis Hypoxia Hyperoxia Alveolar Hyperventilation Ventilatory Failure Values ph <7.35 ph >7.45 PaO 2 <60 PaO 2 >100 PaCO 2 <35 PaCO 2 >50 Primary Blood Gas Classifications Classification ph PaCO 2 HCO 3 - Acute metabolic acidosis N Chronic metabolic acidosis N Acute metabolic alkalosis N Chronic metabolic alkalosis N Primary change 28
H + Metabolic Acidosis H + ph HCO 3- CO 2 Respiratory Compensation ph = pk + log(hco 3 - / 0.03 x PCO 2 ) 29
Hyperventilation CO 2 Effect of hyperventilation Basic Causes of Abnormalities Metabolic acidoses: a. ketoacidoses (diabetic/alcoholic) b. renal failure c. lactic acidosis d. rhabdomyolysis e. toxins (methanol, ethylene glycol, salicylates, paraldehyde) f. diarrhea g. HCl administration 30
HCO 3- H +, ph (HCO 3- ) CO 2 ph = pk + log HCO 3 - / 0.03 x PCO 2 Metabolic Alkalosis 31
Hypoventilation CO 2 Respiratory Compensation Basic Causes of Abnormalities Metabolic alkaloses: a. vomiting/ NG suctioning b. diuretic therapy c. mineralocorticoid activity (Cushing's syndrome, exogenous steroids) 32
Acid-base disorders: diagnosis & management Reasons for metabolic acidosis & alkalosis 33
結果分析 Primary Blood Gas Classifications Classification Acute ventilatory failure (acute respiratory acidosis) Chronic ventilatory failure (compensated respiratory acidosis) Acute alveolar hyperventilation (acute respiratory alkalosis) Chronic alveolar hyperventilation (compensated respiratory alkalosis) Primary change 代償 ph PaCO2 HCO3 N N N N 34
:Hypoventilation CO 2 ph ph = pk + log HCO 3 - / 0.03 x PCO 2 Respiratory Acidosis ph = pk + log HCO 3 - / 0.03 x PCO 2 RENAL COMPENSATION 3 Excretion of acids Reclamation of filtered bicarbonate 35
Basic Causes of Abnormalities Acute ventilatory failure: a. acute airway obstruction b. severe pneumonia/pulmonary edema c. neuromuscular disorders d. CNS depression (drugs, CNS event) e. ventilator dysfunction Chronic ventilatory failure: a. chronic lung diseases 36
Respiratory Alkalosis : Hyperventilation CO 2 ph ph = pk + log HCO 3 - / 0.03 x PCO 2 RENAL COMPENSATION Excretion of bicarbonate RENAL COMPENSATION 37
Basic Causes of Abnormalities Acute alveolar hyperventilation: a. Anxiety b. hypoxia c. drugs (aspirin, catecholamines, progesterone) d. Sepsis e. hepatic encephalopathy ( ) Causes of respiratory acidosis & alkalosis 38
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