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Respiratory Pathophysiology: Arterial Blood Gases (Huda) INTRODUCTION: Importance: diagnosis and management of many acute and chronic medical disorders Interpretation: must always be interpreted in relation to clinical history and status of the patient Components of Arterial Blood Gas: Oxygen: efficiency of oxygenation of blood as it passes through the lungs CO2: efficiency of the respiratory system to remove CO2 (measure of ventilation) pH: with CO2 indicates the acid-base status of the patient OXYGEN: Transport in the Blood: Dissolved (PaO2): measured by arterial O2 tension (PaO2) o Indicator of efficiency of oxygenation of blood as it passes through lung capillaries Hb Bound (SaO2): measured by arterial O2 saturation (SaO2) o Indicates the amount of Hb that is saturated with O2 Oxygen Content Calculation (CaO2): o Equation: CaO2= (1.39 x Hb x SaO2) + (0.003 x PaO2) Dissolved O2: Alveolar Gas Equation: predicts the partial pressure of O2 in the alveolus (PAO2) o Equation: PAO2= PIO2 – (PaCO2/R) R= 0.8 (under normal dietary conditions) Note: can also MULTIPLY PaCO2 by 1.25 PIO2= partial pressure of inspired O2 Equation: PIO2= (FIO2) x (Pb-PH2O) o FIO2= 0.21 o Pb= 760mmHg (at sea level) o PH2O= 47 mmHg Normal: 150mmHg at sea level PaCO2= normally 40 mHg o **PAO2= normally 100 mmHg** Alveolar-Arterial Gradient (A-a Gradient): o PaO2 and PAO2 are not normally the same: due to normal V/Q relationships, presence of physiological shunts, and shape of oxyHb desaturation curve A-a gradient= PAO2-PaO2 o Normal Values: 10mmHg in a healthy 20 year old (ie. PaO2=90mmHg if PAO2=100mmHg) Increases 2.5mmHg per decade due to normal physiological changes in the lung Therefore, PaO2 decreases by 2.5mmHg per decade o Increased A-a Gradient: implies primary parenchymal lung disease OxyHb Dissociation Curve: General: describes the relationship between PaO2 and SaO2 o Sigmoidal Shape: due to configurational changes in Hb Uptake of O2 enhances the uptake of any remaining O2 until Hb is saturated o Physiological Consequences of Sigmoidal Shape: Increases of PaO2 on plateau phase do not really increase SaO2 (already saturated) or total O2 content of the blood Steep middle phase means large changes in saturation for small changes in PaO2 (condition in peripheral tissues to increase release of O2 where needed the most) Nonlinear relationship of PaO2 and SaO2 provides a reserve of O2 in the blood Important PaO2 and SaO2 Combinations: o PaO2 27mmHg= SaO2 50% (P50): indicator of the position of the dissociation curve o PaO2 40mmHg= SaO2 75%: partial pressure/saturation of O2 in mixed venous blood o PaO2 55mmHg= SaO2 88%: partial pressure/saturation of O2 that qualifies patients for home O2 o PaO2 60mmHg= SaO2 90%: value at the beginning of the plateau phase of the curve (above this, there are smaller changes in CaO2- generally considered lower limits of normal) o PaO2 90mmHg= SaO2 97%: Hb near fully saturated Shifts of the Curve: o Right Shift: affinity of Hb for O2 is DECREASED and ability to release O2 is ENHANCED Physiological Importance: normal mechanism for delivering increased O2 during times of O2 deficit Factors Shifting Curve to the Right: Increased PaCO2 (Bohr effect) Decreased pH (increased H+ concentration) Elevated body temperature Increased 2,3-DPG Hemoglobinopathies (may be secondary to increase in 2,3-DPG) o Left Shift: affinity of Hb for O2 is INCREASED and the ability to release O2 is LOWERED Factors Shifting Curve to the Left: Decreased PaCO2 (Bohr effect) Increased pH (decreased H+ concentration) Decreased body temperature Decreased 2,3-DPG Hemoglobinopathies: o Fetal Hb o CarboxyHb (binding of CO) o MetHb (oxidation of Fe moiety from ferrous to ferric state) Seen with congenital deficiencies or oxidant drugs CO2-BICARBONATE SYSTEM: Biologic Buffer System: plays critical role in maintaining relatively narrow range of pH necessary in the body Major Buffer System: CO2-Bicarb system Other Buffers: o Intracellular proteins o Hb o Plasma proteins Relationship of CO2 and Bicarbonate Anion: Bicarbonate Anion: present in most body fluids and constitutes a large reservoir of buffer o H+ + HCO3- H2CO3 (Carbonic Anhydrase) H2O +CO2 Henderson Hasselbach Equation: o Ka= [H+][HCO3-]/[H2CO3] o pH=pKa + log [HCO3-]/[H2CO3] [H2CO3]= 0.03 x PaCO2 Normal Conditions: o pH= 7.4 o pKa= 6.1 o log[HCO3-]/(0.03 x PaCO2)= 1.3 Other Situations: o Metabolic Alkalosis= increased bicarbonate AND pH o Metabolic Acidosis= decreased bicarbonate AND pH o Respiratory Acidosis= increased PaCO2 with decreased pH o Respiratory Alkalosis= decreased PaCO2 with increased pH Transport of CO2 in the Blood (3 Forms): Dissolved CO2: 5% of CO2 in arterial blood (measured by PaCO2) Bicarbonate Anion: 90% of CO2 in arterial blood o CO2 + H2O occurs rapidly in RBCs (presence of CA enzyme) o HCO3- accumulates in RBCs and diffuses into plasma in exchange for Cl- (chloride shift) H+ impermeable and therefore this shift needs to occur to preserve electrical neutrality o H+ buffered by combining to Hb Haldane Effect: buffering enhanced in tissues with low O2 content (Hb deoxygenated) Carbamino Compounds: 5% of CO2 in arterial blood; formed by reaction of CO2 with terminal amino groups of blood proteins o Hb: major CO2 binding protein in the blood CO2 Hb Dissociation Curve: Linear relationship: between CO2 and Hb at physiologic concentrations Haldane Effect: o Curve is shifted to the left if Hb is deoxygenated (enhances the affinity of Hb for CO2) o Curve is shifted to the right if Hb is oxygenated (decreases affinity of Hb for CO2) ACID BASE DISORDERS: Four Primary Disorders: Respiratory Acidosis: primary increase in PaCO2, leading to a decreased pH Respiratory Alkalosis: primary decrease in PaCO2, leading to a increased pH Metabolic Acidosis: primary increase in acid or decrease in base, leading to a decreased HCO3- and pH Metabolic Alkalosis: primary increase in base or decrease in acid, leading to increased HCO3- and pH Compensatory Responses: Essential: physiologic processes are dependent on the pH being kept in a normal range o Body compensates for changes in PaCO2 or HCO3- to adjust the changes in pH back to normal o pH and PaCO2 do not completely go back to normal Metabolic Disturbances: o General: ventilatory system compensates for changes in the acid/base status via the chemoreceptors Adjust ventilation in response to the slightest changes in PaCO2 (negative feedback) o Metabolic Acidosis: if an acid is added to the system, CO2 is formed by HCO3- and H+ combine Increased CO2 Increased ventilation Decreased PaCO2 Increased pH o Metabolic Alkalosis: if a base is added to the system, the formation H+ ions is favored Decreased CO2 Decreased ventilation Increased PaCO2 Decreased pH Respiratory Disturbances: o General: the kidneys will compensate for a chronic change in the PaCO2 by adjusting the renal absorption of HCO3- (takes 7-10 days for compensation) o Respiratory Acidosis: Increased PaCO2 Increased HCO3- absorption (increased acid secretion) o Respiratory Alkalosis: Decreased PaCO2 Decreased HCO3- absorption (decreased acid secretion) COMPENSATION IS NEVER PERFECT: pH never returns to normal INTERPRETING ABGs: PaO2: Normal: 90-100mmHg (healthy 20 year old breathing room air) o Decreases by 2.5mmHg per decade o PaO2= 100 –(age/3) Acid-Base Status: Normal Values: o pH: 7.4 o PaCO2: 40mmHg o HCO3-: 24 meq/L Prediction of Compensatory Response: o Primary Respiratory Disturbance: Changes in pH: Acute: pH will decrease or increase 0.08 units per 10mmHg increase or decrease in PaCO2 Chronic: pH will decrease or increase 0.03 units per 10mmHg increase or decrease in PaCO2 Changes in HCO3- (Chronic Disturbance Only): Acidosis: HCO3- will increase 3meq/L per 10 mmHg increase in PaCO2 Alkalosis: HCO3- will decrease 3meq/L per 10mmHg decrease in PaCO2 o Primary Metabolic Disturbance: Acidosis: PaCO2 will decrease 1-1.5mmHg per 1 mmol/L decrease in HCO3 Alkalosis: PaCO2 will increase 0.5-1mmHg per 1 mmol/L increase in HCO3 Standard Abbreviation of Blood Gases: pH/PaCO2/PaO2/HCO3-/SaO2: o Normal: 7.40/40/90/24/100% Anion Gap: Definition: difference between unmeasured cations and unmeasured anions in the serum o Unmeasured Cations: K+, Ca++, Mg++ o Unmeasured Anions: proteins (albumin), PO4, SO4, organic acids Calculation: AG= [Na+]-[Cl-]-[HCO3-] Normal Value: 10-12meq/L Importance: important in the differential diagnosis of METABOLIC ACIDOSIS o Increased Anion Gap: indicates an increase in unmeasured anions in the blood o Normal AG: implies that there was a loss of base (or ingestion of a pure acid like HCl) Reasons for Increased Anion Gap: o Decreased Unmeasured Cations: Hypokalemia Hypomagnesia Hypocalcemia o Increased Unmeasured Anions: Organic anions: lactate, ketones Inorganic anions: PO4, SO4 Exogenous Anions: salicylates, methanol, polyethylene glycol Differential Diagnosis of Major Acid-Base Disorders: Respiratory Acidosis: o Acute: Drug overdose Stroke Asthma COPD NM syndromes like Guillan Barre o Chronic: Obesity-hypoventilation syndrome COPD Kyphoscoliosis NM syndromes (ALS, MG) Respiratory Alkalosis: o Hypoxemia of any cause o Cortical influences (anxiety, pain, fever) o Disorders of the airway (asthma, COPD) or lung tissue (pulmonary edema, pneumonia) o Drugs (salicylates) o Pregnancy Metabolic Acidosis: o With Anion Gap: Ketoacidosis (diabetic or alcoholic) Lactic acidosis Intoxicants (methanol, ethylene glycol, salicylates) Renal failure o Without Anion Gap: GI bicarb loss (diarrhea) Diuretics Ingestion of HCl Renal tubular acidoses Early renal failure Metabolic Alkalosis: o Chloride Responsive: urine chloride <10mEq/L Volume depletion GI H+ loss (vomiting) Diuretics Ingestion of alkali o Chloride Unresponsive: urine Cl- >20 mEq/L Mineralcorticoid excess (primary aldosteronism) Glucocorticoid excess (Cushing’s Syndrome)