ABG LOKESH 18.8

ARTERIAL BLOOD GASES : 

ARTERIAL BLOOD GASES MODERATOR: DR MD. YAHYA PRESENTER: DR. LOKESH M.B 18/8/09

WATER CHEMISTRY : 

WATER CHEMISTRY Tendency of water to dissociate into components is demostrated by H2O ------ H+ + OH- KW --------- [H+] * [OH-] (1*107) (1*107) 1*1014 pH (puissance hydrogen)= -log [H+] Change of H+/OH- concentration in acid/base shows an inverse relation

HENDERSON- HESSELBACH EQUATION : 

HENDERSON- HESSELBACH EQUATION pH=pKa+ log ( [salt]/[acid] ) pKa is defined as the pH value at which 50% of the compound is ionised. The compound shows maximum buffer activity at pH =pKa For bicarbonate buffer, pH =pKa+ log ([HCO3-] / [H2CO3] ) pH = pKa + log ([HCO3-] / [s*Paco2]) Where, pKa= 6.1, s=0.0301

COMPENSATORY MECHANISMS : 

COMPENSATORY MECHANISMS

BODY BUFFERS : 

BODY BUFFERS A buffer is a substance that readily accepts or donates H+ ions allowing for relatively large H+ ion changes to take place with relatively little change in free ion concentration (pH). Buffer=combination of weak acid+ its anion HA= H+ + A- HA + A- form buffer system Buffer action is maximum if pH=pKa Concentration of compound is high in given compartment Buffering by- Plasma (HCO3- / H2CO3) is immediate Interstitial (HCO3- / H2CO3) --- 15-20 min Intracellular proteins – 2-4 hours

1. BICARBONATE BUFFER : 

1. BICARBONATE BUFFER H2CO3------ H+ + HCO3- (HCO3- / H2CO3) HCL(H++CL-) + HCO3- ----- CL-+ H2CO3(H2O+CO2) NaOH (Na++OH-) + H2CO3 --- NaHCO3+ H2O pKa =6.1 This buffer is very important because- Relatively high concentration is ECF PaCO2 and HCO3- are regulated by kidney and lungs respectively LIMITATION: can buffer only in metabolic acidosis but not respiratory acidosis.

2. PHOSPHATE BUFFER : 

2. PHOSPHATE BUFFER H2PO4----- H+ + HPO4- pKa=6.8 Relatively low concentration in ECF. More active in ICF because: Relatively in high concentration pH of ICF is 6.9(approx) Maximum activity in renal tubular cells.

3. PROTEIN BUFFER : 

3. PROTEIN BUFFER 75% of body’s chemical buffering power is by proteins Though present in ICF, plays an important role in buffering because- ↑ concentration pKa 7.4(approx) Can buffer both respiratory and metabolic acidosis

Slide 9: 

Respiratory acidosis H2CO3----- H+ + HCO3- H+ + Hb ----- HHb HCO3- + K+ ---- KHCO3 AT LUNGS O2 + HHb ---- OHb + H+ KHCO3 ----- K+ + HCO3- H+ + HCO3- --------- H2CO3 (H2O + CO2)

PULMONARY COMPENSATION : 

PULMONARY COMPENSATION Act via stimulation of medullary chemoreceptors ↑ minute ventilation- 1-4l/min ↑ every 1mmhg ↑ in PaCO2 Hyperventilation Hypoventilation- Due to inhibition by ↑ pH But this compensation is generally not predictable as hypoxia stimulates oxygen sensitive chemoreceptors- so PaCO2 never more than 55mmhg.

RENAL COMPENSATION : 

RENAL COMPENSATION Major route of excretion of metabolic acid- 1meq/kg/dl of sulfuric acid , phosphoric acid, incompletely oxidised organic acid. Not appreciable for 12-24 hours. Max effect- 5days H+ exchange is mainly due to- Na-H exchange Carbonic anhydrase enzyme.

Slide 12: 

H2O + CO2 ↓ H2CO3 ↓ H+→ ←Na

RENAL RESPONSE TO SPECIFIC CONDITIONS : 

RENAL RESPONSE TO SPECIFIC CONDITIONS 1. METABOLIC ACIDOSIS: ↑ H+ excretion with NH4 and PO4-2 buffers 2. RESPIRATORY ACIDOSIS: ↑ H+ excretion with ↓ HCO3- excertion 3. METABOLIC ALKALOSIS not seen unless associated with hyponatremia or mineralocorticoid excess <, 4. RESPIRATORY ALKALOSIS: ↓ PaCO2, ↓ H+ excretion ↑ HCO3- reabsorption.

METHOD OF SAMPLE COLLECTION : 

METHOD OF SAMPLE COLLECTION SITE Radial artery is more preferred Modified allens test- limitations: Cannot be performed on an unconscious or uncooperative patient Previous radial artery cannulation obliterates the pulse Inconclusive if blushing appears by 10-15sec (normal <10s) In such cases collateral circulation can be assessed by keeping pulse transducer/ pulse oximeter on pts thumb and occlude ulnar artery. FRESH, HEPARINSED, ANAEROBIC SAMPLE

TECHNIQUE : 

Wash hands. Prepare heparinised syringe with a 22 g needle (or smaller). Put on a clean gloves Place the pts wrist in hyper extended position Clean the skin with alcohol or povidone iodine Palpate the pulse and insert needle, bevel up at 45 degrees angle to the skin (90 degrees for femoral puncture). Observe for flash of blood at hub of needle. Pressure within the arterial system should allow the syringe to fill without aspiration. Withdraw approx 3ml of blood. Remove needle and apply direct pressure for at least 5 min, longer if pt has a history of anticoagulant therapy or coagulopathy. While applying pressure, remove any bubbles from the syringe by holding it upright, allowing the air to float to the top, where it can be easily expelled. Cap the syringe and immediately place it on ice. Properly dispose of equipment and wash hands. TECHNIQUE

TECHNIQUE : 

TECHNIQUE

INTERPRETATION : 

INTERPRETATION

NORMAL VALUES : 

NORMAL VALUES pH 7.35-7.45 PaCO2 35-45 PaO2 80-100 Hco3- 22-26 Base deficit -2 to +2 SaO2 92-99%

STEPWISE APPROACH : 

STEPWISE APPROACH IDENTIFY PRIMARY DISORDER Look each value individually and label it Describe adequacy of oxygenation with PaCO2 and SaO2 Determine acid base status by pH Determine the primary disorder Confirm by base excess

II EVALUATE COMPENSATORY RESPONSE : 

II EVALUATE COMPENSATORY RESPONSE

Slide 21: 

pH=7.10 PaCO2=25mmhg HCO3- = 8mmol/L BE= -20mmol/L Expected PaCO2=(1.5*HCO3) +8±2 =(1.5*8)+8±2 =18-22 Interpretation: partly compensated metabolic acidosis acidosis resipratory alkalosis metabolic acidosis metabolic acidosos

Slide 22: 

pH=7.53 PaCO2=38mmhg HCO3- = 32mmol/L BE= +7mmol/L Expected PaCO2=(0.7*HCO3)+21±2 =(0.7*32)+21±2 41.5-45.5 Interpretation: partly compensated metabolic acidosis

Slide 23: 

pH=7.24 PaCO2=60mmhg EXPECTED pH= 7.40-[0.008*( PaCO2-40)] = 7.40-[0.008*( 60-40)] =7.24 Interpretation: acute non compensated respiratory acidosis

Slide 24: 

pH=7.34 PaCO2=60mmhg EXPECTED pH= 7.40-[0.003*( PaCO2-40)] = 7.40-[0.003*( 60-40)] =7.34 Interpretation: chronic compensated respiratory acidosis

Slide 25: 

pH=7.54 PaCO2=26mmhg HCO3- = 22mmol/L BE= +2mmol/L EXPECTED pH= 7.40+[0.008*(40- PaCO2)] = 7.40+[0.008*(40-26)] =7.51 Interpretation: acute non compensated respiratory alkalosis

Slide 26: 

pH=7.44 PaCO2 =27mmhg HCO3- = 16mmol/L BE= -6 mmol/L EXPECTED pH= 7.40+[0.003*(40- PaCO2)] = 7.40+[0.003*( 40-27)] =7.439 Interpretation: chronic compensated respiratory alkalosis

CORRECTIONS : 

CORRECTIONS FiO2 correction PaO2=FiO2*5 Temperature correction:

Factors affecting blood gases : 

Factors affecting blood gases

METABOLIC ACIDOSIS : 

METABOLIC ACIDOSIS anion gap: difference between major measured cations and major measured anions Na+ - (Cl- + HCO3-) normal value 7-14

CAUSES : 

CAUSES ↑ ANION GAP(>30) Renal fialure Ketoacidosis Diabetes Starvation Lactic acidosis Ingestion of toxins Salicylate Methanol Ethylene glycol Rhabdomyolysis Inborn errors of metabolism NORMAL ANION GAP ↑ GI loss of HCO3- Diarrhoea Anion exchange resins Ureterosigmoidostomy fistulaas ↑ renal loss of HCO3- RTA Carbonic anhydrase inhibitors hypoaldosteronism Dilutional Total parenteral nutrition ↑ intake of chloride containing acids Ammonium chloride Lysine hydrochloride

Clinical features : 

Clinical features Kussmaul respiration Disorientaition Restlessness coma

Slide 32: 

Treatment Control respiration if neceaasry PaCO2 in low 30s NaHCO3 to be given if pH<7.2 NaHCO3=0.3*body weight (in liters)* base deficit Serial blood gas analysis to be done Refractory- hemodialysis with bicarbonate dialysate Large amounts not advisable bec- if CO2 elimination impaired leads to paradoxical intracellular acidosis. Treatment of primary

RESPIRATORY ACIDOSISCAUSES: : 

RESPIRATORY ACIDOSISCAUSES: Alveolar hypoventilation CNS depression Drug induced Obesity hypoventilation Cerebral ischemia Chest wall abnormalities kyphoscoliosis Neuromuscular disorders Neuropathy/myopathy Airway obstruction Foreign body Tumor Laryngospasm Sleep disorders Asthma COPD Parenchymal lung disorders Pulmonary edema Pulmonary emboli Pneumonia Aspiration ILD Ventilator malfunction ↑ CO2 production Large caloric loads Malignant hypethermia Intensive shivering Thyroid storm Prolonged seixure

SYMPTOMS : 

SYMPTOMS Acute CO2 retention Confusion Lethargy Stupor coma

Slide 35: 

TREATMENT ↑ Alveolar ventilation Bronchodialators, Reversal of narcotics, respiratory stimulants(doxapram), ↓ CO2 production whenever possible Mechanical ventilation: indications- pH<7.2 CO2 narcosis Impeding respiratory muscle fatigue NaHCO3 only if- pH<7.1 and hco3 < 15meq Transiently ↑ PaCO2.

Slide 36: 

So buffers that don’t produce CO2 are in search- Carbicarb: 0.3M sodium bicarbonate + 0.3 M sodium carbonate -mainly produce sodium bicarbonate rather than CO2 Tromethamine: Lack Na+ More effective intracellular buffer Both are of no proven benifit

CHROINC RESPIRATORY ACIDOSIS : 

CHROINC RESPIRATORY ACIDOSIS Treatment Normalise PaCO2 Control O2 therapy carefully Drive for respiration is hypoxia

ANESTHETIC CONSIDERATIONS IN ACIDOSIS : 

ANESTHETIC CONSIDERATIONS IN ACIDOSIS Potentate depressant effect of sedatives Circulatory depressant action of volatile & IV anesthetics increased. Succinylcholine to be avoided – ↑ K+ Respiratory acidosis (but not metabolic) ↑ NDM blockade and prevent its antagonism by reversal agents

RESPIRATORY ALKALOSISCAUSES : 

RESPIRATORY ALKALOSISCAUSES Central stimulation Pain anxiety Ischemia Stroke Tumor Infection Fever Drug induced Salicylates Progesterone Peripheral stimulation Hypoxemia High altitude Pulmonary disease Non cardiogenic pulm edema Asthma Pulm embolism Severe anemia Unknown Sepsis Metabolic encephalopathy Iatrogenic Ventilator induced

Slide 40: 

CLINICAL FEATURES Shortness of breath, anxiety, muscle cramps, tetany, perioral tingling, seizures TREATMENT Correct underlying process If pH>7.6, IV HCL, arginine chloride, ammonium chloride

METABOLIC ALKALOSIS : 

METABOLIC ALKALOSIS Chlorine sensitive= urinary chloride<10 GI Vomiting Chloride diarrhoea Villous adenoma Renal Diuretics Posthypercapnic Low chloride intake sweat Cystic fibrosis Chloride resistant= urinary chloride>20 ↑ mineralocorticoid activity Primary hypoadlosteronism Edematous disorders Cushings syndrome Licorice ingestion Bartters syndrome Severe hypokalemia

Slide 42: 

Miscellaneous causes Blood transfusion Acetate containing solutions Alkaline administration with renal insufficiency Hypercalcemia Glucose feed after starvation Clinical features: Apathy, mental confusion, shallow breathing, tetany, muscle spasms

Slide 43: 

TREATMENT Treat primary ↓ minute ventilation to normalise PaCO2 Chloride sensitive- IV saline, (NaCl). Potassium chloirde (KCl) If pH>7.6, IV HCL, arginine chloride, ammonium chloride hemodialysis

ANESTHETIC CONSIDERATIONS : 

ANESTHETIC CONSIDERATIONS Prolong duration of opioid induced respiratory depression due to ↑ binding of opoids ↓ cerebral blood flow leads to cerebral ischemia. Alkalosis + hypokalemia --- atrial and ventricular arrhythmias Potentiation of NDMR (more with hypokalemia)

NEWER CONCEPTS : 

NEWER CONCEPTS

STRONG ION DIFFERENCE (SID) : 

STRONG ION DIFFERENCE (SID) Net charge of fully dissociated cations minus fully dissociated anions SID= (Na+ + K+ + Ca+2 + Mg+2) – (Cl- + A-) SID= 40-44meq/L

Slide 47: 

SID ↑ Alkalosis Concentration diuresis Hypochloremia Nasogastric suction SID↓ Acidosis Dilutional Mannitol infusion Hyperglycemia Ethylene glycol Methanol poisoning Hyperchloremia Diarrhoea Renal failure

Slide 48: 

THANK YOU

Practice ABG’s : 

Practice ABG’s PaO2 90 SaO2 95 pH 7.48 PaCO2 32 HCO3 24 PaO2 60 SaO2 90 pH 7.32 PaCO2 48 HCO3 25 PaO2 95 SaO2 100 pH 7.30 PaCO2 40 HCO3 18 PaO2 87 SaO2 94 pH 7.38 PaCO2 48 HCO3 28 PaO2 94 SaO2 99 pH 7.49 PaCO2 40 HCO3 30 6. PaO2 62 SaO2 91 pH 7.35 PaCO2 48 HCO3 27 PaO2 93 SaO2 97 pH 7.45 PaCO2 47 HCO3 29 PaO2 95 SaO2 99 pH 7.31 PaCO2 38 HCO3 15 PaO2 65 SaO2 89 pH 7.30 PaCO2 50 HCO3 24 10. PaO2 110 SaO2 100 pH 7.48 PaCO2 40 HCO3 30

Answers to Practice ABG’s : 

Answers to Practice ABG’s Respiratory alkalosis Respiratory acidosis Metabolic acidosis Compensated Respiratory acidosis Metabolic alkalosis Compensated Respiratory acidosis Compensated Metabolic alkalosis Metabolic acidosis Respiratory acidosis Metabolic alkalosis