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ABG Ph <7.35 Acidemia Ph>7.45 Alkalemia
BE:Base Excess ,defined as the amount of strong acid (Hcl for BE>0)or strong base(NaoH for BE<0)required to return 1 lit of whole blood to a Pco2=40 mmhg to PH=7.4.It shows nonrespiratory or metabolic component of an acid-base disturbance.BE<0 means metabolic acidosis,BE>0 means metabolic alkalosis
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HCO3=22-26 Physiologic changes to acid-base disturbances:
Buffer system:1)bicarbonate buffer system(H2co3/Hco3) 2)protein buffer system(prH/Pr) 3)hemoglobin buffer system 4)phosphate buffer system 5)ammonia buffer system Ventilation Renal responses These systems try to preserve the proportion of Hco3 to Co2 equal to 20
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The most important buffering system is bicarbonate
CO2+H2O<<>>H2CO3<<>>H+HCO3 base molecule weak conjugated acid The second important buffering system is Hgb These buffering systems try to keep constant the proportion of Hco3 to Co2 equal to 20 VENTILATORY RESPONSE:central chemoreceptors respondto changes in CSF PH.Pripheral chemoreceptors are sensitive to Pao2 RENAL RESPONSE:slow in onset and maximal up to 5 days 1:reabsorption of Hco3 2:excretion of acid 3:production of ammonia
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Sampling From radial ,brachial,femoral artery
Peripheral venous blood is good for Pco2,PH,BE Pvco2 4-6 mmhg higher Phvenous to 0.04 lower Pvo2 is significantly lower depending on the site of venous blood draw,differeces in tissue metabolic activity may alter Pvo2
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Heparinized,bubble free, fresh
Heparine is acidic then falsely lower PH Air bubbles influence on Paco2 and Pao2,then should be removed Delay causes o2 consumption and Co2 generation by metabolic activity of WBC,it can be reduced by place on ice Hypothermia results decrease in Pco2 and Po2 and increase in PH,while Hco3 doesn’t change and so PH increases
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THE EFFECT OF ACIDOSIS AND ALKALOSIS
Acidemia results in decrease in myocardial contractility and increase in catecholeamines. PH<7.1>>>>decrease in myocardial response to catecholamines Respiratory acidosis may produce more rapid and profound myocardial dysfunction than metabolic acidosis because of rapid entrance of co2 to myocard PH>7.6>>>>decrease in cerebral and coronary blood flow because of vasoconstriction In the brain rapid increase in Co2 decrease ph intracellular and then confusion and seizure happens but chronic increase in CO2 till 150 is well tolerated.
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RESPIRATORY ACIDOSIS Increased production: _Hyperthyroidism _Sepsis _Overfeeding Decreased elimination _pul. Dis.(pneumonia,ARDS,edema) _upper airway obst.(laryngospasm,foreign body) _lower airway obst.(asthema,COPD) _Chest wall restriction(obesity,scoliosis,burns) _CNS depression(opioids,CNS lesion) _decreased skeletal muscle strength(myopathy,neuropathy) _restriction of ventilation(rib fractures,flail chest)
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Consequences of resp. acidosis
Metabolic alkalosis may accompany resp. acidosis when the body stores of cl and k are decreased and then reabsorption of Hco3,cause metabolic alkalosis,this makes PH normal and Pco2 high Avoid hyperventilation because of hypocapnea and CNS irritability PH<7.2>>>>intubation Treatment:Kcl administration Decreased renal perfusion in corpulmonal ,COPD >>>metabolic acidosis
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Respiratory alkalosis
Iatrogenic (mechanical hyperventilation) Decreased barometric p. Hypoxia CNS injury Salicylate overdose Hepatic dis. Pregnancy Decreased Paco2,PH increased>>>stimulate chemoreceptors>>>MV decrease _PH>7.6>>>>sedation is required
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Metabolic acidosis Lactic acidosis DKA Renal failure Hepatic failure
Methanol and ethylen glycol intoxication Aspirin intoxication Increased skeletal muscle activity Cyanide poisoning CO poisoning Treatment :cause of acidosis should be treated _insulin and fluid for DKA _improvement of tissue perfusion for lactic acidosis PH<7.1,Hco3<10 meq>>>administration of bicarb life threatening hyperkalemia>>>>bicarb cardiac arrest with hyperkalemia>>>bicarb cardiac arrest with preexisting metabolic acidosis>>>bicarb Administration of bicarb>>>co2 intracellular increase >>>Ph intracellular decrease,admi. Of bicarb shift PH toward normal and this shifts oxyhemoglobin to left >>>O2 delivery to tissues decrease
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Metabolic alkalosis Hypovolemia Vomiting NG suctioning
Diuretic therapy Hco3 administration Hyperaldostronism Chloride wasting diarrhea Treatment : _volume depletion(vomiting,diarrhea)>>>saline _volume overload(mineralocorticoid excess)>>>>spironolacton and Kcl
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Adverse consequences of alkalosis
_Nervous system Decreased cerebral blood flow Seizures Lethargy Delirium Tetany _Cardiovascular system Arteriolar vasoconstriction Decreased threshold for angina pectoris Predisposition to refractory dysrhythmia _ventilation Hypoventilation Hypercapnea Hypoxia _metabolism Hypokalemia,hypocalcemia,hypomagnesemia,hypophosphatemia,glycolysis stimulated
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Adverse consequences of severe acidosis
Nervous system Obtundation Coma Cardiovascular system Impaired myocardial contractility Low CO Hypotension Decreased responsiveness to cathecolamines Decreased threshold for VF Ventilation Hyperventilation Dyspnea Fatigue of respiratory muscles Metabolism Hyperkalemia Insuline resistance Inhibition of anaerobic glycolysis
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Identification of acid base disturbances
Acidosis:PH<7.35 Alkalosis:PH>7.45 _Paco2 high,Hco3 high:resp.acid _Paco2 high,Hco3 normal or low:resp. acidosis plus metabolic acidosis _Paco2 normal,Hco3 low:met.acidosis plus resp.acidosis _Paco2 low,Hco3 low:met.acidosis Paco2 high,Hco3 high:met.alk. Paco2 low,Hco3 low:resp. alk. Paco2 low,Hco3 high:resp.alk. Plus metabolic alkalosis
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