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An in-depth explanation of blood gas analysis, focusing on pH, pCO2, pO2, HCO3, and the role of bicarbonate in maintaining acid-base balance. It covers the concepts of respiratory and metabolic acidosis and alkalosis, as well as their compensatory mechanisms.
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Laura Ibsen, M.D.
Blood Gas Analysis--Insight into the Acid-Base status of the
Patient
The blood gas consists of pH -negative log of the Hydrogen ion concentration: -log[H+]. (also, pH=pK+log [HCO3]/ 0.03 x pCO2). The pH is always a product of two components, respiratory and metabolic, and the metabolic component is judged, calculated, or computed
by allowing for the effect of the pCO2, ie, any change in the pH unexplained by the pCO indicates a metabolic abnormality.
CO +H 0 2 2 ºº H CO 2 3 ºº HCO 3 + H
- +
CO2 and water form carbonic acid or H2CO3, which is in equilibrium with bicarbonate (HCO3-)and hydrogen ions (H+). A change in the concentration of the reactants on either side of the equation affects the subsequent direction of the reaction. For example, an increase in CO2 will result in increased carbonic acid formation (H2CO3) which leads to an increase in both HCO3- and H+ (\pH). Normally, at pH 7.4, a ratio of one part carbonic acid to twenty parts bicarbonate is present in the extracellular fluid [HCO3-/H2CO3]=20. A change in the ratio will affect the pH of the fluid. If both components change (ie, with chronic compensation), the pH may be normal, but the other components will not.
pCO 2 -partial pressure of carbon dioxide. Hypoventilation or hyperventilation (ie, minute ventilation--tidal volume x respitatory rate--imperfectly matched to physiologic demands) will lead to elevation or depression, respectively, in the pCO2. V/Q (ventilation/perfusion) mismatch does not usually lead to abnormalities in PCO2 because of the linear nature of the CO2 elimination curve (ie, good lung units can make up for bad lung units). Diffusion abnormalities almost never are severe enough to effect CO2 elimination. Any change in pCO2 will effect the equilibrium reaction of CO2 and H2O and will effect pH.
pO 2 -partial pressure of oxygen.
HCO -concentration of bicarbonate ion 3 - TCO -total CO2=dissolved CO2 + HCO3- 2 SaO -oxygen saturation, calculated 2
pH, pCO , and pO 2 2 are the primary measurements of the blood gas machine.
Other terms that are used when discussing blood gas analysis Base deficit or excess --the difference between a patients measured serum bicarbonate level and the normal value of 27 (bicarbonate plus carbonic acid). A way of characterizing the acidosis or alkalosis. It is a nonrespiratory reflection of acid-base status. Anion gap --Cations (sodium plus potassium) minus anions (bicarbonate plus chloride). If hydrogen ions accumulate, the hydrogen ion is not accounted for on the cation side, but the decrease in bicarbonate buffer compensation would appear as a bicarb deficit, and the anion gap would increase. Respiratory acid and respiratory acidosis --Carbon dioxide is “respiratory acid” and is the only acid which can be controlled by respiration. When the pCO2 is high, there is a respiratory acidosis. Metabolic acid and metabolic acidosis --Metabolic acids are all the body’s acids except carbon dioxide--they are not controlled by respiration, hence they have to be neutralized,
pH pCO2 HCO3 Base excess
acute metabolic low N low low
acute metabolic high N high high
pH pCO2 HCO3 Base excess
chronic metabolic N low low low
chronic metabolic N high high high
[H+] is maintained between 36-43 nanoequivalents/L (10 -9eq/L) Normal CO2 production is 15,000meq/day (or 15 equivalents). (adult) Nonvolatile acid load (not excreted by lungs) 1 meq/day. This acid load increases in critical illness-burns, starvation, sepsis
Derangements of Acid-Base Homeostasis
How?--Rise in CO2 production (fever, sepsis), or failure of ventilation (CNS causes, muscle weakness, increased dead space) For each 10 mmHg pCO2, pH falls by 0.08 units Renal compensation-hydrogen ion secretion and ammonium secretion increase
predicted [HCO3]=(pCO2-40)x0.3 + 24
How?-result of hyperventilation or decreased CO2 production Causes of hyperventilation in the ICU: iatrogenic, sepsis, pain, acidemia, CNS, liver, pulmonary disease Causes of decreased CO2 production: sedation/paralysis, hypothermia, low carbohydrate diet, brain death delta [H+] = 0.008x delta PCO2, or for fall PCO2 of 10mmHg, pH rises by 0. units. Compensation: renal excretion bicarbonate ion, titratable acid excretion decreases Predicted [HCO3]=(40-PCO2)x0.17 + 40
Renal Tubular Acidosis (RTA) proximal (type II)--HCO3^15, difficult to treat distal (type I)--less severe, can be more easily treated. Renal Failure: Complete renal failure: cant regenerate bicarb, cant excrete unmeasured anions. Bone buffers to [HCO3]= Acute increase in acid during critical illness can be life-threatening (previously compensated acidosis can become clinically important in the face of acute illness)
Pancreatic, bile, small intestinal fluid high in HCO3. Usually renal compensation occurs, except in the case of severe dehydration, very excessive loss (ie, cholera), or renal failure
Lactic acidosis ketoaciosis congenital metabolic defects: organic acidemias, CHO metabolism defects (MCAD) Exogenous: ethylene glycol, methanol, TPN amino acids
V (alveolar minute ventilation)--increased ventilation, hence decreased pCO2A. Predicted pCO2=1.5x[HCO3]+8 +/- 2
abnormalities of free water.
Regulation reflects arterial filling-Q (^) Tand SVR Homeostatic response: sympathetic nerves, renin-angiotensin-aldosterone system, ADH In disease, arterial filling can be dissociated from venous filling (cardiac failure, tamponade, hepatic failure)
Adequate renal function is neccessary for free water regulation ADH controls water homeostasis; release is triggered by hyperosmolality and volume depletion (circulating blood volume) Osmosensors detect change of 1-2% “Volusensors” less sensitive, respond to change of 10%, but with much larger response. Volume will be maintained at the expense of osmolarity if neccessary. Non-osmotic or non-hemodynamic events can change the relationship (slope) between osms and ADH release--pain, drugs, etc.
SIADH -Syndrome of Inappropriate Anti-Diuretic Hormone “Semantic” arguments--is non-osmotic release of ADH “inappropriate” (?) Disorders associated with SIADH--any CNS disturbance (infection, trauma, surgery, etc), increased intrathoracic pressure (ie, as with mechanical ventilation), drugs. It is not uncommon to see hyponatremia in settings of pulmonary disease (ie, RSV). Dx -decreased urine output, along with inappropriately high urinary osmolarity in the face of low serum osmolarity. Euvolemia is prerequisite. Urine sodium will be greater than 20 (indicates adequate or high circulating blood volume). Rx -Fluid restriction (min 0.75L/M2/d) 3% NaCl (0.513 meq/ml) if symptomatic (ie, seizures)-- 0.6 x Kg x (125-Na)meq. (generally 2-3 cc/kg 3% NS)
Cerebral Salt Wasting Occurs after head trauma or cranial surgery Dx -Hyponatremia, high urine Na, high urine volume ADH high in response to volume depletion Rx -salt supplementation--measure urine sodium to estimate needs.
Diabetes Insipidus Absence of ADH release (brain injury) or effect on renal function (nephrogenic DI). May occur post-surgically (pituitary tumors), as a complication of serious brain injury (failure of the pituitary as part of the progression of brain injury). Nephrogenic DI may be congenital or may be a complication of sickle cell disease, pyelonephritis, drug toxicity (lithium, amphotericin), and others. Dx--High urine output of low specific gravity, rising serum sodium
Rx--You need to replace either the free water or the ADH. a. H20 replacement--D5 + 0.2 NS (initially 1:1) to replace urine output. Follow serum sodium and glucose closely. b. ADH replacement--Vasopressin infusion titrated to decrease urine output. Start at 0. milli-units/kg/min, and double infusion until desired urine output is achieved. Monitor serum Na closely, monitor fluid intake closely. Make sure the serum sodium does not fall (most common complication). This is not effective in treating nephrogenic DI. c. DDAVP should not be used in the acute setting, but is appropriate for chronic DI.
Dopamine Low doses dilate renal vasculature High doses constrict renal vasculature Low doses can increase cardiac output, thus increase urine output Dopamine has a direct tubular natriuretic effect-increased Na delivery to the mTAL and macula densa affects JG apparatus and vascular flow.
Acute Renal Failure Cessation of kidney function with or without changes in urine volume Non-oliguric-70%, oliguric 30%. Non-oliguric more common with nephrotoxic injury, oliguric more common with ischemic injury. Pathophysiology involves renal perfusion and tubular dysfunction. “Conversion” or oliguric to non-oliguric renal failure may merely reflect lesser degree of insult, nevertheless, does make manag ement easier. Diagnostic Studies FENa=Una/Pna x Pcr/Ucr x 100 FENa useless in the presence of diuretics (12 hours) RFI=(Una x 100)/Ucr/Pcr. Prerenal vs Intrinsic Renal Failure
“Classic Abnormalities”
c. What could you do about it.
a. What might you find on the next blood gas? b. What might you find on the next electrolytes if you dont alter your ventilation?
a. Why did this happen?? b. Can anything be done about it??
a. What are your first 3 concerns? b. What will you do about them? c. After stabilization, the patient is admitted to the ICU. What electrolyte/water balance abnormalities will you anticipate? d. How would you make the diagnosis?
a. What do you suspect? b. How will you confirm it? c. How will you treat it (2 ways)?
