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 pCO2 indicates a metabolic abnormality.

• 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.

pCO2-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.

pO2-partial pressure of oxygen.

HCO3--concentration of bicarbonate ion
TCO2-total CO2=dissolved CO2 + HCO3-
SaO2-oxygen saturation, calculated

pH, pCO2, and pO2 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, metabolized, or excreted by the kidney. Metabolic acidosis is a pH which is more acid than appropriate for the pCO2.

Possible interpretations of a blood gas

Guidelines for interpretation of acid-base status)--ie, STEPS TO TAKE

1. What is the pH--normal, acidotic, or alkalotic?
2. What is the pCO2--high, normal, or low?
3. What is the bicarbonate--high, normal, or low?
4. Is the primary problem respiratory or metabolic?
5. Is the problem acute, partially compensated, or compensated?

A Couple “rules”

1. For an acute change in pCO2 of 10, the pH will change by 0.08. If all changes in pH can be accounted for by the change in pCO2, then the problem is an acute respiratory acidosis or alkalosis. If not, there is a metabolic component.
2. A pH change of 0.15 corresponds to a base change of 10 meq/L. This only applies to the base changes that are not due to pCO2 changes. First apply rule 1. If there is “unaccounted for” pH change, apply rule 2 to that and determine the degree of metabolic abnormality.
   
   
   • Example--Blood gas 7.26/50. According to rule 1 the pH should be 7.32. The difference between the predicted and actual pH is -0.06 (base deficit). Apply rule 2--0.15/10=0.06/x. Solving for x, x=4 meq/l, which is the base deficit. Thus, there is a combined respiratory and metabolic acidosis.
     
     
3. An immediate increment in plasma HCO3 will occur due to titration of non-bicarb buffers in response to acute hypercapnia. This is approximately 0.1 meq/L for each mmHg increase in pCO2.
4. The only way to have a normal blood gas is to have a normal pH, pCO2, and HCO3. If the pH is normal but the pCO2 and or HCO3 are not, there is a compensated abnormality, or a mixed abnormality (ie respiratory alkalosis and metabolic aciosis). This is still abnormal and requires attention!!!

Why be impressed?

• [H+] is maintained between 36-43 nanoequivalents/L (10-9 eq/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

Buffering--How are acute changes in pH buffered by the body??

1. pCO2/HCO3--pK=6.1, but pCO2 and HCO3 can be independently regulated by lungs and kidneys.
2. Hemoglobin--histidine residues. When in deoxy form, Hg can buffer more acid--CO2 is transported to the lungs as HCO3.
3. Cellular and plasma proteins, intracellular organic phosphates, bone (carbonates and phosphates).

Derangements of Acid-Base Homeostasis

Respiratory acidosis--

• 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 + 2

Respiratory alkalosis

• 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 0.08 units.
• Compensation: renal excretion bicarbonate ion, titratable acid excretion decreases
• Predicted [HCO3]=(40-PCO2)x0.17 + 40

Metabolic Acidosis

• Renal (non anion-gap)
  • 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]=14
    • Acute increase in acid during critical illness can be life-threatening (previously compensated acidosis can become clinically important in the face of acute illness)
• GI Bicarbonate losses (non anion-gap)
  • 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
• Other (anion gap)
  • Lactic acidosis
  • ketoaciosis
  • congenital metabolic defects: organic acidemias, CHO metabolism defects (MCAD)
  • Exogenous: ethylene glycol, methanol, TPN amino acids
• Compensation for metabolic acidosis: Central chemoreceptors cause increased VA(alveolar minute ventilation)--increased ventilation, hence decreased pCO2.
• Predicted pCO2=1.5x[HCO3]+8 +/- 2

Metabolic Alkalosis:

• Initiation phase--excessive HCO3 production (net gain of HCO3 or net loss of H+)
  • excess renal production: mineralacorticoid excess, steroids stimulate distal nephron acidification (H+ ions excreted, HCO3- produced)
  • vomiting/NG suction--loss of Cl- and volume--secondary hyperaldosteronism and renal acidification, plus attempt to retain volume and Na leads to Na/H+ exchange and increased HCO3 resporbtion. (H+, Cl loss, mineralacorticoids, volume contraction all contribute)
  • Bicarbonate, acetate, lactate, citrate administration
• Maintenence phase
  • Normal kidneys in a normal host can excrete all filtered bicarbonate
  • Factors which maintain alkalosis: volume depletion, hypochloremia, mineralacorticoid excess, decreased GFR
  • Check urinary chloride--low in volume depletion (“chloride responsive”), high in mineralacorticoid excess (“chloride resistant”)
  • Potassium depletion almost always accompanies alkalosis (metabolic or respiratory), and may in itself contribute to metabolic alkalosis (as K moves out of cells, H+ moves into cells).
• Compensation
  • There is some evidence that patients will hypoventilate in an “attempt” to compensate for a metabolic alkalosis. The degree to which a given patient or disease process is likely to compensate not well defined.

Electrolytes: Interactions with Acid Base and Volume Abnormalities

It is important to realize that acid-base status, electrolytes status, and volume status interact and inter-relate, both on a purely chemical means and through the bodies “homeostatic” mechanisms.

Magnesium: Renal loss increased with Na and Ca flux through nephron. Hyperaldosteronism, via increase Na delivery, increased Mg wasting.

Calcium: acidosis increases IONIZED Ca, alkalosis decreases ionized Ca. (Hydrogen ions compete for calcium binding sites). As the pH changes, the ionized calcium (the part that is important will change changes). Raising the pH (more alkalotic) causes decreased ionized Ca, lowering the pH (more acidotic) causes increased ionized Ca. This can be important acutely during resusitation when bicarb is used, or during attempts to induce alkalosis in order to effect pulmonary hypertension.

Phosphate: phosphate is taken into cells when glycolysis is stimulated (eg, glucose administration after starvation, hyperal, anorexia, etc.)

Potassium: acidosis causes extracellular K to increase, alkalosis K to decrease. Respiratory or metabolic alkalosis leads to renal K excretion. Hyperaldosteronism increases renal K excretion.

Sodium: Na homeostasis closely linked with volume homeostasis, except in cases of abnormalities of free water.

Volume Homeostasis

Regulation reflects arterial filling-QT and 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)

Free Water (there is no free water)

• 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.
  1. H20 replacement--D5 + 0.2 NS (initially 1:1) to replace urine output. Follow serum sodium and glucose closely.
  2. ADH replacement--Vasopressin infusion titrated to decrease urine output. Start at 0.5 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.
  3. 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 management 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”

1. Bronchiolitis--hyponatremia
2. Severe asthma--respiratory alkalosis, metabolic acidosis
3. Diarrhea--metabolic acidosis (bicarb loss)
4. Pyloric stenosis--hypochloremic metabolic alkalosis
5. Mineralacorticaoid deficiency--young male infant with hyperkalemia, hyponatremia, shock
6. Diabetec--metabolic acidosis, respiratory alkalosis, hyper or hypokalemia

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This page created October 17, 2001 at 1150 PDT by KT