3. Regulation of Acid-Base Balance
Less critical because the kidneys have more time to provide for ongoing compensation -Renal compensation, which works over a longer period, includes increased excretion of H+ and restoration of HCO3-. -Other renal buffer system such as the use of ammonium (NH4) will also provide a secondary response.
Chronic respiratory acidosis
will provide data needed to evaluate acid-base status and begin steps toward intervention.
ABG measurements
Affect concentration of electrolytes in both ECF (extracellular fluid) and ICF (intracellular fluid)
Acid-base changes
Changes in potassium (K+), Chloride. (Cl-), and sodium (Na+) may accompany
Acid-base disorders
The buffer system is not adequate to control the acidosis, respiratory rate and depth will increase (hyperventilation). This allows large amounts of CO2 to be expired.
Acidosis
The kidney regulatory system do not have time to compensate, since these only begin to react within 12-24 hours
Acute respiratory acidosis
H+ + HCO3- <-> H2CO3 <-> CO2 + H2O the bicarbonate-carbonic acid buffer system
As the buffer system reacts with fixed acids, H2CO3 is produced. H2CO3 readily dissolves to CO2 and H2O. Therefore, the lungs will accommodate the increased load of acids by increasing rate and depth of breathing and by expiring the CO2. The kidney helps with this buffer system by either reabsorbing HCO3- or regenerating additional HCO3- from CO2 and H2O
Symptoms of respiratory alkalosis
Cardiovascular system symptoms: cardiac arrhythmias Respiratory system symptoms: frequent yawning and deeper breaths Central nervous system symptoms: lightheaded ness, mental confusion, anxiety, and seizures. Other symptoms: cold and clammy extremedied
ongoing metabolic acidosis relies on carbonate from bone to buffer the acid load. This results in growth failure in children and renal osteodystrophy in adults.
Chronic renal disese symptoms in metabolic acidosis
the disease caused by either the absence or inefficient use of the hormone insulin
Diabetes mellitus
-must be treated quickly and accurately to prevent coma and death - providing adequate insulin, fluids, and electrolytes allows the correction of the metabolic acidosis and prevents these complications
Diabetic keto acidosis treatment
one of the most common causes of lactic acidosis results in metabolic acidosis due to both increased production of and inability to metabolize ketones
Diabetic ketoacidosis
typically develops as a result of infections or because the patient does not take adequate amounts of insulin
Diabetic ketoacidosis
Most common cause of metabolic acidosis
Diarrhea
The kidney cant use bicarbonate as a buffer since it cannot be excreted at the same time as the hydrogen ions. It uses ___ and ____ to prevent damage from acidic urine
Dibasic phosphate and ammonium
Both function to accept H+ in order to control acid-base balance -in a situation where large load of fixed acids is produced, the kidneys will respond by increasing formation of acids within the buffer system.
Dibasic phosphate and sulfur
Important buffer system within red blood cells and tubules of the kidney - excretion of H+ could potentially make urine acidic that excretion would by physically damaging to the kidney - phosphate helps with this buffer system by either reabsorbing HCO3- or regenerating additional HCO3- from CO2 and H2O
Disodium/monosodium phosphate (Na2HPO4)
Hydrogen ions and bicarbonate
Electrolytes
Lab values in acute respiratory failure: compensatory mechanisms or secondary responses allow the pH to remain normal but serum bicarbonate and arterial pCO2
Elevated
Lab values in acute respiratory failure: pCO2
Elevated
HCO3- levels in metabolic alkalosis
Elevated >26mEq/L
this may occur in a patient who is respiratory-compromised and is unable to respond to a situation producing a metabolic disorder. This could also occur in situations of drug overdose where different medications cause both respiratory and metabolic responses.
Ex of when a mixed acid-base disorder may occur
Henderson-Hasselbalch equation
Explains the interrelationship between H2CO3, HCO3-, and pH. In humans, the pH, or the ratio of acids to bases, is 1 part H2CO3 to 20 parts HO3-. For pH to remain within normal range, the ratio has to be maintained. Any change in H2CO3 must be accompanied by a proportional change in HCO3-. If one part of the equation changes without the other and the ratio is not maintained, pH will move out of the normal range.
As renal function declines, other mechanisms to correct acid-base disturbance such as production of NH4+ may
Fail
In chronic kidney disease the ability to restore bicarbonate may
Fail
The largest source of base is ______ which is regulated primarily by the kidneys.
HCO3,
May be lost from an ileostomy or from pancreatic, biliary, or intestinal fistulas
HCO3-
Kidney responds by reducing the amount of HCO3- reabsorbed
Kidneys respond to alkalosis
Controlling both H+ and HCO3- ions
Kidneys role in maintenance of pH homeostasis
deep and labored respirations
Kussmaul's respirations.
When NAD concentration is decreased compared to NADH + H*, the scale leans in the direction of lactic acid production and not pyruvic acid production. Conditions that result in decreased concentrations of NAD include decreased oxygenation of the tissues, excessive ketone body production (as in diabetes), and metabolism of ethanol.
Lactic Acid Production
occurs as a result of increased production of lactate or ketoacids
Lactic acidosis
Have ability to change respiratory rate and depth of breathing to control either release or retention of CO2, and hence assist in acid-base balance -this control system is very sensitive and can respond spontaneously
Lungs
Evaluation of pH in humans
Measures that ratio of acids to bases - If both acids and bases increase or decrease in same proportion pH remains the same - when one changes out of proportion, then there is a pH change
All types of acidosis that are not caused by excessive CO2 -results from either excessive loss of base (HCO3-) or an excessive gain of fixed (nonvolatile) acids -can be acute or chronic -uses AG calculation to determine the origin of the disorder
Metabolic acidosis
Conditions that result in excess loss of bicarbonate from the gastrointestinal system or from renal excretion of bicarbonate can result in
Metabolic acidosis
occurs when there is retention of fixed acids or excessive loss of bases.
Metabolic acidosis
result of excessive loss of fixed acids or retention of bases.
Metabolic alkalosis
-lasting longer than 24 hours -a secondary renal response (compensation) occurs -kidneys reduce their secretion of H+ (which also reduces regeneration of HCO3-) and increase their excretion of bicarbonate (HCO3-)
Pathophysiology for chronic respiratory alkalosis
Allow the person to replace the carbon dioxide "blown off" while hyperventilating
Rebreathing into a paper bag
Renal regulatory control is slower than respiratory regulation and may take up to several days to fully respond to imbalances
Renal vs regulatory control responses
Occurs when there is an excess of acid in relationship to base caused by retention of carbon dioxide. -generally occurs when the lungs are not able to expire CO2 - as CO2 levels rise hypercapnia occurs (more carbonic acid H2CO3 is formed) and pH shifts towards acidosis
Respiratory acidosis
Respiratory conditions such as pneumonia, acute pulmonary edema, or pneumothorax can result in
Respiratory acidosis
is a result of retention of CO2
Respiratory acidosis
Four major types of simple acid-base disorders
Respiratory acidosis Respiratory alkalosis Metabolic acidosis Metabolic alkalosis (Combinations and mixes of these disorders can occur) (The only combination not possible is respiratory acidosis and respiratory alkalosis because hypoventilation and hyperventilation cannot happen together)
-the major cellular buffering defense available is expiration of CO2 by the lungs, but this buffering system is typically insufficient -Body stores of HCO3- are released in order to maintain appropriate ratio of CO2 to HCO3-, keeping pH in a normal range.
Respiratory acidosis pathophysiology
Characterized by a relative excess amount of base (HCO3-) as a reduction of CO2 -the acid-base disturbance is generally a result of conditions causing hyperventilation - rapid breathing results in a decreased PaCO2
Respiratory alkalosis
Result in an inability to maintain adequate oxygenation or release of carbon dioxide.
Respiratory diseases such as chronic obstructive pulmonary disease
Major cause of respiratory acidosis
Respiratory dysfunction (this is why the buffering system is typically insufficient
include deep labored breaths which are referred to as Kussmaul breathing.
Respiratory symptoms in metabolic acidosis
Respiratory: high levels of H+ in the blood stimulate respiratory centers in the brain. Lungs: respond by increasing reate and depth of breathing Kidneys: behin their compensatory response by increasnig their excretion of H+ and retention of HCO3- Renal: comensation is much slower than respiratory, and if the kidney disease is present, effectiveness of the compensaiton is decreased
Responses of different systems to meabolic acidosis
-situations that increase the amount of acid, such as administration of ammonium chloride (used for treatment of metabolic alkalosis) and rapid administration of IV saline -accidental poising with substances such as salicylate (aspirin), ethylene glycol (anti-freeze), or formaldehyde
Result in metabolic acidosis
By conserving bicarbonate (HCO3-) urinary excretion of positively charged cations (Na*, K*, NH,*) increases
Second, the renal system compensates by
-no specific -determined by condiotons of volume deficit or electrolyte abnormalities
Signs and symptoms in metabolic alkalosis
Lab values in acute respiratory failure: bicarbonate levels
Slightly elevated if renal composition just began
with its reliance on fat stores, can also increase synthesis of ketoacids and result in acidosis
Starvation
are not as clear as those of other acid-base disturbances.
Symptoms of metabolic acidosis
Acid bases disturbances are difficult to assess and figure out the origin because
The body attempts to self-correct changes in pH by compensatory or secondary responses
Changes in pH (specifically CO2 levels) are detected in
The cerebrospinal fluid by respiratory center in the brain.
Direct stimulation of respiratory center in the brain malignancy Stroke Hyper metabolic state (like fever and sepsis) Drugs (theophylline, salicylates, progesterone, doxapram, and catecholamines, and anxiety and other emotions distress) As an adaptive response to high oxygen demands during strenuous physical activity
Things that cause hyperventilation
Without adequate insulin, there is an increased dependence on lipids as the primary fuel source. The increased rate oflipolysis results in the production of ketones: aceto-acetic acid and hydroxybutyric acid. These ketone bodies are acids that lower serum pH. The kidney reacts by excreting the ketone bodies in the urine (ketonuria). The increased levels of hydrogen ions are buffered by plasma bicarbonate.
This combination of events results in metabolic acidosis.
A healthy, normally functioning kidney will reabsorb the majority of all HCO3- that is needed. This function requires the kidney to secrete H+ which combines with HCO3- forming H2CO3. H2CO3 dissolves to form CO2 and H2O which then forms HCO3- and free H+. This allows for constant regeneration of bicarbonate, which is needed to buffer the fixed acids being continuously released
To maintain a pH (kidneys)
focuses on correcting the underlying conditions causing respiratory changes
Treatment for respiratory acidosis
Correction of the underlying cause is the only significant treatment -correction of hypoxemia by providing oxygen therapy would be 1st step -if the cause if psychological hyperventilation, rebreathing of CO2 can correct the symptoms
Treatment for respiratory alkalosis
focused on the underlying cause of the acidosis. Correcting pH too quickly can cause additional complications. The goal is to raise systemic pH to a safe level.
Treatment of metabolic acidosis
In chloride-responsive metabolic alkalosis, correcting volume imbalance with isotonic saline with added KCL will correct alkalosis. Metabolic alkalosis that does not involve a fluid deficit requires treatment of underlying causes before alkalosis can be corrected. In severe conditions, use of a carbonic anhydrase inhibitor will enhance HCO, excretion.
Treatment of metabolic alkalosis
The largest source of acid within the body is
carbonic acid.
There will be no change in pH if the ratio remains stable, but
changes in either portion of the ratio will result in changes in pH.
Stored blood contains _____ as a perservitive
citrate
Increased secretion of aldosterone causes the kidney to increase reabsorption of sodium. This is accompanied by secretion of H*, which increases regeneration of HCO3.
example of non-volume-related alkalosis is in the condition of primary or secondary hyperaldosteronism.
a result of hyperventilation and a subsequent decrease in CO, levels
respiratory alkalosis
- primary buffer system in extracellular fluid (ECF) - accommodates more than 80% of the required buffering in the ECF - H+ + HCO3- <-> H2CO3 <-> CO2 + H2O
the bicarbonate-carbonic acid buffer system
serve as compensatory or secondary mechanisms in acid-base imbalance.
the respiratory and renal systems
Common Causes of Metabolic Alkalosis
• Loss of acid • Vomiting • Nasogastric suctioning • Hypokalemia • Excessive base • Intravenous therapy • Blood transfusion • Excessive or chronic use of antacids
How pH works in humans
-if both acids and bases increase or decrease In the same proportion then pH will remain steady -if one changes out of proportion then there is a change in pH - just because pH is in normal range, it does not exclude the possibility of an acid-base disturbance
High levels of ketoacids lead to an increase in the
plasma anion gap.
Symptoms of respiratory acidosis
-alteration in respirations include increased respiratory rate (hyperventilation) and an increase in depth of respirations -other symptoms result from the change in oxygenation in the brain and/or a decrease in neurotransmission these include restlessness, apprehension, lethargy, muscle twitching, tremors, convulsions, and finally a coma
Labs for both chronic and actuate respiratory alkalosis
-electrolyte imbalances -low serum levels of K+ and Ca+ as well as high levels of CL-
Physiological means of accommodating all the hydrogen ions it constantly produces
1) chemical buffers 2) respiratory regulation of pH 3) kidney regulation of pH
Effectiveness or the power of the particular buffer is determined by
1) its association with a cellular salt (pK) 2) its overall concentration in the fluid compartment
The pH is maintained in a ratio of
20:1 base to acid within body fluids.
Minimum pH of urine in humans
4.5
Normal pH in humans is
7.35-7.45.
Reference range for calculus AG is
8-16 mEq/L
pH levein in metabolic alkalosis
>7.45
pH level in acute respiratory alkalosis
>7.45 and PaCO2 is decreased
pH level in chronic respiratory alkalosis
>7.45 and plasma HCO3- is low
Cannot cross back across the cell membrane so H+ is trapped and exerted back into the urine
Ammonium (NH4+)
Fistula
An abnormal connection between organs
Injury or trauma to the chest wall can potentially result in
An inability to expire adequate amounts of carbon dioxide
Represents the difference between unmeasured anions and cations
Anion gap
Affect ventilation and thus the ability to release CO2
Any factor that inhibits the medullary respiratory center
Common labs to asses acid-base balance
Arterial blood gases (ABGs) and serum chemistries
Hydrogen ions secretion coupled with bicarbonate reabsorption in a kidney tabular cell
Because the disappearance of a filtered HCO3- from the tubular fluid is coupled with the appearance of another HCO3- in the plasma. HCO3- is considered to have been reabsorbed
Why are both base excess and HCO3 are measure but both values are not evaluated
Because they both directly correlate
Carbonic acid dissociates to
Bicarbonate and free H+
Reacts with free H+ ions in order to maintain acid-base equilibrium -present in all body fluids (extracellular and intracellular)
Buffer
The lab values for acid-base balance include arterial measures of
CO2 and O2 (PaCO2 and PaO2)
The lungs are the primary regulators of
CO2 levels.
Transport and Exchange of Carbon Dioxide and Oxygen
CO2 picked up at the tissue level is transported in the blood in three ways: 1) physically dissolved 2) bound to the hemoglobin (Hb), and 3) as bicarbonate ion (HCO3-). Hemoglobin is present only in the red blood cells, as is carbonic a hydrate, the enzyme that catalyzes the production of HCO3-. The H+ generated during the production of HCO3- also binds to Hb. Bicarbonate moves by facilitated diffusion down its concentration gradient out of the red blood cells into the plasma, and chloride (CL-) moves by means of the same passive carrier into the red blood cell down the electrical gradient created by the outward diffusion of HCO3-
Chronic conditions such as sleep apnea or acute events such as cardiac arrest
Can affect normal ventilation
Medications such as opiates or sedatives
Can inhibit respirations
Disease that affect musculature of the respiratory system and chest wall such neurological conditions such as myasthenia gravis or extreme obesity seen in Pickwickian syndrome
Can result in poor ventialtion
Diffuses into the blood as it is produced through out the body
Carbon dioxide
CO2 will combine with water forming
Carbonic acid
Oxygenated hemoglobin gives up the H+ to HCO3- to generate
Carbonic acid (HCO3)
Can result in excessive loss of base while inhibiting production of carbonic acid in the kidney. In the condition fo renal tubular acidosis, ability to reabsorb bicarbonate is decreased
Carbonic anhydride inhibitors such as the drug acetazolamide/ diamoz (used as an anti seizures medication)
affected by decreased contractility and response to catecholamines. Vasodilation may cause hypotension and dysrhythmias.
Cardiovascular symptoms in metabolic acidosis
can be categorized as either those conditions involving fluid imbalance (alka- losis with volume decrease) or those without fluid imbalances (alkalosis without volume contraction).
Clinical situations resulting in alkalosis
would include hyperaldosteronism, excessive use of corticosteroids, blood transfusions, chronic use of antacids, and excessive administration of sodium bicarbonate.24
Conditions leading to alkalosis that do not involve fluid imbalance
include prolonged vomiting, nasogastric (NG) suction, or use of diuretics.
Conditions that involve fluid imbalance
In the condition of renal tubular acidosis, the ability to absorb bicarbonate is
Decreased
Lab values in acute respiratory failure: pH
Decreased
one of the most serious acute complications of type 1 diabetes mellitus
Ketoacidosis
may result when the kidney or liver fails to convert lactate to pyruvate.
High levels of lactate
Commonly a result of a reduction in serum oxygen levels (hypoxemia)
Hyperventilation
Can be a result of respiratory diseases such pneumonia, asthma, pulmonary embolism, or pulmonary edema, or of exposure to high altitudes
Hypoxemia
it is possible the body will convert the citrate to bicarbonate. This potentially could lead to metabolic alkalosis.
If an individual receives a large amount of transfused blood
Electorlyte levels in metabolic alkalosis
Imblanced K+ <3.5mEq/L Cl- <98mEq/L
The chemical buffer system Phosphate Buffer System function
Important urinary buffer; also buffers ICF
Respiration's will slow, CO2 concentrations will increase, and pH will normalize.
In a situation where PaCO2 has decreases (alkalosis)
hypoxemia is present; this reduced level of oxygen is responsible for most symptoms associated with acidosis - a more acute onset will result in increased severity of symptoms
In both acute and chronic repiratory acidosis
as pH lowers, respiratory ventilation changes to accommodate the need to reduce pCO,, Respirations are deep and labored
In diabetic ketoacidosis
The kidney will increase secretion of H+ and increase the amount of HCO3- reabsorbed.
Kidney response to acidosis
there is both a fluid loss and a subsequent decrease in K* levels. To maintain serum K+ levels within a safe range, the kidney will excrete H* in exchange for K*. Even though K* may increase, the loss of H results in generation of more bicarbonate. This further contributes to alkalosis.
In situations where there is also volume depletion, such as in use of diuretics,
Lab values in acute respiratory failure: serum electrolytes
Increase in serum Ca+, K+, and possibly CL- due to changes in renal control
A pH of <7.35 or >7.45
Indicates acidosis or alkalosis
may be seen in post- operative patients who are experiencing ileus. It removes gasric secretions in prevention of vomitting or aspiration
NG suction
-a base -formed in renal tubular cells from the amino acid glutamine. -free H+ combines with it to form ammonium (NH4+)
NH3 (ammonia)
AG calculation
Na+ - (CL- + HCO3-)
Disodium/monosodium phosphate (Na2HPO4) buffer system
Na2HPO4 + H+ <-> NaH2PO4 + Na+
will affect the ability of the respiratory system to respond to changes in pH. The second line of defense is a secondary response "compensation"; this is coordinated by the kidneys
Nervous system controls respiration, or muscles that assist in breathing
lethargy and stupor with eventual coma are observed as the pH falls in cerebrospinal fluid.
Neurological symptoms in metabolic acidosis
Overall schema of maintenance of acid-base balance
On the usual mixed diet, pH us threatened by production of strong acids (ex. Sulfuric, hydrochloric, and phosphoric), which result mainly from protein metabolism. These strong acids are buffered by chemical buffers in the body. Removal of extra H+s and the accompanying anions from the body is accomplish by renal excretion. When the kidneys excrete H+s, they add new bicarbonate to the blood, thereby restoring depleted body buffer bases. The respiratory system eliminates CO2 produced by metabolism. CO2 is not a threat to acid-base balance, provided its partial pressure in arterial blood is kept at a normal value.
Stoma
Opening in the body
-within first 24 hours -is a shift of acid from the ICF to the ECF with an accompanying movement of bicarbonate into cells in exchange for chloride -Additional H+ is synthesized by an increase in lactic acid derived from pyruvate within cells. - Shifts in H+ are generally not adequate to handle a continued decrease in PaCO2
Pathophysiology of acute respiratory alkalosis
When H levels increase, the bicarbonate- carbonic acid buffer system is stimulated. This shift of H into ECF reduces serum K+ at the same time in order to maintain equilibrium between the ECF and ICF.
Pathophysiology of metabolic acidosis
begins with the underlying event that causes either an excessive loss of acid or accumulation of base. This could be, for example, prolonged vomiting that results in decreased concentration of HCI". Normally, the kidney will compensate for the decrease in nonvolatile acid by generating Ht and decreasing reab- sorption of bicarbonate. In order for metabolic alkalosis to progress, other events need to occur that prevent adequate compensation by the kidney.
Pathophysiology of metabolic alkalosis
Other lab values for acid-base balance include
Ph, CO2, HCO3, base excess, and anion gap
Focus treatment on increasing oxygenation through administration of oxygen or provision of mechanical ventilation -It's crucial to realize that hypoxemia may be providing the stimulus for ventilation -If oxygen therapy reduces hypoxemia, ventilation may acutely decline without this stimulus
Presence of hypoxemia treatment for respiratory acidosis
The chemical buffer system Bicarbonate-carbonic acid buffer system function
Primary ECF buffer against non-carbonic-acid changes
The chemical buffer system Protein Buffer system function
Primary ICF buffer; also buffers ECF
The chemical buffer system Hemoglobin Buffer System function
Primary buffer against carbonic acid changes
- Protein present in the plasma can act as buffers; their contributions are most important intracellularly - acts in the same fashion as the bicarbonate-carbonic acid buffer system in that protein accepts the H+. - Many proteins can also release the H+ if alkalinity increases - the proteins' ability to act in both situations increases the effectiveness of this buffer system
Protein buffer system
a mixed disorder should be suspected when PaCO, and HCO3 are not consistent with the measured pH. Or it may be present when the compensatory/secondary response is exaggerated. For example, metabolic alkalosis and respiratory acidosis may occur when a patient with chronic obstructive pulmonary disease receives diuretics.
When examining ABGs for a mixid acid-base disorder
We measure concentration of CO, as an indirect measure of acidity. Concentration of CO2 is expressed
as PaCO2.
pH is the ratio of
bases to acids.
Most important buffer in the blood
hemoglobin
In both starvation and chronic alcoholism, synthesis of ketoacids is
increased
Presence of an excessive amount of base (HCO3) results in -genrally, this acid-base distrubance is caused by a loss of nonvolatile acids or the excessive administration of bicarbonate transfusion within whole blood
metabolic alkalosis
The scale for measuring acidity or alkalinity ofa fluid is the measurement
of pH.
The levels of CO2 in the blood controls the
pH of the cerebrospinal fluid