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8/8/2019 Acid Base Balance Final
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and nursing care.
4.4.Discuss metabolic alkalosis.
4.4.1.enumerate the different etiological factors of
metabolic alkalosis.
4.4.2.list its different defining characteristics
4.4.3discuss in brief its treatment and nursing care
4.5.Identify two different samples for mixed acid-base imbalances.
4.5.1.identify respiratory alkalosis plus metabolic acidosis.
4.5.2.identify respiratory acidosis plus metabolic acidosis.
ACID-BASE BALANCE
A. The overall acid-base balance of the body is maintained by controlling the H+
concentration of body fluids, especially extracellular fluid.
1. The normal pH of extracellular fluid is 7.35-7.45.
2. Homeostasis of pH is maintained by buffer systems, exhalation of carbon dioxide,
and kidney excretion.
B. The Actions of Buffer Systems
1. Most buffer systems of the body consist of a weak acid and the salt of that acid (which
functions as a weak base); together they function to prevent rapid, drastic changes in the
pH of a body fluid by changing strong acids and bases into weak acids and bases. Buffers
work within fractions of a second.
2. The important buffer systems include the protein system, the carbonic acid-bicarbonate
system, and the phosphate system.
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a. The protein buffer system is the most abundant buffer in body cells and
plasma. Inside red blood cells the protein hemoglobin is an especially
good buffer for carbonic acid.
b. The carbonic acid-bicarbonate buffer system is an important regulator
of blood pH and is based on the bicarbonate ion.
c. Thephosphate buffer system is an important regulator of pH, both in
red blood cells and in the kidney tubular fluids.
C. Exhalation of Carbon Dioxide
1. The pH of body fluids may be adjusted by a change in the rate and depth
of respirations, which usually takes from 1 to 3 minutes.
a. An increase in the rate and depth of breathing causes more carbon
dioxide to be exhaled, thereby increasing pH.
b. A decrease in respiration rate and depth means that less carbon
dioxide is exhaled, causing the blood pH to fall.
2. The pH of body fluids, in turn, affects the rate of breathing (Figure 27.7).
The kidneys excrete H+
and reabsorb HCO3-to aid in maintaining pH.
1. Cells in the PCT and collecting ducts secrete hydorgen ions into the tubular fluid.
2. In the PCT Na+/H
+antiporters secrete H
+and reabsorb Na
+(Figure 26.13).
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3.The apical surfaces of some intercalated cells include proton pumps (H+
ATPases) that
secrete H+
into the tubular fluid and HCO3
antiporters in their basolateral membranes to
reabsorb HCO3
(Figure 27.8).
4. Other intercalated cells have proton pumps in their basolateral membranes and Cl
/HCO3
antiporters in their apical membranes.
5. These two types of cells help maintain body fluid pH by excreting excess H+ when pH is
too low or by excreting excess HCO3 when the pH is too high.
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A-Metabolic Acidosis
(HCO3 deficit)
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Low PH, elevated H + ions concentration
Low plasma bicarbonate concentration.I n compensation :
The lungs hyperventilate to decrease the
Pa Co2 concentration.
Anion Gap
Metabolic acidosis can be divided into two forms depending on the value of the
serum anion gap.
AG=Na ( CL + HCO3 )
Normally =12 + 2 m Eq / L
There are other anions in the body fluids that are not accounted for in the equation,
including anionic proteins ,phosphates, sulfates, and organic anions ( such as ketonesand lactic acids ).
Normally the sum of these unmeasured anions should be no greater than 12 + 2
mEq/L however ,in some situations ,these anions are markedly increased and theAG is greater than expected. These situations are referred to as high AG metabolic
acidosis.If the primary problem is direct loss of bicarbonate, gain of chloride, or decreased
renal ammonia production ,the AG will be within normal limits.
Causes of high or normal AG metabolic acidosis :-
Most commonly seen in
*Significant cardiopulmonary problems
*Sepsis
When intracellular ( IC) O2 is not available ,energy is produced by the anaerobic
metabolic pathways, producing lactate and hydrogen ions ( which in turn form lactic acid
in the blood stream.
*Accumulation of lactic acid produces a
profound decrease in PH
The normal arterial lactate level is 7.45
Bicarbonate > 26 m Eq /L
Pa CO2 > 45 mmHg ( compensatory).
Serum Cl relatively lower than Na.
Example of patient with vomiting
PH = 7.62
HCO3 = 45mEq/ L
paCO2 = 48 mmHg
BE = 16 mEq /L
Blood gases show an increase in PH, an elevation of bicarbonate level ,compensatory
hypoventilation ( PaCO2 ),depilated patients may develop marked hypoxemia as a
result of hypoventilation, Base excess is always positive.*Metabolic alkalosis can be acute orchronic.
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Expected directional changes in blood gases forUncompensated,partly compensated
metabolic alkalosis
Imbalance PH HCO3 PaCo2 BE
Uncompensated(acute) N
Partly compensated(sub)
Completely compensated N
(chronic )
Treatment and nursing care
-Treatment is aimed at reversal of the underlying disorders. Sufficient chloride must be
supplied for the kidneys to absorb sodium with chloride ( allowing the excretion of excess
bicarbonate).
- Restoration of normal fluid volume byadministration of sodium chloride fluids ( continued fluid depletion serves to maintain
the alkalosis).
Respiratory Acidosis
(H2CO3 Excess)
Can be either acute or chronic. The acute imbalance is particularly dangerous. Because
renal compensation is very slow ( bicarbonate level remain normal ).Therefore the high
PaCO2 can quickly produce a sharp decrease in plasma PH.
Etiological Factors:
Acute respiratory acidosis:Sudden hypercapnea ( elevated PaCo2) can cause sudden increased pulse and respiration
rate, BP, mental cloudiness and a feeling of fullness in the head e.g.:
Acute pulmonary edema
aspiration of foreign bodyAtelectasis
PneumothoraxOverdosage of sedatives
Position on OR table that interfere with
respiration.Cardiac arrestSevere pneumonia
Laryngospasm
Mechanical ventilation improperly regulated.
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Chronic Respiratory Acidosis
*Patients with COPD may not develop symptoms of hypercapnia because compensatorychanges have had time
to occur.
*The respiratory center becomes relatively insensitive to CO2 as a respiratory stimulant,lowering hypoxemia as the major drive for respiration.
*Excessive O2 administration removes the stimulus of hypoxemia and the patient develops
acute ventilatory failure unless the situation is quickly reversed.
Etiological factors
-Emphysema
-Cystic fibrosis
-Advanced multiple sclerosis
-Bronchiectasis
-Bronchial asthma
Factors favoring hypoventilation-Obesity
-Tight abdominal binders or dressings-Postoperative pain as in high abdominal or
chest incisions).-Abdominal distension from cirrhosis or bowel
obstruction.
Defining characteristics:
Acute respiratory acidosis:
- Feeling of fullness in the head ( PaCO2) causes cerebrovascular vasodilatation andincreased cerebral blood flow, particularly when higher than 60 mm Hg ).
- Mental cloudiness- Dizziness- Palpitation- Muscular twitching- Convulsions- Warm, flushed skin- Unconsciousness- Ventricular fibrillation may be first sign in anesthetized patient ( related to
hyperkalemia ).
- ABGs : PH < 7.35Pa CO2 > 45mmHg ( primary)Hco3 normal or only slightly elevated
Chronic Respiratory Acidosis :
Weakness
Dull headache
Symptoms of underlying disease process
ABGs:
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-PH < 7.35 or within lower limits ofnormal
-paCO2 > 45 mmHg ( primary).-HCO3 > 26mEq/L (compensatory)
Expected Directional Changes in blood gases in respiratory acidosis
Imbalance PH PaCO2 HCO3 BE
Uncompensated N N
( acute)
partly compensated
Completely compensated N
Treatment and Nursing Care:
-Treatment is directed at improving ventilation: Exact measures vary with the cause ofinadequate ventilation
Bronchodilators help reduce bronchialspasms.
Antibiotic are used for respiratoryinfections.
Pulmonary hygienic measures are used
when necessary to get ride the respiratory
tract of mucous and purulent drainage.
Adequate hydration ( 2-3L/day) is
indicated to keep the mucous membrane
moist and thereby facilitate removal of
secretions.
Supplemented O2 is used as necessary.
A mechanical respirators , used cautiously
may improve pulmonary ventilation .
overzealous use of a mechanical respirator
may cause such rapid excretion of CO2 that
the kidney will be unable to eliminate excessbicarbonate with sufficient rapidity to prevent
alkalosis and convulsions for this reason theelevated Paco2 must be decreased slowly.
Respiratory Alkalosis
( H2Co3 deficit)
Carbonic acid deficit
Is always due to hyperventilation blowing off CO2 and hence a decrease in plasma
( H2CO3) content.
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Etiological Factors-Extreme anxiety (most common cause)
-High fever-Hypoxemia
-Early salicylate intoxication (stimulates
respiratory center.
-Pulmonary emboli-Thyrotoxicosis
-Excessive ventilation by mechanical
ventilators.
-Pregnancy ( high progesterone level sensitizes the respiratory center to CO2;
physiological).
Defining characteristics;
-Light headiness ( a low PaCo2 causes
cerebral vasoconstriction and thus decreased
cerebral blood flow).
-Inability to concentrate
-Those of decreased calcium ionization ( numbness and tingling of extremities andcircumoral parathesia; more likely to occur if respiratory alkalosis develops rapidly ).
-Hyperventilation syndrome:
Tinnitus
Palpitation
Sweating
Dry mouth
Tremulousness
Pericardial pain ( tightness)
Nausea and vomiting
Epigastric pain
Blurred vision
Convulsions and loss of consciousness
( may be partly due to cerebral ischemia,
caused by cerebral vasoconstriction ).
ABGs:
PH > 7.45Paco2 < 35 mmHg ( primary)
Hco3 < 22 mEq/L ( compensatory)
As with respiratory acidosis ,acute and chronic conditions can occur in respiratoryalkalosis ;
In the acute stage ,the PH is elevated above normal as a result of a low Pco2 and a
normal bicarbonate level.e.g.; PH of a patient with acute respiratory alkalosis :
In the compensated state ,the kidneys have had time to lower the bicarbonate level
Example: Patient with chronic respiratory alkalosis
PH =7.40
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Pa Co2 =30 mmHgHco3 =18 mEq / L
BE = -5 m Eq/L
Expected directional changes in blood gases in Uncompensated ,Partly compensated,
andCompletely compensated respiratory alkalosis are listed:
Imbalance PH PaCo2 Hco3 BE
Uncompensated N N
Partly compensated
Completely compensate N
Treatment and Nursing Care:
If the cause is anxiety instruct the patient to breath more slowly or to breath into aclosed system. Sedative may be required to relieve hyperventilation in very anxious
patients.
If alkalosis is severe enough to cause fainting ,the increased ventilation will cease andrespiration will revert to normal.
Treatment for other causes of respiratory
alkalosis is directed at correcting the
underlying problems.
E-Mixed Acid-base
In some clinical situations the patient may have two or more primary acid-base
disturbances simultaneously. Some examples are listed:
Examples of combinations of mixed acid-base disorders:
Metabolic acidosis /respiratory acidosis
Respiratory acidosis / metabolic alkalosis
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In summary
ACIDOSIS (PARAMETER) ALKALOSIS
RESPIRATORY ACIDOSIS N
METABOLIC ACIDOSIS N
RESPIRATORY ALKALOSIS N
METABOLIC ALKALOSIS N
COMPENSATION FOR ACID-BASE
IMBALANCE
RESPIRATORY ACIDOSIS N
COMPENSATION
METABOLIC ACIDOSIS N
COMPENSATION
RESPIRATORY ALKALOSIS N
COMPENSATION
METABOLIC ALKALOSIS N
COMPENSATION
pH pCO2 HCO3
pH pCO2 HCO3
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General Nursing management
of acid-base imbalances
1-Note any history of renal, endocrine or respiratory disease or diabetes mellitus
2-Assess the patient for symptoms of acid-base imbalance include dysnea, anxiety,
confusion, dizziness, lightheadness, seizures and change in weight.
3-List any medications the patient is taking.
4-Observe the patient's appearance in terms of reponsiveness, signs of distress
5-Take the vital signs and weigh the patient
6-Pay especial attention to the rate,depth and rhythm of respiration
7-Test muscle strength and sensory function in extremities.
8-Evaluate mental status
9-Note the results of blood gases.
Specific nursing care of respiratory acidosis
-Measure paCO2 levels in arterial blood gases
-Observe the patient for signs of respiratory distress including
restlessness,anxiety,confusion, and tachycardia
-Frequently note the rate ,depth and rhythm of respiration for example the patient with a
head injury or drug overdose may have slow respirations that contribute to carbon dioxide
retention
-Assess level of consciousness, including orientation to person, time and place to detect
changes in mental status
-Encourage fluid intake to loosen secretions and keep mucous membrane moist
-Position patients with the head elevated 30 degrees to promot comfort and ensure optimal
gas exchange
-Frequent suctioning if needed
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-Give antibiotic and bronchodilator if ordered.
Specific nursing care of Respiratory alkalosis
-Assess the underlying cause
- Reassure the patient and give sedative if ordered
-Encourage the patient to breath slowly which will retain carbon dioxide through breathing
in a paper bag
-Allow the patient to have uninterrupted rest , because hyperventilation can result in
fatigue.
Specific Nursing care of Metabolic acidosis
-Assess the underlying cause
-Monitor the blood gases if patient is ventilated or comatosed
-Initiate intravenous infusion of sodium bicarbonate might be ordered based on arterial
blood gases
-Reassure and orient confused oatients
Specific nursing care of metabolic alkalosis
-Assess vital signs
-Monitor blood gases especially the level of bicarb
-assess if patient took massive sodium bicarb or massive blood transfusion
-Assess patient for excessive vomiting, diuretics, prolonged nasogastric suctioning and
massive doses of antiacids.
-Assess the reflexes as the patient may develop hyperactive reflexes , and numbness of
extremities
-Keep accurate intake and output records including fluid removed by suction
-Use isotonic saline solutions for irrigating nasogastric tube rather than water because the
use of water result in loss of electrolytes