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

acid base balance final

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