NURSING NOTES

1. 1
Definition: PH:- PH refers to the negative logarithm of the H+
concentration. It is used to express acidity or alkalinity. Indicates a
reciprocal relationship i.e.
pH = H+
Determination of acid base status:
It is difficult to determine the acid base status in the extra cellular fluid of
a person by direct methods.
Indirect methods: By using Sir Henderson-Hasselbalch.
Equation:
It determines PH of the fluid (concn
HCO3
-
& CO2)
PH is calculated as follows:
pH =pK + Log HCO3
-
CO2
Where pK is constant with PH of 6.1.
Thus
pH = 6.1 + Log HCO3
-
CO2
PH compatible to life: - 6.8 -7.8.
Regulatory systems of Acid Base balance:
Acid Base balance
Buffer system Respiratory Mech. Renal Mech.
- HCO3
-
Buffer.
- Phosphate Buffer.
- Protein Buffer.

2. 2
Buffer System:
Definition:
Buffer: It is a solution which resists the change in the pH
which may be expected to occur by addition of acid or base.
1) BICARBONATE BUFFER SYSTEM: This is a buffer system in
extra cellular fluid. Mainly consist of weak acid & salt base.
Mechanism of action:
1) HCL +NAHCO3 H2CO3 + NACL.
Thus change
Prevented in pH.
2) NAOH + HCO3 H2O + NAHCO3.
2) PHOSPHATE BUFFER: It is useful in intra cellular fluid. (RBC
and other cells) as concn
of phosphate is more in ICF than ECF.
Mechanism of action:
1) HCL +NA2HPO4 NAH2PO4 + NACL.
Thus change
Prevented in pH.
2) NAOH + NAH2PO4 NA2HPO4 + H2O.
- Phosphate buffer is more powerful than bicarbonate buffer.
- It is also useful in tubular fluids of kidney.
3) PROTEIN BUFFER:
- Present in blood (both plasma & hemoglobin).
- Hemoglobin is the most effective protein buffer.
- In RBC acid base balance, is maintained by a process called
chloride shifts.
- Chloride shifts in & out of the cell in response to the level of
oxygen present in the blood.

3. 3
RESPIRATORY REGULATORY MECHANISIM:
LUNGS:
- They are the bodies second defence mechanism to maintain acid
base balance.
- Regulate carbon dioxide in the blood.
CO2 + H2O H2CO3 H+
+ HCO3
-
Entire reaction is reversed in the lungs when CO2 is removed from
the blood into the alveoli of the lungs & CO2 is blown off by
ventilation.
So- In acidosis pH decreases respiratory rate & depth increases.
In alkalosis pH increases respiratory rate & depth decreases.
RENAL REGULATORY MECHANISIM:
- Ultimate correction of acid base imbalance is dependent on the
kidneys, even though the renal excretion of acids & alkali is
very slow.
- Compensation requires a few hours to several days.
- They reabsorb the bicarbonate in acid excess & excrete it in
case of acid deficit.
- In addition kidneys use phosphate ions to excrete H+
ions by
forming phosphoric acid.
- Kidney also uses ammonia mech. To regulate acid base
balance- certain amino acids are chemically changed within the
renal tubules into ammonia which in presence of H+
ions form
ammonia & are excreted in the urine.

4. 4
ACID BASE DISTURBANCES:
There are 4 types of acid base disturbances:
1) Metabolic acidosis.
2) Respiratory acidosis.
3) Metabolic alkalosis.
4) Respiratory alkalosis.
Metabolic acidosis:
- It is also called as primary alkali deficit.
- Cause when there is reduction in bicarbonate ion.
Primary compensatory mech.
When first line of defence fails respiratory mech. comes into
action.
Respiratory center stimulated by acidosis.
Deep, rapid breathing
Increased ventilation.
CO2 lost.
Decreased H2CO3.
- However increased ventilation causes reduction in pCO2 which
in turn depresses the respiratory center.
- Thus two opposing forces are working. i.e. acidosis-respiratory
center stimulated. Low pa CO2 - respiratory center depressed.
Therefore respiratory compensation is only partial.

5. 5
Secondary compensatory mech.:
Attempt to correct the disturbances as follows:
- Increasing the formation of ammonia. To excrete H+ ion.
- HCO3
Etiology:
1. Endogenous production of excessive acid as occurring in:
- DKA
- Lactic acidosis.
- Starvation.
- Fever.
- Violent exercise.
2. Ingestion of acidifying salts:
- Dietary
- Administration of excessive quantities of acids. e.g. aspiren,
HCL.
3. Renal insufficiency:
- Retention of acids normally produced.
- Factors like decreased GFR with retention of acids.
4. Abnormal loss of HCO3:E.g. severe diarrhea.
Sign & symptoms:
1. Hyper ventilation.
2. Kausmauls respiration.
3. CNS depression- stupor, dullness, coma, headache, convulsions.
4. Hyperkalemia.
5. Twitching.
Management:
Assess for nausea, vomiting, LOC.
- Monitor IO chart.
- Prepare Iv solution such as NS + HCO3 etc.
- Initiate safety measures.
- Monitor K+ level closely.
- Diet given should be low in protein & high in calories.

6. 6
 For DKA:
- Insulin administration.
 For renal failure:
- Dialysis.
Respiratory acidosis:
- It is a state of relative excess of acid in body fluids resulting
from retention or excessive production of CO2.
- It is also called as primary [H2CO3] excess.
- The underlying abnormality here is increased H2CO3 in blood,
which follows decrease elimination of CO2 in pulmonary
alvcoli.
- If excretion of CO2 through lungs is impaired more CO2 will
accumulate in blood resulting in excess (H2CO3 formation)
H+
+ HCO3
-
H2CO3 CO2 + H2O
- This results in lowering the ratio of HCO3 ions, i.e. pH
decreases & is described as respiratory acidosis.
Compensatory mech.:
Respiratory mech.:
- In this condition the respiration becomes secondary & renal
mech. becomes of prime importance.
- Increased stimulation to respiratory centre by increased paCO2
results in hyperventilation.
- This mech. Becomes secondary in importance as the problem
may with respiratory center, depression or some pathology on
lungs.
- This compensatory mech. becomes less effective.
Renal mech.:
- More HCO3
-
ions are reabsorbed from tubules in response to
raised p CO2 in blood.
- Ratio HCO3
-
= 20 is restored.
HCO3 1

7. 7
Etiology:
1. Conditions in which there is depression of respiration.
a. Damage to CNS:
- Brain damage: Trauma, inflammation / CNS lesions.
- Drug poisoning like morphine & barbiturates.
- Excessive anesthesia.
b. Loss of ventilatory functions due to increased
intrathoracic pressure or loss of elasticity.
- Pulmonary & mediastinal tumor.
- Emphysema.
- Cyst.
2. Condition causing impairment of diffusion of CO2 across
alveolar memb.
- Emphysema.
- Pulmonary edema.
3. Conditions in which there is an obstacle to the escape of CO2
from the alveoli.
- Obstruction to respiratory tract.
- Laryngeal obstruction, asthma, bronchitis, COPD.
- Rebreathing from a closed space.
4. A condition in which pulmonary blood flows is on
fussicient.
- Certain congenital heart disease.
5. Excessive CO2 production.
- Hypermetabolism of CHO for energy. E.g. enteral
feeds, parenteral nutrition.
6. Iatrogenically (from inadequate mech. ventilation) or from
excessive O2 supply which causes CO2 retention.
Sign & symptoms:
1. Hyper ventilation.
2. Hypotension.
3. Mental status changes- drowsiness, confusion, tremor,
lethargy, ultimately coma.
4. Headache, restlessness, diaphoresis.
5. Rapid, irregular pulse.
6. Hyperkalemia.
7. Cyanosis as hypnosis becomes more acute.

8. 8
Management:
1. Underlined causes are treated-to treat pneumonia-antibiotics, drug
overdose-narcotic antagonist, and toxins-dialysis.
2. Respiratory support-mechanical ventilation with low tidal
volume,O2 supplementation (at low flow rate) .
3. Administration of exogenous alkali-if renal functions are adequate-
administration of NAHCO3.
Metabolic alkalosis:
- It is a state of relative excess of base in body fluids resulting
from retention from a gain of HCO3 or loss of acids.
Mechanism of action
Respiratory mech.:
- Excess of HCO3 accumulation increases the pH.
- Respiratory centre inhibited by alkalosis causing irregular
breathing.
- Ratio of bicarbonate & carbonic acid is restored.
- Howe ever decreased ventilation raises pCO2 which stimulates
respiratory centre & respiratory compensation is incomplete.
Renal mech.:
- Increase excretion of HCO3.
- Increase excretion of K+.
- Decrease excretion of non volatile acids.
- Reduced NH3 formation.
Etiology:
1. Loss of acid.
2. Loss of intestinal fluids.
3. Post hypercapnic metabolic alkalosis.
4. Over correction of acidosis.
5. Massive transfusion of whole blood.
6. Treatment of hypovolemia.
7. Hyperaldosteronism.

9. 9
Sign & symptoms:
1. Hypo ventilation.
2. Hypokalemia.
3. Mental status changes- drowsiness, confusion, lethargy, seizures,
restlessness, numbness.
4. Hypocalcaemia.
Management:
1. Underlined causes are treated- replacement of loss fluids &
electrolytes & support of renal function.
2. Administration of acetazolamide- it is a diuretic that inhibits
carbonic anhydrases & promote the loss of bicarbonate in urine.
3. Administration of exogenous acid- in severe alkalemia IV
Administration of acid or precursor. Enhances compensation. Risk
of acid infusion includes local tissue injury, hypervolemia, osmolar
imbalances, hyperkalemia.
Respiratory alkalosis:
- It is a state of relative excess of base in body fluids resulting
from increased respiration eliminates of CO2.
Mechanism of action:
- Increased loss of CO2 – decrease H2CO3 (hyperventilation).
- HCO3
-
.= pH increased.
HCO3
- Decreased pa CO2 less H+
ions.
- Exchange is reduced causing decrease in HCO3
-
reabsorption.
Compensatory mech.: main compensation is kidney.
- Excretion of alkali (HCO3
-
).
- Decreased excretion of H+.
- Decreased excretion of NH3.
- Retention of CL-
in blood.

10. 10
Etiology:
1. Alveolar hyperventilation.
2. High altitude.
3. Pulmonary fibrosis.
4. Hysteria.
5. Over ventilation by mech. Ventilation.
6. Salicylates.
7. Hypoxia acid deficit.
Sign & symptoms:
1. Headache.
2. Lightheadedness.
3. Mental status changes.
4. Paresthesia.
5. Hypokalemia, Hypocalcemia.
5. Tetany, convulsion.
Management:
1. Provide emotional support reassurance to the client.
2. Encourage appropriate breathing pattern.
3. Assist with breathing technique, breathing aids as
Prescribed:
a. Voluntary holdings of breath.
b. Rebreath exhaled CO2.
c. Rebreathing mask as prescribed.
d. CO2 Breath as prescribed.
4. Provide cautious care with ventilator client so that they are
Not forced to take breaths too deeply, rapidly.
5. Monitor electrolyte values K & Ca level.
6. Ca glucorate for tetancy.

11. 11
ARTERIAL BLOOD GASES:
1. Obtain vital signs.
2. Determine whether the client has an arterial line in place.
3. Perform the Allen test to determine the presence of collateral
circulation.
4. Assess factors that may affect the accuracy of the results, such as
changes in the O2 settings, suctioning within the last 20 minutes,
and client activities.
5. Provide emotional support to the client.
6. Assist with the specimen draw by preparing a heparinized.
7. Apply pressure immediately to the puncture site following the
blood draw; maintain pressure for 5 minutes or for 10 minutes if
the client is taking anticoagulants.
8. Appropriate labeling on speamen.
9. On lab form, records clients’ temperature & O2 supply (type).
NURSING MANAGEMENT OF CLIENT:
1. Assessment.
- Vital sign.
- ECG monitoring.
- I/O charting.
- Monitor ABG, BUN, Creatinine, serium electrolyte.
2. Institute safety measure in client.
3. O2 supplementation.
4. Administration of alkali / acids.
5. Ventilatory care.

12. 12
BIBLIOGRAPHY:
1. Joycee N Black, medical surgical nursing, volume 1, 6th
edition,
saunders emprints of elseres Philadelphia 2001, Page no 259-271.
2. Brunner & Suddarthi, text book of medical surgical nursing, 10th
edition, lippincott Williams & wilkins, London 2004, Page no 278-
281.
3. K Sembulingam, essential of medical physiology, 2nd
edition,jaypee publication, new Delhi, reprint 2004, Page no 24-27.
4. Barbara Kozier, Fundamentals of nursing, vol-2, 7th
edition,
pearson education, Indian reprint 2004, saurabh printers pvt ltd.
Page no-1360 to 1361.
5. Ross & Wilson, Anatomy & physiology in health & illness, 9th
edition, Elsvier churchill living stone publication, Page no-21
To 23, 59.
6. Potter & Perry, Fundamentals of nursing, 6th
edition, Mosby,
emprint of Elsevier, Indian reprint 2005, Page no-1143 to 1146.
7. Lindi Anne Silvestri, comprehensive review for NCLEX; 2nd
edition, saunders-elsena 2002, reprint India 2005, Noida, Page no
85-91.
8. U Satyanarayana, text book of biochemistry, 3rd
edition, revised,
reprint 2007, arunabhasen publication, Page no 468-477.
9. Carlor Taylor, Card Lillin fundamentals of nursing, 6th
edition,
wolfers kluwer, vol-1, new Delhi reprint 2008, Page no 1680-1681
& 1685-1696.
10. Sue C.Pelacene, Patricia K. Ladner, fundamentals of nursing,
Thomson publication, 3rd
edition, Indian reprint 2007, Page no 983.

13. 13
WEBSITE’S:
1. Needham, A. 2004. Comparative & environmental physiology
acidosis & alkalosis.
2. Medline plus medical encyclopedia: respiratory acidosis.
3. EMedince-respiratory acidosis:Article by Jackie A Hayes
(http://www.emedicine.com/MED/ topic 2008 htm). Retrived on
2008-12-2006.
4. Hobler KE, Carey LC. Effect of acute progressive hypoxemia on
cardiac output & plasma excess lactate. Ann surg.1973 Feb;
177(2):199-202.
5. Hobler KE, Napodano RJ, tolerance of swine to acute blood
volume deficits.
6. J Trauma, 1974 Aug: 14(8):716-8.
7. Clinical physiology of acid-base & electrolyte disorders by Rose,
post (http://books.mcgrawhill.com/getbook.php?isbn=0071346821
& template=medical).
8. Intensive care medicine by Irwin & Rippe
(http://www.1ww.com/product/?0-7817-3548-3).

14. 14
SEMINAR
ON
ACID BASE
BALANCE
Submitted to: Mrs. Agnes Swamy
Associate Professor
Submitted By: Ms Pranali A Samudre.
First Year M.Sc. Nursing

15. 15
GENERAL OBJECTIVE:
At the end of the seminar, the students will have in-depth knowledge of
topic & will utilize it is their nursing practice.
SPECIFIC OBJECTIVE:
At the end of the seminar, the students will be able to:
1. Tell what is meant by acid base balance.
2. Review the regulatory mechanisms in body for maintaining
acid base balance.
3. Discuss the different acid base imbalances in the body & its
management.
- Respiratory Acidosis.
- Respiratory Alkalosis.
- Metabolic Acidosis.
- Metabolic Alkalosis.
4. Discuss the nursing management in acid base imbalance.

16. 16