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ACID-BASE BALANCE

GRACIELA LOU F. MANA-AY,RN,MAN


• The body normally maintains a steady balance between the acids
produced during normal metabolism and the bases neutralize and
promote the excretion of the acids.
• pH- the hydrogen concentration of a solution
• Values
Neutral pH- 7.0
Acidic - <7.0
Alkaline - >7.0
• Normal levels: 7.35-7.45
 <7.35 – ACIDOSIS
 >7.45 – ALKALOSIS
• NORMAL ARTERIAL BLOOD GASES:
• pH: Hydrogen ion concentration: 7.35–7.45
• PCO2: Partial pressure of carbon dioxide: 35–45 mm Hg
• PO2: Partial pressure of oxygen: 80–100 mm Hg
• HCO3−: Bicarbonate: 22–26 mEq/L
ACID-BASE REGULATION
1. BUFFER SYSTEM
-fastest-acting system
-primary regulator of acid-base balance
-chemically change strong acids into weaker acids or bind acids to
neutralize their effect.

2. CHEMICAL BUFFERS
-Immediate-acting;
-Combine with offending acid or base to neutralize harmful effects until
another system takes over;
-Includes the ff: Bicarbonate buffer, Phophate buffer and Protein buffer.
ACID-BASE REGULATION
3. RESPIRATORY SYSTEM
-lungs help maintain a normal pH by excreting CO2 and water;
-CO2 is acidic;
-Lungs regulate blood levels of CO2;
-CO2+ H2O = Carbonic Acid
-HIGH CO2 = slower breathing
-LOW CO2 = faster breathing
-Twice as effective as chemical buffers, but effects are temporary compensatory
mechanism of respiratory system:
>Altering the rate and depth of breathing to:
-BLOW OFF CO2 (through HYPERventilation)
- RETAIN CO2 (through HYPOventilation)
-increase RR – decrease blood pH
-decrease RR – increase blood pH
ACID-BASE REGULATION
3. RENAL SYSTEM
-Kidneys to reabsorb and conserve all of the HCO3.
-HCO3 – filter and excrete a portion of the acid.
-the kidneys normally excrete acidic urine (average pH is 6)
-Compensatory mechanism of the renal system: (compensate for acidosis)
>the kidneys can reabsorb all the HCO3 and eliminate excess H.
increase urine pH = increase blood pH
decrease urine pH = decrease blood pH
ALTERATIONS IN ACID-BASE BALANCE
1. RESPIRATORY IMBALANCES
2. METABOLIC IMBALANCES

ACIDOSIS - CO2, HCO3, pH


ALKALOSIS - CO2, HCO3, pH
RESPIRATORY ACIDOSIS
• Respiratory acidosis is an acid–base imbalance that occurs when:
o pH is decreased—below 7.35
o partial pressure of carbon dioxide (PCO2) is increased—greater
than 45 mm Hg.
• Carbon dioxide builds up in the blood because the client has
some disorder, which causes the client to hypoventilate and
retain carbon dioxide.
• Since the client retains this acid, this causes the pH to go down.
RESPIRATORY ACIDOSIS
• CAUSES:
o Respiratory Arrest;
o Some drugs: narcotics, sedatives, hypnotics, anesthesia and ecstasy;
o Sleep apnea;
o Excessive alcohol;
o Surgical incision (abdominal and broken ribs);
o Collapsed lung (pneumothorax, hemothorax);
o Weak respiratory muscles (MG, GBS);
o Airway obstruction (poor cough mechanism, laryngeal spasm);
o Brain trauma (medulla);
o High-flow O2 in chronic lung disease; and
o Severe respiratory distress syndrome.
RESPIRATORY ACIDOSIS
• SIGNS and SYMPTOMS:
o Hyperkalemia
o Decreased muscle tone, decreaded DTRs
o Hypotension
o Restlessness; tachycardia
o Arrhythmias
o Cardiac arrest
o Acidic urine
o Warm skin
RESPIRATORY ACIDOSIS
• DANGER SIGNS

Respiratory acidosis is brought on by different things. What can harm


your client is dependent on the initial cause of the imbalance. So don’t
forget to focus on the initial problem.

o Respiratory arrest.
o Arrhythmias: leading to cardiac arrest and shock.
o Severe decrease in LOC.
RESPIRATORY ACIDOSIS
• ABG RESULTS
o Compensated
pH Normal
PaCO2 >45
HCO3 > 26

o Uncompensated
pH < 7.35
PaCO2 >45
HCO3 Normal
RESPIRATORY ACIDOSIS
• MANAGEMENT
o Treat the cause.
o Airway clearance: possible intubation.
o Mechanical ventilation with PEEP.
o Goal is to have the client blow off the excess CO .
2

o Administer drugs to open up the airways and thin out secretions so


o they can be coughed up.
o Increase fluids to liquefy secretions so they can be coughed up more
easily.
RESPIRATORY ACIDOSIS
• MANAGEMENT

o Oxygen therapy.
o Respiratory therapy: breathing treatments.
o Elevate head of bed (HOB) for lung expansion.
o Monitor ABGs.
o Monitor for electrolyte imbalances.
o Monitor pulse oximetry.
o Administration of Pulmocare: a tube feeding sometimes used to
decrease
o CO2retention.
RESPIRATORY ALKALOSIS
• Respiratory alkalosis is an acid–base imbalance where:
o PCO2 is less than 35 mm Hg
o pH is greater than 7.45.
• Basically, the pH is increased and the CO2 is decreased.
• The only way the PCO2 can decrease in the blood is through excessive
exhalation—hyperventilation.
• When the lungs are impaired, the kidneys compensate with their own
chemicals—bicarbonate and H+.
RESPIRATORY ALKALOSIS
• The kidneys will retain H+ because this is acid. We want to keep acid
in order to replace the acid being lost from the hyperventilation.
• The kidneys will excrete bicarbonate because this is base. This
excretion of the base will help raise acid levels and restore the body
to a normal pH.
• Respiratory alkalosis means that the client has lost excessive CO2
(acid), thus making the client alkalotic.
RESPIRATORY ALKALOSIS
• CAUSES:
o Hysteria; anxiety
o High mechanical ventilator setting
o Aspirin overdose
o Pain (having a baby)
o Fever
o Sepsis
o High Altitudes
o Anemia
RESPIRATORY ALKALOSIS
• SIGNS and SYMPTOMS:

o Hyperventilation
o Light-headedness, dizziness,
fainting
o Rapid pulse
o Hypokalemia
o Arrhythmias
RESPIRATORY ALKALOSIS
• DANGER SIGNS

What harms your client is totally dependent on what causes


the respiratory alkalosis.
For example, if the cause is due to an aspirin overdose, then
specific complications for this event exist. Remember to focus
on the cause of the imbalance.
-Life-threatening arrhythmias.
-Seizures.
RESPIRATORY ALKALOSIS
• ABG RESULTS
o Compensated
pH Normal
PaCO2 < 35
HCO3 < 22

o Uncompensated
pH > 7.45
PaCO2 < 35
HCO3 Normal
RESPIRATORY ALKALOSIS
• MANAGEMENT
o Treat the cause.
o Monitor vital signs, especially respirations.
o Monitor electrolytes.
o Administer antianxiety medications as ordered.
o Place on mechanical ventilator to control respiratory rate in severe cases.
o Monitor ABGs.
o Calm the client.
o Have client breathe into paper bag or rebreather mask to encourage CO2
retention.
METABOLIC ACIDOSIS
• Metabolic acidosis is an acid–base imbalance where:
o pH is less than 7.35
o bicarbonate level is less than 22 mEq/L.

• Acid (H+ ions) builds up in the body, or too much bicarbonate has
been lost from the body.
• Basically, the pH is decreased and the bicarbonate level is decreased.
The less bicarb you have in the body, the more acid you will be.
• In metabolic disorders, the problem is not with the lungs but with the
kidneys.
METABOLIC ACIDOSIS
• The decrease in the alkaline substances (bases) causes a build up of
acids in the body, causing acidosis.
• Which organ will compensate? The lungs will compensate by
increasing respirations in an effort to blow off excess CO2 (acid) and
therefore increase pH.
• The lungs will start compensating in just few minutes, but it’s not
enough to correct the imbalance at this point.
METABOLIC ACIDOSIS
• CAUSES:

o Diabetic ketoacidosis,
malnutrition, starvation
o Lactic acidosis
o Shock
o Kidney illness
o GI Illness, Diarrhea
o Drugs: Diamox, Aldactone
o Aspirin overdose
METABOLIC ACIDOSIS
• SIGNS AND SYMPTOMS
o Hyperkalemia
o Arrhythmias
o Increased respiratory rate
o Headache, decreased LOC, Coma
o Muscle twitching and burning,
oral numbness, weakness, flaccid paralysis
(severe hyperkalemia)
o Weakness, flaccid paralysis, tingling
and numbness in the arms and legs
METABOLIC ACIDOSIS
• DANGER SIGNS

The initial problem or cause associated with metabolic


acidosis will determine the complications to watch out for.
A couple of universal precautions are:
-Life-threatening arrhythmias.
-Cardiac arrest.
METABOLIC ACIDOSIS
• ABG RESULTS
o Compensated
pH Normal
PaCO2 < 35
HCO3 < 22

o Uncompensated
pH < 7.35
PaCO2 Normal
HCO3 < 22
METABOLIC ACIDOSIS
• MANAGEMENT

o Monitor ABGs.
o Treat the cause.
o Monitor and manage hyperkalemia.
o Monitor and manage arrhythmias.
o Monitor and manage hypercalcemia.
o Administer sodium bicarbonate IV to decrease acidity of blood.
o Monitor LOC closely.
o Administer lactated Ringers (LR) given IV to increase base level.
o Institute seizure precautions (brain doesn’t like it when the pH
is messed up).
METABOLIC ALKALOSIS
• Metabolic alkalosis is an acid–base imbalance where:
o pH is greater than 7.45
o bicarbonate level is greater than 26 mEq/L.

• There is an excess of base in the body and a loss of acid. Basically, pH


is increased and bicarbonate is increased.
• The lungs did not cause the problem; that is why it is a metabolic
problem and not a respiratory one.
METABOLIC ALKALOSIS
• Metabolic means the “kidneys”, which involve bicarbonate and H+.
• The lungs compensate by retaining CO2 by means of
hypoventilation.
• This compensates for the alkalosis and helps the pH go down into
normal range.
METABOLIC ALKALOSIS
• CAUSES:

o Vomiting; bulimia; Nasogastric (NG) tube suctioning


o Excess antacid ingestion
o Blood transfusions
o Sodium bicarbonate
o Thiazide and loop diuretics
o Baking soda
o Hypokalemia
o Activation of renin–angiotensin system
o Steroids
o Dialysis
o Licorice
METABOLIC ALKALOSIS
• SIGNS AND SYMPTOMS

o Arrhythmias; flattened T-wave


o Decreased respirations, hypoventilation
o Hypokalemia
o Tightening of muscles, tetany, LOC
changes, seizures, tingling in fingers and toes
o LOC changes
o Hepatic encephalopathy
METABOLIC ALKALOSIS
• DANGER SIGNS

Metabolic alkalosis can cause the following life-threatening


illnesses:
-Arrhythmias.
-Cardiac arrest.
-Seizures.
METABOLIC ALKALOSIS
• ABG RESULTS
o Compensated
pH Normal
PaCO2 > 45
HCO3 > 26

o Uncompensated
pH > 7.45
PaCO2 Normal
HCO3 > 26
METABOLIC ALKALOSIS
• MANAGEMENT

o Treating the cause of the acid–base imbalance (antiemetics for


vomiting etc.).
o Monitoring ABGs for further complications.
o Treating arrhythmias.
o Stopping client bicarbonate intake.
o Monitoring potassium levels and correcting hypokalemia.
o Monitoring respirations and LOC.
METABOLIC ALKALOSIS
• MANAGEMENT

o Assessing for hypotension.


o Treating dehydration if present.
o Assessing DTRs.
o Administering ammonium chloride IV in severe cases to increase
acidity (increases H+).
o Administering acetazolamide (Diamox) to increase excretion of
bicarbonate through the kidneys
RENAL FAILURE
Assessment and Diagnostic Methods
• Urine output measurements
• Renal ultrasonography, CT and magnetic resonance
imaging
(MRI) scans
• BUN, creatinine, electrolyte analyses
RENAL FAILURE - Loss of kidney function

Type:
Acute – sudden onset
Chronic – gradual onset (ex. Due to Diabetes, or chronic
hypertension)

The signs and symptoms of RENAL FAILURE is due to retention


of wastes & fluid, and inability of the kidneys to regulate
electrolytes
ACUTE RENAL FAILURE
an abrupt reduction in renal function with elevation of BUN and
plasma creatinine levels, reversible (meaning – can be reversed to
previous functioning state)
Causes
- Infection
- Medications
- Obstruction
STAGES:
1. Oliguric Phase
• Duration: 8 – 15 days
• Decreased GLOMERULAR FILTRATION RATE ( <400mL/day) – thus
it is called OLIGURIC phase
• Hyperkalemia
• Sodium normal / decreased
• Fluid overload
• Elevated BUN & creatinine
• acidosis
STAGES:
2. Diuretic Phase
• GLOMERULAR FILTRATION RATE begins to increase (4-5L/day) –
thus it is called DIURETIC PHASE
• Hypokalemia, hyponatremia, hypovolemia – (LOW)
• Gradual decline in BUN and creatinine
• Hypotension(due to excessive dieresis), tachycardia, improvement
in LOC
STAGES:
3. Recovery Phase
• Slow process: complete recovery may take 1-2 years
• Urine volume is normal
• Increase LOC; BUN is stable & normal;
• Progressive loss and ongoing deterioration in kidney function that
occurs slowly over time
CLASSIFICATION OF CAUSES

a. PRE-RENAL – (“pre” meaning the cause is before the kidney


like decrease cardiac output which decreases blood delivery to the
kidney)
b. INTRARENAL – (“intra” meaning the cause is within the
KIDNEY itself like infection in the kidney)
c. POSTRNAL – (“post” meaning the cause is after the kidney like
problems in the lower ureters, bladder, or urethra)
NURSING MANAGEMENT
• Monitor for complications.
• Assist in emergency treatment of fluid and electrolyte imbalances.
• Assess progress and response to treatment; provide physical and emotional support.
• Keep family informed about condition and provide support

Monitoring Fluid and Electrolyte Balance


• Screen parenteral fluids, all oral intake, and all medications for hidden sources of potassium.
•Monitor cardiac function and musculoskeletal status for signs of hyperkalemia.
• Pay careful attention to fluid intake (IV medications should be administered in the smallest volume
possible), urine output, apparent edema, distention of the jugular veins, alterations in heart sounds and
breath sounds, and increasing difficulty in breathing.
• Maintain daily weight and intake and output records.
• Report indicators of deteriorating fluid and electrolyte status immediately. Prepare for emergency
treatment of hyperkalemia. Prepare patient for dialysis as indicated to correct fluid and electrolyte
imbalances.
NURSING MANAGEMENT
Reducing Metabolic Rate
• Reduce exertion and metabolic rate during most acute stage with bed rest.
• Prevent or treat fever and infection promptly.
Promoting Pulmonary Function
•Assist patient to turn, cough, and take deep breaths frequently.
• Encourage and assist patient to move and turn.
Preventing Infection
• Practice asepsis when working with invasive lines and catheters.
•Avoid using an indwelling catheter if possible.
NURSING MANAGEMENT
Providing Skin Care
• Perform meticulous skin care.
• Bath the patient with cool water, turn patient frequently, keep the skin clean and well
moisturized and fingernails
trimmed for patient comfort and to prevent skin breakdown.
Providing Psychosocial Support
• Assist, explain, and support patient and family during hemodialysis treatment; do not
overlook psychological
needs and concerns.
• Explain rationale of treatment to patient and family.
CHRONIC RENAL FAILURE
Stages of CHRONIC RENAL FAILURE (DRE)

I : Diminished renal reserved


II: Renal insufficiency
III: End Stage
I. DIMINISHED RENAL RESERVE
• Renal function mildly / moderately impaired
• No accumulation of metabolic waste
• The healthier kidney compensates
• Nocturia and polyuria
II. RENAL INSUFFICIENCY
• Metabolic waste begins to accumulate
• Oliguria and edema occur
• DISTINCT SIGN – anemia (presence of anemia
distinguishes CRF from ARF; ARF usuallyno
anemia); Epogen/Epokein – synthetic
erythropeitin given through SQ injection to
correct anemia
III. END STAGE
• Excessive accumulation of metabolic wastes
• Kidneys unable to maintain homeostasis
• Dialysis / other renal replacement therapy
CLINICAL MANIFESTATIONS of CRF
Hypertension
Restrict Sodium & fluids; administer diuretics / anti Hypertensives
Hypervolemia
I&O monitoring, wt monitoring, edema, hypertension, CHF, pulmonary edema, fluid
restriction, diuretics, low sodium, avoid antacids / cold remedies (sodium bicarbonate –
contains sodium causeing water retention), skin care for edema
Hypovolemia
I&O monitoring, wt monitoring, hypotension, dehydration, sodium supplement
Potassium retention
Dysrhythmias, low potassium diet, meds to lower K, dialysis (to remove accumulated
potassium or other wastes products of the body)
CLINICAL MANIFESTATIONS of CRF
Phosphorus retention
Aluminum hydroxide preparation or other phosphate binders to remove
phosphorus
WARNING: aluminum causes CONSTIPATION
Low calcium
Calcium supplements, activated vitamin D administration
Metabolic acidosis
Alkalynizers, ABG monitoring
Anemia
Epoetin (Epogen) injection/ folic acid , BT when necessary
CLINICAL MANIFESTATIONS of CRF
GI bleeding
Hgb & hct monitoring ; stool occult blood
Pruritus
Monitor skin breakdown, rash; good skin care; no soaps, anti pruritus
Muscle cramps
Monitor electrolytes / replacement, administer heat & massage
Insomia / fatigue
Adequate rest, comfort measures / backrubs
Neurological changes
Confusion, LOC ; safe & hazard free environment
TREATMENT AND MANAGEMENT
Renal replacement therapy with dialysis or transplantation.
Conservative management of renal insufficiency and by renal replacement therapy
with dialysis or transplantation.
Dietary protein restriction and blood pressure normalization.
Dialysis and Transplantation
• Dialysis or renal replacement therapy is indicated when
advanced uremia or serious electrolyte imbalances are present.
• The choice between dialysis and transplantation is dictated by
age, related health problems, donor availability, and personal
preference.
• There are two broad categories of dialysis: hemodialysis and
peritoneal dialysis
Hemodialysis
• A hemodialysis system, or artificial kidney,
consists of three parts: a blood compartment,
a dialysis fluid compartment, and a cellophane
membrane that separates the two
compartments.
• Most persons are dialyzed three times each
week for 3 to 4 hours; treatment is determined
by kinetic profiles, referred to as Kt/V values,
which consider dialyzer size, dialysate, flow
rate, time of dialysis, and body size.
Peritoneal Dialysis
• The thin serous membrane of the peritoneal
cavity serves as the dialyzing membrane.
• A Silastic catheter is surgically implanted in the
peritoneal cavity below the umbilicus to provide
access.
• The catheter is tunneled through subcutaneous
tissue and exits on the side of the abdomen
• Peritoneal dialysis can be performed at home or in
a center, by an automated or manual system, and
on an intermittent or continuous basis
Dietary Management
• Dietary intervention is needed, with careful regulation of protein intake, fluid
intake to balance fluid losses, and sodium intake, and with some restriction of
potassium.
• Adequate intake of calories and vitamins is ensured. Calories are supplied with
carbohydrates and fats to prevent wasting.
• Protein is restricted; allowed protein must be of high biologic value (dairy
products, eggs, meats).
• Fluid allowance is 500 to 600 mL of fluid or more than the previous day’s 24-hour
urine output.
•Vitamin supplementation.
Dietary Management
• The goal of dietary treatment is to provide • Potassium. Dietary restriction of potassium
optimum nutrition while maintaining becomes mandatory. Using salt substitutes
tolerable levels of metabolic wastes. that contain potassium, or ingesting fruits,
fruit juice, chocolate, potatoes, or other high-
• Protein. Restriction of dietary proteins may potassium foods can cause hyperkalemia.
decrease the progress of renal impairment in
persons with advanced renal disease. • Sodium and Fluid Intake. The sodium and
fluid restrictions depend on the kidneys’
• Carbohydrates, Fat, and Calories. With renal ability to excrete sodium and water and must
failure, adequate calories in the form of be individually determined.
carbohydrates and fat are required to meet
energy needs. This is particularly important
when the protein content of the diet is
severely restricted.
NURSING MANAGEMENT
Promoting Home- and Community-Based Care
Teaching Patients Self-Care
• Provide ongoing explanations and information to patient and family concerning ESRD,
treatment options, and potential
complications; monitor the patient’s progress and compliance with the treatment
regimen.
• Refer patient for dietary counseling and assist with nutritional planning.
• Teach patient how to check the vascular access device for patency and appropriate
precautions, such as avoiding venipuncture and blood pressure measurements on the arm
with the access device.
• Teach patient and family what problems to report: signs of worsening renal failure,
hyperkalemia, access problems
NURSING MANAGEMENT
• Assess fluid status and identify potential sources of imbalance.
• Implement a dietary program to ensure proper nutritional intake
within the limits of the treatment regimen.
• Promote positive feelings by encouraging increased self-care
and greater independence.
• Provide explanations and information to the patient and family
concerning ESRD, treatment options, and potential complications.
• Provide emotional support.
NURSING MANAGEMENT
Continuing Care
• Stress the importance of follow-up examinations and
treatment.
• Refer patient to home care nurse for continued monitoring and
support.
• Reinforce the dietary restrictions required, including fluid,
sodium, potassium, and protein restriction.
• Remind the patient about the need for health promotion
activities and health screening.

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