Fluid,electrolyte, and acid base imbalance

Report
Zoya Minasyan, RN, MSN-Edu
Purpose
 Maintain a balance between acids and bases to achieve
homeostasis: State of equilibrium
 Health problems lead to imbalance
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Diabetes mellitus
Vomiting and diarrhea
Respiratory conditions
Chemotherapy- N/V
pH
 Measure of H+ ion concentration
 Blood is slightly alkaline at pH 7.35 to 7.45.
 <7.35 is acidosis.
 >7.45 is alkalosis.
Range of pH
The normal range of plasma pH is 7.35 to 7.45. A normal pH is maintained by a ratio of 1 part
carbonic acid to 20 parts bicarbonate.
Regulators of Acid/Base
 Metabolic processes produce acids that must be
neutralized and excreted.
 Regulatory mechanisms
 Buffers
 Respiratory system
 Renal system
Regulators of Acid/Base
 Buffers: Act chemically to neutralize acids or change
strong acids to weak acids
 Primary regulators
 React immediately
 Cannot maintain pH without adequate respiratory and
renal function
 The buffers in the body include
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carbonic acid–bicarbonate
monohydrogen- dihydrogen phosphate
intracellular and plasma protein
hemoglobin
Regulators of Acid/Base
 Respiratory system: Eliminates CO2
 Respiratory center in medulla
controls breathing.
 Responds within minutes/hours to changes in acid/base.
 Increased respirations lead to
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increased CO2 elimination
decreased CO2 in blood.
Regulators of Acid/Base
• When released into circulation, CO2 enters RBCs and
combines with H2O to form H2CO3.
• This carbonic acid dissociates into hydrogen ions and
bicarbonate.
• The free hydrogen is buffered by hemoglobin molecules,
and the bicarbonate diffuses into the plasma.
• In the pulmonary capillaries, this process is reversed, and CO2
is formed and excreted by the lungs.
• As a compensatory mechanism, the respiratory system acts
on the CO2 + H2O side of the reaction by altering the rate
and depth of breathing to “blow off” (through
hyperventilation) or “retain” (through hypoventilation)
CO2.
• If a respiratory problem is the cause of an acid-base
imbalance (e.g., respiratory failure), the respiratory system
loses its ability to correct a pH alteration.
Regulators of Acid/Base
 Renal system: Eliminates H+ and reabsorbs HCO3 Reabsorption and secretion of electrolytes (e.g., Na+, Cl)
 Responds within hours to days
Regulators of Acid/Base
• The three mechanisms of acid elimination are
• secretion of small amounts of free hydrogen into the
renal tubule,
• combination of H+ with ammonia (NH3) to form
ammonium (NH4+), and
• excretion of weak acids.
• The body depends on the kidneys to excrete a portion of
the acid produced by cellular metabolism.
• Thus the kidneys normally excrete acidic urine (average
pH equals 6).
• As a compensatory mechanism, the pH of the urine can
decrease to 4 and increase to 8.
Alterations in Acid-Base Balance
 Imbalances occur when compensatory mechanisms
fail.
 Classification of imbalances
 Respiratory: Affect carbonic acid concentration
 Metabolic: Affect bicarbonate
Respiratory Acidosis
 Carbonic acid excess caused by
 Hypoventilation
 Respiratory failure
 Compensation
 Kidneys conserve HCO3- and secrete H+ into urine.
Respiratory Acidosis
• Hypoventilation results in a buildup of CO2
• carbonic acid accumulates in the blood
• Carbonic acid dissociates, liberating H+, and a decrease
in pH occurs.
• If CO2 is not eliminated from the blood, acidosis results
from the accumulation of carbonic acid.
• In acute respiratory acidosis, the renal compensatory
mechanisms begin to operate within 24 hours.
Respiratory Alkalosis
 Carbonic acid deficit caused by
 Hyperventilation
 Hypoxemia from acute pulmonary disorders
Metabolic Acidosis
 Base bicarbonate deficit caused by
 Ketoacidosis
 Lactic acid accumulation (shock)
 Severe diarrhea
 Kidney disease
 Metabolic acidosis (base bicarbonate deficit) occurs
when an acid other than carbonic acid accumulates in
the body, or when bicarbonate is lost from body fluids.
 Compensatory mechanisms
 Increased CO2 excretion by lungs
 Kussmaul respirations (deep and rapid)
 Kidneys excrete acid
Metabolic Alkalosis
 Base bicarbonate excess caused by
 Prolonged vomiting or gastric suction
 Gain of HCO3-
 Compensatory mechanisms
 Decreased respiratory rate to increase plasma CO2
 Renal excretion of HCO3-
Blood Gas Values
 Arterial blood gas (ABG) values provide information
about
 Acid-base status
 Underlying cause of imbalance
 Body’s ability to regulate pH
 Overall oxygen status
Interpretation of ABGs
 Diagnosis in six steps:
 Evaluate pH.
 Analyze PaCO2.
 Analyze HCO3-.
 Determine if CO2 or HCO3- matches the alteration.
 Decide if the body is attempting to compensate.
Normal Blood Gas Values
Sample ABG Interpretation
Acid-Base Mnemonic—ROME
 Respiratory
 Opposite
 Alkalosis↑ pH ↓ PaCO2
 Acidosis ↓ pH ↑ PaCO2
 Metabolic
 Equal
 Acidosis ↓ pH ↓ HCO3
 Alkalosis↑ pH ↑ HCO3
Interpretation of ABGs
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pH 7.18
PaCO2 38 mm Hg
PaO2 70 mm Hg
HCO3- 15 mEq/L
What is this?
 Metabolic acidosis
Interpretation of ABGs
 pH 7.58
 PaCO2 35 mm Hg
 PaO2 75 mm Hg
 HCO3- 50 mEq/L
 What is this?
 Metabolic alkalosis
Question
A patient with an acid-base imbalance has an altered
potassium level. The nurse recognizes that the potassium
level is altered because:
1. Potassium is returned to extracellular fluid when
metabolic acidosis is corrected.
2. Hyperkalemia causes an alkalosis that results in
potassium being shifted into the cells.
3. Acidosis causes hydrogen ions in the blood to be
exchanged for potassium from the cells.
4. In alkalosis, potassium is shifted into extracellular fluid
to bind excessive bicarbonate.
24
Answer
 Answer: 3
 Rationale: Changes in pH (hydrogen ion concentration)
will affect potassium balance.
 In acidosis,
 hydrogen ions accumulate in the intracellular fluid (ICF),
 and potassium shifts out of the cell to the extracellular fluid to
maintain a balance of cations across the cell membrane.
 In alkalosis,
 ICF levels of hydrogen diminish,
 and potassium shifts into the cell.



If a deficit of H+ occurs in the extracellular fluid, potassium will shift
into the cell.
Acidosis is associated with hyperkalemia
Alkalosis is associated with hypokalemia.
Fluid volume deficit
 Can occur with
 Abnormal loss of body fluids
Diarrhea, hemorrhage, polyuria
 Inadequate fluid intake
 Shift of fluid from plasma into interstitial space
• Treatment
 Correct the underlining cause
 Replace the fluid and electrolyte (LR or NS isotonic solutions)
Fluid volume excess
 May result from
 excessive intake of fluid
 Abnormal retention of fluids(heart failure, renal failure)
 Shift of fluid from interstitial fluid into plasma fluid
o Collaborative care
o
o
o
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ID primary cause
Diuretics and fluid restriction
Restriction of Na intake
Fluid excess may result to ascites or pleural effusion, and
paracentesisi or thoracentsis may be necessary.
Commonly prescribed crystalloid solutions
 Dextrose in water
 5% isotonic
 10% hypertonic
 Saline
 0.45% hypotonic
 0.9% isotonic
 3.0% hypertonic
 Dextrose in Saline
 5% in 0.225% isotonic
 5% in 0.45% hypertonic
 5% in 0.9% hypertonic
 Multiple Electrolyte Solutions
 Ringer’s solution- isotonic, includes CL, Na, K, Ca
 Lactated Ringer’s solution- isotonic-Na, K, Cl, Ca, and
lactate(the precursor of bicarbonate)
CVADs (central venous access device)
 Catheters placed in large blood vessels of people who
require frequent access to the vascular system
 Subclavian vein, jugular vein
 Three different methods
 Centrally inserted catheter(by MD)
 Peripherally inserted central catheter
 Implanted ports( by MD)
CVADs
 Permit frequent, continuous, rapid, or intermittent
administration or monitoring
 Indicated for patients with limited peripheral vascular
access or need for long-term vascular access
Centrally Inserted Catheter
 Inserted into a vein in the neck, chest, or groin with tip
resting in the distal end of the superior vena cava
 Single, double, triple, or quad lumen
 Nontunneled or tunneled
Central .Venous Catheter
PICC
 Central venous catheters inserted into a vein in the
arm
 Single or multilumen, nontunneled
 For patients who need vascular access for 1 week to 6
months
 Complications include catheter occlusion and
phlebitis.
Copyright © 2011, 2007, 2004, 2000, 1996, 1992,
1987, 1983 by Mosby, Inc., an affiliate of Elsevier
Inc.
PICC
Implanted Infusion Ports
 Central venous catheter connected to an
implanted, single or double subcutaneous injection
port
 Port is metal sheath with self-sealing silicone
septum.
Implanted Infusion Port
Implanted Infusion Port
 Port accessed with special Huber-point needle
 Advantages
 Good for long-term therapy
 Low risk of infection
 Cosmetic discretion
 Care requires regular flushing.
 Complication: (table 17-21 page 330)
 Cath occlusion(kinked, precipitate build up)
 Embolism( dislodgment of thrombus, air entry, cath
breaking)
 Cath related infection
 Cath Migration
Nursing Management
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Inspect catheter and insertion site.
Assess pain.
Change dressing and clean according to institution policies.
Change injection caps.
Flushing is important.
• Catheter and insertion site assessments include inspection of the
site for redness, edema, warmth, drainage, and tenderness or pain.
Observation of the catheter for misplacement or slippage is
important.
• Transparent dressing or gauze may be used.
• Discuss cleaning techniques with chlorhexidine-based
preparations, povidone-iodine, and isopropyl alcohol
• Teach the patient to turn the head to the opposite side of the
CVAD insertion site during cap change.
• Flushing: Use a normal saline solution in a syringe that has a
barrel capacity of 10 mL or more to avoid excess pressure on the
catheter. If resistance is felt, force should not be applied.
Removing CVADs
 Should be done according to policy and procedures.
 Gently withdraw.
 Apply pressure.
 Ensure that catheter tip is intact.

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