Acid Base Balance

INTRODUCTION
ü Plasma pH is an indicator of hydrogen

ion (H+) concentration and measures
Ø Acid-base disturbances are alkalinity and acidity of the blood.
commonly encountered in • ↑H+ concentration = ↓pH = ACID
clinical practice, especially • ↓H+ concentration = ↑pH = ALKALINE
in critical-care units (CCU).
Ø Identification of the specific
acid-base imbalance is
important in discovering the ü Homeostatic mechanism keep pH within
underlying cause of a normal range (7.35-7.45).
disorder and in the • BUFFER SYSTEM
determination of • LUNGS
appropriate treatement.
• KIDNEYS
INTRODUCTION
DONATE ACID Strong HCL

HCL
H2SO4 Weak H2CO3
H+
H2CO3
Strong NaOH
HCO3
ACCEPTS BASE Weak HCO3
INTRODUCTION
ACID
Volatile Fixed
H2CO3 Catabolism:
-Protiens and Phospolipids
(H2SO4 / H3PO4)
BUFFERED
Excreted via
q Prevent major changes in th pH
of the body fluids by removing or
releasing H+.
q They act quickly, and serves as the
first aid in maintaing acid-base balance.
q They are extremely efficient, and
different systems work at different rates.
q It takes only seconds for the
chemical buffers in the blood to make
adjustments to pH.
q The buffer systems functioning in blood
plasma include plasma proteins,
phosphate, and bicarbonate and
carbonic acid buffers.
Weak Acid Conjugate Base
HA A-
v A Buffer Solution resist

Weak Base Conjugate Acid the change in pH.
B BH+ v If a hydrogen ion is
added the buffer
BUFFER PAIR attaches to it reversibly.
v If hydrogen ion
concentration is high
the reaction shift to the
right.
H+ + A - HA v In contrast, if its low

the reaction shifts to
the left.
B I C A R B O N AT E
P H O S P H AT E
PROTEINS
Bicarbonate-Carbonic Acid Buffer
Base (A+ ) - BICARBONATE (HCO3-)

Acid (HA) - CARBONIC ACID (H2CO3) or
CARBON DIOXIDE (CO2)
20 (HCO3-) : 1 (H2CO3)
If the ratio is altered the pH changes. it is the ratio

of HCO3- to H2CO3 that is important in maintaining
the balance and not the absolute value.
EXTRACELLULAR
FLUID
Bicarbonate-Carbonic Acid Buffer
Phosphate Buffer
These are minor buffers that can

be inorganic or organic
INORGANIC ORGANIC
H2P4- / HPO4- ATP / ADP

Ø They are also Ø Are more
extracellular intracellular
buffers. buffers.
Ø but are more a
urinary buffer.
INTRACELLULAR URINARY SYSTEM
FLUID
Phosphate Buffer
Phosphates are found in the blood in two HCl + Na2HPO4→NaH2PO4 + NaCl

(strong acid) + (weak base) → (weak acid) + (salt)
forms: sodium dihydrogen phosphate
(Na2H2PO4−), which is a weak acid, and
NaOH + NaH2PO4→Na2HPO4 + H2O
sodium monohydrogen phosphate (Na2HPO42-),
which is a weak base. (strong base) + (weak acid) → (weak base) + (water)
v When Na2HPO42- comes into contact with a strong acid, such as HCl, the base
picks up a second hydrogen ion to form the weak acid Na2H2PO4− and sodium
chloride, NaCl.
v When Na2HPO42− (the weak acid) comes into contact with a strong base, such as
sodium hydroxide (NaOH), the weak acid reverts back to the weak base and
produces water. Acids and bases are still present, but they hold onto the ions.
Protein Buffer
v Nearly all proteins can function as

buffers.
v Proteins are made up of amino acids,
which contain positively charged
amino groups and negatively charged
carboxyl groups.
v The charged regions of these
molecules can bind hydrogen and
hydroxyl ions, and thus function as
buffers.
v Buffering by proteins accounts for
two-thirds of the buffering power of
the blood and most of the buffering
within cells.
Protein Buffer
Hgb H+ H2 O
H2CO3
HCO3 CO2
HEMOGLOBIN
q Hemoglobin is the principal protein inside of red

blood cells and accounts for one-third of the
mass of the cell.
q During the conversion of CO2 into bicarbonate,
hydrogen ions liberated in the reaction are
buffered by hemoglobin, which is reduced by the
dissociation of oxygen.
q This buffering helps maintain normal pH. The CO2
process is reversed in the pulmonary capillaries CO2 + H2O = H2CO3
H+ Hgb
to re-form CO2, which then can diffuse into the HCO3-

air sacs to be exhaled into the atmosphere.
Cl-
VOLATILE ACIDS
vAerobic cellular respiration, which results in the release of

carbon dioxide, produces volatile acid. Carbonic acid
(H2CO3) is created when the body's water-carbon dioxide
mixture reacts.
v“Volatile” refers to the fact that carbon dioxide is expired
by the lungs.
vThe lungs are responsible for the regulation of the levels of
volatile acids in the body fluids.
§ The main byproduct of metabolism, carbon dioxide (CO2), is continuously
created inside of the cells.
§ It exits the cells and enters the bloodstream via interstitial fluid. Here, it
dissolves and produces carbonic acid (H2CO3). It is subsequently transferred to
the lungs after being buffered.
§ CO2 is reformed in the lung tissue, diffuses into the alveoli, and is expelled. The
main byproduct of metabolism, carbon dioxide (CO2), is continuously created
inside of the cells.
§ It exits the cells and enters the bloodstream via interstitial fluid. Here, it
dissolves and produces carbonic acid (H2CO3). It is subsequently transferred to
the lungs after being buffered.
§ CO2 is reformed in the lung tissue, diffuses into the alveoli, and is expelled.
§ While the water (H2O) created by the reaction is dispersed into the body's
overall water pool, acid is expelled from the body through the lungs as carbon
dioxide (CO2). As the body requires, these equilibrium reactions can be changed
to the right to eliminate acid (as CO2) or to the left to make more acid (H+).
Ø The respiratory center is activated if there is a
hydrogen ion (H+) concentration imbalance. The
lungs respond to the body's desire to expel excess
acid (H+ ions) by speeding up respiration (known as
HYPERVENTILATION) to expel more acid as CO2.
Ø The lungs can slow down respiration (a process
known as HYPOVENTILATION) in order to hold onto
more CO2 if the body needs to retain acid (H+ ions)
to balance an excessively alkaline pH.
Ø Rapid changes in blood pH and hydrogen ion (H+) concentration
trigger an immediate respirator y response. After an abrupt
change, the lungs, acting alone, can quickly adjust the H+
concentration. However, the respiratory system only functions
between 50% and 75% of the time, meaning that the lungs
cannot raise the pH to its usual level of around 7.40 on their
own.
Ø This is because the stimulation to the respirator y center is
eliminated as the hydrogen ion concentration returns to normal.
For instance, the respiratory system can quickly raise the blood
pH to a range of 7.20–7.30 if it lowers unexpectedly from
7.40–7.00. To fur ther restore the balance, the kidneys and
buffering systems must work.
Ø In a case such as this, medical tr eatment may
include attempting to mimic the body’s own
r espir ator y r esponse to the acidic pH. As an
illustration, deliberately inducing hyperventilation in
patients who have long been in cardio-respirator y
arrest.
Ø The renal regulation of the body’s acid-base balance addresses the
metabolic component of the buffering system.
Ø Whereas the respiratory system (together with breathing centers in the
brain) controls the blood levels of carbonic acid by controlling the
exhalation of CO2, the renal system controls the blood levels of
bicarbonate.
Ø A decrease of blood bicarbonate can result from the inhibition of
carbonic anhydrase by certain diuretics or from excessive bicarbonate
loss due to diarrhea.
Ø Blood bicarbonate levels are also typically lower in people who have
Addison’s disease (chronic adrenal insufficiency), in which aldosterone
levels are reduced, and in people who have renal damage, such as
chronic nephritis.
Ø Finally, low bicarbonate blood levels can result from elevated levels of
ketones (common in unmana ged diabetes mellitus), w hich bind
bicarbonate in the filtrate and prevent its conservation.
Bicarbonate ions, HCO3–, found in the filtrate, are
essential to the bicarbonate buffer system, yet the
cells of the tubule are not permeable to bicarbonate
ions. The steps involved in supplying bicarbonate
ions to the system are summarized as folows:
Step 1: Sodium ions are reabsorbed from the filtrate in exchange

for H+ by an antiport mechanism in the apical membranes of cells
lining the renal tubule.
Step 2: The cells produce bicarbonate ions that can be shunted to
peritubular capillaries.
Step 3: When CO2 is available, the reaction is driven to the
formation of carbonic acid, which dissociates to form a bicarbonate
ion and a hydrogen ion.
Step 4: The bicarbonate ion passes into the peritubular
capillaries and returns to the blood. The hydrogen ion is secreted
into the filtrate, where it can become part of new water molecules
and be reabsorbed as such, or removed in the urine.
Ø It is also possible that salts in the filtrate, such as sulfates,
phosphates, or ammonia, will capture hydrogen ions.
Ø If this occurs, the hydrogen ions will not be available to combine

with bicarbonate ions and produce CO2.
Ø In such cases, bicarbonate ions are not conserved from the filtrate
to the blood, which will also contribute to a pH imbalance and
acidosis.
Ø The hydrogen ions also compete with potassium to exchange with
sodium in the renal tubules.
Ø If more potassium is present than normal, potassium, rather than the

hydrogen ions, will be exchanged, and increased potassium enters the
filtrate.
Ø When this occurs, fewer hydrogen ions in the filtrate participate in the
conversion of bicarbonate into CO2 and less bicarbonate is conserved.
Ø If there is less potassium, more hydrogen ions enter the filtrate to be

exchanged with sodium and more bicarbonate is conserved.
Ø Chloride ions are important in neutralizing positive ion
charges in the body.
Ø If chloride is lost, the body uses bicarbonate ions in

place of the lost chloride ions.
Ø Thus, lost chloride results in an increased

reabsorption of bicarbonate by the renal system.
Compensation Mechanisms
Ø Various compensatory mechanisms exist to maintain blood pH within

a narrow range, including buffers, respiration, and renal mechanisms.
Ø Although compensatory mechanisms usually work very well, when
one of these mechanisms is not working properly (like kidney failure
or respiratory disease), they have their limits.
Ø If the pH and bicarbonate to carbonic acid ratio are changed too
drastically, the body may not be able to compensate.
Ø Moreover, extreme changes in pH can denature proteins.
Ø Extensive damage to proteins in this way can result in disruption of
normal metabolic processes, serious tissue damage, and ultimately
death.
Respiratory Compensation
Ø Respiratory compensation for metabolic acidosis increases the respiratory rate to

drive off CO2 and readjust the bicarbonate to carbonic acid ratio to the 20:1 level.
Ø This adjustment can occur within minutes.
Ø Respiratory compensation for metabolic alkalosis is not as adept as its compensation
for acidosis.
Ø The normal response of the respiratory system to elevated pH is to increase the
amount of CO2 in the blood by decreasing the respiratory rate to conserve CO2.
Ø There is a limit to the decrease in respiration, however, that the body can tolerate.
Hence, the respiratory route is less efficient at compensating for metabolic alkalosis
than for acidosis.
Metabolic Compensation
Ø Metabolic and renal compensation for respiratory diseases that can create acidosis
revolves around the conservation of bicarbonate ions.
Ø In cases of respiratory acidosis, the kidney increases the conservation of bicarbonate
and secretion of H+ through the exchange mechanism discussed earlier.
Ø These processes increase the concentration of bicarbonate in the blood,
reestablishing the proper relative concentrations of bicarbonate and carbonic acid.
Ø In cases of respiratory alkalosis, the kidneys decrease the production of bicarbonate
and reabsorb H+ from the tubular fluid.
Ø These processes can be limited by the exchange of potassium by the renal cells,
which use a K+-H+ exchange mechanism (antiporter).
Analysis of Arterial Blood Gas
PARAMETER ARTERIAL BLOOD MIXED VENOUS BLOOD
pH 7.35 - 7.45 7.32 - 7.42
PCO2 35 - 34 mm Hg 38 - 52 mm Hg
PO2 >80 mm Hg 24 - 48 mm Hg
HCO3- 22 - 26 mEq/L 19 - 25 mEq/L
Base Excess/Deficit ±2 mEq/L ±5 mEq/L
Sa02% >94% 65 - 75%

q Lab tests for pH, CO2 partial pressure (pCO2),and HCO3– can
identify acidosis and alkalosis, indicating whether the
imbalance is respiratory or metabolic, and the extent to which
compensatory mechanisms are working.
q The blood pH value, as shown, indicates whether the blood is
in acidosis, the normal range, or alkalosis. The pCO2 and total
HCO3– values aid in determining whether the condition is
metabolic or respiratory, and whether the patient has been
able to compensate for the problem. MIXED
ARTERIAL
q The table lists the conditions and laboratory results PARAMETER
BLOOD
VENOUS
BLOOD
that can be used to classify these conditions. pH 7.35 - 7.45 7.32 - 7.42
q Metabolic acid-base imbalances typically result from PCO2 35 - 34 mm Hg 38 - 52 mm Hg
kidney disease, and the respiratory system usually PO2 >80 mm Hg 24 - 48 mm Hg
responds to compensate. HCO3- 22 - 26 mEq/L 19 - 25 mEq/L
Base
±2 mEq/L ±5 mEq/L
Excess/Deficit
Sa02% >94% 65 - 75%
pH
7.35 - 7.45 =Normal
<7.35 =Acidosis PaCO2
>7.45 =Alkalosis 35 - 45 mm Hg=Normal
>45 mm Hg =Acidosis
<35 mm Hg =Alkalosis
HCO3 PARAMETER
ARTERIAL
MIXED
VENOUS
22 - 26 mEq/L =Normal BLOOD
BLOOD
<22 mEq/L =Acidosis pH 7.35 - 7.45 7.32 - 7.42
>26 mEq/L =Alkalosis PCO2 35 - 34 mm Hg 38 - 52 mm Hg

PO2 >80 mm Hg 24 - 48 mm Hg
HCO3- 22 - 26 mEq/L 19 - 25 mEq/L
Base
±2 mEq/L ±5 mEq/L
Excess/Deficit
Sa02% >94% 65 - 75%
FIRST WORD SECOND WORD
(Respiratory or Metabolic) (Alkalosis or Acidosis)
EXAMPLE:
1
To detrmine SECOND WORD, § pH = 7.5 = ALKALOSIS
RULE identify the pH level. § pH = 7.25 = ACIDOSIS
§ pH = 7.11 = ACIDOSIS
2
EXAMPLE:
§ pH + HCO3 = METABOLIC To detrmine FIRST WORD, find
RULE
§ pH + PaCO2 = RESPIRATORY the pair of the second word.
EXAMPLE:
§ pH = 7.27 ACIDOSIS
§ HCO3 = 30 mEq/L ALKALOSIS pH + PaCO2 = RESPIRATORY
§ PaCO2 = 48 mm Hg ACIDOSIS
“RESPIRATORY ACIDOSIS”
ANSWER:
1
§ pH = 7.32
§ HCO3 = 28 mEq/L
§ PaCO2 = 51 mm Hg
ANSWER:
2 § pH = 7.48
§ HCO3 = 27 mEq/L
§ PaCO2 = 48 mm Hg
ANSWER:
3
§ pH = 7.30
§ HCO3 = 18 mEq/L
§ PaCO2 = 29 mm Hg
ANSWER:
4 § pH = 7.57
§ HCO3 = 17 mEq/L
§ PaCO2 = 32 mm Hg
Metabolic acidosis is problematic, as lower-than-normal amounts

of bicarbonate are present in the blood. The pCO2 would be normal at
first, but if compensation has occurred, it would decrease as the body
reestablishes the proper ratio of bicarbonate and carbonic acid/CO2.
Respiratory acidosis is problematic, as excess CO2 is present in the

blood. Bicarbonate levels would be normal at first, but if compensation
has occurred, they would increase in an attempt to reestablish the
proper ratio of bicarbonate and carbonic acid/CO2.
Alkalosis is characterized by a higher-than-normal pH. Metabolic

alkalosis is problematic, as elevated pH and excess bicarbonate are
present. The pCO2 would again be normal at first, but if compensation
has occurred, it would increase as the body attempts to reestablish the
proper ratios of bicarbonate and carbonic acid/CO2.
Respiratory alkalosis is problematic, as CO2 deficiency is present in

the bloodstream. The bicarbonate concentration would be normal at first.
When renal compensation occurs, however, the bicarbonate
concentration in blood decreases as the kidneys attempt to reestablish
the proper ratios of bicarbonate and carbonic acid/CO2 by eliminating
more bicarbonate to bring the pH into the physiological range.
DETERMINATION OF DEGREE OF COMPENSATION
FULLY COMPENSATED
PARTIALLY COMPENSATED
UNCOMPENSATED
DETERMINATION OF DEGREE OF COMPENSATION
1 DETERMINE pH if pH is within normal range = COMPENSATED

if ph is abnormal proceed with number 2
2 LOOK for other PARAMENTER without normal = PARTIALLY COMPENSATED

with normal = UNCOMPENSATED
1 2 3
ANSWER: ANSWER: ANSWER:
§ pH = 7.14 § pH = 7.47 § pH = 7.43
§ HCO3 = 15 mEq/L § HCO3 = 56 mEq/L § HCO3 = 19 mEq/L
§ PaCO2 = 20 mm Hg § PaCO2 = 36 mm Hg § PaCO2 = 20 mm Hg
Disorders of the Acid - Base Balance
ü Normal arterial blood pH is restricted to a very narrow range of 7.35 to
7.45.
ü A person who has a blood pH below 7.35 is considered to be in acidosis
(actually, “physiological acidosis,” because blood is not truly acidic until
its pH drops below 7), and a continuous blood pH below 7.0 can be fatal.
Acidosis has several symptoms, including headache and confusion, and
the individual can become lethargic and easily fatigued.
ü A person who has a blood pH above 7.45 is considered to be in alkalosis,
and a pH above 7.8 is fatal. Some symptoms of alkalosis include cognitive
impairment (which can progress to unconsciousness), tingling or
numbness in the extremities, muscle twitching and spasm, and nausea
and vomiting.
ü Both acidosis and alkalosis can be caused by either metabolic or
respiratory disorders.
ü As discussed earlier, the concentration of carbonic acid in the blood is
dependent on the level of CO2 in the body and the amount of CO2 gas
exhaled through the lungs.
ü Thus, the respiratory contribution to acid-base balance is usually
discussed in terms of CO2 (rather than of carbonic acid).
ü Remember that a molecule of carbonic acid is lost for every molecule of
CO2 exhaled, and a molecule of carbonic acid is formed for every
molecule of CO2 retained.
Metabolic Acidosis (Base Bicarbonate Deficit)
v Is a common clinical disturbance characterized by a low pH (increased H+

concentration) and a low plasma bicarbonate concentration.
v Can be produced by a plasma bicarbonate concentration.
v It can be divided into two forms, according to the values of the serum anion gap: high
anion gap acidosis and normal anion gap acidosis.
v The anion gap refers to the difference between the sum of all measured positively
charged electrolytes (cations) and the sum of all negatively charged electrolytes
(anions) in the blood.
v sum of measured cations is typically greater than the sum of measured anions, there
normally exists a gap referred to as anion gap.
v The anion gap can be calculated by either of the following equations:
vPotassium is often omitted from the equation because of its low level in
the plasma; therefore, the second equation is used more often than the
first (Emmett & Szerlip, 2015).
vNormal value of an anion gap: 8-12 mEq/L (8-12mmol/L) w/o potassium
in the equation.
vIf potassium is included in the equation, the normal value for the anion
gap is 12 to 16 mEq/L (12-16mmol/L).
vUnmeasured anions: <16mEq/L
vA low or negative anion gap may be attributed to hypoproteinemia.
Physical Assessment Findings:

CLINICAL MANIFESTATION ü decreased BP
ü Headache ü cold and clammy skin
ü dysrhythmias, and shock.
ü Confusion ü Chronic metabolic acidosis is usually seen
ü Drowsiness with chronic kidney disease.
ü Respiratory rate and depth
DIAGNOSTIC FINDINGS
ü Nausea ü ABG
ü Vomiting ü Calculation of the anion gap
ü Peripheral vasodilation and ü ECG
decreased cardiac output occur The cardinal feature of metabolic acidosis is a

when the pH drops to <7. decrease in serum bicarbonate level.
MEDICAL MANAGEMENT For management of vomiting

ü Treatment for metabolic acidosis works in (common to metabolic acidosis):
three main ways: ü position the patient to prevent
1. excreting or getting rid of excess acids aspiration.
2. buffering acids with a base to balance ü Prepare for possible seizures and
blood acidity administer appropriate precautions.
3. preventing the body from making too ü Provide good oral hygiene after
many acids
incidences of vomiting.
ü IV sodium bicarbonate
ü Insulin, diabetes medications, fluids,
ü Use sodium bicarbonate washes to
electrolytes (sodium, chloride, potassium) if neutralize acid in the patient's mouth
diagnosed with diabetes ü Monitor serum potassium level.
ü Hemodialysis
Metabolic Alkalosis (Base Bicarbonate Excess)
Causes of metabolic
v Is a clinical disturbance characterized by a high pH and a high alkalosis:
plasma bicarbonate concentration. a. Loss of stomach acids
v It can be produced by a gain of bicarbonate or a loss of H+ b. Excess of antacids
c. Diuretics
d. Potassium deficiency
(hypokalemia)
There are two kinds of metabolic alkalosis: e. Reduced volume of blood in the
arteries (EABV).
f. Heart, kidney, or liver failure
Ø Chloride-responsive alkalosis results from loss of hydrogen g. Genetic causes:
ions, usually by vomiting or dehydration. § Bartter syndrome
§ Gitelman syndrome
§ Liddle syndrome
Ø Chloride-resistant alkalosis results when your body retains § Glucocorticoid remediable
too many bicarbonate (alkaline) ions, or when there’s a shift of aldosteronism
§ Apparent mineralocorticoid
hydrogen ions from your blood to your cells. excess
Symptoms of metabolic alkalosis:

Ø Metabolic alkalosis may not show any symptoms.
Ø People with this type of alkalosis more often complain of the Assessment and Diagnostic
underlying conditions that are causing it. Findings:
Ø These can include:
§ -vomiting ü Understanding pH levels (elevation
§ -diarrhea of ABGs reveals a pH greater than
§ -swelling in the lower legs (peripheral edema) 7.45 and a serum bicarbonate
§ -fatigue concentration greater than 26
mEq/L)
Severe cases of metabolic alkalosis can cause: ü Urine Analysis (urine chloride
Ø agitation levels)
Ø disorientation ü Chloride-responsive
Ø seizures ü Chloride-resistant
Ø coma
Medical Management:
ü Restoring normal fluid

volume by administering
normal saline
ü Proton pump inhibitors
ü Carbonic Anhydrase
Respiratory Acidosis (Carbonic Acid Excess)
Ø Respiratory acidosis is a clinical disorder in which the pH is less

than 7.35 and the PaCO2 is greater than 42 mm Hg. It may be
either acute or chronic.
Ø Respiratory acidosis is always due to inadequate excretion of CO2
with inadequate ventilation, resulting in elevated plasma CO2
concentrations and, consequently, increased levels of carbonic
acid.
Causes
ü Acute Respiratory Acidosis
ü Chronic Respiratory Acidosis
ü Upper respiratory obstruction
ü Defect in the pulmonary gas exchange
ü Defect in the pulmonary gas exchange
Signs and Symptoms

q There is often breathlessness.
q The patient is restless. Lab diagnosis of respiratory
q There is a headache, dyspnoea, and tachypnea. acidosis:
q There is apprehension followed by lethargy. q pH = <7.35 to 7.45.
q The patient will have disorientation. q paCO2 = >45 mm Hg.
q There are muscle twitching and tremors. q HCO3– = Normal (in the acute
q Skin will be warm and flushed due to raised CO2 stage).
causing vasodilatation. q HCO3– = Increased (in the
q There may be hypertension or hypotension. chronic stage).
q There are atrial and ventricular arrhythmias.
q The patient will have convulsions and ultimately
goes into a coma.
Medical Management Nursing Management

ü In anxious patients, anxiolytics may Ø Teach patient breathing techniques to slow
be necessary. down breathing, holding
Ø breath…”rebreathing into a paper bag or
ü For Infectionius disease antibiotics
re-breather mask
targeting sputum or blood cultures Ø Watch potassium levels (hypokalemia.
are appropriate. Ø Closely watch patients on mechanical
ü In embolic disease, anticoagulation is ventilation to ensure breaths are not
necessary. hyperventilating the patien
ü Ventilator support may be necessary Ø Provide sedation and pain medication, as
for patients with acute respiratory indicated.
failure, acute asthma Ø Administer CO2, or use rebreathing mask
as indicated.
Respiratory Alkalosis (Carbonic Acid Deficit)
Ø Respiratory alkalosis is a clinical condition which the arterial ph

is Greater than 7.45 and The paco is less than
Sign and symptoms
Ø Respiratory alkalosis is the most common acid-base abnormality 1. Confusion
with no discrimination between genders 2. light-headedness,
3. dizziness,
4. anxiety,
What causes respiratory alkalosis? 5. chest pain
Ø Respiratory alkalosis is caused by hyperventilation ,which 6. Wheezing
causes excessive loss or blowing off off CO2 7. hemoptysis
Ø Any lung disease that leads to shortness of breath can also 8. trauma
cause respiratory alkalosis (such as pulmonary embolism and
asthma
Treatment of respiratory acidosis NURSING CONSIDERATIONS

Treatment of the pulmonary causes: ● Be alert for critical changes in the patient’s respiratory, CNS,
ü If there is obstruction by the foreign body, remove that and cardiovascular functions. Report such changes as well as
immediately. any variations in ABG levels or electrolyte status immediately.
ü There may be a need for mechanical ventilators. Also, maintain adequate hydration.
ü Give bronchodilators. ● Maintain a patent airway and provide adequate
ü If there is pneumonia, then start antibiotics. humidification if acidosis requires mechanical ventilation.
ü If there is pneumothorax, then put chest tube. Perform tracheal suctioning regularly and vigorous chest
ü In the case of pulmonary embolism, start thrombolytic physiotherapy if ordered. Continuously monitor ventilator
and anticoagulants. settings and respiratory status.
ü Remove the secretions by bronchoscopy. ● To prevent respiratory acidosis, closely monitor patients
ü Treatment of chronic obstructive pulmonary disease with COPD and chronic CO2 retention for signs of acidosis.
(COPD): Also, administer oxygen at low flow rates.
ü Give O2 at a slow rate. ● Closely monitor all patients who receive opioids and
ü Start bronchodilators. sedatives. Instruct patients who have received a general
ü Start corticosteroids. anesthetic to turn, cough, and perform deep-breathing
ü You can also give I/V sodium bicarbonate. exercises frequently to prevent the onset of respiratory
ü Other drugs are needed for the treatment of the cause. acidosis.
Complex Acid - Base Disorder
q Involve more than one primary process.

q In these mixed disorders, values may be deceptively normal.
q Thus, when evaluating acid-base disorders, it is important to determine whether
changes in Pco2 and HCO3− show the expected compensation.
q If not, then a second primary process should be suspected of causing the abnormal
compensation. .
q The anion gap should always be calculated; elevation almost always indicates a
metabolic acidosis. A normal anion gap with a low HCO3−, and high serum chloride
(Cl−) indicates a non-anion gap (hyperchloremic) metabolic acidosis.
q If metabolic acidosis is present, a delta gap is calculated to identify concomitant
metabolic alkalosis, and Winters formula is applied to determine whether respiratory
compensation is appropriate or reflects a second acid-base disorder.
• Respiratory acidosis is suggested by Pco2> 40

mm Hg; HCO3− should compensate by increasing 3
to 4 mEq/L ( 3 to 4 mmol/L) for each 10-mm Hg
rise in Pco2 sustained for 4 to 12 hours (there may
be no increase or only an increase of 1 to 2 mEq/L
[1 to 2 mmol/L], which slowly increases to 3 to 4
mEq/L [3 to 4 mmol/L] over days).
• Greater increase in HCO3− implies a primary • Metabolic alkalosis is suggested by HCO3−>
metabolic alkalosis; lesser increase suggests no 28 mEq/L (> 28 mmol/L).
time for compensation or coexisting primary • The Pco2 should compensate by increasing
metabolic acidosis. about 0.6 to 0.75 mm Hg for each 1 mEq/L (1
mmol/L) increase in HCO3− (up to about 55 mm
Hg).
• Greater increase implies concomitant
respiratory acidosis; lesser increase,
respiratory alkalosis.
• Respiratory alkalosis is suggested by Pco2<

38 mm Hg. The HCO3− should compensate over 4
to 12 hours by decreasing 4 to 5 mEq/L (4 to 5
mmol/L) for every 10 mm Hg decrease in Pco2.
• Lesser decrease means there has been no time
for compensation or a primary metabolic
alkalosis coexists.
• Greater decrease implies a primary metabolic
acidosis.
• Nomograms (acid-base
maps) are an alternative way
to diagnose mixed disorders,
allowing for simultaneous
plotting of pH, HCO3−, and
Pco2.
Mixed disturbances: mixed disturbances are very common and may have
opposing or additive effects on blood [H+]
Opposing disturbances: Additive disturbances:

[1] Respiratory alkalosis and metabolic
acidosis: this combination occurs for example if
[1] Respiratory acidosis and metabolic
heart failure with pulmonary congestion is combined acidosis: this combination occurs in
with renal failure, and in salicylate poisoning. The latter respiratory failure associated with circulatory
condition is associated with initial respiratory alkalosis failure.
due to stimulation of the ventilation by the
salicylate but later complicated by metabolic acidosis. [2] Respiratory alkalosis and metabolic
alkalosis: this combination can occur as a
[2]. Respiratory acidosis and metabolic complication of respiratory failure if excessive
alkalosis: this combination occurs in patients with
ventilatory failure and edema (as in corpulmonale) that
artificial ventilation is given and K and/or Cl ions
is overtreated with diuretics is causing K and / or depletion is induced by excessive diuretic
Cl ions depletion. This combination is commonly therapy.
associated with intracellular acidosis.
Parenteral Fluid Therapy
When no other route of administration is available, fluids are given

by IV in hospitals, outpatient diagnostic and surgical settings,
clinics, and homes to replace fluids, administer medications, and
provide nutrients.
PURPOSE
Ø To provide water, electrolytes, and nutrients to meet daily requirements
Ø To replace water and correct electrolyte deficits
Ø To administer medications and blood products
IV solutions contain dextrose or electrolytes mixed in various

proportions with water. Pure, electrolyte-free water can never
be given by IV because it rapidly enters red blood cells and
causes them to rupture.
TYPES OF INTREVENOUS SOLUTIONS
Ø Solutions are often categorized as isotonic, hypotonic, or hypertonic,

according to their total osmolality
Ø Isotonic if the total electrolyte content (anions + cations) is between
250 and 375 mEq/L.
Ø Hypotonic if the total electrolyte content is less than 250 mEq/L.
Ø Hypertonic if the total electrolyte content is greater than 375 mEq/L.
Ø The nurse must also consider a solution’s osmolality, keeping in
mind that the osmolality of plasma is approximately 300 mOsm/L
(300 mmol/L). For example, a 10% dextrose solution has an
osmolality of approximately 505 mOsm/L.
ISOTONIC FLUIDS
q Have a total osmolality close to that of the ECF.

q Do not cause red blood cells to shrink or swell.
q Composition may or may not approximate that of the ECF.
q Expand the ECF volume.
q One liter of isotonic fluid expands the ECF by 1 L; but, expands the
plasma by only 0.25 L because it is a crystalloid fluid.
q 3 L of isotonic fluid is needed to replace 1 L of blood loss.
q Patients with hypertension and heart failure should be carefully
monitored for signs of fluid overload.
ISOTONIC FLUIDS
D5W NSS OTHER

Ø D5W may be both isotonic Ø Contains water, salt, and chloride. Ø Several other solutions contain
and hypotonic. Ø Solution remains within the ECF. ions in addition to sodium and
Ø Initially isotonic solution, Ø Often used to correct an chloride and are somewhat
extracellular volume deficit but is similar to the ECF in composition.
then disperses as a not identical to ECF. Ø Lactated Ringer solution contains
hypotonic fluid Ø Used with administration of blood potassium and calcium in
Ø Patient is at risk for transfusions and to replace large addition to sodium chloride.
increased intracranial sodium losses, such as in burn Ø Used to correct dehydration and
pressure. injuries. sodium depletion and replace GI
Ø Hyperglycemia can result. Ø Not used for heart failure, losses. Lactated Ringer solution
Ø Used mainly to supply water pulmonary edema, renal contains bicarbonate precursors
impairment, or sodium retention. as well. These solutions are
and to correct an increased Ø Normal saline does not supply marketed, with slight variations,
serum osmolality. calories. under various trade names.
ISOTONIC FLUIDS
Nursing Considerations for Isotonic Solutions
a. Document baseline data.

b. Observe for signs of fluid overload.
c. Monitor manifestations of continued hypovolemia.
d. Prevent hypervolemia.
e. Elevate the head of the bed at 35 to 45 degrees.
f. Elevate the patient’s legs.
g. Educate patients and families.
h. Close monitoring for patients with heart failure.
HYPOTONIC SOLUTIONS
q One purpose is to replace cellular fluid, because it is hypotonic

compared with plasma.
q Another, to provide free water for excretion of body wastes.
q Hypotonic sodium solutions are used to treat hypernatremia and
other hyperosmolar conditions.
q Half-strength saline (0.45% sodium chloride) solution is
frequently used.
q Multiple-electrolyte solutions are also available.
q Excessive infusion can lead to intravascular fluid depletion,
decreased blood pressure, cellular edema, and cell damage.
q These solutions exert less osmotic pressure than the ECF.
HYPOTONIC SOLUTIONS
Nursing Considerations for Hypotonic Solutions

b. Do not administer in contraindicated conditions.
c. Risk for increased intracranial pressure (IICP).
d. Monitor for manifestations of fluid volume deficit.
e. Warning on excessive infusion.
f. Do not administer along with blood products.
HYPERTONIC SOLUTIONS
q When normal saline solution or lactated Ringer solution contains 5% dextrose, the total
osmolality exceeds that of the ECF.
q Dextrose is quickly metabolized, and only the isotonic solution remains. Therefore, any
effect on the intracellular compartment is temporary.
q Similarly, with hypotonic multiple-electrolyte solutions containing 5% dextrose, once the
dextrose is metabolized, these solutions disperse as hypotonic fluids.
q Higher concentrations of dextrose, such as 50% dextrose in water, are strongly
hypertonic and must be given into central veins so that they can be diluted by rapid
blood flow.
q Saline solutions are also available in osmolar concentrations greater than that of the
ECF.
q These solutions draw water from the ICF and cause cells to shrink.
q If given rapidly or in large quantity, they may cause an extracellular volume excess and
precipitate circulatory overload and dehydration.
q These solutions must be given cautiously and usually only when the serum osmolality
has decreased to dangerously low levels.
q Hypertonic solutions exert an osmotic pressure greater than that of the ECF.
HYPERTONIC SOLUTIONS
Nursing Considerations for Isotonic Solutions

b. Watch for signs of hypervolemia.
c. Monitor and observe the patient during administration.
d. Verify order.
e. Assess health history.
f. Prevent fluid overload.
g. Do not administer peripherally.
h. Monitor blood glucose closely.
OTHER INTRAVENOUS THERAPY
q When the patient is unable to tolerate food, nutritional requirements are often met using the IV route.
q Solutions may include high concentrations of glucose (such as 50% dextrose in water), protein, or fat to
meet nutritional requirements.
q The IV route may also be used to administer colloids, plasma expanders, and blood products).
q Examples of blood products include whole blood, packed red blood cells, albumin, and cryoprecipitate.
q Many medications are also delivered by the IV route, either by continuous infusion or by intermittent bolus
directly into the vein.
q Because IV medications enter the circulation rapidly, administration by this route is potentially hazardous.
q All medications can produce adverse reactions; however, medications given by the IV route can cause these
reactions quickly after administration, because the medications are delivered directly into the bloodstream.
q Administration rates and recommended dilutions for individual medications are available in specialized
texts pertaining to IV medications and in manufacturers’ package inserts; these should be consulted to
ensure safe IV administration of medications.
Nursing Management of the Patient Receiving
Intravenous Therapy
q In many settings, the ability to perform venipuncture to gain access to the venous
system for administering fluids and medication is an expected nursing skill.
q This responsibility includes selecting the:
a. appropriate venipuncture site
b. type of cannula
c. being proficient in the technique of vein entry.
q The nurse should demonstrate competency in and knowledge of catheter placement
according to the Nurse Practice Act applicable in their state and should follow the rules
and regulations, organizational policies and procedures, and practice guidelines of that
state’s board of nursing.
Intravenous Therapy: Systemic Complications
Overloading the circulatory system with excessive IV fluids causes
increased blood pressure and central venous pressure. FLUID OVERLOAD
Signs and symptoms include:
ü moist crackles on auscultation of the lungs NURSING MANAGEMENT
ü cough ü Decreasing the IV rate
ü restlessness ü Monitoring vital signs frequently
ü distended neck veins
ü Assess breath sounds
ü edema
ü weight gain ü Placing the patient in a high Fowler
ü dyspnea, and rapid, shallow respirations. position.
ü Contact primary provider immediately.
Possible causes include rapid infusion of an IV solution or hepatic, cardiac,
or renal disease. Complication can be avoided by using an
infusion pump and by carefully monitoring
The risk of fluid overload and subsequent pulmonary edema is especially
all infusions. Complications of circulatory
increased in older patients with cardiac disease; this is referred to as
circulatory overload overload include heart failure and
pulmonary edema
Ø The risk of air embolism is rare but ever-present.
Ø It is most often associated with cannulation of central veins AIR EMBOLISM
and directly related to the size of the embolus and the rate of
entry. NURSING MANAGEMENT
Ø Air entering into central veins gets to the right ventricle, ü Immediately clamping the cannula and replacing a
where it lodges against the pulmonary valve and blocks the leaking or open infusion system
flow of blood from the ventricle into the pulmonary arteries. ü p[lace the patient on the left side in the
Ø Manifestations of air embolism include: Trendelenburg position
ü palpitations ü Assess vital signs and breath sounds
ü dyspnea ü Administering oxygen.
ü continued coughing
ü jugular venous distension Air embolism can be prevented by using locking adapters on
ü wheezing, and cyanosis all lines, filling all tubing completely with solution, and using an
ü hypotension air detection alarm on an IV infusion pump. Complications of
air embolism include shock and death. The amount of air
ü weak,rapid pulse necessary to induce death in humans is not known; however,
ü altered mental status the rate of entry is probably as important as the actual volume
ü chest, shoulder, and low back pain. of air.
Ø Pyogenic substances in either the infusion solution or the IV
administration set can cause bloodstream infections. INFECTION
Ø Signs and symptoms include:
ü abrupt temperature elevation shortly after the infusion is
started Ø In severe sepsis, vascular collapse
ü backache and septic shock may occur.
ü headache
Ø Infection ranges in severity from
ü increased pulse and respiratory rate
ü nausea and vomiting
local involvement of the insertion
ü diarrhea site to systemic dissemination of
ü chills and shaking, organisms through the
ü general malaise. bloodstream, as in sepsis.
Ø Additional symptoms include: Ø Measures to prevent infection are
ü erythema essential at the time the IV line is
ü edema, inserted and throughout the entire
ü induration or drainage at the insertion site.
infusion.
INFECTION
Prevention includes the following:
Ø Performing careful hand hygiene before every contact with any part of the infusion system or the patient
Ø Examining the IV containers for cracks, leaks, or cloudiness, which may indicate a contaminated solution Using strict aseptic
technique
Ø Firmly anchoring the IV cannula to prevent to-and-fro motion (e.g., a catheter stabilization device will help). Sutureless securement
devices avoid disruption around the catheter entry site and may decrease the degree of bacterial contamination
Ø Inspecting the IV site daily and replacing a soiled or wet dressing with a dry sterile dressing (antimicrobial agents that should be used
for site care include 2% tincture of iodine, 10% povidone–iodine, alcohol, or chlorhexidine gluconate, used alone or in combination)
Ø Disinfecting injection/access ports with antimicrobial solution before and after each use
Ø Removing the IV cannula at the first sign of local inflammation, contamination, or complication
Ø Replacing the peripheral IV cannula according to agency policy and procedure
Ø Replacing the IV cannula inserted during emergency conditions (with questionable asepsis) as soon as possible
Ø Infusing or discarding medication or solution within 24 hours of its addition to an administration set
Ø Changing primary and secondary continuous administration sets according to agency policy and procedure, or immediately if
contamination is suspected
Ø Using administration sets with a twist-lock design
Intravenous Therapy: Local Complications
INFILTRATION and EXTRAVASATION

Ø The unintentional administration of a nonvesicant solution or medication into surrounding tissue. o
Ø OccurS when the IV cannula dislodges or perforates the wall of the vein.
Ø Characterized by edema around the insertion site, leakage of IV fluid from the insertion site, discomfort and coolness in
the area of infiltration, and a significant decrease in the flow rate.
Ø When the solution is particularly irritating, sloughing of tissue may result.
Ø Close monitoring of the insertion site is necessary to detect infiltration before it becomes severe.
Ø Is usually easily recognized if the insertion area is larger than the same site of the opposite extremity but is not always
so obvious.
Ø Common misconception is that a backflow of blood into the tubing proves that the catheter is properly placed within the
vein. However, if the catheter tip has pierced the wall of the vessel, IV fluid will seep into tissues and flow into the vein.
Although blood return occurs, infiltration may have occurred as well.
Ø A more reliable means of confirming infiltration is to apply a tourniquet above (or proximal to) the infusion site and
tighten it enough to restrict venous flow. If the infusion continues to drip despite the venous obstruction, infiltration is
present.

NURSING MANAGEMENT
Ø As soon as detected infusion should be stopped,
Ø Discontinue IV catheter
Ø Apply sterile dressing to the site after careful inspection to determine the extent of infiltration. The
infiltration of any amount of blood product, irritant, or vesicant is considered the most severe. The
Ø IV infusion should be started in a new site or proximal to the infiltration site if the same extremity must be
used again.
Ø A warm compress may be applied to the site if small volumes of noncaustic solutions have infiltrated over
a long period.
Ø If the solution was isotonic with a normal pH; the affected extremity should be elevated to promote the
absorption of fluid.
Ø If the infiltration is recent, hypertonic or had an increased pH, a cold compress may be applied to the area.


Ø Extravasation is similar to infiltration, with an inadvertent administration of vesicant or irritant solution or medication
into the surrounding tissue.
Ø Medications such as vasopressors, potassium and calcium preparations, and chemotherapeutic agents can cause:
ü pain
ü burning, and redness at the site
ü Blistering
ü inflammation, and necrosis of tissues can occur.
Ø Older patients, comatose or anesthetized patients, patients with diabetes, and patients with peripheral vascular or
cardiovascular disease are at greater risk for extravasation; other risk factors include high pressure infusion pumps,
palpable cording of vein, and fluid leakage from the insertion site.
Ø The extent of tissue damage is determined by the concentration of the medication, the quantity that extravasated, the
location of the infusion site, the tissue response, and the duration of the process of extravasation.

NURSING MANAGEMENT
Ø Stop infusion and notify provider promptly.
Ø The agency’s protocol to treat extravasation is initiated.
Ø The protocol often specifies infiltration of the infusion site with an antidote prescribed after
assessment by the provider, removal of the cannula, and application of warm compresses to
sites of extravasation from alkaloids or cold compresses to sites of extravasation from
alkylating and antibiotic vesicants.
Ø The affected extremity should not be used for further cannula placement.
Ø Thorough neurovascular assessments of the affected extremity must be performed frequently.

NURSING MANAGEMENT
Ø Reviewing the institution’s IV policy and procedures and incompatibility charts and checking with the
pharmacist before administering any IV medication, whether peripherally or centrally, are recommended
to determine incompatibilities and vesicant potential to prevent extravasation.
Ø Careful, frequent monitoring of the IV site, avoiding insertion of IV devices in areas of flexion, securing the
IV line, and using the smallest catheter possible that accommodates the vein help minimize the incidence
and severity of this complication.
Ø when vesicant medication is given by IV push, it should be given through a side port of an infusing IV
solution to dilute the medication and decrease the severity of tissue damage if extravasation occurs.
Ø Extravasation is rated as grade 4 on the infiltration scale. Complications of an extravasation may include
blister formation, skin sloughing and tissue necrosis, functional or sensory loss in the injured area, and
disfigurement or loss of limb.
PHLEBITIS
Ø Inflammation of a vein, can be categorized as chemical, mechanical, or bacterial; but two or more of these
types of irritation often occur simultaneously.
Ø Chemical phlebitis can be caused by an irritating medication or solution, rapid infusion rates, and
medication incompatibilities.
Ø Mechanical phlebitis results from long periods of cannulation, catheters in flexed areas, catheter gauges
larger than the vein lumen, and poorly secured catheters.
Ø Bacterial phlebitis can develop from poor hand hygiene, lack of aseptic technique, failure to check all
equipment before use, and failure to recognize early signs and symptoms of phlebitis.
Ø Other factors include poor venipuncture technique, catheter in place for a prolonged period, and failure to
adequately secure the catheter.
PHLEBITIS
Ø Phlebitis is characterized by a reddened, warm area around the
insertion site or along the path of the vein, pain or tenderness at
the site or along the vein, and swelling.
Ø The incidence of phlebitis increases with the length of time the
IV line is in place, the composition of the fluid or medication
infused (especially its pH and tonicity), catheter material,
emergency insertions, the size and site of the cannula inserted,
ineffective filtration, inadequate anchoring of the line, and the
introduction of microorganisms at the time of insertion.
Ø The Infusion Nurses Society (INS) has identified specific
standards for assessing phlebitis.
Ø Phlebitis is graded according to the most severe presenting
indication
PHLEBITIS
NURSING MANAGEMENT
Ø Treatment consists of discontinuing the IV line and restarting it in
another site, and applying a warm, moist compress to the affected
site.
Ø Phlebitis can be prevented by using aseptic technique during
insertion, using the appropriate-size cannula or needle for the vein,
considering the composition of fluids and medications when
selecting a site, observing the site hourly for any complications,
anchoring the cannula or needle well, and changing the IV site
according to agency policy and procedures.
THROMBOPHLEBITIS NURSING MANAGEMENT

Ø Discontinuing the IV infusion
Ø Apply cold compress first to decrease the flow of blood
Ø Thrombophlebitis refers to the presence of a and increase platelet aggregation
clot plus inflammation in the vein. It is Ø Followed by a warm compress;
evidenced by : Ø Elevate the extremity
ü localized pain, Ø Restarting the line in the opposite extremity.
ü redness, warmth, and swelling around the
If the patient has signs and symptoms of
insertion site or along the path of the vein, thrombophlebitis, the IV line should not be flushed. The
ü immobility of the extremity because of catheter should be cultured after the skin around the
discomfort and swelling, catheter is cleaned with alcohol. If purulent drainage
ü sluggish flow rate, exists, the site is cultured before the skin is cleaned.
ü fever, Thrombophlebitis can be prevented by avoiding trauma to
ü malaise, the vein at the time the IV line is inserted, observing the
ü leukocytosis. site every hour, and checking medication additives for
compatibility.
HEMATOMA NURSING MANAGEMENT

Ø Remove the needle or cannula and applying light
pressure with a sterile, dry dressing
Ø Hematoma results when blood leaks into
Ø Apply ice for 24 hours to the site to avoid extension
tissues surrounding the IV insertion site.
of the hematoma
Ø Leakage can result if the opposite vein wall is
Ø Elevate the extremity to maximize venous return, if
perforated during venipuncture, the needle
tolerated; assessing the extremity for any
slips out of the vein, a cannula is too large for
circulatory, neurologic, or motor dysfunction
the vessel, or insufficient pressure is applied
Ø Restarting the line in the other extremity if
to the site after removal of the needle or
indicated.
cannula.
Ø The signs of a hematoma include ecchymosis,
A hematoma can be prevented by carefully
immediate swelling at the site, and leakage of inserting the needle and by using diligent care with patients
blood at the insertion site. who have a bleeding disorder, are taking anticoagulant
medication, or have advanced liver disease
CLOTTING and OBSTRUCTION

NURSING MANAGEMENT
Ø Blood clots may form in the IV line as a result ü Infusion must be discontinued and restart in
of kinked IV tubing, a very slow infusion rate, another site with a new cannula and
an empty IV bag, or failure to flush the IV line administration set.
after intermittent medication or solution ü Tubing should not be irrigated or milked.
administrations. ü Neither the infusion rate nor the solution
Ø The signs are decreased flow rate and blood container should be raised, and the clot should
backflow into the IV tubing. not be aspirated from the tubing.
Clotting of the needle or cannula may be prevented by not allowing the IV solution bag to run
dry, taping the tubing to prevent kinking and maintain patency, maintaining an adequate flow rate, and
flushing the line after intermittent medication or other solution administration.
In some cases, a specially trained nurse or physician may inject a thrombolytic agent into the
catheter to clear an occlusion resulting from fibrin or clotted blood.
Promoting Home, Community-Based,
and Transitional Care
Educating Patients About Self-Care
q At times, IV therapy must be given in the home setting, in which case much of
the daily management rests with the patient and family.
q Education becomes essential to ensure that the patient and family can
manage the IV fluid and infusion correctly and avoid complications.
q Written instructions as well as demonstration and return demonstration help

reinforce the key points for all of these functions.
Continuing and Transitional Care

q Home infusion therapies cover a wide range of treatments, including antibiotic,
analgesic, and antineoplastic medications; blood or blood component therapy; and
parenteral nutrition.
q When direct nursing care is necessary, arrangements are made to have an infusion
nurse visit the home and administer the IV therapy as prescribed.
q In addition to implementing and monitoring the IV therapy, the nurse carries out a
comprehensive assessment of the patient’s condition and continues to educate the
patient and family about the skills involved in overseeing the IV therapy setup.

q Any dietary changes that may be necessary because of fluid or electrolyte
imbalances are explained or reinforced during such sessions.
q Periodic laboratory testing may be necessary to assess the effects of IV therapy

and the patient’s progress.
q Blood specimens may be obtained by a laboratory near the patient’s home, or a

home visit may be arranged to obtain blood specimens for analysis.

q The nurse collaborates with the case manager in assessing the patient, family, and
home environment
ü Develop a plan of care in accordance with the patient’s treatment plan and level of
ability
ü Arrange for appropriate referral and follow-up if necessary.
q Any necessary equipment may be provided by the agency or purchased by the patient,
depending on the terms of the home care arrangements.
q Appropriate documentation is necessary to assist in obtaining third-party payment for

the service provided.

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INTRODUCTION

ü Plasma pH is an indicator of hydrogen

DONATE ACID Strong HCL

v A Buffer Solution resist

H+ + A - HA v In contrast, if its low

Base (A+ ) - BICARBONATE (HCO3-)

If the ratio is altered the pH changes. it is the ratio

These are minor buffers that can

H2P4- / HPO4- ATP / ADP

Phosphates are found in the blood in two HCl + Na2HPO4→NaH2PO4 + NaCl

v Nearly all proteins can function as

q Hemoglobin is the principal protein inside of red

to re-form CO2, which then can diffuse into the HCO3-

vAerobic cellular respiration, which results in the release of

Step 1: Sodium ions are reabsorbed from the filtrate in exchange

Ø If this occurs, the hydrogen ions will not be available to combine

Ø If more potassium is present than normal, potassium, rather than the

Ø If there is less potassium, more hydrogen ions enter the filtrate to be

Ø If chloride is lost, the body uses bicarbonate ions in

Ø Thus, lost chloride results in an increased

Ø Various compensatory mechanisms exist to maintain blood pH within

Ø Respiratory compensation for metabolic acidosis increases the respiratory rate to

PARAMETER ARTERIAL BLOOD MIXED VENOUS BLOOD

pH 7.35 - 7.45 7.32 - 7.42

HCO3- 22 - 26 mEq/L 19 - 25 mEq/L

Base Excess/Deficit ±2 mEq/L ±5 mEq/L

Sa02% >94% 65 - 75%

<22 mEq/L =Acidosis pH 7.35 - 7.45 7.32 - 7.42

>26 mEq/L =Alkalosis PCO2 35 - 34 mm Hg 38 - 52 mm Hg

Metabolic acidosis is problematic, as lower-than-normal amounts

Respiratory acidosis is problematic, as excess CO2 is present in the

Alkalosis is characterized by a higher-than-normal pH. Metabolic

Respiratory alkalosis is problematic, as CO2 deficiency is present in

1 DETERMINE pH if pH is within normal range = COMPENSATED

2 LOOK for other PARAMENTER without normal = PARTIALLY COMPENSATED

v Is a common clinical disturbance characterized by a low pH (increased H+

Physical Assessment Findings:

decreased cardiac output occur The cardinal feature of metabolic acidosis is a

MEDICAL MANAGEMENT For management of vomiting

Symptoms of metabolic alkalosis:

ü Restoring normal fluid

Ø Respiratory acidosis is a clinical disorder in which the pH is less

Signs and Symptoms

Medical Management Nursing Management

Ø Respiratory alkalosis is a clinical condition which the arterial ph

Treatment of respiratory acidosis NURSING CONSIDERATIONS

q Involve more than one primary process.

• Respiratory acidosis is suggested by Pco2> 40

• Respiratory alkalosis is suggested by Pco2<

Opposing disturbances: Additive disturbances:

When no other route of administration is available, fluids are given

IV solutions contain dextrose or electrolytes mixed in various

Ø Solutions are often categorized as isotonic, hypotonic, or hypertonic,

q Have a total osmolality close to that of the ECF.

D5W NSS OTHER

Nursing Considerations for Isotonic Solutions

a. Document baseline data.

q One purpose is to replace cellular fluid, because it is hypotonic