ACID-BASE IMBALANCE

Basics

• Hydrogen ions-pH
• Acid- Hydrogen donors
• Base- Hydrogen acceptors
 Regulatory system
• First line- Blood buffers
• Second line- Respiratory regulation
• Third line- Renal regulation
 Buffers
• Fastest acting regulatory system
• Resist changes in pH when an acid or alkali
added.
• Hemoglobin system- Chloride shift
• Plasma protein system-
• Carbonic acid –bicarbonate system-Primary
buffer system
7.4- 20 parts of bicarbonate: 1 part of carbonic acid
• Phosphate buffers- Neutralizes excess hydrogen
ions
 Lungs
• Second defense
• 13000-30000 m Eq/day
• 10- 30 seconds
• Acidosis- pH decreased, hydrogen ions increased
(hypoventilation)
Compensatory- inactivation of hydrogen ions
Neutralized by bicarbonate - carbonic acid formed and
reduced to carbon dioxide and water and exhaled
• Alkalosis- pH increased, hydrogen ions decrease
( Hyperventilation)
Compensatory- CO2 retained and carbonic acid neutralizes
excess base
 Kidneys
• Third defense
• 50 mEq/day
• Compensation requires a few hours to several
days
• Acidosis- Excess hydrogen ions secreted into
renal tubule
• Alkalosis- Excess bicarbonate move into renal
tubule
 Potassium
Acidosis- Potassium moves outside- Hyperkalemia
Alkalosis- Potassium moves into the cells-
Hyporkalemia
 ABG : Normal parameters
Blood pH:
• Normal: 7.35-7.45
• Acidosis: <7.35
• Alkalosis: >7.45
CO2 (carbon dioxide):
• Normal: 35-45 mmHg
• Acidosis: >45 mmHg
• Alkalosis: <35 mmHg
• (CO2 lab value ALWAYS indicates a RESPIRATORY issue)
HCO3 (bicarbonate):
• Normal: 22-26 mEq/L
• Acidosis: <22 mEq/L
• Alkalosis: >26 mEq/L
• (HCO3 lab value ALWAYS indicates a METABOLIC issue)
 When solving ABG problems always
ask these 3 Questions
• Is it a respiratory or metabolic problem?
• Is this alkalosis or acidosis?
• Is this uncompensated, partially
compensated, or fully compensated?
 ROME
• ROME stands for
• Respiratory
• Opposite
• Metabolic
• Equal
CO2 ↑, pH↓ : Respiratory acidosis
CO2  ↓, pH ↑: Respiratory alkalosis
HCO3 ↓  , pH ↓  : Metabolic acidosis
HCO3  ↑, pH ↑  : Metabolic alkalosis
Problem 1: pH 7.28, CO2 50, HCO3 24
Problem 2: pH 7.30, CO2 40, HCO3 18
Problem 3: pH 7.42, CO2 26, HCO3 18
Problem 4:pH 7.51, CO2 47, HCO3 32
Problem 5: pH 7.37, CO2 32, HCO3 17
 Problem 6: pH 7.3, PaCO2 68 mm Hg,
HCO3 28 mmol/L, and PaO2 60 mm Hg.
• pH 7.0, PaO2 90 mm Hg, PaCO2 23 mm Hg,
and HCO3 12 mmol/L; other results are Na+
126 mmol/L, K+ 5 mmol/L, and Cl- 95
mmol/L.
•  pH 7.6, PaO2 120 mm Hg, PaCO2 31 mm Hg,
and HCO3 25 mmol/L. 
• pH 7.5, PaO2 85 mm Hg, PaCO2 40 mm Hg,
and HCO3 34 mmol/L
•  pH 7.10, PaCO2 70 mm Hg, and HCO3 24
mEq/L
• pH 7.39, PaCO2 27 mmHg, and HCO3 19
mEq/L. What does this mean?
• pH 7.57, PaCO2 37 mmHg and HCO3 30
mEq/L.
• pH 7.61, PaCO2 22 mmHg, and HCO3 25
mEq/L
•  pH 7.35, PaCO2 72 mmHg, and HCO3 38
mEq/L. 
 Anion gap
 The anion gap measures the
difference—or gap—between
the negatively charged and
positively charged electrolytes
in your blood.
 If the anion gap is too high, your
blood is more acidic than normal.
 If the anion gap is too low, your
blood isn't acidic enough.
 A normal anion gap is < 12.
(HAGMA) 
Glycols (ethylene glycol,
propylene glycol)
Oxoproline (pyroglutamic acid,
the toxic metabolite of
excessive acetaminophen or
paracetamol)
L-Lactate (standard lactic acid
seen in lactic acidosis)
D-Lactate (exogenous lactic
acid produced by gut bacteria)
Methanol (this is inclusive of
alcohols in general)
Aspirin (salicylic acid)
Renal Failure (uremic acidosis)
Ketones (diabetic, alcoholic
and starvation ketosis)
Non-anion gap metabolic acidosis
(NAGMA),
• H = hyperalimentation (e.g., starting
TPN).
A = acetazolamide use.
R = renal tubular acidosis (Type I = distal;
Type II = proximal; Type IV = HCO3 loss and
replaced with Cl-
hyporeninemic hypoaldosteronism) anion gap normal
D = diarrhea
U = uretosigmoid fistula (because the
colon will waste bicarbonate).
P = pancreatic fistula (because of alkali
loss–the pancreas secretes a bicarbonate-
rich fluid).
 Base excess/deficit
• Base excess (BE) was introduced by Siggaard-Andersen in 1960 
• Base excess is defined as the amount of strong acid that must be
added to each liter of fully oxygenated blood to return the pH to
7.40 at a temperature of 37°C and a pCO2 of 40 mmHg
• Base deficit (ie. a negative base excess) is defined by the amount
of strong base that must be added.
• Normal values range from -2 to +2 mEq/L.
• A high base excess (> +2mmol/L) -Primary metabolic alkalosis or
a compensated respiratory acidosis.
• A low base excess (< -2mmol/L) -Metabolic acidosis or a
compensated respiratory alkalosis.
 Electrolyte imbalance

Electrolyte : These are substances that once they

enter and dissolve in water (hence our blood)
they produce an electrical charge (become ions),
which helps with electrical signaling in the body
and other important processes.
 Electrolytes in the extracellular fluid
• Sodium- Primary cation in the ECF
• Calcium
• Chloride- Primary anion in the ECF
• Bicarbonate
 Electrolyte in the intracellular
fluid
• Potassium- Primary cation in the ICF
• Magnesium
• Phosphate
 Sodium

Cation
 Types
• Euvolemic hyponatremia -- total body water
increases, but the body's sodium content stays
the same
• Hypervolemic hyponatremia -- both sodium
and water content in the body increase, but the
water gain is greater
• Hypovolemic hyponatremia -- water and
sodium are both lost from the body, but the
sodium loss is greater
 Euvolemic Hyponatremia 
• Euvolemic Hyponatremia is where the water in
the body normal but the sodium loss
• The causes include: SIADH (Syndrome of
inappropriate antidiuretic hormone secretion)
which is due to the increased amount of
secretion of antidiuretic hormone.
• This hormone retains water in the body which
dilutes sodium.
• Other causes: diabetes insipidus, adrenal
insufficiency, Addison’s disease et
 Hypovolemic Hyponatremia 
• Hypovolemic Hyponatremia is where the
patient has lost a lot of fluid and sodium.
•  Causes: vomiting, diarrhea, NG suction,
diuretic therapy, burns, sweating.
 Hypervolemic Hyponatremia
• Hypervolemic Hyponatremia  is where the
body has increased in fluid and sodium.
 Causes: congestive heart failure, kidney
failure, IV infusion of saline, liver failure etc.
 Hyponatremia
• Low sodium in the blood (less than 135 mEq/L)
Causes:
• Not consuming enough sodium
• Diuretics “thiazides”
• Vomiting (GI suction…rich in sodium and
potassium)
• Diarrhea
• Sweating
 Remember “NO Na+”
• Na+ excretion increased with renal problems, NG
suction (GI system rich in sodium), vomiting, diuretics,
sweating, diarrhea, decreased secretion of aldosterone
(wasting sodium)
• Overload of fluid with congestive heart failure,
hypotonic fluids infusions, renal failure (dilutes sodium)
• Na+ intake low through low salt diets or nothing by
mouth
• Antidiuretic hormone over secreted **SIADH
(syndrome of inappropriate antidiuretic hormone
secretion…remembers retains water in the body and
this dilutes sodium)
 Causes……
– Aldosterone: regulates blood pressure and causes
water and sodium to be kept by the kidneys but in
turn excretes potassium
• (Addison’s Disease)
• Low amount of aldosterone: would cause the kidneys to not
reabsorb much sodium and drop blood levels and in turn
would cause the kidneys to keep potassium (leading to
hyperkalemia)
– SIADH (Syndrome of Inappropriate Antidiuretic
Hormone Secretion): too much ADH is released
causing the body to retain water which dilutes the
sodium level.
– Overload of fluid (dilutes sodium) with congestive
heart failure, hypotonic fluids infusions, renal failure.
Signs and Symptoms of Hyponatremia
• Seizures & Stupor (decrease in
consciousness…confusion)
• Abdominal cramping
• Lethargic
• Tendon reflexes diminished,
trouble concentrating
• Loss of urine & appetite, Lithium
toxicity
• Orthostatic hypotension,
overactive bowel sounds
• Shallow respirations (happens
late due to skeletal muscle
weakness)
• Spasms of muscles
Nursing Interventions for
Hyponatremia
 Hypernatremia
• Hypernatremia: excessive sodium in the
blood 
• Normal sodium levels: 135 to 145
mEq/L (>145 sodium is hypernatremic)
 Causes of Hypernatremia
• Remember the phrase “HIGH SALT”
• Hypercortisolism (Cushing’s Syndrome),
hyperventilation
• Increased intake of sodium (oral or IV route)
• GI feeding (tube) without adequate water supplements
• Hypertonic solutions
• Sodium excretion decreased (body keeping too much
sodium) and corticosteroids
• Aldosterone overproduction (Hyperaldosteronism…
Conn’s Syndrome)
• Loss of fluids (dehydrated) infection (fever), sweating,
diarrhea, and diabetes insipidus
• Thirst impairment
 Signs & Symptoms of Hypernatremia
• Remember:  FRIED 
• Fatigue
• Restless, really agitated
(confused….central nervous system
changes)
• Increased reflexes (progress to
seizures and coma)
• Extreme thirst (*big sign)
• Decreased urine output, dry
mouth/skin
 Management
• Restrict sodium intake
• Keep patient safe because they will be confused and
agitated.
• Doctor may order to give isotonic or hypotonic
solutions such as 0.45% NS (which is hypotonic and
most commonly used).
• Give hypotonic fluids slowly because brain tissue is at
risk due to the shifting of fluids back into the cell
(remember the cell is dehydrated with hypernatremia)
and the patient is at risk for cerebral edema)
• In other words, the cell can lyse if fluids are
administered too quickly.
• Educate patient and family about sign and symptoms
of high sodium level and proper foods to eat.
Nursing management
 Calcium
• Calcium plays a huge role in bone and teeth
health along with muscle contraction/nerve
transmission, cell, and blood clotting.
• Calcium is absorbed in the GI system (so a diet
rich in calcium is essential for maintaining
calcium blood levels), and it’s stored in the
bones.
• Therefore, if blood levels drop the bones will
release some calcium in the blood to help
maintain levels, but this can be unhealthy
overtime and lead to osteoporosis.
• Vitamin D helps play a role in calcium
absorption.
• Phosphorus and calcium affect each other in
the opposite way.
• For instance, if phosphorus levels are high in
the blood, calcium will decrease and vice versa
• Normal calcium level: 8.5  to 10.5 mg/dL
 Causes of Hypocalcemia
• Remember “Low Calcium”
• Low parathyroid hormone
This is due to the destruction or removal
parathyroid gland (any surgeries of the neck ex:
thyroidectomy you want to check the calcium
level) Professors love to ask this on an exam.
• Oral intake inadequate (alcoholism, bulimia etc.)
• Wound drainage (especially GI System because
this is where calcium is absorbed)
• Celiac’s & Crohn’s Disease cause malabsorption of
calcium in the GI track
• Acute Pancreatitis
• Low Vitamin D levels (allows for calcium to be
reabsorbed)
• Chronic kidney issues (excessive excretion of
calcium by the kidneys)
• Increased phosphorus levels in the blood
(phosphorus and calcium do the opposite of each
other)
• Using medications such as magnesium
supplements, laxatives, loop diuretics, calcium
binder drugs
• Mobility issues
 Signs & Symptoms of Hypocalcemia
• Remember “CRAMPS”
• Confusion
• Reflexes hyperactive
• Arrhythmias (prolonged QT
interval and ST interval) Note:
definitely remember prolonged QT
interval)
• Muscle spasms in calves or feet,
tetany, seizures
• Positive Trousseau’s
• Signs of Chvostek’s
 Management
• Safety (prevent falls because patient is
at risk for bone fractures, seizures
precautions, and watch for laryngeal
spasms)
• Administer IV calcium as ordered (ex:
10% calcium gluconate)….give slowly as
ordered (be on cardiac monitor and
watch for cardiac dysrhythmias).
• Assess for infiltration or phlebitis
because it can cause tissue sloughing
(best to give via a central line).
• Also, watch if patient is on Digoxin
cause this can cause Digoxin toxicity.
• Administer oral calcium with Vitamin D
supplements (given after meals or at
bedtime with a full glass of water)
• If phosphorus level is high (remember
phosphorus and calcium do the
opposite) the doctor may order
aluminum hydroxide antacids to
decrease phosphorus level which in
turn would increase calcium levels.
• Encourage intake of foods high in
calcium:
 Hypercalcemia
• Meaning of Hypercalcemia: excessive calcium
in the blood
• Normal calcium levels in the blood: 8.6 to 10.0
mg/dL (>10.0 is hypercalcemia)
 Causes of Hypercalcemia
• Remember “High Cal”
• Hyperparathyroidism (high parathyroid hormone
causes too much calcium to be released into the blood)
• Increased intake of calcium (excessive use of oral
calcium or Vitamin D supplements)
• Glucocorticoids usage (suppresses calcium absorption
which leaves more calcium in the blood)
• Hyperthyroidism
• Calcium excretion decreased with Thiazide* diuretics &
renal failure, cancer of the bones
• Adrenal insufficiency (Addison’s Disease)
• Lithium usage (affects the parathyroid and causes
phosphate to decrease and calcium to increase)
 Signs & Symptoms of Hypercalcemia

• “The body is too WEAK”

• Weakness of muscles (profound)
• EKG changes shortened QT interval (most
common) and prolonged PR interval
• Absent reflexes, absent minded
(disorientated), abdominal distention from
constipation
• Kidney Stone formation
 Management
• Keep patient hydrated (decrease chance of renal stone
formation)
• Keep patient safe from falls or injury
• Monitor cardiac, GI, renal, neuro status
• Assess for complaints of flank or abdominal pain & strain
urine to look for stone formation
• Decrease calcium rich foods and intake of calcium-
preserving drugs like thiazides, supplements, Vitamin D
• Administer calcium reabsorption inhibitors: Calcitonin,
Bisphosphonates, prostaglandin synthesis inhibitors (ASA,
NSAIDS)
• Prepare patient for dialysis
 Potassium
• The normal potassium level is 3.5 to 5.1
mEq/L.
• Unlike sodium that is an extracellular
electrolyte that is found in the blood plasma,
potassium is most abundant in the cells of the
body; it is primarily an intracellular electrolyte.
• This electrolyte promotes and facilitates
electrical impulses that are necessary for
muscular contractions and also for the normal
functioning of the brain.
 Nursing Interventions for
Hypokalemia
• Watch heart rhythm (place on cardiac
monitor…most are already on telemetry),
respiratory status, neuro, GI, urinary output
and renal status (BUN and creatinine levels)
• Watch other electrolytes like Magnesium (will
also decrease…hard to get K+ to increase if
Mag is low), watch glucose, sodium, and
calcium all go hand-in-hand and play a role in
cell transport
• Administer oral Supplements for potassium with
doctor’s order: usually for levels 2.5-3.5…give
with food can cause GI upset
• IV Potassium for levels less 2.5 (NEVER EVER
GIVE POTASSIUM via IV push or by IM or subq
routes)
• -Give according to the bag instruction don’t
increase the rate…has to be given slow…
patients given more than 10-20 meq/hr should
be on a cardiac monitor and monitored for EKG
changes
• -Cause phlebitis or infiltrations
• Don’t give LASIX, demadex , or thiazides (waste
more Potassium) or Digoxin (cause digoxin
toxicity) if Potassium level low…notify md for
further orders)
• Physician will switch patient to a potassium
sparing diuretic Spironolactone (Aldactone),
Dyazide, Maxide, Triamterene
• Instruct patient to eat Potassium rich foods
 Hyperkalemia
• Meaning of hyperkalemia: excessive
potassium in the blood
• Normal Potassium is 3.5 to 5.1. Anything
higher 7.0 or higher is very dangerous!
Nursing Interventions for Hyperkalem
• Monitor cardiac, respiratory, neuromuscular,
renal, and GI status
• Stop IV potassium if running and hold any PO
potassium supplements
• Initiate potassium restricted diet and
remember foods that are high in potassium
• Remember the word POTASSIUM for food rich
in potassium
• Prepare patient for ready for dialysis. Most
patient are renal patients who get dialysis
regularly and will have high potassium.
• Kayexalate is sometimes ordered and given PO or
via enema. This drug promotes GI sodium
absorption which causes potassium excretion.
• Doctor may order potassium wasting drugs like
Lasix or Hydrochlorothiazide
• Administer a hypertonic solution of glucose and
regular insulin to pull the potassium into the cell
 Magnesium
• Normal Levels of Magnesium: 1.6 to 2.6 mg/dL (>2.6
hypermagnesemia)
• Magnesium plays a role in: major cell functions like
transferring and storing energy, regulation of
parathyroid hormone PTH (which also plays a role in
calcium levels).
• Magnesium also plays a role in the metabolism of
carbs, lipids, and proteins, and blood pressure
regulation.
• Magnesium is absorbed in the small intestine and
excreted via the kidneys (any issues with these systems
can cause magnesium level issues).
 Hypermagnesemia
• Normal Levels of Magnesium: 1.6 to 2.6
mg/dL (>2.6 hypermagnesemia)
 Causes
• Remember “MAG”
• Hypermagnesemia is less common than
hypomagnesemia.
• It typically happens when you are trying to correct
hypomagnesemia with magnesium sulfate IV infusion.
However, other causes can include:
• Magnesium containing antacids and
laxatives***(Mylanta, Maalox)
• Addison’s disease (adrenal insufficiency)
• Glomerular filtration insufficiency (<30mL/min) renal
failure. This is because the kidneys are keeping too
much magnesium.
 SIGNS AND SYMPTOMS
• Lethargy (profound)
• EKG changes with prolonged PR & QT interval
and widened QRS complex
• Tendon reflexes absent/grossly diminished
• Hypotension
• Arrhythmias (bradycardia, heart blocks)
• Respiratory arrest
• GI issues (nausea, vomiting)
• Impaired breathing (due to skeletal weakness)
• Cardiac arrest
 Nursing Interventions for
Hypermagnesemia
• Monitor cardiac, respiratory, neuro system, renal
status. Put patient on cardiac monitor (watch for EKG
changes)
• Ensure safety due to lethargic/drowsiness
• Prevention:
• Avoid giving Magnesium containing antacids/laxative
to patients with renal failure
• Assess for hypermagnesemia during IV infusions of
magnesium sulfate for hypomagnesemia (sign and
symptom would be diminished/absent deep tendon
reflexes)
• Withhold foods high in magnesium, such as:
 Hypomagnesemia
• Normal Levels of Magnesium: 1.6 to 2.6
mg/dL (<1.6 hypomagnesemia)
 Signs & Symptoms of
Hypomagnesemia
• Trouesseau’s (positive due to hypocalcemia)
• Weakness
• Irritability
• Torsades de pointes (abnormal heart rhythm that leads to sudden
cardiac death…seen in alcoholism) Tetany (seizures)
• Cardiac changes (moderate loss: Tall T-waves and depressed ST
segments*** severe loss: prolonged PR & QT interval (prolong of
QT interval increases patient’s risk for Torsades de pointes) with
widening QRS complex, flattened t-waves, Chvostek’s sign (positive
which goes along with hypocalcemia)
• Hypertension, hyperreflexia
• Involuntary movements
• Nausea
• GI issues (decreased bowel sounds and mobility)
 Causes
• Remember “Low Mag”
• Limited intake Mg+ (starvation)
• Other electrolyte issues cause low mag levels (hypOkalemia
, hypOcalcemia)
• Wasting Magnesium kidneys (loop and thiazide diuretics &
cyclosporine…stimulates the kidneys to waste Mag)
• Malabsorption issues (Crohn’s, Celiac, proton-pump
inhibitors drugs “Prilosec, Nexium, Protonix”…drug family
ending in “prazole” Omeprazole, diarrhea/vomiting)
• Alcohol (due to poor dietary intake, alcohol stimulates the
kidneys to excreted mag, acute pancreatitis)
• Glycemic issues (Diabetic Ketoacidosis, insulin
administration)
 Nursing Interventions for
Hypomagnesemia
• Monitor cardiac, GI, respiratory, neuro status. Place on a cardiac monitor
(watching for any EKG changes prolonging of PR interval and widening
QRS complex)
• May administer potassium supplements due to hypokalemia (hard to get
magnesium level up if potassium level is down)
• Administering calcium supplements (oral calcium supplements w/
Vitamin-D or 10% Calcium Gluconate)
• Administer Magnesium Sulfate IV route. Monitor Mg+ level closely
because patient can become magnesium toxic (***Watch for depressed
or loss of deep tendon reflexes)
• Place patient in seizure precautions
• Oral forms of Magnesium may cause diarrhea which can increase
magnesium loss so watch out for this
• Watch other electrolyte levels like calcium and potassium
• Encourage foods rich in Magnesium:
Fluids