University or Jordan

Faculty of Nursing
Research Title:

Acid- base Imbalance and

its Impact on Electrolytes

Prepared by:
Majdi Muhanna & Naif Hammed Almutairi
ID # 8050992 ID # 8051936

Under Supervision
Dr. Mohammad Khatatbeh
Faculty of Medicine
1st semester
2005 - 2006
Objective
Identify the major four Acids base Disorder: respiratory
acidosis alkalosis, metabolic acidosis alkalosis and mixed
acid-base disorder.
Equilibrium of HCO3/CO2 buffer system at a ratio of 20/1 to
achieve normal PH= 7.4.
Identify Base excess base deficit and anion gap for
confirming acid base disorders.
Acid-base imbalance and relation to electrolyte changes.
ECG changes in relation to electrolyte disturbance.
Describe poly morphous ventricular tacky cardiac (Torsades
de pointes) cause and treatment.
Identify some electrolyte imbalance.
 Acid-Base Disorder

Acid-Base Path Physiology

Acid-Base Disturbance and Impact on Electrolyte

Introduction
Disturbance in acid-base balance are common
clinical problem that range in severity from mild to
life threatening, the acute toxicity of acid-base
derangements will primarily involve the heart and the
brain, the four primary acid-base disorder's:
Metabolic acidosis
Metabolic Alkalosis
Respiratory acidosis
Respiratory alkalosis
Mixed acid-base disorders.
Acids
An acid is a substance containing one or more [H+] ions
that can be liberated in solution (proton donor) metabolic
process in the body result the formation of two types of
acids: Volatile and nonvolatile. Volatile acid can
change between liquid and gaseous, states. Carbon
dioxide major end products of carbohydrates, fats,
amino acids and the ability to react with water to form
H2CO3:

CO2 + H2O H2CO3 H+ + HCO3-

Bases
In contrast to an acid a base is a substance that can
capture or combine with [H+] from a solution (proton
acceptors).

H+ + HCO3- H2CO3
Buffers
The term buffer describes chemical substances that
minimize the pH change in a solution caused by the addition
of either an acid or a base. A buffer is a mixture of a weak
acid and its alkali salt (or a weak base and it acid salt).
Four main buffer pairs or systems in the body help to
maintain the constancy of the pH:
Bicarbonate-Carbonate acid system (NaHCO3 and H2CO3).
Disodium-monosodium phosphate buffer system (Na2HPO4, &
NaH2PO4).
Hemoglobin oxy- hemoglobin buffer system in Red blood cells.
Protein buffer system
The HCO3/CO2 Buffer System
Acid-base homoeostasis centers depend on the regulation of
the HCO3-/CO2 buffer system.
Because acid-base regulation center's on the HCO3-/CO2 buffer
pair, all acid-base are classified as being either respiratory (too
much / too little CO2) or metabolic (too much / too little HCO3-)

Where: pK is the carbonic acid dissociation

At a body pH of 7.4 the ratio of HCO3- to H2CO3 must be 20: 1
 Base Excess
The base excess defined as the amount of acid
in mmol required to restore 1 letter of blood to its
normal pH at a PaCO2 of 5.3 kPa (40 mmHg).
Base excess >+2 = metabolic of alkalosis
measured pH greater than predicated pH mean
metabolic alkalosis is present.
Base deficit <-2 = metabolic acidosis measured
pH less than calculated pH: mean metabolic
acidosis is present.
Anion Gap
The term anion gap (AG) represents the
concentration of all unmeasured anions in the
plasma. The equivalent of cations in a solution
always balances the equivalents of anion. the
real balance is given by the equation:
[Na+] + [Other Cations] = [Cl] + [HCO3] + [Other
Anions]
Rearranging:
[Na+][(Cl-)+(HCO3-)] =[Other Anions][Other Cations]
=(Anion Gap)
Normal range 10-15 mg/L a gap >15 suggest
metabolic acidosis.Other reference considers 8 16
mg/L normal AG.
Acid-Base Imbalance
1. Many conditions that cause a disturbance in the body pH
such as vomiting and diarrhea are dominated clinically by
abnormalities in fluid and electrolyte balance and it is the
dehydration rather than the pH change that required
immediate attention rather than acid base correction.
2. The same apply for hypocalcaemia where ensuring proper
hydration rather than trying to correct the serum calcium.
Similarity adequate fluid and electrolyte to replacement will
permit correction of any associated pH abnormality in the
majority of patients.
3. However, there are occasions when the pH disorder
dominates the clinical picture and it is necessary to administer
base or less commonly acid, these include the acute acidosis:
server hypovolemic shock, diabetic keto acidosis, the over
dose of an exogenous acid and cardiac arrest and the acute
Alkalosis of alkali over dose, pyloric stenosis and congital
metabolic alkalosis in rare cases.
Acidosis
I. Respiratory Acidosis:
Increase in CO2 (PaCO2) will lead to respiratory
acidosis and decrease pH (pH) and normal [HCO3].
1) Interfere with gas exchange in the lung like
pneumonia from drugs, trauma and tumour.
2) Depressed the drive to ventilation respiratory
center from drugs, trauma and tumour.
3) Interfere with mechanics of ventilation like
pheneric paralysis and diaphragmatic fatigue.
Acidosis
II. Non Respiratory (Metabolic Acidosis):
Increase in non volatile acids in the body:

Decrease in HCO3 will lead to metabolic acidosis

and decrease in PH (pH)
The main causes for metabolic acidosis

1. Interfere with normal excretion of the acid (fixed)

like renal failure.
2. Excessive loss of base like diarrhea, diuretic's,
vomiting.
3. Excessive production of endogenous acid like
fasting starvation, D.M, Hyper catabolic state,
infection, burn and fever.
4. Ingestion of acidifying compound like Aspirin and
ammonium chloride.
5. Increase Anion gap: Increased acid production
lactic acidosis (shock or cardio pulmonary arrest)
diabetic keto acidosis, acute chromic renal failure.
Alkalosis
I. Respiratory Alkalosis:
Excessive elimination of CO2 by the lungs due to:
1. Voluntary in appropriate hyper ventilation hysteric
cause (very common).
2. Involuntary in appropriate hyper ventilation cause
by fever or Thyrotoxicosis, meningitis, head
trauma and or brain tumor.
3. In case of salicylate poisoning true acidosis
(metabolic acidosis) hyper ventilation for over
compensation and leading to respiratory alkalosis.
Note:
Compensation: Always exist before any over
deviation in plasma pH occurs.
Over compensation: A temporary phenomenon
likes dramatic increase in ventilation.
Alkalosis
II. Metabolic Alkalosis:
Metabolic alkalosis (HCO3- excess) is a system disorder
characterized by a primary increase in the plasma HCO3-
concentration resulting in an increase in the pH (decrease in
the [H+])
Respiratory compensation consists of rising of PaCO2 by
hypoventilation: however the degree of hypoventilation limited
because respiration continues to be driven by hypoxia.
Vomiting or Nasogastic suction
Loop or thiazide type diuretics.
Mineralocorticoid excess hyper aldosternism, cushings
syndrome
Hypokalemia and hypochloremia
 (Mixed acid base Disorders)

Mixed acid-base disorders are condition in which at

least two of the simpler acid-base disturbance coexist
and occur in the presence of complex media problem.
These mixed disturbances include:
1. Metabolic acidosis plus respiratory acidosis:
Cardio pulmonary arrest
COPD goes it shock
CRF with pulmonary edema
DKA receive potent opiate or barbiturate
 (Mixed acid base Disorders)
1. Metabolic Alkalosis plus respiratory alkalosis:
COPD who is hyper ventilated on a respiratory
Head trauma patient with hyper ventilation with diuretics
Metabolic acidosis plus respiratory alkalosis lactic
acidosis complicating septic shock
Metabolic Alkalosis plus respiratory acidosis (COPD)
who is vomiting or treated with N.G suction or potent
diuretics.
2. Metabolic acidosis plus respiratory alkalosis lactic
acidosis complicating septic shock
3. Metabolic Alkalosis plus respiratory acidosis (COPD) who
is vomiting or treated with N.G suction or potent
diuretics.
Hyper Kalaemia and Acidosis:
1. In hyper kalaemia excess plasma K+ enters the cell
and displaces cellular H+ which then appears in the
plasma causing an acidosis.
2. In acidosis excess plasma H+ enters the cells and
displaces cellular K which then appears in the plasma
causing hyper kalaemia.
3. In the distal Nephron where K+ and H+ exchange for
Intralumiral Na+:
Hyper kalaemia (K+) dominate the exchange so that
K+ appears in excessive amount in the urine and H+
return to body causing Secondary Acidosis.
In acidosis the plentiful amounts of H+ dominate the
exchange and K+ is retained causing Secondary
Hyperkalaemia.
Hypo Kalaemia and Alkalosis
1. In Hypokalaemia K+ cell enter plasma and displaces
plasma H+ enter the cell causing alkalosis.
2. In Alkalosis excess cell H+ enter plasma and displaces
plasma K+ causing hypo kalaemia.
3. In distal nephorn hypo kalaemia excessive amount of
H+ appears in the urine causing Secondary
Alkalosis.
4. In Alkalosis returning H+ to compensate Alkalosis and
displacing K+ in the urine causing Secondary
Hypokalaemia.
Hyperchloraemic & Metabolic Acidosis

In the case of diarrhea, renal tubular acidosis and

Aldosteron deficiency represents the loss of
HCO3 from either the kidney (Renal-tubular
Acidosis = RTA) or the G.I tract in either case the
HCO3 is lost in exchange for Cl-, this result hyper
chloraemia and normal anion gap because each
lost in HCO3 is replaced by Cl -.
Hypochloraemic & Metabolic Alkalosis

Decrease Cl (Cl -) Frees Na from NaCl

leads to more Na come from NaHCO3
increase (HCO3 -) leading Metabolic
Alkalosis.
Cause: Loss of HCl from vomiting of pyloric
stenosis mainly.
Sodium & pH Disturbance

Na+ is the predominant cations combined with

plasma HCO3- and is the principal cation involve in
the bicarbonate buffer system.
Therefore, any fall in sodium plasma results in a fall
in the salt / acid ratio of this system, and
consequence fall in pH NaHCO3 / CO2 ratio.
 Potassium Imbalances
I. Hypo Kaleamia:
Metabolic alkalosis
Treatment of DKA with insulin
and glucose.
Antibiotic and magnesium
(Mg++) depletion.
Hypo kalemia augments the
effect of digitalis often resulting
in toxic effects.
The major effect of hypokalemia
on cardiac conduction is
prolonged depolarization
resulting in flattered T-waves.
The U-wave increases, ST
segment depression occurs with
sever hypokalemia.
 Potassium Imbalances
I. Hyper Kalemia:
The most common causes is inadequate renal
excretion
Poor vein puncture technique leads to blood cell lyses
Metabolic acidosis
Rapid transfusion of aged blood
Endogenous source of K+ over loading might be
internal bleeding with release of K+ during hemolytic of
RBC.
Hypocalcemia, hyponatreamia, acedemia, and a rapid
rise of serum K+ enhance the toxic effects of hyper
kalemia (CRF). hypernatremia and hypercalcemia
counteract the effects of hyperkalemia on the
membrane potential
That's why treatment by CaCl or Ca-gluconate. 500ml
10% glucose with 10U insulin and sodium bicarbonate
I.V to correct Acidosis.
 Potassium Imbalances
I. Hyper Kalemia (cont..):
Cardiac arrest is the most feared complication of hyper kalemia
ECG charge include peaking or tenting T-waves, prolong PR
interval and widening of the (QRS) complex
Clinical sign of cardiovascular: cardiac dysrrythmias, Brady
cardiac, complete heart block, ventricular fibrillation
 Calcium Homeostasis
In the ECF and cytosol, Ionized Calcium (Ca++) is
essential for a variety of cellular processes ionized
calcium influences cardiac contractility and
automaticity via slow calcium channels in the heart
muscle.
Calcium is important in the property of
adhesiveness that binds cells together in enzyme
activity and blood coagulation, the calcium in
plasma is in three forms:
1. Bound to proteins
(principally albumin)
2. Complexed with small
ligands (Phosphate,
citrate and Sulphate)
3. Ionized Calcium (Ca++)
Calcium Homeostasis
The ionized calcium in plasma is physiologically active and
clinically important in defining hypocalcemia and
hypercalcemia (Ca++, Ca++).
I. Reduction of pH (acidosis) will decline calcium binding,
so that more of the total serum calcium is ionized, and
less is bound to albumin in condition of acidosis.
II. Alkalosis (higher pH) less ionized Ca++ and more bound
to albumin.
Note:
Thus, signs and symptoms of hypocalemia are more
likely to occur when associated with alkalosis, but are
masked when associated with acidosis, so we have to
compare ionized Ca++ and serum calcium.
PTH secretion occurs in response to hypocalcemia and
is suppressed by hypercalcemia, excessive PTH causes:
hypercalcemia and hypophosphatemia and deficiency of
PTH cause hypocalcemia and hyperphosphatemia.
Hypophosphatemia
One of the most common causes of severs
hypophosphatemia is prolonged intensive hyper
ventilation causing respiratory alkalosis intracellular
alkalosis activates phosphofructokinase and
increases phosphorylation glucose and serum
phosphate moves into the cells to be consumed in
the process.
Hyperphosphatemia

Acidosis (Respiratory or metabolic) reduces

phosphorylation and may cause phosphates to
diffuse out of the cell, phosphate like wise released
from RBCs in hemolysis.
Note: Phosphate-binding antacids such as magnesium
hydroxide (Maalox) should never be used for the
treatment of hyperphosphatemia in patient with renal
failure because a fatal hyper magnesmia may result.
Magnesium Homeostasis

Magnesium is required for the synthesis nucleic

acid and proteins, decreasing acetylcholine
resulting in curare like, facilitates transportation of
Na, K causing secondary hypokalemia and it
influence on PTH decrease secretion causing
Hypocalcemia , so hypocalcemia can occur as a
result of hypomagnesaemia Mg++.
Hypomagnesemia
Hypocalcemia also frequently accompanies
hypomagnesemia because of magnesium deficit
interfere with the decrease of release of PTH, The
most common cause if Hypomagnesemia is
chronic alcoholism and alcoholic with drawal.
Renal transplant patients are also given
cyclosporine to prevent organ rejection; this
drug causes increased renal tubular excretion
of magnesium.
Cardiac dysrrhythmias include premature
ventricular contraction PVCs and a trial or
ventricular fibrillation ECG changes that may be
noted include prolong PR and QT intervals,
wide QRS complex flat or inverted T-waves and
ST segment depression.
Hyper Magnesemia
Almost occur due to patient with renal failure who has
ingested magnesium containing drugs (antacids Maalox)
or laxatives such as milk magnesium).
Also, administration of Mg++ to treat eclampsia (toxemia
of pregnancy) is another result for hypermagnesemia.
Mg is standard treatment for preclampsia and eclampsia
and may cause intoxication in both mother and neonate.
Mg excess suppress acetylcholine thus reducing muscle
excitability and cause hypotention by relaxing smooth
muscle and reducing vascular resistance by displacing
calcium from the vascular surface.
Treatment

Instituting peritoneal dialysis or hemodialysis

with magnesium free dialysate may be the
treatment of choice for patient with renal
failure.In patient with normal renal function
saline and furosemide to provide hydration and
promote diuresis with elimination of excess
Mg++. Calcium-gluconate (A Magnesium
Antagonist).
Summary
1. Emesis and hyper aldosteronism causing metabolic alkalosis leading
to hypo kalaemia hypo magnesium hypo chloraemia.
2. Respiratory acid-base causes only small changes in the plasma [K]
therefore if the [K] changes with PaCo2 change look for a cause other
than the simple acid-base disturbance.
3. Hyper kalaemia is due lack of oxygen (cell destruction) or lack of
insulin.
4. Hyper kalaemia and hyper chloraemia in metabolic acidosis stimulate
aldosteron release and result in loss of extra [k] in the urine.
5. K shift into cells in metabolic alkalosis but not in respiratory
alkalosis.
6. The magnitude of H+ shifting is much smaller with respiratory acid-
base disorder do not expect hypo kalaemia in patient with respiratory
alkalosis K can shift into cell during metabolic alkalosis.
7. It's important to remember that diuretics digitalis and hypo kalaemia
are potentially lethal combination.
8. Torsades de pointes due to hypo kalaemia hypo magnesium and may
be due to hypo calcaemia.