DEFINITIONS: ACID, BASE, BUFFER

Acid - a substance that can yield a hydrogen ion or hydronium ion when
dissolved in water
Base - a substance that can yield hydroxyl ion
Dissociation constant - e strengths of acids and bases, their ability to
dissociate in water
pK - negaive log of the ionization constant is also the pH in which the
protonated and unprotonated forms are present in equal concentrations
Strong acids - pK values of less than 3.0
Strong bases - pK values greater than 9.0
Buffer - combination of a weak acid (e.g. carbonic acid - H 2CO3) or weak base
(HCO3) and its salt, is a system that resists changes in pH

ACID-BASE BALANCE
Maintenance of Hydrogen

Normal concentration of H - 3644 nmol/L (pH, 7.347.44)

The body controls and excretes H through exquisite mechanisms that involve
the lungs and kidneys
Increase in H concentration decreases the pH
Decrease in H concentration increases the pH
Acidosis - pH below the reference range (less than 7.34)
Alkalosis - pH above the reference range (greater than 7.44)

Buffer Systems: Regulation of H

First line of defense against extreme changes in H concentration

When acid is added to the bicarbonatecarbonic acid system, the HCO3 will
combine with the H from the acid to form H2CO3
When a base is added, H2CO3 will combine with the OH group to form
H2O and HCO3
Why Bicarbonate-Carbonic Acid System is still an Important Buffer:
o H2CO3 dissociates into CO2and H2O, allowing CO to be eliminated by the
lungs and H as water
o changes in CO2modify the ventilation rate
o HCO3 concentration can be altered by the kidneys
o Immediately counters the effects of fixed nonvolatile acids by binding
the dissociated hydrogen ion
Other Buffers:
o Hpo4 H2PO4 - plays a role in plasma and red blood cells and is
involved in the exchange of sodium ion in the urine H filtrate
HendersonHasselbalch equation:
o Depicts or shows the interrelationship of the lungs and kidneys in
maintaining pH
o Numerator (HCO3) Kidney function
o Denominator (pCO2 which represents H2CO3) Lung function

Regulation of Acid-Base Balance: Lungs and Kidneys

Carbon dioxide end product of most aerobic metabolic processes

Dissociation of H2CO3 = increase HCO3 concentration
LUNGS:
o Process:
Inspired O2 is bound to haemoglobin form oxyhemglobin
H which is carried on haemoglobin in venous blood is released
to recombine with HCO3 and forms H2CO3
H2CO3 dissociates into H2O and CO2
CO2 is eliminated through ventilation
o Decreased Ventilation or Disease - lungs do not remove CO2 at the
rate of its production which causes H concentration increases
o Hyperventilation faster release of CO2 than production which
causes decrease H concentration
Kidneys:
o Excrete variable amounts of acid or base
o Main role in maintaining acid-base homeostasis is to reclaim HCO 3
o proximal tubules main site of HCO3 reclamation
o Process:
Na in the glomerular filtrate is exchanged for H in the tubular
cell
H combines with HCO3 in the filtrate to form H2CO3
H2CO3 dissociates into H2O and CO2 by carbonic anhydrase
CO2 diffuses into the tubule and reacts with H2O to reform
H2CO3 and then HCO3
HCO3 is reabsorbed in the blood along with Na
In Alkalotic condition the kidney excretes HCO3
o The body produces a net excess of 50100 mmol/L of acid each day
o blood or plasma HCO3 level is higher than 2630 mmol/L, HCO3 will be
excreted

ASSESSMENT OF ACID-BASE HOMEOSTASIS

The Bicarbonate Buffering System

Also referred as an open system

In this buffer system the dissolved CO2 (dCO2) is in equilibrium with CO2 gas
dCO2 controlled by the lungs, it is the respiratory component
Lungs - participate rapidly in the regulation of blood pH through
hypoventilation or hyperventilation
Kidneys (formerly known as metabolic component) controls
concentration of HCO3

Henderson-Hasselbalch Equation

A is proton acceptor, or base (e.g. HCO 3)

HA is proton donor, or weak acid (e.g. H2CO3)
pK is pH at which there is an equal concentration of protonated and un
protonated species
pK of the bicarbonate buffering system is 6.1. (Body Temp)
H2CO3 & CO2 equilibrium: 1:800

Acid-Base Disorders: Acidosis and Alkalosis

Acidemia Blood pH is less than the reference range, it reflects excess acid
Alkalemia - pH greater than the reference range, reflects an excess of base
Primary Respiratory Acidosis or Alkalosis - a disorder caused by
ventilatory dysfunction
Nonrespiratory Disorder (formerly known Metabolic Acidosis or
Alkalosis) disorder resulting from a change in the bicarbonate level
Compensation
o restoration of acid-base homeostasis whenever an imbalance occurs
o It is accomplish by altering the factor not primarilyaffected by the
pathologic process
o Imbalance is of Nonrespiratory Origin - body compensates by
altering ventilation
o Disturbances of the Respiratory Component - kidneys
compensate by selectively excreting or reabsorbing anions and cations
o Compensation of the Lungs - compensate immediately, but the
response is short term and often incomplete
o Compensation of the Kidney - slower to respond (24 days),
however, but the response is long term and potentially complete
o Fully Compensated pH has returned ti the normal range (20:1)
o Partially Compensated - pH is approaching normal

Acidosis

Primary Nonrespiratory Acidosis there is a decrease in bicarbonate (24

mmol/L), resulting in a decreased pH
o May be caused by the direct administration of an acid-producing
substance (e.g. ammonium chloride, calcium chloride) or by excessive
formation of organic acids
o also seen with reduced excretion of acids (renal tubular acidosis)
o Excessive loss of bicarbonate from diarrhea or drainage from a biliary,
pancreatic, or intestinal fistula

Compensation mechanism: hyperventilation (an increase in the rate

or depth of breathing)
Primary respiratory acidosis - results from a decrease in alveolar
ventilation (hypoventilation),causing a decreased elimination of CO 2 by the
lungs
o May be seen in patients with COPD & bronchopneumonia
o Also seen in drugs that causes hypoventilation (e.g. arbiturates,
morphine, or alcohol)
o Seen in decreased cardiac output (congestive heart failure)
o Compensation occurs through nonrespiratory processes:
Kidney increase excretion of H and reclamation of HCO 3
Takes days or weeks for maximal compensation occur
Primary Nonrespiratory Alkalosis - results from a gain in HCO3, causing
an increase in the nonrespiratory component and pH
o Result from the excess administration of sodium bicarbonate or
ingestion of bicarbonate-producing salts
o Excessive loss of acid through vomiting, nasogastric suctioning, or
prolonged use of diuretics
o Compensation: hypoventilation
Primary respiratory alkalosis - excessive elimination of CO2 by the lungs
o Causes:
Hypoxia
Chemical Stimulation of the respiratory center by drugs
Increase in the environmental temperature
Fever, hysteria (hyperventilation)
Pulmonary emboli
Pulmonary fibrosis
o Compensation: excretion of HCO3 in the urine and reclaiming H to
the blood by the kidney
o

OXYGEN AND GAS EXCHANGE

Oxygen and Carbon Dioxide

Evaluation of a patients oxygen status is possible using the partial pressure

of oxygen (pO2) measured along with pH and pCO2 in the blood gas analysis
Requirement for Adequate Tissue Oxygenation:
o available atmospheric oxygen
o adequate ventilation
o gas exchange between the lungs and arterial blood
o loading of O2 onto haemoglobin
o adequate haemoglobin
o adequate transport (cardiac output)
o release of O2 to the tissue
Dead Space Air air retained from the previously expired breath, which are
found in the airways, it dilutes the air being inspired
pO2 in the alveoli - averages is about 110 mm Hg
Factors that Influence pO2 in the Alveoli:

Fraction of Inspired Oxygen (FiO2) percentage of O2 in the

inspired air
o Amount of pCO2 in the expired air dilutes the inspired air
o The ratio of the volume of inspired air to the volume of the dead space
air
Factors Influence the Amount of O2
o Destruction of the alveoli
o Pulmonary edema
o Airway blockage
o Inadequate blood supply
o Diffusion of CO2 and O2
o

Oxygen Transport

Hemoglobin transports most of O2

1 Adult haemoglobin can combine with 4 molecules of O2
Factors that Affects the Total Amount of O2 Loaded to Hemoglobin:
o The concentration and type(s) of hemoglobin present
o The presence of interfering substances
o The pH & temperature of the blood
o The levels of pCO2 and 2,3-diphosphoglycerate (2,3-DPG)
Blood Hemoglobin Exists in 1 of 4 Conditions:
o Oxyhemoglobin O2 bound to hemoglobin
o Deoxyhemoglobin haemoglobin not bound to O2
o Carboxyhemoglobin haemoglobin bound to CO2
o Methemoglobin haemoglobin unable to bind O2 because iron is in
an oxidized rather than reduced state

Quantities Associated With Assessing a Patients Oxygen Status

Four
o
o
o

Parameters Used to Assess Oxygen Status:

Oxygen saturation (SO2)
Fractional (percent) oxyhemoglobin (Fo2Hb)
Trends in oxygen saturation assessed by transcutaneous, pulse
oximetry (SpO2) assessments
o Amount of O2 dissolved in plasma (pO2)
Oxygen saturation
o represents the ratio of O2 that is bound to the haemoglobin, compared
with the total amount of hemoglobin capable of binding O 2
Fractional (or percent) oxyhemoglobin

o
o

Ratio of the concentration of oxyhemoglobin to the concentration of

total hemoglobin (ctHb)
cdysHb - represents hemoglobin derivatives that cannot reversibly
bind with O2 but are still part of the total hemoglobin measurement

Partial Pressure of Oxygen Dissolved in Plasma (pO2) - accounts for

little of the bodys O2 stores
o Normal Range: 90 to 95 mm Hg
Pulse Oximetry
o These devices pass light of two or more wavelengths through the
tissue in the capillary bed of the toe, finger, or ear
Hemoglobin Oxygen (Binding) Capacity - maximum amount of O2 that
can be carried by hemoglobin in a given quantity of blood
Oxygen Content - total O2in blood and is the sum of the O 2 bound to
haemoglobin and the amount dissolved in the plasma

HemoglobinOxygen Dissociation

increased H concentration and pCO2 levels = change in the molecular

configuration of O2Hb (facilitating O2 release)
If O2 tension is below 60 mm Hg O2 is released rapidly from haemoglobin
Factors Affecting the Affinity of O2:
o Hydrogen ion activity
o pCO2 and CO levels
o Body temperature
o 2,3-DPG
Oxidative metabolism increases the Following: (Causes right shift of
the dissociation curve)
o Temperature
o H,Co2 and 2,3-DPG concentration
Decreased Affinity of Hemoglobin promotes release of Oxygen
In the Lungs temperature, H, pCO2, and 2,3-DPG decrease relative
tissue level (shifting the oxygen-dissociation curve slightly to the left which
enhances O2 binding to hemoglobin)
chains of the Hemoglobin bind 2,3-DPG = dissociation of
Oxyhemoglobin causing shifts to the right, it causes subsequent
enhancement of oxygen release
Dyshemoglobins (COHb or MetHb) - can also affect oxyhemoglobin
dissociation
Elevation of CO shifts the curve to the left