Dellon Durga

Acid Base Disorders.

Serum pH alone neither defines a specific disease nor specifies an appropriate therapy.
Instead, the underlying cause of the abnormality must be assessed, with the results of the
assessment providing the key to resuscitation. A patient’s acid-base status, whether
respiratory or metabolic, can only be evaluated within that patient’s clinical context.

Arterial vs. venous blood gas (ABG or VBG) analysis: In most cases, a VBG analysis serves
as an adequate surrogate for an ABG. Because the precise pH is minimally significant, the
difference between ABG and VBG rarely has a clinical consequence. The most important
therapy when treating disturbances in acid-base physiology is to identify and treat the
underlying cause.

Serum pH is a measurement of the activity of free protons in the plasma. A pH value of 7.4
corresponds to a H+ concentration of 39.8  nmol/L. The actual pH or concentration of
H+ matters far less than the underlying cause of the acid-base abnormality. Any acid-base
schema should endeavor to identify the causative factors relating to the acid-base
perturbations and then strive to correct these rather than to directly correct the pH.
Acidemia and alkalemia are direct measures of the serum H+ concentration. When the pH is
<7.35, an acidemia is present. When the pH is >7.45, an alkalemia is present.

It is a commonly held belief that acidemia negatively affects a patient’s cardiac function and
response to vasopressor agents. This dogma is based on animal models that have never been
validated in human studies. In contrast, a number of clinical trials have demonstrated that
correcting the serum pH without intervening with regard to the underlying problem does not
correct the hemodynamic dysfunction. Instead, it is likely that the cause of the cardiac
dysfunction and vasopressor resistance in the animal model studies was actually the
underlying disease leading to the acidosis in question.

Acidosis and alkalosis are used to define the type of physiological processes that are
occurring within the patient. Attempts to determine whether these are primary or secondary
processes will not be emphasized, because they tend to be neither clinically helpful nor
accurate. For example, a patient presents with a metabolic acidosis secondary to DKA. Blood
gas analysis reveals that he also has a decreased partial pressure of CO2 (pCO2). The
traditional approach would state that this is a compensatory process secondary to the DKA.
The traditional approach would then require clinicians to determine whether the patient is
appropriately compensating using Winter’s Formula. Typically, such processes are
cumbersome, confusing, and, more importantly, inaccurate, and do not aid clinical decision-
making. Clinicians do not intubate a patient secondary to the results of the Winter’s Formula
but rather based on the patient’s actual appearance.
CO2, while not an acid itself, functions as one through the formation of carbonic acid: CO2 +
H2O ⇄ H2CO3 ⇄ H+ + HCO3−

It is important to know a patient’s pCO2 to aid in our understanding of his/her current

respiratory function and how the patient is handling his/her metabolic demand. The typical
assumption is that the pCO2 will guide therapy (eg, intubation or non-invasive ventilation
[NIV]). However, this assumption is not always valid. Studies have failed to determine an
association between pH and/or pCO2 and the patient’s need for NIV or intubation, or the
patient’s mortality. Hence, it is important to place the patient’s pCO2 in its proper clinical
context, and medical decisions should not be made based on this value alone.

Respiratory alkalosis represents a state in which ventilation outpaces CO2 production. This

state typically occurs when an alternative process is driving the patient’s respiratory rate. For
example:

 Metabolic acidosis.
 Disease processes that lead to a hypoxic respiratory drive, increasing the patient’s
ventilation with no increase in CO2 production.
 Anxiety attack.
 Typically, respiratory alkalosis is associated with noticeable tachypnea, and it is the
clinician’s responsibility to identify the underlying cause of this increased respiratory
rate rather than directly trying to decrease the minute ventilation or balance the pH.

Most cases of respiratory acidosis fall into one of two categories:

“Won’t breathe”
 Respiratory mechanics are intact but the patient has lost his/her central drive to
maintain CO2 hemostasis.
 Patients presenting with an opioid overdose are the classic example of “won’t
breathe.” A key component of the opioid toxidrome is suppression of the central
respiratory drive. Patients no longer respond appropriately to an increasing pCO2.

“Can’t breathe”
 Central respiratory drive is intact but the patient’s work of breathing has outpaced the
patient’s ability to maintain CO2 hemostasis.
 These cases can be divided into:
o Increased CO2 production (eg, DKA, salicylate intoxication, sepsis).
o Increased work of breathing (eg, asthma, pneumonia, acute respiratory distress
syndrome).
o A decrease in the patient’s ability to manage the respiratory workload (eg,
neuromuscular disorders, muscular atrophy
Metabolic acidosis occurs in one of two ways: an increase in the chloride anion in relation to
the sodium cation. An increase in the “unmeasured anions” (AG) in relation to sodium.
Metabolic alkalosis occurs in one of two ways: A decrease in the chloride anion in relation to
the sodium cation. A decrease in the “unmeasured anions” in relation to sodium.

AG = [Na+] − ([Cl−] + [HCO3−]), which quantifies the role of other unmeasured anions with
respect to a patient’s acid-base status. Low AG value: Alkalosis. Typically due to a decrease
in albumin. Often seen in patients with chronic malnutrition. Also seen in processes with
unmeasured cations (eg, lithium ingestion or multiple myeloma).

High AG value. AG values greater than normal will be filled by an unmeasured anion. Most
of these cases are due to a serious underlying pathology. Clinicians should seek to identify all
of the anions that fill the gap as well as the underlying cause of the elevated AG value.
 V/Q Mismatch

Oxygenation is the process of oxygen diffusing passively from the alveolus to the pulmonary
capillary, where it binds to hemoglobin in red blood cells or dissolves into the plasma.
Insufficient oxygenation is termed hypoxemia. This is to be differentiated from hypoxia,
which is an abnormally low oxygen content in a tissue or organ.

Arterial oxygen saturation (SpO2 and SaO2) — SaO2 is a direct measurement of the

percent of oxyhemoglobin (oxygen saturated hemoglobin) in the blood using lab tests on
arterial blood while SpO2 is a noninvasive measurement of the percent of saturated
hemoglobin in the capillary bed using co-oximetry with a pulse oximeter.

Arterial oxygen tension (PaO2) — A small amount of the oxygen that diffuses from the
alveolus to the pulmonary capillary dissolves into the plasma. The arterial oxygen tension
(PaO2) is the amount of oxygen dissolved in the plasma, which is measured by arterial blood
gas. Similar to oxygen saturation, an abnormal PaO2 has not been precisely defined because a
threshold below which tissue hypoxia predictably occurs has not been identified. However, it
seems reasonable to consider a PaO2 <80 mmHg abnormal, although the value should not be
considered in isolation

A-a oxygen gradient — The alveolar to arterial (A-a) oxygen gradient is a common measure
of oxygenation ("A" denotes alveolar and "a" denotes arterial oxygenation). It is the
difference between the amount of the oxygen in the alveoli (ie, the alveolar oxygen tension
[PAO2]) and the amount of oxygen dissolved in the plasma (PaO2) 

A-a oxygen gradient = PAO2 - PaO2

Hypoxemia does not necessarily indicate tissue hypoxia. It can be caused by hypoventilation,
ventilation-perfusion mismatch, right-to-left shunt, diffusion impairment, reduced inspired
oxygen tension, genetic disorders of hemoglobin oxygen affinity, and other hemoglobin
issues which affect oxygen delivery.

V/Q mismatch — Ventilation-perfusion (V/Q) mismatch refers to an imbalance of blood

flow and ventilation. It causes the composition of alveolar gas to vary among lung regions:

●Lung regions with low ventilation compared to perfusion will have a low alveolar oxygen
content and high CO2 content

●Lung regions with high ventilation compared to perfusion will have a low CO2 content and
high oxygen content

In the normal lung, there is V/Q mismatch because perfusion and ventilation are
heterogeneous. Both ventilation and perfusion are greater in the bases than in the apices
(when in an upright position). However, the difference between apical and basilar ventilation
is smaller than the difference between apical and basilar perfusion. As a result, the V/Q ratio
is higher in the apices than in the bases. V/Q mismatch is responsible for the normal
physiologic occurring A-a gradient.
In the diseased lung, V/Q mismatch increases because heterogeneity of both ventilation and
perfusion worsen. The net effect is hypoxemia. Hypoxemia due to V/Q mismatch can be
corrected with low to moderate flow supplemental oxygen and is characterized by an
increased A-a gradient. Common causes of hypoxemia due to V/Q mismatch include
obstructive lung diseases, pulmonary vascular diseases, and interstitial diseases.