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Lactate is a byproduct of glycolosis, which is an anaerobic glucose metabolism occurring in the cellular cytoplasm.  Pyruvate is also generated through glycolosis and is broken down through the Krebs cycle to create energy (Sharma 2007).  The liver’s lactate to glucose conversion ability decreases when there are elevated blood levels of lactose (Sharma 2007).   Once the liver can no longer maintain the lactate to glucose conversion, acidosis begins. With adequate oxygen, adenosine triphosphate (ATP) metabolites are recycled and cytosolic lactate concentration increases without acidosis (Sharma 2007).  Hypoxia prompts cells to utilize anaerobic energy to create ATP resulting in lactate and hydrogen (Sharma 2007).  Sepsis accounts for most cases of lactic acidosis (Sharma 2007).

Arterial blood gasses need to be drawn in order to identify the current condition of our patient as well as a full assessment.  Continued monitoring would be warranted during critical states of illness.  Signs of impaired tissue perfusion consist of hypotension, peripheral vasoconstriction, and oliguria (Sharma 2007).  Signs of septic shock include tachypnia, hypotension, and decreased mental status (Sharma 2007). The appropriate treatment for this patient is to treat the underlying cause of the acidosis, in other words, treat the pneumonia.  In the case of lactic acidosis, sodium bicarbonate may be given to balance the pH.  ABG and patient monitoring are necessary to ensure appropriate treatment is being administered.

SIRS, Sepsis, and Lactic Acidosis

Our patient, who has symptoms indicative of pneumonia, is at a risk to develop a pH disturbance.  Respiratory acidosis may result from the lung infection or lactic acidosis may develop in response to septic shock.

            The balance of acids and bases are important in the human body.  The power of hydrogen (pH) is how we measure the acid base balance. A higher pH reading is less acidic than a lower pH reading (Huether & McCance, 2008).  PH is balanced in several ways by our bodies and measured in the blood.  The main organs that regulate blood pH are the lungs and kidneys according to T.L.Bland (personal communication, Feb.13, 2008).

            The body’s normal metabolism generates acids, which require elimination in order to maintain normal pH.  An imbalance may result in acidosis, when the pH is less than 7.35, or alkalosis when the pH is greater than 7.45.  The lungs respond accordingly by retaining carbon dioxide (CO2) if the alkalosis occurs or breathing out more CO2 if acidosis occurs.  The kidneys respond to ph changes with bicarbonate which is a base that increases the pH or the kidneys give off acids in the urine if the pH is acidic.  The compensatory lungs improve results in minutes while the kidney compensatory mechanism requires hours to days although both responses may occur simultaneously (http://labtestsonline.org/understanding/conditions/acidosis.html). 

            Acid base disorders are divided into acidosis (low pH) or alkalosis (high pH).  The disorders are identified as respiratory or metabolic according to the factor that has changed.  For example CO2 concentration changes indicate respiratory while bicarbonate concentration (HCO3-) changes indicate metabolic changes.   The respiratory and metabolic entities may compensate each other in order for the body to work in harmony (http://labtestsonline.org/understanding/conditions/acidosis.html).

            According to T.L. Bland, the arterial blood gasses (ABG’s) respond to severe pneumonia with low pH resulting in acidosis with slightly elevated HCO3 and partial pressure of CO2 in arterial blood (Paco2) when tissue hypoxia is severe enough to produce lactic acid.  Lactic acidosis can also occur with septic shock (Huether & McCance 2008). Tissue hypoxia results when the body’s demand for oxygen is higher than the supply.  Anaerobic metabolism creates lactic acid build up resulting in lactic acidosis.

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Looking at SIRS more specifically, there are four key response mediators at work - neutrophils, macrophages, platelets, and endothelial cells. Some are working directly on platelet aggregation; others are stimulated to produce the chemical mediators.  There are five sub-groups of these chemical mediators, cytokines, plasma enzyme cascades, lipid mediators; toxic oxygen related mediators, and two unclassified mediators, nitric oxide and proteases. In a synergistic effort to fight the triggering mechanism, our body mounts a hormonal response as well. The stress hormones catecholamines, glucagon, cortisol and growth hormone are released along with suppression of the thyroid gland and a hormonal suppression of the fluid electrolyte and balances (Kleinpell and Burns 2007).

Sepsis is a manifestation of SIRS in the presence of a known infection, usually bacterial in nature (Pugin 2008). Each year approximately 215,000 deaths are reported due to severe sepsis.  It is also associated with a mortality rate of 28%-50%. Annually, it is estimated that cost of treating patients with sepsis is about 16 billion dollars yearly just in the US.  Risk factors for sepsis include extremes of age, surgical or invasive procedures, malnutrition, and use of broad-spectrum antibiotics, chronic illness, immune deficiency disorders and increasing numbers of drug resistant microorganisms (Kleinpell 2003).

As a manifestation of SIRS, sepsis has a continuation of the systemic exposure of the pro-inflammatory cytokines. This can overwhelm the actions of the anti-inflammatory cytokines. Excessive systemic inflammation occurs, leading to impaired tissue function and organ damage. The pro-inflammatory cytokines (interleukin and tumor necrosis factor-?) that are now being produced without regulation by the anti-inflammatory cytokines stimulate the release of tissue factor, a cell surface glycoprotein produced by the monocytes and endothelial cells. This action triggers the coagulation pathway (Kleinpell 2003), which can lead to DIC.