Page 443 - Clinical Small Animal Internal Medicine

41 Approach to the Patient with Shock 411

Lactate
Box 41.1 Endpoints of resuscitation. Each of these
VetBooks.ir values must be interpreted within the clinical context Because lactate is a byproduct of anaerobic metabolism,
as improvement in an isolated variable may not
has a relatively short half‐life and can be measured read­
indicate complete resolution of shock
ily, it is a very useful biomarker for shock. Lactate meas­
urement is an inexpensive adjunct to traditional physical
Normalization of heart rate
● exam endpoints and its use has become standard of care
Normalization of respiratory rate
● in human medicine.
Improvement of pulse quality
● In most cases, elevations in lactate occur secondary to
Normalization of capillary refill time
● anaerobic metabolism, so by measuring the concentra­
Blood pressure
● tion of lactate in a blood sample, the clinician can form
Improvement of blood lactate concentration
●
an idea of whether or not anaerobic metabolism is occur­
● ScvO 2
ring. Occasionally, neoplastic or endocrine diseases can
cause the production of lactate to be higher than the
body’s ability to metabolize it, leading to elevation of
include physical exam findings or biochemical variables blood lactate concentration. Similarly, significant liver
(Box 41.1). These should be evaluated before, during, disease or liver failure can reduce lactate clearance and
and after therapy has been instituted. lead to hyperlactatemia. When lactate is elevated due to
Normalization of heart rate, respiratory rate, and causes other than anaerobic metabolism, it is termed
CRT as well as improvement of pulse quality have been type B hyperlactatemia. Occasionally, strenuous exercise
traditionally used by clinicians to judge if resuscitation can cause hyperlactatemia. This appears clinically in
is complete. These endpoints are intuitive because patients with prolonged seizures or patients that require
they coincide with the findings that are initially used to aggressive restraint during examination or blood collec­
determine if a patient is in shock. It follows that when tion. These possibilities should be considered when a
those findings normalize, resolution of shock has been patient has a high blood lactate concentration but no
achieved. The reality is more complex as physical exam other clinical signs that would indicate the presence of
endpoints can normalize while inadequate oxygen shock. This is an uncommon occurrence in veterinary
delivery is ongoing at the cellular and subcellular level. medicine and an animal presented in shock with blood
Therefore, the use of endpoints that include evaluation lactate elevation should be assumed to have inadequate
of cellular oxygen usage such as lactate, base excess, oxygen delivery until proven otherwise.
and hemoglobin saturation should be incorporated The finding of elevated lactate alone does not neces­
into all shock treatment plans. In practice, resuscita­ sarily mean that global oxygen delivery is inadequate as
tion should continue until there is resolution of the local perfusion abnormalities can have significant impact
physical exam endpoints, at which time analysis of the on lactate concentration. Although absolute lactate con­
biochemical endpoints should be performed. If those centration can be correlated with patient outcomes, lac­
endpoints have been reached then resuscitation is tate clearance following resuscitative efforts is probably a
complete; if biochemical derangements persist then better prognostic indicator and patients with persistently
resuscitation efforts should continue until resolution is elevated lactate concentrations despite aggressive treat­
achieved. ment should be considered to have a worse prognosis. As
with all resuscitation endpoints, the results of lactate
measurement must be interpreted in light of the patient’s
Blood Pressure clinical condition.
Blood pressure can be measured in a variety of ways but
is most commonly performed using a Doppler with
sphygmomanometer or a digital monitor with oscilllo­ Mixed Venous or Central Venous Oxygen Saturation
metric capability. Unfortunately, blood pressure is an Measurement of venous hemoglobin saturation can pro­
unreliable predictor of perfusion as it is influenced by the vide meaningful insight into the consumption of oxygen
compensatory mechanisms previously discussed. In fact, within the body. The hemoglobin saturation of venous
a patient can have significant microcirculatory hypoper­ blood is expected to be lower than that of arterial blood.
fusion while maintaining normal blood pressure. If this difference is greater than expected, it may indicate
However, hypotension does occur as shock progresses that oxygen‐starved tissues are removing more oxygen
and when present should be aggressively treated with a than usual from each hemoglobin molecule. This is best
target of returning the systolic blood pressure to at least explained by the oxygen extraction ratio (OER), which is
90 mmHg and MAP to 60 mmHg. simply the mathematical ratio of the amount of oxygen