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Approach to the Patient with Shock

James W. Barr, DVM, DACVECC

Blue Pearl Veterinary Partners, Tampa, FL, USA

Shock is a clinical entity that veterinarians come into con­ diastolic filling of the heart and subsequent decrease in
tact with regularly and is defined as inadequate delivery or cardiac output. It is possible for patients to fit more than
usage of oxygen at the cellular and subcellular level. The one category and limiting classification to a single cate­
result of cellular and tissue hypoxia is the central driver of gory can lead the clinician astray. For instance, patients
the pathology of shock. Subsequently, resolving this that are septic may have shock that has characteristics of
hypoxia must be the clinician’s primary focus to effectively hypovolemic, cardiogenic, and distributive etiologies.
treat a patient in shock. Cellular hypoxia results in the fail­ In addition to categorizing etiology, shock can be char­
ure of energy‐dependent mechanisms. When cells lack acterized by severity as either compensated or decom­
the necessary energy, dysfunction of the organelles occurs pensated. The sympathetic nervous system attempts to
which ultimately results in the death of the cell. When compensate for perceived decreases in intravascular vol­
cells die, organs become dysfunctional and compensatory ume and/or blood pressure, generating some of the clini­
mechanisms meant to be protective instead exacerbate cal signs associated with shock. While the etiologies
injury and lead to the death of the organism. vary, there are commonalities in the clinical signs of
Classically, shock has been defined as lack of organ shock. The recognition of shock centers on identifying
perfusion resulting from the impaired ability of the car­ the compensatory mechanisms the patient displays in
diovascular system to deliver oxygen to the tissues of the response to decreased oxygen delivery. If a patient is in
body. This can result from many diseases, but the global the compensated phase of shock, the sympathetic nerv­
effects are similar regardless of cause. There are clinical ous system has been activated and the subsequent
situations in which the delivery of oxygen to the tissues is increases in chronotropy, inotropy, and systemic vascu­
normal or increased whilst the tissues are unable to use lar resistance (SVR) will all converge to increase oxygen
the oxygen presented to them that can lead to shock. delivery. Patients in compensated shock will often have a
This, fortunately, is not recognized often in veterinary normal blood pressure and mentation on presentation,
medicine so this chapter will focus on the failure of oxy­ but will likely have other clinical signs suggestive of
gen delivery rather than failure of oxygen utilization. shock such as tachycardia and tachypnea. If the initiating
It is often helpful to classify shock states according to cause of shock has been removed then patients in com­
their underlying etiology. This enables formation of a pensated shock may not progress further.
general treatment plan. In general, shock can be classified If the underlying etiology of shock is severe or persis­
as hypovolemic, cardiogenic, distributive, or obstructive. tent, compensatory mechanisms will be unable to restore
Hypovolemic shock occurs when intravascular volume is oxygen delivery and the patient will progress to decom­
reduced, resulting in decreased cardiac output. This can pensated shock. These animals will have profound clini­
include whole‐blood loss (hemorrhagic shock) or loss of cal signs including depressed mentation, cold extremities,
plasma volume. Cardiogenic shock is a result of poor car­ thready pulses, and hypotension. If left untreated,
diac function that reduces cardiac output. Distributive patients in decompensated shock will generally progress
shock develops from inappropriate vasodilation and to an irreversible shock state in which compensatory
decreased resistance to blood flow lowering blood pres­ mechanisms cease to function. This is termed autoregu-
sure despite normal or even increased cardiac output. latory escape and results from global vasodilation as oxy­
Obstructive shock is a result of physical impedance of gen‐starved tissues finally demand blood flow. Clinical

Clinical Small Animal Internal Medicine Volume I, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical