May 2025

In this VETgirl online veterinary continuing education blog, Lexi Dickens, BS, LVT, RVT, VTS (ECC), reviews shock in veterinary medicine.  In Part 1, we focus on the pathophysiology, stages, and types of shock. This is a two-part blog, so make sure to check out Part 2 HERE for more on emergency and critical care!

By Lexi Dickens, BS, LVT, RVT, VTS (ECC)
Senior Patient Care Training Coordinator, BluePearl Pet Hospital, Cary, NC

Understanding Shock, Part 1

Shock can be defined as an inadequate delivery of oxygen (DO2) to maintain cellular energy production. This can be the result of a variety of causes including but not limited to decreased perfusion or a lack of oxygen supply.1-4 The body requires appropriate perfusion and oxygen delivery to tissues to fulfill and maintain normal function.

Pathophysiology

To understand how the body compensates while in a state of shock, we must first understand how it maintains hemostasis under normal circumstances. The “tree of life”, a metaphorical example of the heart’s vascular system, focuses on many of the mechanisms that provide perfusion and oxygen to tissues throughout the body. 3, 4

The first aspect of the tree of life is DO2 = CaO2 x CO with DO2 representing the amount of oxygen delivered to the tissues each minute, CaO2 representing oxygen content of arterial blood, and CO representing cardiac output.2, 3 CaO2 is determined by three values: hemoglobin (Hb), oxygen saturation of arterial blood (SaO2), and the partial pressure of oxygen in arterial blood (PaO2).3,4 Cardiac output is further explained with CO = HR x SV, where HR represents heart rate and SV represents stroke volume, or the volume of blood that is pumped with each beat.2 Stroke volume is determined by preload, the stretch of the left ventricle wall caused by filling of the ventricle just before it contracts, afterload, the resistance the heart must overcome to expel the blood from the ventricle into systemic circulation, and contractility, the ability of the myocardium to contract adequately.

Another important factor in the “tree of life,” which includes cardiac output, is the equation MAP= CO x SVR, with MAP representing mean arterial pressure, and SVR representing systemic vascular resistance.3, 4 SVR is the overall resistance of the arterioles that the heart must pump against.

 

The “tree of life” explains how the body compensates in a state of imbalance. For example, it is common to see tachycardia when a patient is hypovolemic, such as with severe dehydration or hemorrhage. That can be explained with the equation CO= HR x SV; for example, the body is sympathetically increasing heart rate to increase CO. The SV is decreased in hypovolemia, which will cause the HR to increase in an effort to maintain CO.

Stages of Shock

Clinical presentation of a patient can vary based on what stage of shock they are in. Shock can be broken into three phases: compensatory, early decompensatory, and late decompensatory.2, 3

Types of Shock

Shock is a secondary disorder trigged by an internal or external factor and can be categorized based on etiology. There are multiple classifications, with some being more prevalent in veterinary patients.

  • Hypovolemic shock is the most common type of shock seen in small animal veterinary patients. The cause is a decrease in circulating intravascular volume due to a severe loss such as hemorrhage (e.g., hemoabdomen), third spacing (e.g., ascites), burns, or severe gastrointestinal losses secondary to persistent vomiting or diarrhea. Patients with hypovolemic shock have a significantly decreased preload or stroke volume, resulting in a decrease in cardiac output.1, 2, 4 Clinical signs for a patient with decreased perfusion can include hypotension, tachycardia, weak pulses, pale mucous membranes, and cold extremities.1
  • Obstructive and Distributive shock are similar in the fact that there is an adequate circulating volume as well as a maldistribution of blood volume; however, they have different etiologies. In obstructive shock, there is a physical obstruction stopping appropriate volume distribution. Some common causes can be gastric dilatation volvulus (GDV), feline aortic thromboembolism (FATE), gastric torsion, or caval syndrome. Distributive shock occurs when there is inappropriate systemic vasodilation and decreased vascular resistance resulting in pooling of blood and decreased cardiac output. Common causes of this can be SIRS, sepsis, or excessive catecholamine release.1, 2 Clinical presentation is often similar to that of hypovolemic shock; however there will also be clinical signs specific to the primary disorder (e.g., a distended abdomen and unproductive retching with GDV).
  • Cardiogenic shock is most simply explained as pump failure. The heart does not have appropriate mechanical function and cannot produce appropriate cardiac output to maintain perfusion and oxygen delivery.2,6 This can be caused by congestive heart failure, arrhythmias, or abnormalities of the heart such a valvular disease or cardiomyopathies like dilated cardiomyopathy (DCM) or hypertrophic cardiomyopathy (HCM). Less commonly medications that decrease contractility in excessive doses can cause cardiogenic shock.1 Clinical presentation for these patients can be different than other forms of shock as they often present with signs of congestive heart failure such as dyspnea, pulmonary edema, and muddy or cyanotic mucous membranes.2, 6

Next week, tune back in for part 2 of this blog, where we’ll focus specifically on treatment of shock.

Abbreviations

CaCO2: oxygen content of arterial blood
CO: cardia output
DCM: dilated cardiomyopathy
DIC: disseminated intravascular coagulation
DO2: oxygen delivery
FATE: feline aortic thromboembolism
GDV: gastric dilatation volvulus
Hb: hemoglobin
HCM: hypertrophic cardiomyopathy
HR: heart rate
MAP: mean arterial pressure
PaO2: partial pressure of oxygen in arterial blood
RAAS: renin-angiotensin-aldosterone system
SaO2: oxygen saturation of arterial blood
SIRS: systemic inflammatory response syndrome
SNS: sympathetic nervous system
SV: stroke volume
SVR: systemic vascular resistance
VO2: oxygen consumption

References

  1. Laforcade, A., & Silverstein, D. C. Shock. In Small Animal Critical Care Medicine (2nd ed), 26–30. Wiley; 2015.
  2. Arenth, J., Norkus, C. Shock and Initial Stabilization. In Veterinary Technician’s Manual for Small Animal Emergency and Critical Care (2nd ed), 17-34. Wiley; 2019.
  3. Cooper, E. (2018). Pathophysiology of Shock. In Textbook of Small Animal Emergency Medicine (eds K.J. Drobatz, K. Hopper, E. Rozanski and D.C. Silverstein); 2016. https://doi.org/10.1002/9781119028994.ch152
  4. Kuo, K., & Palmer, L. Pathophysiology of hemorrhagic shock. J Vet Emerg and Crit Care, 32(S1), 22-31; 2022. https://doi.org/10.1111/vec.13126
  5. Cooper, Edward. Hypotension. In Small Animal Critical Care Medicine (2nd ed), 46-50. Wiley; 2015.
  6. Brown, A., Madell, Cardiogenic Shock. In Small Animal Critical Care Medicine (2nd ed), 210-225. Wiley; 2015.

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