Page 572 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

560 FLUID THERAPY

TABLE 23-2 Circulatory Shock—Categorization

Mechanism Cardiac Output Blood Volume Systemic Vascular Resistance Capillary Flow
Hypovolemia Decreased Decreased Increased Decreased
Cardiogenic Decreased Normal/increased Increased Decreased
Distributive Increased Normal/increased Decreased Decreased
Note in clinical medicine, patients commonly have more than one mechanism of circulatory shock occurring simultaneously.

blood volume and maximize perfusion of vital organs 4. Tachycardia as part of the sympathetic, compensatory
during the acute insult. Tachycardia and increases in response.
systemic vascular resistance will contribute to the mainte­ 5. Poor pulse quality due to vasoconstriction and
nance of a normal MAP in the face of volume loss (see decreased stroke volume.
Figure 23-1). 41,53,124 This phase is also known as compen­ 6. Decreased extremity temperature compared with
satory shock. There does appear to be some species the core body temperature as a result of peripheral
variability in the nature of the hemodynamic responses to vasoconstriction.
circulatory shock. In the dog it has been reported that there Moderate, normotensive hemorrhage in experimental
is little change in left ventricular contractility in association dogs occurs with the loss of less than 30% of blood
60
with the increase in sympathetic tone. In addition plasma volume. As the degree of hemorrhage increases there is
epinephrine is not elevated during this normotensive hem­ a precipitous decrease in MAP and heart rate. In experi­
orrhage in dogs. 39 mental dog studies, this usually occurs when following
The renin-angiotensin system (RAS) is also stimulated the removal or loss 30% of blood volume. This hypoten­
by hemorrhage and the associated decrease in cardiac out­ sive phase is associated with central inhibition of sympa­
put. Renin release will be activated by the increase in sym­ thetic outflow and the animals cannot be salvaged despite
pathetic tone occurring as part of the baroreceptor administration of the shed blood and additional volume
response. In addition the afferent arteriole of the kidney support. 41,124 This is also known as decompensated or
is itself a baroreceptor and may sense the decrease in irreversible shock. Although decompensated shock is
ECV directly. Plasma renin cleaves the plasma protein marked by bradycardia, the hypotension is independent
angiotensinogen, generating angiotensin I. Angiotensin of the bradycardia because it does not improve with atro­
I is rapidly converted to angiotensin II by angiotensin pine-induced tachycardia. The activity of the RAS
converting enzyme, which is present in the endothelium continues to increase during hypotensive hemorrhage.
of the lung. Angiotensin II is one of the most potent In some species, including cats, rabbits, and rats, there
vasoconstrictors of the body contributing to increases in is evidence that the sympathoinhibition seen with severe
systemic vascular resistance. Angiotensin II also stimulates hemorrhage is stimulated by cardiac or cardiopulmonary
the release of aldosterone. Both angiotensin II and aldo­ receptors and transmitted via the vagus nerve. 41 In con­
sterone stimulate renal sodium retention in an effort to trast there is no apparent role of cardiopulmonary
augment blood volume (see Chapter 3). 11,55 As men­ receptors in the generation of sympathoinhibition in
tioned above, carotid sinus baroreceptor off-loading also dogs, the cause of the failure of sympathetic-mediated
stimulates the release of vasopressin (antidiuretic vasoconstriction in uncompensated shock in dogs is cur­
hormone) from the hypothalamus, which causes vasocon­ rently unknown. 129 Additionally, there may be a relative
striction and renal water conservation. Baroreceptor vasopressin deficiency following prolonged shock states,
responses mediate changes on a minute-to-minute basis further exacerbating the hypotension. 40,78 Cardiac out­
and are vital to surviving an acute injury or insult. put and arterial blood pressure fall to zero with loss of
The RAS responses take 10 minutes to an hour to have 35% to 45% of total blood volume and is rapidly fatal. 53
benefit and are more important in attempting to return The clinical hallmark of decompensated shock is bra­
the system back to the preinjury state and recovery. 53 dycardia and for this reason bradycardia (not due to con­
The pathophysiology above explains the six classic duction disturbances) may be a poor prognostic indicator
clinical signs of hypovolemic shock. in canine patients presenting in circulatory shock. In con­
1. Decreased mentation due to inadequate perfusion of trast bradycardia (or inappropriate normocardia) is not
the brain. uncommon in cats having circulatory shock and does
2. Pale mucous membranes as a result of arteriolar con­ not appear to carry any prognostic significance in this spe­
striction and decreased blood volume in the capillary cies. The mechanism of bradycardia in hemodynamically
beds. unstable cats is unknown. It can occur in mild to
3. Prolonged capillary refill time because the moderate cases of shock and the heart rate generally
vasoconstricted arterioles delay the return of blood increases as the animal is resuscitated. 13,122 Hypothermia
to the capillaries of the mucous membranes. is recognized to cause bradycardia and is common in