Page 436 - Clinical Small Animal Internal Medicine

404 Section 5 Critical Care Medicine

signs of autoregulatory escape include venous pooling, Chemoreceptors are sensory organs responsible for
VetBooks.ir bradycardia, and hypotension unresponsive to fluids or monitoring the blood for appropriate concentrations of
key chemicals, primarily oxygen and carbon dioxide. The
vasopressors and eventual death.
There are some specific treatments for each type of
cation, sense oxygen tension and the partial pressure of
shock, but key similarities exist between all categories. carotid bodies, which are located near the carotid bifur­
The ultimate goal in the treatment of shock is to restore carbon dioxide (CO 2 ) in arterial blood. The aortic body,
homeostasis by ensuring adequate oxygen delivery to the located in the aortic root, senses pressure in addition to
tissues. For the most part, these treatments do not oxygen and carbon dioxide tension and pH of arterial
address the underlying cause of shock; rather, they are blood. These chemoreceptors send signals to the medulla
nonspecific augmentations of oxygen delivery. The ideal oblongata to regulate breathing and blood pressure and
treatment of shock would prevent death, allow the are a potent mechanism by which respiratory rate and
patient time to heal from the initiating insult, and limit heart rate are controlled.
ongoing injury as much as possible.
Compensatory Mechanisms

Pathophysiology of Shock and Effect During shock, hypoxia is sensed centrally which prompts
on Organ Systems the firing of the respiratory center efferent nerves,
increasing the respiratory rate in an effort to raise the
amount of fresh gas presented to the alveoli to ensure
Cellular Effects of Hypoxia
oxygen extraction from the atmosphere is maximized.
Shock occurs due to failure of oxygen delivery to the tis­ Control of cardiac output is regulated by the autonomic
sues which results in cellular and mitochondrial hypoxia. nervous system. The sympathetic branch of the auto­
The resulting anaerobic metabolism leads to a significant nomic nervous system acts on the areas of the heart that
decrease in production of adenosine triphosphate (ATP) have pacemaking capability (i.e., sinoatrial node, atria,
with generation of lactate as a byproduct causing acido­ atrioventricular node ventricles). Sympathetic stimula­
sis at both local and systemic levels. tion results in an increase in sinoatrial node rate of firing,
The ATP deficiency that occurs during shock has numer­ decrease in atrioventricular node delay, and increase in
ous detrimental effects on the cell. ATP‐dependent trans­ speed of the spread of an action potential through the
port proteins cease to function and membrane gradients of specialized myocardial conduction system. Sympathetic
electrolytes are lost. This results in cellular swelling, cellu­ stimulation directly increases the strength of contractility
lar death, and ultimately organ dysfunction if enough cel­ through the action of epinephrine stimulating beta‐1‐
lular death occurs. Cell death resulting from hypoxia is adrenergic receptors. Indirectly, sympathetic stimulation
usually necrotic and not apoptotic, and can therefore increases inotropy by increasing vascular tone through
induce an inflammatory response. This organ failure, if not arteriolar vasoconstriction, increasing resistance to blood
corrected in time, results in the death of the organism. flow (systemic vascular resistance) and blood pressure.
Preferential vasoconstriction shunts blood flow away
from peripheral sites and to the brain and heart, increas­
Sensors of Cardiovascular Homeostasis
ing preload and causing a reflex increase in inotropy.
In order to maintain homeostasis, volume, pressure The parasympathetic branch of the autonomic nerv­
(baroreceptors), and chemical status (chemoreceptors) of ous system regulates chronotropy (heart rate). Para­
the blood must be monitored at all times. This is the job sympathetic stimulation slows the heartbeat with little
of afferent sensors in various parts of the body capable of effect on the strength of ventricular contractions. In
sensing a change in one or more of these variables. These shock, parasympathetic tone is reduced to increase the
sensors send signals primarily to the autonomic nervous heart rate. The net result of the increase in sympathetic
system and if an abnormality is detected, cause physio­ tone and decrease in parasympathetic tone is increased
logic responses intended to reestablish homeostasis. inotropy and chronotropy. As a consequence, most
Baroreceptors are mechanoreceptors located within patients in shock exhibit tachycardia. Patients with
the walls of vessels that are excited with stretch of the hyperkalemia or in the decompensatory phase of shock
vessel wall (pressure) and are important for the beat‐ may demonstrate bradycardia, however.
to‐beat regulation of blood pressure. The information Other less immediate compensatory mechanisms are
collected by baroreceptors is used to regulate the func­ also activated during shock. The renin‐angiotensin‐
tion of the heart, vascular smooth muscle tone, and aldosterone system (RAAS) is activated and a nonos­
endocrine responses aimed at managing intravascular motic release of antidiuretic hormone in response to
volume. hypotension occurs. Both of these responses attempt to