Page 38 - Basic Monitoring in Canine and Feline Emergency Patients

blood volume. In addition to the RAAS system, if the perfusion pressure should increase, the arte-
ADH release also contributes to water reabsorp- rial vasculature will constrict to ‘block’ increased
VetBooks.ir tion in the renal collecting ducts as well as vasocon- blood flow to tissues and help maintain more con-
stant organ perfusion.
striction, and helps maintain an appropriate blood
The ability of an organ to autoregulate blood
volume and pressure (Fig. 2.4). The RAAS is a com-
mon site of pharmacologic intervention in patients flow varies. For example, the renal, cerebral, and
with hypertension (see Section 2.4, Interpretation coronary circulatory beds exhibit excellent
of the Findings). autoregulation while the skeletal muscle circula-
tory bed shows only moderate autoregulation and
the cutaneous circulatory bed offers almost no
Regulation of mean arterial pressure: Local autoregulation.
regulation of vascular tone
In addition to the various factors controlling sys-
temic vascular tone and blood volume, the circula- Measuring the blood pressure
tory system has the ability to regulate vascular tone The diastolic pressure measured within the vessels
within individual tissues in order to deliver a rela- is relatively constant when measured in the aorta
tively constant flow of blood to organs over a wide extending distally to the larger peripheral arteries.
range of arterial pressures. This ‘autoregulation’ In contrast, the systolic pressure and MAP increase
causes arterial blood vessels in a particular organ over this same range in healthy patients. Again, the
or tissue bed to dilate when exposed to lower per- pulse pressure (which is appreciated clinically dur-
fusion pressure. The resulting arterial dilation ing physical examination), is the difference between
improves blood flow to that tissue bed. Conversely, the systolic and diastolic pressures.

JG cells detect drop in Macula densa in DRT Retain water
afferent arteriole detect decreasing DRT
pressure sodium concentration Retain sodium
(DRT)

Renin released Aldosterone
from JG cells
ADH release release (adrenal
(pituitary gland) gland)
Vasoconstriction
(including
efferent renal
vessels)
Renin enters ACE (lungs)
bloodstream
Angiotensinogen Angiotensin I Angiotensin II

Fig. 2.4. A diagrammatic representation of the steps involved in the renin−angiotensin−aldosterone system (RAAS).
The juxtaglomerular (JG) cells in the kidney detect a drop in the afferent arteriole pressure. In addition, the macula
densa within the distal renal tubules (DRT) can sense a decrease in urine sodium concentration. Either change
leads to the JG cells releasing renin. In the bloodstream, renin cleaves circulating angiotensinogen to angiotensin I.
Angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE), which lies predominantly in the
pulmonary endothelium. Angiotensin II has multiple effects which can improve blood pressure: (i) vasoconstriction
leading to increased systemic vascular resistance; (ii) release of aldosterone from the adrenal gland which leads
to sodium and subsequent water retention in the DRT; and (iii) release of antidiuretic hormone (ADH) which leads
directly to water retention. Water retention leads to increased circulating volume and improved cardiac output.

30 D.S. Foy