Page 37 - Basic Monitoring in Canine and Feline Emergency Patients

BP
VetBooks.ir CO SVR

Vascular &
SV HR tissue factors
Neurohormonal
(–) (–) factors
Afterload
Preload
Contractility

Fig. 2.3. A diagrammatic representation of the various factors affecting the cardiac output (CO) and systemic blood
pressure (BP). The cardiac output represents the blood ejected out of the left ventricle into the systemic circulation
over time. One of the determinants of the arterial blood pressure is the volume of blood that leaves the heart (CO).
The other determinant of the blood pressure is the vascular tone or systemic vascular resistance (SVR). As the
SVR increases, the blood pressure increases and as the SVR decreases, the vessels dilate and the blood pressure
decreases. The cardiac output is in turn made up of the stroke volume (SV) and the heart rate (HR). The SV is the
blood volume that leaves the left ventricle and enters the aorta during a ventricular contraction while the HR is the
number of ventricular contractions over time. The SV increases as more blood is returned to the ventricle (the preload
increases). The SV is also increased when the heart contracts more vigorously (has increased contractility) and
when the afterload (pressure that the heart is pumping against) is lower (shown in the diagram by a minus (–) sign).
Typically, as the heart rate increases, the CO increases. However, as shown in the diagram by the minus sign (−), if
the heart rate increases too much, the ventricle does not have adequate time to relax and it will not fill completely (i.e.
a decreased preload), leading to a decreased SV and decreased CO. Neurohormonal factors can have a wide array
of effects on CO and BP. For example, systemic nervous system stimulation may improve SVR, increase HR, and
increase contractility. In addition, the renin–angiotensin–aldosterone system may lead to improved SVR and improved
water retention, which leads to increased preload. Local tissue factors (such as hypoxia or increased activity) can have
regional effects on SVR.

Once released into the bloodstream, renin acts
Regulation of mean arterial pressure:
Blood volume on circulating angiotensinogen and cleaves angio-
tensinogen to angiotensin I. Angiotensin converting
Extrinsic factors not only play a role in the mainte- enzyme (ACE) lies predominantly in the pulmonary
nance of vascular tone, but also in the regulation of endothelium and further cleaves angiotensin I to
blood volume. The renin–angiotensin–aldosterone angiotensin II. The formation of angiotensin II is
system (RAAS) is involved in blood pressure regu- critical to the clinical effects of the RAAS as angio-
lation through control of both vascular tone and tensin II acts as a potent vasoconstrictor (increasing
blood volume. The first component of the system SVR and blood pressure). At the same time, angio-
(renin) is stored in the juxtaglomerular cells in the tensin II is involved in controlling blood volume. It
kidney, which are associated with the renal afferent stimulates sodium reabsorption within the kidney,
arteriole. A drop in the renal afferent arteriole pres- increases aldosterone release from the adrenal cor-
sure leads to the release of renin. The juxtaglo- tex, and stimulates release of antidiuretic hormone
merular cells can also release renin in response to (ADH, vasopressin) from the pituitary gland.
sympathetic nervous system stimulation. Furthermore, Aldosterone also leads to sodium reabsorption
cells (called the macula densa) within the distal largely in the distal tubule and collecting ducts of the
renal tubules sense sodium and chloride concentration; kidney. As water generally follows sodium, reabsorp-
a decrease in distal tubule sodium concentration tion of sodium by any mechanism will lead to reten-
also leads to renin release. tion of water and, subsequently, an increase in

Blood Pressure Monitoring 29