Blood Pressure Regulation
Blood Pressure Regulation
Blood Pressure Regulation
Three major components of the circulatory system: blood volume, cardiac pump, and vasculature.
They must respond effectively to complex neural, chemical, and hormonal feedback systems to
maintain an adequate blood pressure (BP) and perfuse body tissues.
BP is regulated through a complex interaction of neural, chemical, and hormonal feedback
systems affecting both cardiac output and peripheral resistance.
This relationship is expressed in the following equation: Mean arterial BP = CO × PR
Cardiac output is a product of the stroke volume (the amount of blood ejected from the left
ventricle during systole) and heart rate.
Peripheral resistance is primarily determined by the diameter of the arterioles.
Tissue perfusion and organ perfusion depend on mean arterial pressure (MAP), or the average
pressure at which blood moves through the vasculature.
MAP must exceed 65 mm Hg for cells to receive the oxygen and nutrients needed to metabolize
energy in amounts sufficient to sustain life.
True MAP can be calculated only by complex methods; however, most digital BP machines provide
a MAP reading to guide clinical decisions.
BP is regulated by baroreceptors (pressure receptors) located in the carotid sinus and aortic arch.
These pressure receptors are responsible for monitoring the circulatory volume and regulating
neural and endocrine activities.
When BP drops, catecholamines (epinephrine, norepinephrine) are released from the adrenal
medulla. These increase heart rate and cause vasoconstriction, restoring BP. Chemoreceptors,
also located in the aortic arch and carotid arteries, regulate BP and respiratory rate using much
the same mechanism in response to changes in oxygen and carbon dioxide (CO2 ) concentrations in
the blood. These primary regulatory mechanisms can respond to changes in BP on a moment-to-
moment basis.
The kidneys regulate BP by releasing renin, an enzyme needed for the eventual conversion of
angiotensin I to angiotensin II, a potent vasoconstrictor. This stimulation of the renin–angiotensin
mechanism and the resulting vasoconstriction indirectly lead to the release of aldosterone from
the adrenal cortex, which promotes the retention of sodium and water (hypernatremia).
Hypernatremia then stimulates the release of antidiuretic hormone (ADH) by the pituitary gland.
ADH causes the kidneys to retain water further in an effort to raise blood volume and BP. These
secondary regulatory mechanisms may take hours or days to respond to changes in BP.
The relationship between the initiation of shock and the responsiveness of primary and secondary
regulatory mechanisms that compensate for deficits in blood volume, the pumping effectiveness
of the heart, or vascular tone, which may result because of the shock state, is noted in Figure 11-2.
Beginning with ventricular systole, the pressure inside the ventricles rapidly increases, forcing
the AV valves to close. As a result, blood ceases to flow from the atria into the ventricles, and
regurgitation (backflow) of blood into the atria is prevented.
The rapid increase in pressure inside the right and left ventricles forces the pulmonic and aortic
valves to open, and blood is ejected into the pulmonary artery and aorta, respectively.
The exit of blood is at first rapid; then, as the pressure in each ventricle and its corresponding
artery equalizes, the flow of blood gradually decreases.
At the end of systole, pressure within the right and left ventricles rapidly decreases. As a result,
pulmonary arterial and aortic pressures decrease, causing closure of the semilunar valves.
These events mark the onset of diastole, and the cardiac cycle is repeated.
Chamber pressures can be measured with the use of special monitoring catheters and
equipment. This technique is called hemodynamic monitoring.
Cardiac Output
Cardiac output refers to the total amount of blood ejected by one of the ventricles in liters per
minute. The cardiac output in a resting adult is 4 to 6 L/min but varies greatly depending on the
metabolic needs of the body. Cardiac output is computed by multiplying the stroke volume by the
heart rate. Stroke volume is the amount of blood ejected from one of the ventricles per heartbeat. The
average resting stroke volume is about 60 to 130 mL
Cardiac Cycle
The cardiac cycle refers to the events that occur in the heart from the beginning of one
heartbeat to the next. The number of cardiac cycles completed in a minute depends on the heart rate.
Each cardiac cycle has three major sequential events: diastole, atrial systole, and ventricular systole.
These events cause blood to flow through the heart due to changes in chamber pressures and
valvular function during diastole and systole.
During diastole, all four heart chambers are relaxed. As a result, the AV valves are open and the
semilunar valves are closed. Pressures in all of the chambers are the lowest during diastole, which
facilitates ventricular filling. Venous blood returns to the right atrium from the superior and
inferior vena cava, then into the right ventricle. On the left side, oxygenated blood returns from the
lungs via the four pulmonary veins into the left atrium and ventricle.
Toward the end of this diastolic period, atrial systole occurs as the atrial muscles contract in
response to an electrical impulse initiated by the SA node. Atrial systole increases the pressure
inside the atria, ejecting the remaining blood into the ventricles. Atrial systole augments ventricular
blood volume by 15% to 25% and is sometimes referred to as the atrial kick. At this point,
ventricular systole begins in response to propagation of the electrical impulse that began in the SA
node some milliseconds earlier.