Physiology of Blood Pressure Regulation

1

What are the two components of measured blood pressure and what do they represent?

An individual’s blood pressure, or systemic arterial pressure, refers to the pressure measured within large arteries in the systemic circulation. This number splits into systolic blood pressure (SBP) and diastolic blood pressure (DBP). SBP refers to the maximum pressure within the large arteries when the heart contracts to propel blood through the body. DBP describes the lowest pressure within the large arteries during heart relaxation between beatings.

2

What is mean arterial pressure and its hemodynamic determinants?

Mean arterial pressure (MAP) is the average blood pressure during a single cardiac cycle. As mentioned in the formula above, MAP is the product of cardiac output (CO) and systemic vascular resistance (SVR) plus the central venous pressure (CVP). CVP can typically be neglected due to the small value. Interestingly, the fraction of time spent in a cardiac cycle between systole and diastole is two thirds and one third, respectively; therefore when noninvasive blood pressure (NIBP) is measured via a cuff, MAP can be estimated as ⅔ SBP + ⅔ DBP, and its normal value falls within the range of 65 to 100 mm Hg.

3

What factors determine CO?

The volume of blood being pumped per minute through the circulatory system is defined as CO and is directly proportional to both the heart rate (HR), that is the number of beats per minute, and stroke volume (SV), which is the amount of blood pumped from the ventricles per beat. Therefore it is represented by the formula:

External influences, specifically, the autonomic nervous system, determines the HR through altering the spontaneous depolarization of the cardiac pacemaker cells in the sinoatrial (SA) node. On the other hand, SV is the difference between left ventricular end diastolic volume (EDV) and end systolic volume (ESV), of which the former is determined by venous return and the latter inversely by cardiac contractility.

4

Define the Frank-Starling law of the heart?

This law defines an integral intrinsic mechanical property of the myocardium. The Frank-Starling law states that, for a fixed total load, SV increases as cardiac filling increases. Therefore an increase in preload will increase EDV and SV due to the increase in extent of cardiac sarcomere shortening during contraction.

5

What are the determinants of SVR?

Poiseuille law states that the velocity of the steady flow of a fluid through a narrow tube (as a blood vessel or a catheter) is directly proportional to the pressure and the fourth power of the radius of the tube and inversely to the length of the tube and the coefficient of viscosity. Thus a small change in arterial diameter will result in a significant increase in SVR, making this mechanism the predominant factor responsible for sizeable changes in MAP. The vasoconstriction and vasodilation mechanisms are mediated through the autonomic nervous system and through the effect of various hormones discussed in this chapter.

6

What are the primary mechanisms involved in the short-term regulation of blood pressure?

The predominant mechanism for the short-term regulation of blood pressure occurs via the autonomic nervous system, which subsequently moderates changes to CO and SVR. The autonomic nervous system can be divided into two pathways—the parasympathetic and sympathetic nervous systems.

• Parasympathetic Nervous System: The cardiovascular effects of the parasympathetic nervous system are primarily mediated by the efferent fibers of the vagus nerve (cranial nerve [CN] X). Although the cardiac pacemaker cells of the SA node exhibit automaticity, they can be influenced by agents that augment their rate of firing. The pacemaker cells of the SA node are innervated by the vagus nerve, which mainly acts to decrease chronotropy via the release of acetylcholine and activation of muscarinic receptors located on cardiac pacemaker cells. As previously noted, this can decrease CO and thus decrease blood pressure.

• Sympathetic Nervous System: The cardiovascular effects of the sympathetic nervous system are mediated via the release of catecholamines—epinephrine and norepinephrine. The effects of these catecholamines causes direct and indirect stimulation of their target organs via the release of norepinephrine at peripheral synapses located within the vascular smooth muscle cells and cardiac myocytes and the release of epinephrine and norepinephrine from chromaffin cells located within the adrenal medulla. Their effect is moderated via the activation of α and β adrenergic receptors located at the membranes of their target tissues. Their overall effect is to increase vascular resistance via activation of α ₁ receptors located within the vascular smooth muscle and to increase chronotropy and contractility via activation of β ₁ receptors located on the cardiac pacemaker cells and cardiac myocytes, respectively. Activation of these receptors leads to an increase in CO and SVR, resulting in an overall increase in blood pressure ( Fig. 6.1 ).

  

7

What is the role of the baroreceptor reflex in regulation of MAP?

The baroreceptor reflex describes an important way by which the body attempts to maintain a constant blood pressure in the face of acute changes. This homeostatic mechanism relies on the actions of specialized neurons known as baroreceptors, which are stretch-sensitive mechanoreceptors primarily located at the bifurcation of the internal and external carotid arteries and aortic arch. These baroreceptors respond mainly to passive stretching of the arterial wall. The baroreceptors in the carotid sinuses are innervated by the sinus nerve of Haring, a branch of the glossopharyngeal nerve (CN IX), which synapses in the nucleus tractus solitarius (NTS) located in the dorsal medulla. The baroreceptors in the aortic arch are alternatively innervated by the aortic nerve, a branch of the vagus nerve (CN X), which also synapses in the NTS. Together, these comprise the afferent limb of a negative feedback system known as the baroreceptor reflex loop. The efferent limb of the baroreceptor reflex loop starts at the level of the NTS, which modifies the activity of the sympathetic and parasympathetic in the medulla to exhibit autonomic control of the cardiovascular system to maintain a constant blood pressure ( Fig. 6.2 ).

8

What is the role of chemoreceptors in the regulation of blood pressure?

Carotid body chemoreceptors have been implicated in the mechanism of hypertension correlated with sleep apnea syndrome in which a reversible diurnal elevation of blood pressure occurs as a result of periods of brief hypoxic episodes. Additionally, an accumulation of partial pressure of carbon dioxide (pCO ₂ ) within the cerebral vasculature in the case of cerebral ischemia leads to the activation of the sympathetic system, thereby increasing blood pressure to facilitate cerebral perfusion. The primary role of chemoreceptors is to maintain arterial pH, pCO ₂ , and partial pressure of oxygen (pO ₂ ) by regulating respiratory activity. Chemoreceptors are primarily located in the periphery at the carotid and aortic bodies and centrally in the cardiovascular regulatory center within the medulla. Like baroreceptors, chemoreceptors in the carotid and aortic bodies are innervated by branches of the glossopharyngeal nerve (CN IX) and vagus nerve (CN X), respectively. Their action is mediated via the chemoreceptor reflex such that decreased arterial pO ₂ (hypoxemia), increased arterial pCO ₂ (hypercapnia), and decreased arterial blood pH (acidemia) results in decreased parasympathetic outflow to the heart and increased sympathetic tone, resulting in an increased CO via increased HR and SV, systemic vasoconstriction, and an increased respiratory rate to facilitate gas exchange. Additionally, an accumulation of pCO ₂ within the cerebral vasculature in case of cerebral ischemia leads to the activation of the sympathetic system, thereby increasing blood pressure to facilitate cerebral perfusion.