Blood Pressure Physiology
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Arterial blood pressure is created by the combined forces, and complex interactions, of cardiac output, systemic vascular resistance (resistance produced mainly in the arterioles), and viscosity of the blood.
The arterial blood pressure is the force causing blood to flow through the arteries, into the capillaries, then back to the heart via the veins.
The left ventricle contracts (systole), ejecting blood into the aorta, creating a pressure pulse. This is the measurement known as systolic blood pressure. Part of the blood that is ejected during systole remains within the distended arteries, and rebounds during diastole (relaxation of the ventricle), creating the diastolic blood pressure. An adequate blood pressure is required for normal blood flow; however the presence of a normal arterial blood pressure does not guarantee that blood flow is normal.
Physiological Mechanisms to Maintain Normal Blood Pressure
There are both immediate and long-term physiological mechanisms which react in order to maintain blood pressure within normal limits. These are:
1) Autonomic nervous system (ANS) responses
2) Capillary fluid shift mechanism
3) Hormonal responses
Autonomic nervous system (ANS) responses
Normal circulatory homeostasis depends upon there being a basal level of activity in both the sympathetic and parasympathetic nervous systems - the ANS is controlled by the cardioinhibitory and vasomotor centres within the medulla oblongata . The ANS is the most rapidly responding regulator of blood pressure.
Stimulus for activation
A drop in cardiac output results in a drop in arterial blood pressure, which is sensed by baroreceptors (pressure-sensitive nerve endings) located in the carotid sinus and aortic arch. A drop in signals from the baroreceptors to the vasomotor centre (VMC) of the brainstem in response to perceived hypoperfusion leads to a centrally controlled increase in activity of the sympathetic nervous system and an increased release of adrenaline from the adrenal medulla.
Response to stimulus
Adrenaline released from the adrenal medulla into the circulation, and noradrenaline released at nerve terminals, stimulate cardiac and vascular alpha and beta-receptors, resulting in vasoconstriction of both the arterial and venous side of the circulation (alpha-receptors) and increased contractility of the heart (beta-receptors).
Alpha Effects increase arterial blood pressure and protects perfusion of essential vascular beds (cerebral and coronary) but the increased systemic vascular resistance leads to increased afterload and decreased cardiac output, with increased myocardial oxygen demand. It is likely to exacerbate hypoperfusion of non-essential vascular beds.
Beta Effects stimulate the release of adenylate cyclase, which generates intracellular cyclic AMP. This in turn has many intracellular effects, including increasing the rate and magnitude of the contractions in intracellular calcium fibres. This has positive inotrope (increased myocardial contractility which increases cardiac output), positive chronotrope (increased heart rate), and positive luisitrope (improved diastolic relaxation) effects, and stimulates renin release from the Juxtaglomerular apparatus (JGA). These effects lead to an increased rate and strength of cardiac contraction, and improved myocardial relaxation. This process does, however, increase myocardial oxygen consumption (increased heart rate and increased work due to inotropic stimulation) and increased intracellular calcium can lead to calcium overload that in turn can result in cardiac rhythm disturbances and cell death. Chronic stimulation leads to down-regulation of the system.
NOTE There is a strong correlation between the severity of heart failure and the degree of stimulation of the adrenergic system. Veterinary studies have confirmed greater stimulation of the adrenergic system in patients with more advanced heart disease. Human studies have demonstrated a worse prognosis in those patients with higher levels of circulating noradrenaline.
Capillary Fluid Shift Mechanism
The maintenance of normal pressures within the arterial and venous circulations is essential for the maintenance of normal fluid homeostasis. The Starling hypothesis describes the state whereby the equilibrium of fluid exchange across the capillary wall (between the blood and the interstitial fluid) is determined by the hydrostatic pressures and oncotic pressures that exist across the capillary wall. This fluid exchange is controlled by the capillary blood pressure, the interstitial fluid pressure and the colloid osmotic pressure of the plasma. Normally there is a net loss of fluid from the capillary at the arteriolar end, and a net gain at the venous end, resulting in almost perfect fluid balance being maintained. Any net fluid movement from the intravascular to the extracellular space can be compensated for by lymphatic drainage. Low blood pressure results in fluid moving from the interstitial space into the circulation, helping to restore blood volume and blood pressure.
Hormonal responses exist for the purpose of both lowering and raising blood pressure. They act in various ways, including vasoconstriction, vasodilation and alteration of blood volume.
Renin-Angiotensin-Aldosterone System (RAAS)
The juxtaglomerular apparatus of the kidneys plays an important role in the control of blood volume and blood pressure via the RAAS - Renin is released from this area. The stimulus for renin release into the circulation includes;
- local baroreceptors in the afferent renal arteriole - a drop in renal blood flow stimulates renin release
- cardiac and arterial baroreceptors responsd to reduced local perfusion, initiating beta-1 mediated effects via innervation of the juxtaglomerular apparatus (JGA)
- decreased chloride delivery to the macula densa is detected by chemoreceptors - a drop in glomerular filtration rate (GFR) detected as a drop in chloride presented at the macula densa leads to increased reabsorption in the proximal convoluted tubule.
Renin then leads to the cleavage of circulating Angiotensinogen (produced by the liver) to angiotensin I, and then angiontensin converting enzyme (ACE) catalyses the production of angiotensin II from angiotensin I - this occurs mainly in the lungs. ACE is bound to endothelial cells throughout the vascular system. Angiotensin II acts as a stimulus to aldosterone release from the zona glomerulosa of the adrenal cortex, which in turn leads to sodium and water retention in the cortical collecting duct of the renal tubule.
NOTE This system is responsible for the long-term maintenance of blood pressure, but is also activated very rapidly in the presence of hypotension.
Vascular Hormal Effects
Angiotensin II is a potent vasoconstrictor which causes an increase in mean arterial pressure, and the direct stimulation of sodium retention in the proximal convoluted tubule of the kidney via the increased synthesis and release of aldosterone. Aldosterone stimulates reabsorption of sodium and chloride, and the secretion of potassium and protons. Initially, the effects are advantageous by protecting perfusion to essential vascular beds and expanding the circulation fluid volume, and therefore increasing contractility by the Starling mechanism. As systemic vascular resistance increases, however, there is increased myocardial work and increased myocardial oxygen demand. Expanded circulatory volume ultimately results in congestion of vascular beds once the Starling mechanism is overwhelmed in the failing heart. Angiotensin II and aldosterone also effect genetic expression, which may lead to a progression of the myocardial dysfunction present. They therefore play a role in the progression of hypertrophy and fibrosis.
Kidney and Fluid Balance Mechanisms
The kidneys help to regulate the blood pressure by increasing (when blood pressure falls) or decreasing (when blood pressure rises) the blood volume, and also by the renin-angiotensin system described above. The kidney-fluid system is the main method of the long-term control of blood pressure. In addition to the RAAS sytem, renal blood flow is regulated by:
- Pressure Diuresis: As arteriolar blood pressure increases, so flow through the kidneys also increases and this increases filtration rate and urinary output
- Pressure Natriuresis: If renal perfusion pressure is increased then sodium excretion increases i.e. sodium excretion increases when blood pressure increases. If more sodium is excreted less water is reabsorbed therefore the ECF volume decreases and blood pressure decreases. The actual mechanism is not clear but it is thought to involve a direct effect of the pressure on the renal interstitium.
Local Regulators of Blood Flow
Individual vascular beds have the ability to regulate blood flow according to the demands of the organ being supplied. Alterations in vasculature at this level probably contribute to the pathophysiology of heart failure, but are more difficult to establish because levels of regulators are regionally variable and cannot therefore be assessed systemically. These changes are induced by various vasoregulatory substances:
- Endothelin: A polypeptide factor involved in local regulation of blood flow. Manufactured in the vascular endothelium and active locally.
- Prostaglandin/Prostacyclin: Locally produced vasodilatory substances.
- Nitric Oxide (EDRF - endothelin derived relaxation factor): A locally produced vasodilator. Myocardial dysfunction is associated with dysfunction of this system.
Methods of Blood Pressure Measurement
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