BLOOD PRESSURE

Blood Pressure

Introduction to Blood Pressure 

Blood pressure (BP) is the force exerted by the blood as it presses against and attempts to stretch the walls of blood vessels. While blood exerts this force throughout the entire vascular system, when the term "blood pressure" is used without qualification, it generally refers to systemic arterial pressure. 

The SI unit of pressure is the pascal (Pa), but physiologists often express pressure in millimeters of mercury (mm Hg). The circulatory system is slightly overfilled with blood, meaning its contents are more than its capacity, which causes the blood to exert this outward force.

Types of Blood Pressure in the Body

1. Systemic Arterial Pressure

    ◦ Systolic Blood Pressure (SP): This is the maximum pressure reached during the cardiac cycle. It is produced with each systole (contraction) of the left ventricle, as approximately 70-80 mL of blood is ejected into the aorta and its branches. The highly elastic vessels stretch and accommodate this stroke volume, causing the pressure to rise sharply.

    ◦ Diastolic Blood Pressure (DP): This is the minimum pressure reached during the cardiac cycle. During diastole (relaxation) of the heart, the large elastic vessels recoil, moving the accommodated blood down the arterial tree. These vessels act as "secondary pumps" to maintain pressure and blood flow during diastole. Clinically, greater importance is often attached to DP because this pressure is exerted consistently, making diastolic hypertension potentially more dangerous than systolic hypertension due to sustained damage to vessel walls.

    ◦ Pulse Pressure (PP): This is the difference between systolic and diastolic pressures (SP - DP). It varies directly with stroke volume and inversely with arterial compliance.

    ◦ Mean Arterial Pressure (MAP): This is the average of all pressures measured during the cardiac cycle. It is not a simple arithmetic mean because diastole is longer than systole. A reasonable approximation can be calculated as one-third of pulse pressure plus diastolic pressure (e.g., if SP=120, DP=80, MAP ≈ 1/3(40) + 80 = 93 mm Hg). The MAP (approximately 95 mm Hg in systemic large arteries) provides the driving force (pressure head) for blood flow through arteries, capillaries, and veins, ensuring tissue perfusion.

2. Capillary Pressure: This is also referred to as capillary hydrostatic pressure. In human skin, it is approximately 35 mm Hg at the arteriolar end and 15 mm Hg at the venular end. Fluid exchange across capillary walls (filtration and absorption) is influenced by the balance between hydrostatic and osmotic forces.

3. Venous Pressure: Pressures progressively fall along the circulatory system, reaching nearly zero in the right atrium. In a standing person, the pressure in any vein below the heart is increased, and above the heart, it is decreased by gravity, with a factor of 0.77 mm Hg/cm.

4. Mean Circulatory Filling Pressure: If the heart were suddenly stopped in an experimental animal, blood would redistribute throughout the vascular tree, exerting a pressure of 8-10 mm Hg, known as the mean circulatory filling pressure.

Factors Affecting Blood Pressure

The degree of pressure exerted by blood on vessel walls is determined by:

• Pumping action of the heart (Cardiac Output).

• Peripheral resistance.

• Elasticity of large blood vessels (Arterial Compliance).

• Volume of circulating blood.

• Viscosity of blood.

The last three factors (elasticity, volume, viscosity) typically do not participate in short-term BP control.

Factors Required for the Regulation of Blood Pressure

Blood pressure is primarily a product of

 BP= CO X TPR

Cardiac output (CO) and total peripheral resistance (TPR). 

Cardiac Output (CO): CO = Heart Rate (HR) × Stroke Volume (SV).

1. Heart Rate (HR)

    ◦ Controlled by the autonomic nervous system: sympathetic stimulation increases HR, and parasympathetic (vagal) activity decreases HR. An increase in HR typically reduces diastole duration, potentially affecting ventricular filling, but also enhances contractility by increasing calcium influx.

2. Stroke Volume (SV)

    ◦ Preload: The load on the heart that determines the length of cardiac muscle cells prior to contraction, typically represented by end-diastolic volume (EDV) or pressure. Increased preload (e.g., from increased venous return) leads to an increase in stroke volume, as described by the Frank-Starling relationship. Central venous pressure (CVP) acts as the heart's preload.

    ◦ Afterload: The load the heart experiences as it ejects blood, primarily aortic pressure for the left ventricle. Increased afterload requires the ventricle to work against higher pressure, resulting in a decrease in stroke volume.

    ◦ Contractility (Inotropism): The intrinsic ability of cardiac muscle to generate force at a given length. It is directly related to intracellular Ca$^{2+}$ concentration. Positive inotropic agents (e.g., sympathetic stimulation, norepinephrine) increase contractility, causing the ventricle to develop greater tension and increase stroke volume by decreasing end-systolic volume. Negative inotropic agents (e.g., beta-blockers) decrease contractility.

Total Peripheral Resistance (TPR):

• Arteriolar Tone: This is the greatest site of resistance to blood flow and pressure drop in the arterial system.

    ◦ Local Control (Intrinsic): Arterioles exhibit autoregulation, maintaining constant blood flow over a range of perfusion pressures, especially in organs like the heart, brain, and kidney. This involves myogenic mechanisms (stretch-sensitive channels depolarizing VSMCs and causing contraction), and local chemical factors (e.g., interstitial PO${2}$, PCO${2}$, pH, K$^{+}$, lactic acid, adenosine) that cause vasodilation or constriction.

    ◦ Extrinsic Control (Neural and Humoral):

        ▪ Sympathetic Nervous System: Sympathetic vasoconstrictor nerve fibers maintain basal tone in resistance vessels. Norepinephrine (released from sympathetic nerves and adrenal medulla) and epinephrine (from adrenal medulla) cause vasoconstriction (via alpha-adrenergic receptors) or vasodilation (via beta-adrenergic receptors).

        ▪ Humoral Agents: Angiotensin II is a potent vasoconstrictor that increases blood pressure. Nitric oxide (NO) is an endothelium-derived relaxing factor (EDRF) that causes vasodilation by activating guanylyl cyclase in vascular smooth muscle, increasing cGMP. Bradykinin and histamine generally lower blood pressure.

Regulation of Blood Pressure: Short-term and Long-term

Blood pressure is maintained within a relatively narrow range in normal individuals through a complex interplay of various regulatory mechanisms. These are typically categorized into short-term (neural) and long-term (hormonal and fluid balance) mechanisms.

1. Short-term Regulation (Moment-to-moment / Minute-to-minute)

    ◦ Baroreceptor Reflex (Sino-aortic mechanism): This is a fast, neural negative feedback system that maintains arterial blood pressure minute-to-minute.

        ▪ Location: Stretch receptors (baroreceptors or pressoreceptors) are located in the walls of the carotid sinus (near the common carotid artery bifurcation) and the aortic arch.

        ▪ Mechanism: An increase in arterial pressure stretches these receptors, increasing their firing rate. These impulses are carried via afferent fibers in the glossopharyngeal (IX) and vagus (X) nerves to the vasomotor center in the brainstem (nucleus of the tractus solitarius in the medulla).

        ▪ Response: The vasomotor center coordinates responses to restore BP to a set point (about 100 mm Hg).

            • Decreased parasympathetic (vagal) outflow to the heart.

            • Increased sympathetic outflow to the heart and blood vessels.

            • Results in: increased heart rate, increased contractility and stroke volume (increasing CO), vasoconstriction of arterioles (increasing TPR and arterial pressure), and vasoconstriction of veins (increasing venous return and CO via Frank-Starling).

        ▪ Adaptation: Baroreceptors adapt to sustained pressure changes, making them less effective for long-term regulation.

    ◦ Chemoreceptors: Peripheral chemoreceptors (carotid and aortic bodies) are stimulated by a decrease in blood oxygen tension (Pao${2}$) and an increase in blood carbon dioxide tension (Paco${2}$). Central chemoreceptors in the medulla oblongata also respond to CO$_{2}$/pH changes. Stimulation increases respiration rate and depth, but also causes peripheral vasoconstriction.

    ◦ CNS Ischemic Response (Cushing's Reflex): Severe hypotension can lead to cerebral ischemia, which induces a pronounced sympathetic nervous stimulation of the heart, arterioles, and veins. This strong response aims to increase blood pressure, but severe, prolonged ischemia eventually depresses brainstem cardiovascular centers, leading to loss of sympathetic tone and further BP reduction.

2. Long-term Regulation (Days, Weeks, Months, Years)

    ◦ Renal-Body Fluid Volume System: The kidney is the major organ that regulates extracellular fluid (ECF) volume and thus blood volume, which is crucial for long-term blood pressure control. Overhydration leads to fluid excretion, while dehydration causes reduced urine output.

    ◦ Hormonal Mechanisms:

        ▪ Renin-Angiotensin-Aldosterone System (RAAS): This is a slow, hormonal mechanism for long-term BP regulation by adjusting blood volume. Renin release (stimulated by reduced kidney perfusion pressure, sympathetic activity, decreased NaCl delivery to macula densa) leads to angiotensin II production (a potent vasoconstrictor that increases BP). Angiotensin II also stimulates aldosterone release, which promotes Na$^{+}$ and water retention by the kidneys.

        ▪ Arginine Vasopressin (AVP) / Antidiuretic Hormone (ADH): Secreted by the posterior pituitary, AVP secretion is stimulated by increased plasma osmolality and decreased blood volume/pressure. AVP increases water permeability in the kidney collecting ducts, promoting water reabsorption and increasing blood volume.

        ▪ Natriuretic Peptides (ANP and BNP): 

Atrial Natriuretic Peptide (ANP) and Brain Natriuretic Peptide (BNP) are released from atrial and ventricular myocytes, respectively, when the heart chambers are distended (e.g., by increased blood volume). They act to reduce blood pressure and increase the excretion of NaCl and water by the kidneys.

Clinical Conditions in Which Cardiac Output is Changed

Cardiac output is a key determinant of blood pressure, and its alterations are central to many clinical conditions:

• Increased Cardiac Output (High Output States):

    ◦ Exercise: CO increases significantly (4-5 fold), primarily by increasing both heart rate and stroke volume, leading to higher arterial pressure.

    ◦ Hyperthyroidism: Causes increased heart rate, myocardial contractility, and reduced systemic vascular resistance, resulting in elevated cardiac output [115b, 431].

    ◦ Pregnancy: Associated with about a 40% increase in CO due to positive chronotropic and inotropic effects. Peripheral resistance decreases due to progesterone, leading to a rise in pulse pressure.

    ◦ Sympathetic Stimulation: Generally increases heart rate and contractility, which can lead to increased cardiac output.

• Decreased Cardiac Output (Low Output States):

    ◦ Heart Failure: The heart cannot provide adequate blood flow. This can result from impaired contractility (cardiac function curve shifts downward), leading to increased residual volume in ventricles. Patients may have small arterial pulse pressures.

    ◦ Hemorrhage: Acute blood loss reduces blood volume, significantly decreasing venous return and thus cardiac output.

    ◦ Valvular Stenosis (e.g., Aortic Stenosis, Mitral Stenosis): Narrowing of the aortic valve increases afterload, reducing stroke volume ejected from the left ventricle. Mitral stenosis impedes left ventricular filling, reducing end-diastolic volume and stroke volume.

    ◦ Valvular Regurgitation (e.g., Aortic Regurgitation, Mitral Regurgitation): Incompetent valves allow backward blood flow, impacting net forward stroke volume and affecting pressure dynamics.

    ◦ Arrhythmias:

        ▪ Profound Bradycardia: Excessively slow heart rates (e.g., sick sinus syndrome, complete AV block) can lead to inadequate ventricular filling and significantly decrease cardiac output [48, 215b, 433].

        ▪ Excessively High Tachycardia: Heart rates above ~200 bpm can also decrease CO, as filling time becomes too short.

    ◦ Hypovolemia: A general decrease in blood volume (e.g., from severe dehydration or hemorrhage) directly reduces cardiac output by lowering preload.

    ◦ Hypothyroidism: Leads to sluggish cardiac activity, slow heart rate, and diminished cardiac output [121b, 527].

    ◦ Pharmacological Agents: Drugs like beta-blockers (e.g., propranolol) reduce heart rate and contractility, thus decreasing cardiac output.

Methods of Recording Blood Pressure

1. Direct Measurement:

    ◦ In hospital intensive care units, arterial BP can be measured directly by introducing a needle or catheter into a peripheral artery. This allows for continuous, precise measurement. Micropipettes can be used to measure capillary pressure in exposed organs.

2. Indirect Measurement (Sphygmomanometry): 

This is the common clinical method.

    ◦ An inextensible cuff with an inflatable bag is wrapped around the arm (usually), inflated above systolic pressure to occlude the artery, and then slowly deflated.

    ◦ Palpatory Method: The physician detects the pulse by feeling the radial artery at the wrist. The pressure at which the pulse is first felt (as the cuff deflates) represents the systolic pressure. This method may slightly underestimate SP.

    ◦ Auscultatory Method (using Korotkoff Sounds): A stethoscope is used over the brachial artery in the antecubital space to detect a series of sounds as the cuff deflates. Auscultatory Method (Korotkoff, 1905).

        ▪ Phase I (Systolic): Sharp tapping sounds indicate blood spurting through the compressed artery. The pressure at which these sounds are first heard is the systolic pressure.

        ▪ Phase IV (Diastolic, first): The sounds become muffled and softer. This point is often favored as the diastolic pressure.

        ▪ Phase V (Diastolic, second): The sounds disappear completely.

    ◦ Oscillometric Method (Digital Blood Pressure Monitors): These battery-operated units (palm-top or wrist) work on the oscillometric principle, automatically translating pulse wave oscillations into systolic and diastolic pressures, and heart rate. They are easy to use by laypersons but should be periodically checked against standard sphygmomanometers.