Cardiovascular System: Blood Vessels PDF

Summary

This document provides an overview of the cardiovascular system, focusing on blood vessels. It details the functions of arteries, veins, capillaries, and arterioles, as well as blood flow and pressure regulation. The document also discusses factors influencing blood flow resistance and the role of different mechanisms in controlling blood flow.

Full Transcript

## Cardiovascular System: Blood Vessels The vascular system has a major function in regulating blood pressure and distributing blood flow to the various tissues. Elaborate branching and regional specializations of blood vessels enable efficient matching of blood flow to metabolic demand in individ...

## Cardiovascular System: Blood Vessels The vascular system has a major function in regulating blood pressure and distributing blood flow to the various tissues. Elaborate branching and regional specializations of blood vessels enable efficient matching of blood flow to metabolic demand in individual tissues. - **Arteries**: vessels that carry blood away from the heart. - **Veins**: vessels that carry blood back to the heart. ### The Vascular System - **Large artery**: low resistance, conducting vessels. - **Large vein**: low resistance, high-capacitance vessels. - **Arteriole**: main resistance vessels, controls distribution of blood flow. - **Venule**: WBCs released into tissues during inflammation and infection; capacitance vessels. - **Capillary**: exchange of gases, fluid, nutrients; uptake of waste and secretory products from cells. ### Hemodynamics Flow rate is directly proportional to the pressure difference between two points and inversely proportional to the resistance. $F = \Delta P / R$ Where: * $F$ = flow rate * $\Delta P$ = pressure difference * $R$ = resistance Example Calculation: * $P_1$ = 100 mmHg * $P_2$ = 10 mmHg * $\Delta P$ = 90 mmHg * Flow rate = 10 mL/min ### Hemodynamics Hemodynamics describe the relationship among blood pressure, blood flow, and resistance to flow. - **Blood pressure** (P) denotes the force exerted by blood on vessel walls (measured in mmHg), which is generated by the contraction of the heart. - **Blood Flow** (F) is always from a region of higher pressure to one of lower pressure. Depends on pressure difference (ΔP), measured as volume/time. - The relation between flow and pressure difference also depends on **resistance** (R), due to friction between blood and vessel walls. ### Determinants of Resistance The three main determinants of resistance are: - **Blood Viscosity** (normally constant, depends on hematocrit and proteins). - **Vessel Length** (constant). - **Vessel Diameter** (most important). Resistance is directly proportional to viscosity and the vessel's length, and inversely proportional to the fourth power of the vessel's radius. ### 2- Arteries Large arteries have thick walls full of elastic tissue → Act as Elastic Tubes → High compliance (stretch easily). Function as low-resistance tubes to conduct blood and **pressure reservoir** to maintain blood flow during diastole. After ventricular contraction, stretched arterial walls recoil passively, and blood continues to move into arterioles during diastole. ### Arterial Pressure: Fluctuations - **Systolic pressure** (SP) - The maximum arterial pressure reached during peak ventricular ejection. - **Diastolic pressure** (DP) - Minimum arterial pressure that occurs just before ventricular ejection begins. - **Pulse Pressure**: The difference between SP and DP. ### Circulation Pressures - Highest systemic arterial systolic/diastolic pressures are 120 and 80 mmHg. - Highest pulmonary arterial systolic/diastolic pressures are 25 and 10 mmHg. ### Mean Arterial Pressure (MAP) Arterial pressure is continuously changing throughout the cardiac cycle. The average pressure during the cycle, referred to as the **mean arterial pressure (MAP)**, is NOT the value halfway between SBP and DBP. This is because diastole lasts about twice as long as systole. Therefore, DBP will have a larger effect on MAP. $MAP = 1/3 SBP + 2/3 DBP$ It is the average pressure driving blood into the tissues averaged over the entire cardiac cycle. ### Measuring Blood Pressure Measured using a **Sphygmomanometer**. An inflatable cuff containing a pressure gauge is wrapped around the upper arm, and a **stethoscope** is placed over the brachial artery just below the cuff. - The cuff is inflated with air to a pressure greater than SBP → No sound. - The cuff is deflated slowly → blood flows when reach SBP → First sound. - With further deflation → when pressure decreases to DBP → No sounds. The sounds heard when measuring BP are called **Korotkoff's sounds**. ### 3- Arterioles Arterioles have two major functions: 1. Determining the relative blood flow to individual organs. 2. Determining the mean arterial pressure (MAP). **Blood flow** (F) is a function of the pressure gradient (ΔP) and the resistance to flow (R). Arteriolar radii in individual organs can be independently adjusted (control resistance to control flow). $F_{organ} = MAP / Resistance_{organ}$ ### Arterioles Because MAP is the same throughout the body, differences in flow (blood distribution) between organs depend on relative arteriole resistances. Arterioles contain smooth muscle, which can either: - **Relax** and cause the vessel radius to increase (**vasodilation**). - **Contract** and decrease the vessel radius (**vasoconstriction**). Arteriolar smooth muscles possess spontaneous activity called **intrinsic tone**. The mechanisms controlling vasoconstriction and vasodilation in arterioles fall into two categories: 1. **Local controls**. 2. **Extrinsic (reflex) controls**. ### Arteriolar Tone: Local Controls **Local controls**: Independent of nerves or hormones → organs alter their own arteriolar resistances (E.g. paracrine signals). **Classification**: - **Active hyperemia**: Increased blood flow when metabolic demand increases. - **Flow Autoregulation**: To maintain flow, due to changes in supply or pressure. - **Reactive hyperemia**: Following complete occlusion of blood flow. - **Response to Injury**: Cause vasodilation, part of inflammation (Eicosanoids). ### Arteriolar Tone: Local Controls **Active hyperemia**: Depends on chemoreceptors for O2 and metabolic products (E.g. CO2, H+, adenosine, K+, Eicosanoids and bradykinin). **Flow Autoregulation**: Depends on chemoreceptors and baroreceptors (monitor vessel wall stretch / BP). Can cause vasodilation or vasoconstriction. **Muscle stretch** → dilation / ↑ → constriction (**myogenic responses**) ### Arteriolar Tone: Extrinsic Controls - **Sympathetic Neurons** (Norepinephrine) → Vasoconstriction - **Other Autonomic Neurons** (Nitric Oxide) → Vasodilation **Hormones:** - **Epinephrine** (adrenal medulla) → Part of sympathetic → Vasoconstrictor - **Angiotensin II** → Part of the RAAS system → Vasoconstrictor - **Vasopressin** (Antidiuretic hormone) → Vasoconstrictor - **Atrial Natriuretic Peptide** → Vasodilator ### Arteriolar Tone: Extrinsic Controls - **Thirst** - **Hyperosmolality** - **Hypernatremia** - **Hypovolemia** - **Hypervolemia** → **Brain** → **ADH** - **Angiotensinogen** → **Renin** → **Angiotensin I** → **ACE** → **Angiotensin II** → **Artery** → **Vasoconstriction** - **Renal perfusion Pressure** → **Kidney** → **Aldosterone** → **Na+ retention** - **Heart** → **ANP** → **Renal Na and H2O excretion** → **Vasodilation** ### Arteriolar Tone: Extrinsic Controls **Renin-Angiotensin-Aldosterone Pathway** 1. **Dehydration**, **Na+ deficiency**, or **hemorrhage** → 2. **Decrease in blood volume** → 3. **Decrease in blood pressure** → 4. **Juxtaglomerular cells of kidneys** → 5. **Increased renin** → 6. **Liver** → **Angiotensinogen** → 7. **Increased angiotensin I** → 8. **Lungs** (ACE = Angiotensin Converting Enzyme) → 9. **Increased angiotensin II** → 10. **Adrenal cortex** → 11. **Increased aldosterone** → 12. **In kidneys, increased Na+ and water reabsorption** → 13. **Increased blood volume** → 14. **Blood pressure increases until it returns to normal** → 15. **Vasoconstriction of arterioles** → 16. **Increased K+ in extracellular fluid** ### Arteriolar Tone: Endothelium Endothelial cells respond to various substances and mechanical stimuli. They secrete several **paracrine chemicals** that diffuse to the adjacent vascular smooth muscle and induce either relaxation or contraction. - **Nitric Oxide** (endothelium-derived relaxing factor): Paracrine vasodilator. - **Prostacyclin** (prostaglandin 12): Vasodilator - **Endothelin-1 (ET-1)**: Vasoconstrictor. ### 4- Capillaries At any given moment, 5% of the total blood is flowing through the capillaries. This 5% that is performing the ultimate purpose of the entire circulatory system, the **exchange of nutrients, metabolic products, and cell secretions**. Each individual capillary is only about 1 mm long with an inner diameter of about 8 µm, just wide enough for an erythrocyte to squeeze through. The endothelial cells of a capillary are not attached tightly to each other but are separated by narrow, water-filled spaces termed **intercellular clefts**. ### Capillary Networks - **Intercellular clefts** - **Endothelial cell** - **Enlargement of capillary** - **To veins** - **Metarteriole** - **Smooth muscles** - **Arteriole** - **Precapillary sphincters** - **Capillaries** - **Venule** ### Capillary Networks **Microcirculation**: Composed of arterioles, capillaries, and venules. Blood flow through capillaries depends very much on the state of the other vessels that constitute the microcirculation. In some tissues, blood enters capillaries not directly from arterioles but from vessels called **Metarterioles**, which connect arterioles to venules. The site at which a capillary exits from a metarteriole is surrounded by a ring of smooth muscle, the **Precapillary Sphincter**, which relaxes or contracts in response to local metabolic factors. ### Velocity of Capillary Blood Flow When a continuous stream (artery) moves through consecutive sets of tubes (capillaries), the velocity of flow decreases as the sum of cross-sectional areas of tubes increases. **Maximizes time for substance exchange.** ### Capillary Exchange **Definition**: The movement of substances between blood and interstitial fluid. ### Capillary Exchange: Mechanisms - **Diffusion**: The most important → exchange of nutrients and gases down the concentration gradient (Through membranes and intercellular clefts). - **Transcytosis**: By Endocytosis and Exocytosis. E.g. Some hormones. - **Bulk Flow**: Down the pressure gradient (Filtration and Reabsorption). - **Mediated Transport**: In some tissues (E.g. the brain). ### Bulk Flow Across the Capillary Wall - **Bulk Flow**: Movement of large amounts of material (protein-free plasma) in the same direction from an area of high pressure to an area of low. - The **function** of bulk flow is the **distribution of extracellular fluid volume**. - **Filtration** is movement of material into interstitial fluid promoted by blood hydrostatic pressure & interstitial fluid osmotic pressure. - **Reabsorption** is movement from interstitial fluid into capillaries promoted by blood colloid osmotic pressure. Balance of these pressures (**Starling Forces**) is **Net Filtration Pressure**. ### Edema **An abnormal accumulation of fluid in the interstitial spaces** ### Edema: When Filtration > Reabsorption 1. **Excess Filtration** (↑ Hydrostatic pressure or size of intercellular clefts) - Increased arterial pressure or venous pressure. - Increased permeability of capillaries (E.g. inflammation). 2. **Inadequate Reabsorption** (↓ Blood colloid pressure) - Decreased level of plasma proteins (↓ synthesis or ↑ loss of proteins). - E.g. Liver disease, burns, malnutrition, kidney disease, lymphatic vessel block ### 5- Venules - **Blood flow** (Capillaries → Venules → Veins → Heart). - **Exchange of materials** also occurs between the interstitial fluid and venules. - The permeability to macromolecules is **greater for venules than capillaries**. - Venules & Veins have large blood capacity → they are **capacitance vessels**. - Site of **leucoctye migration** into tissues during inflammation and infection. ### 6- Veins - The force driving venous return is the pressure difference between peripheral veins (initially 10-15 mmHg) and the right atrium (0 mmHg). - The low pressure difference is adequate due to **low resistance** (large vein diameters). Thus, a major function of the veins is to act as low-resistance conduits for blood flow from the tissues to the heart. - Peripheral veins of arms and legs contain **valves that permit one-way flow** - Their diameters are reflexively altered by changes in blood volume, thereby **maintaining peripheral venous pressure and venous return to the heart**. ### Determinants of Venous Pressure - The main determinants of pressure within a vein are: The **volume of blood** within it and the **compliance of its walls**. - **Venules and Veins** contain most of blood volume (around 60%) → have thin compliant walls to help accommodate large volumes with little pressure. - The main mechanisms that increase venous pressure and flow are: - **Vasoconstriction** (by the sympathetic nervous system) - **The Respiratory Pump** - **The Skeletal Muscle Pump** ### Blood Volume Distribution - **Heart**: 9% - **Arteries**: 11% - **Arterioles and Capillaries**: 7% - **Venules and Veins**: 61% - **Pulmonary Circulation**: 12% **NOTE**: Arteriole constriction reduces forward flow, whereas vein constriction increases forward flow. ### Determinants of Venous Pressure **Skeletal muscle pump** - Contraction of muscles compresses the vein, the distal valve closes while the proximal valve opens, and blood flows to the heart. **Respiratory pump** - Decreased thoracic pressure and increased abdominal pressure during inhalation, moves blood into thoracic veins and the right atrium. ### 7- Regulation of Blood Pressure The mean systemic arterial pressure (MAP) is the product of: 1. **cardiac output** (CO) 2. **total peripheral resistance** (TPR) $MAP = CO \times TPR$ TRP is the combined resistance to flow of all the systemic blood vessels. For this reason, TPR is also known as systemic vascular resistance (SVR). Deviation in MAP will elicit homeostatic reflexes so that CO and/or TPR will change in the direction required to minimize the initial change in MAP. **MAP Change** → **Input** → **Cardiovascular Center** → **Output** → **Correction** ### Regulation of Blood Pressure The cardiovascular centre is the main region for nervous system regulation of the heart and blood vessels. **INPUT TO CARDIOVASCULAR CENTRE** (nerve impulses) - **From higher brain centres**: cerebral cortex, limbic system, and hypothalamus. - **From proprioceptors**: monitor joint movements. - **From baroreceptors**: monitor blood pressure - **From chemoreceptors**: monitor blood acidity (H+), CO2, and O₂. **OUTPUT TO EFFECTORS** (increased frequency of nerve impulses) - **Heart**: decreased rate. - **Heart**: increased rate and contractility - **Blood vessels**: vasoconstriction. ### Baroreceptor Reflexes Arterial receptors that respond to changes in pressure. Sensory neurons that are highly sensitive to stretch. E.g. Found in Aorta Arch & Carotid Sinus. Serve as pressure sensors, or **baroreceptors** because the degree of wall stretching is directly related to pressure in the artery. ### Arterial Baroreceptor Reflex Lower MAP → Less stretch → Less baroreceptors and cardiovascular center activity. This leads to: - ↑ sympathetic and ↓ parasympathetic activity to the heart (higher HR and SV). - ↑ sympathetic activity to vessels and ↑ angiotensin II and vasopressin (vasoconstriction → higher resistance and higher venous return). - Increased MAP induces the opposite. ### Long-Term Regulation: Blood Volume Baroreceptor reflexes adapt and cannot set long-term arterial pressure. The major mechanism for long-term regulation is through blood volume. **Blood volume** → **venous pressure** → **return** → **EDV (Preload)** → **SV** → **CO**. **Regulation**: An increase in pressure causes a decrease in blood volume. An increase in the blood volume for any reason increases the blood pressure, which tends to bring the blood volume back down. Blood pressure can stabilize, in the long run, only at a value at which blood volume is also stable. ### Other Cardiovascular Reflexes Stimuli acting upon receptors other than baroreceptors can initiate reflexes that cause changes in arterial pressure (**chemoreceptors & proprioceptors**). E.g. stimuli that cause an increase in blood pressure: - Decreased arterial O2 concentration, increased arterial CO2 concentration, decreased blood flow to the brain, and pain originating in the skin.

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