Hemodynamics and Venous Return Lecture Notes PDF

PHYSIOLOGY LECTURE | TRANS 4 LE Hemodynamics and Venous Return DR. JUNE CATHLEEN C. CASTILLO, DPBA | Lecture...

PHYSIOLOGY LECTURE | TRANS 4 LE Hemodynamics and Venous Return DR. JUNE CATHLEEN C. CASTILLO, DPBA | Lecture Date (11/20/2023) | Version 4 03 OUTLINE → Maintaining internal HOMEOSTASIS: an appropriate I. Circulatory System VI. Venous Return environment needed by the body for the survival and optimal A. Systemic Circulation vs. A. Venous System function of the cells. Pulmonary Circulation B. Venous Compliance The body tends to maintain its HOMEOSTASIS through its B. Overview Of The C. Venous Return own regulating and control mechanisms Circulatory System D. Factors that can cause II. Hemodynamics transient changes in Venous SYSTEMIC CIRCULATION A. Blood Flow Return Systemic arteries carry blood rich in oxygen from the heart to B. Hemodynamics E. Venous Valves the body tissues. And from the tissues which now contain III. Blood Pressure F. Central Venous Pressure deoxygenated blood is returned to the heart through systemic A. Blood Pressure G.Influence of CVP and PVP veins. It continues to the pulmonary circuit. 💬 IV. Regulation of Arterial Blood on VR 84% of the blood volume circulates in the systemic circulation. Pressure H. CVP and Cardiac Output 64% of it is in the venous system= 46% were in the small A. Intrinsic and Extrinsic I. CVP Estimation by PE veins and 18% were in the large veins Control of Vascular Tone VII. Review Questions B. Arterial Baroreceptors VIII. References PULMONARY CIRCULATION C. Neural Control Pulmonary arteries carry deoxygenated blood to the lungs for V. Autonomic Nervous System gas exchange releasing CO2 and acquiring oxygen making the A. Immediate Control blood oxygenated. Pulmonary veins will carry freshly oxygenated B. Intermediate Term Control blood from the lungs back to the heart returning to systemic C. Renal Blood Volume circulation. Pressure Control 16% of the blood volume circulates in the pulmonary circulation. → Approximately half percent are in pulmonary circulation and ❗️ Must Know 💬 Lecturer 📖 Book 📋 Previous Trans half is in the heart. SUMMARY OF ABBREVIATIONS CO Cardiac Output TPR Total Peripheral Resistance KE Kinetic Energy PE Potential Energy Pdyn Dynamic Pressure PLat Static Pressure CVP Central Venous Pressure PVP Pulmonary Venous Pressure VR Venous Return NTS Nucleus of the tractus solitarius RVLM Rostral Ventrolateral Medulla RAAS Renin-angiotensin-aldosterone system Figure 1. Simplified Diagram of the Circulatory System SNS SV Sympathetic Nervous System Stroke volume 💬 💬 oxygenated Imagine the circulatory system as a closed loop of tubes. As blood was pumped out of the heart from left ventricle, SVR Systemic Vascular Resistance blood is carried by your aorta and then your arteries LEARNING OBJECTIVES ✔ ✔ Describe the component parts of the circulatory system. Explain the effects of the determinants of blood pressure. 💬 Inthrough into the tissues. your tissue level, there would be oxygen and nutrient exchange your capillaries, and then deoxygenated blood would go ✔ Demonstrate the procedures for determining blood pressure to your venous circulation and enter the right atrium then through Correlate the Korotkoff sounds to pressure changes in the blood 💬 ✔ the vena cavas. vessels. The deoxygenated blood would be carried by your pulmonary ✔ Compare the intrinsic and extrinsic mechanisms of regulating artery to the lung for oxygenation, and then oxygenated blood blood pressure would be carried by your pulmonary vein into the left atrium and Distinguish the venous system from the arterial system. 💬 ✔ left ventricle. ✔ Describe the mechanisms that return blood to the heart. The heart would pump the newly oxygenated blood and the cycle ✔ Describe the venous return curve. goes on again. ✔ Explain the relationship between venous return, cardiac output, and circulatory pressures. I. CIRCULATORY SYSTEM A. SYSTEMIC CIRCULATION VS PULMONARY CIRCULATION CIRCULATORY SYSTEM Basic Function: serve the needs of the body: → via transport of nutrients to the body including oxygen, → transport of waste products away from the body, → Transport of hormones from one part of the body to another Figure 2. Structure of Blood Vessels LE 1 TG 1 | Verdillo, Versoza, Vicencio, Vicente, Villamil, TE | Ramos, R., Seriña, M. AVPAA | Vivero, M. PAGE 1 of TRANS 1 E. Villanueva, I. Villanueva 22 PHYSIOLOGY | LE1 Hemodynamics and Venous Return | Dr. June Cathleen C. Castillo, DPBA 💬 💬 Artery carries oxygenated blood. Arteriole, which are small arteries that lead into your capillaries. → → Pulmonary artery Aorta Capillaries are where the exchange of nutrients and oxygen → Brachiocephalic happen. Deoxygenated blood would flow back into the heart → Subclavian through your venules and veins, which are capacity vessels. → Common carotid artery → Common iliac artery B. OVERVIEW OF THE CIRCULATORY SYSTEM BLOOD VESSELS MUSCULAR ARTERY Main Function: Distribute and exchange nutrients and waste Farther from the heart, where the surge of blood has dampened, products. the percentage of elastic fibers in an artery’s tunica intima All blood vessels are distensible decreases and the amount of smooth muscle in its tunica → Accommodate pulsatile output of the heart media increases. Compliance = distensibility x volume Their thick tunica media allows muscular arteries to play a → Blood vessels become less compliant as humans age regulatory role in vasoconstriction and vasodilation. Arteries and Veins share common structure that consist of three In contrast, their decreased quantity of elastic fibers limits their 📖 layers: Tunica Intima ▪ Innermost layer, lined by a single layer of specialized ability to expand. Fortunately, because the blood pressure has dampened by the time it reaches these more distant vessels. 📖 semipermeable epithelium called endothelium. Tunica Media There is no “line of demarcation” where an elastic artery suddenly becomes muscular. ▪ Middle layer consisting chiefly of concentric layers of → There is a gradual transition as the vascular tree repeatedly 📖 helically arranged smooth muscle cells. Tunica Externa/Adventitia branches. → Muscular arteries branch to distribute blood to the vast network ▪ Outermost layer, It is a connective tissue consisting primarily of arterioles. For this reason, a muscular artery is also known of type I collagen fibers and elastic fibers. as a distributing artery. → Lumen ▪ Examples of muscular arteries ▪ A hollow passageway through where blood flows. − Brachial artery − Radial artery Compared to arteries, veins have larger lumens, thinner walls, − Popliteal artery less smooth muscle, and elastic tissue making it look more − Femoral artery collapsed under the microscope. Arterioles have thicker walls than veins and venules because ARTERIOLE they are closer to the heart and receive blood that is surging at a Also called as “resistance vessels” far greater pressure. Small lumen averaging 30 um or less in diameter Critical in slowing down or resisting blood flow and, thus, causing a substantial drop in blood pressure → Very small artery that leads to a capillary Arterioles have the same three tunics as the larger vessels, but the thickness of each is greatly diminished. → The critical endothelial lining of the tunica intima is intact. → The tunica media is restricted to one or two smooth muscle cell layers in thickness. → The tunica externa remains but is very thin. The muscle fibers in arterioles are normally slightly contracted, causing arterioles to maintain a consistent muscle tone—in this case referred to as vascular tone. Arterioles are the primary site of both resistance and regulation of blood pressure. Figure 3. Anatomy of (a) Artery and (b) Vein. The precise diameter of the lumen of an arteriole at any given ARTERIES moment is determined by neural and chemical controls, and Distributes oxygenated blood from the heart to the body tissues vasoconstriction and vasodilation in the arterioles are the primary Have strong vascular walls because they receive blood at high mechanisms for distribution of blood flow. velocity Metarteriole arises from terminal arteriole, it has a precapillary Contains elastin which allows them to stretch and recoil. sphincter allowing control of inflow of blood to the capillary bed. Composed of smooth muscle which allows them to constrict and vasodilate Serve as conduit by absorbing the pressure generated by systolic contraction Tunica media is the thickest and most conspicuous part of the artery. Thick walls help withstand high pressure from the blood ejected by the heart, especially from the vessels closest from the heart, for example the aorta. Arteries with thicker walls have greater amounts of elastic fiber. ELASTIC ARTERIES Arteries with thick walls contain a high percentage of elastic fibers. Allows the vessels to expand as blood pumps from the ventricle then will recoil. Also called conducting artery, because it contains a larger diameter of lumen that enables it to accept larger volumes of blood from the heart and conduct it to smaller branches Figure 4. Different Types of Arteries Contains high elastin content, >10mm in diameter, near the heart Examples of elastic arteries: PHYSIOLOGY Hemodynamics and Venous Return PAGE 2 of 22 PHYSIOLOGY | LE1 Hemodynamics and Venous Return | Dr. June Cathleen C. Castillo, DPBA CAPILLARIES VENULES Main Function: exchange of gasses and other substances Extremely small veins, generally 8–100 um in diameter. (occurs in the capillaries between the blood and the surrounding Multiple venules join to form veins. cells and their tissue or interstitial fluid) The walls of venules consist of endothelium, a thin middle layer Primary exchange vessel & microscopic channel that supplies with a few muscle cells and elastic fibers, plus an outer layer of blood to the tissues themselves in a process called perfusion. connective tissue fibers that constitute a very thin tunica externa. → Normal adult contains billions of capillaries. Venules as well as capillaries are the primary sites of emigration With highest cross-sectional area and surface area compared to or diapedesis other vessels → Diapedesis The diameter of a capillary lumen ranges from 5–10 um; the ▪ Process through which WBCs adhere to the endothelial smallest are just barely wide enough for an erythrocyte to squeeze lining of the vessels and then squeeze through adjacent through. cells to enter the tissue fluid Slow flow along the capillaries, but makes nutrient exchange SUMMARY OF BLOOD VESSELS optimal due to more time of exchange Vessels closest to the heart would be predominantly elastic, and have higher elastic tissue content. To withstand the high pressure of blood going out of the heart all arteries have thick walls Muscularity will increase as diameter decreases until terminal arteriole, where smooth muscle predominates. Capillaries are composed of a single layer of cell making them the best site for gas exchange. Short tubes that are one cell thick. After blood passes through the capillaries for gas exchange it passes through an increasing size of blood vessels. Near the heart the number of veins decreases and the thickness and composition of the vein wall change. Figure 5. Structure of arterioles, capillaries, and venules. In a capillary bed, arterioles give rise to metarterioles. Precapillary sphincters located at the junction of a metarteriole with a capillary regulate blood flow. A thoroughfare channel connects the metarteriole to a venule. An arteriovenous anastomosis, which directly connects the arteriole with the venule, is shown at the bottom. Figure 7. Internal diameter, wall thickness, and relative amounts of VEINS the principal components of the vessel walls of the various blood vessels that constitute the circulatory system. Table 1. Arteries vs. Veins Arteries Veins Except for PULMONARY Except for PULMONARY ARTERY, arteries carry VEINS, carry oxygen-poor oxygen-rich blood from the blood from the body tissues heart to the tissues back to the heart More elastic tissues and Usually with large lumen smooth muscle in tunica media compared to veins Thinner walls compared to arteries Look collapsed under the microscope (Less smooth muscle and elastic tissue) Figure 6. Anatomy of Different Types of Veins. Capacitance vessels; blood vessels that conduct blood towards the heart. Compared to arteries, these are thin-walled with large and irregular lumens. Tunica media is less pronounced compared to that of the artery. Low-pressure vessels → Larger veins are commonly equipped with valves. → Valves promote the unidirectional flow of blood toward the heart and prevent backflow toward the capillaries caused by the inherent low blood pressure in veins as well as the pull of gravity. PHYSIOLOGY Hemodynamics and Venous Return PAGE 3 of 22 PHYSIOLOGY | LE1 Hemodynamics and Venous Return | Dr. June Cathleen C. Castillo, DPBA DISTRIBUTION OF BLOOD VOLUME II. HEMODYNAMICS Approximately half of the pulmonary circulation takes place in A. BLOOD FLOW the heart (end diastole) and another half in pulmonary Quantity of blood that passes a given point in the circulation in a circulation. given period of time Overall blood flow in the total circulation of an adult person at rest is about 5000 ml/min B. HEMODYNAMICS Physics of fluid flow through vasculature VELOCITY → the distance that a particle of fluid travels with regard to time, and it is expressed in units of distance per unit time (e.g. cm/sec) FLOW → rate of displacement of a volume of fluid over time (volume per unit of time e.g. cm3/sec) VELOCITY AND CROSS-SECTIONAL AREA Figure 8. Distribution of Blood (in percentage of total blood) in the Different Parts of the Circulatory System Table 2. Distribution of Blood Volume. Absolute Relative Volume Location Volume (mL) (mL) Systemic Circulation Aorta and large arteries 300 6.0 Small arteries 400 8.0 Capillaries 300 6.0 Figure 9. Velocity and Cross-sectional Area of the Blood Small veins 2300 46.0 Vessels Large veins 900 18.0 Total 4200 84.0 Cross-sectional area significantly increases at the level of Pulmonary Circulation capillaries due to the number of capillaries that are in parallel with Arteries 130 2.6 each other. Blood velocity is at the lowest point at the level of capillary Capillaries 110 2.2 Total cross-sectional area is at its peak at the level of capillaries. Veins 200 4.0 Total 440 8.8 Heart (End Diastole) 360 7.2 Total 5000 100 CONCEPT CHECKPOINT Q1. The pointed peripheral vessel carries which kind of blood? In a rigid tube, velocity (V) and flow (Q) are related to one another ❗ by the cross sectional area (A) of the tube: V = Q/A Velocity of blood is directly proportional to the blood flow and is inversely proportional to the cross sectional area thus velocity decreases as blood traverses the arterial system and is at minimum at the capillaries and increases progressively towards the venous system. A. Oxygenated B. Deoxygenated BERNOULLI’S PRINCIPLE Answer: A. Oxygenated Sum of potential, kinetic, and pressure energy per unit mass of an The other is vein. To answer, identify the structure first and know incompressible, non-viscous fluid remains constant. the function. Blood has mass and velocity → Kinetic Energy (KE) of flowing blood → proportionate to mean velocity PHYSIOLOGY Hemodynamics and Venous Return PAGE 4 of 22 PHYSIOLOGY | LE1 Hemodynamics and Venous Return | Dr. June Cathleen C. Castillo, DPBA → Potential Energy (PE) → Pressure exerted laterally against Dynamic Component of Pressure the walls of the vessel → P = pv^2/2 → The total energy (E) of the blood flowing within the vessel → Where (assuming no gravitational effects) ▪ P is Pressure ▪ E = KE + PE ▪ p is density of the fluid → Increase in KE ➔ a reciprocal decrease in the magnitude of PE ▪ v is the velocity ➔ decrease in the lateral pressure. Dynamic Pressure is increased in narrow areas meaning there will → An increase in velocity leads to a decrease in lateral be an increase in velocity at the site of stenosis. pressure. → Causing low lateral pressure to the vessel wall = Vessel Velocity is inversely proportional to area. ❗ collapse. Clinical Pearl: At narrow areas of constriction (e.g. vessel embolus or atherosclerotic plaque), noted with high velocity which is associated with high kinetic energy and thus, high Pdyn. → Increase in Pdyn → Decrease in lateral pressure → Decreased perfusion of distal segments after the obstruction. CASE SCENARIO You are a 25-year old healthy medical intern on duty at the ER today. Figure 10. Flow of Kinetic and Potential Energy Your first patient at the ER, Tatay Lito, came in with a complaint of severe left leg pain. After doing a doppler ultrasound, they found a blockage along his distal femoral artery. Figure 11. Bernoulli’s Principle in Relation to Stenosis Clinical Application: Stenosis → Narrowing of vessel → The cross-sectional area of the vessel would decrease, and will be inversely proportional to the velocity. → Velocity will increase and lead to an increased Kinetic energy which will significantly decrease the potential energy. Q2. Which law of physics explains the poor circulation → After passing through stenosis, KE will revert back to its distally after a point of vessel stenosis/blockage? pre-stenosis state, but due to turbulence and stenosis that occur and lead to energy loss, PE will not fully revert back to its A. Bernoulli’s Principle original state and will remain decreased B. Poiseuille’s Law ▪ Low lateral pressure to the vessel wall → vessel collapse Answer: A. Bernoulli’s Principle → Post-stenosis will lead to decreased flow to the distal To answer, familiarize yourself with the laws and principles segment. involved in Hemodynamics. It can also be Poiseuille’s law RELATIONSHIP BETWEEN VELOCITY AND PRESSURE because it is the relationship of radius to your flow, but Bernouilli’s principle is the best answer because post stenosis will lead to decreased flow in the distal segment due to low lateral pressure to the vessel wall causing vessel collapse. Space intentionally left blank Figure 12. Effect of Pressure and Velocity Total P = PDyn + PLat → PDyn = Blood flow with velocity. → PLat = Pressure exerted against the vessel wall. PHYSIOLOGY Hemodynamics and Venous Return PAGE 5 of 22 PHYSIOLOGY | LE1 Hemodynamics and Venous Return | Dr. June Cathleen C. Castillo, DPBA LAMINAR FLOW VS. TURBULENT FLOW LAMINAR FLOW Normal flow of blood: concentric layers of blood moving along ❗️ ❗️ blood vessels Slowest: near the vessel wall due to friction (higher resistance) Fastest: at the center of the stream Table 3. Laminar Flow vs. Turbulent Flow Laminar Flow Turbulent Flow Type of motion wherein fluid Fluid elements do not remain moves as a series of confined in a specific lamina individual layers, each layer moving in different velocity. Center tube with highest Rapid and radial mixing velocity, velocity decreases parabolically towards the vessel wall ❗️ Figure 14. Poiseuille’s Law. ❗️Biggest determinant of the flow is vessel diameter Vessels are NOT Rigid. Flow is PULSATILE. This layer in contact to Vortices (swirls) are present vessel wall→ “motionless” Distribution of velocities is chaotic Greater force needed to push fluid out of the tube → increase work of heart Table 4. Reynold’s Number Type of Flow Reynold’s Number Laminar Flow 3000 💬 Laminar flow can be computed using Reynold’s Number. Figure 14. A. Demonstration of the effect of vessel diameter on blood flow. B, Concentric rings of blood flowing at different velocities; the farther away from the vessel wall, the faster the flow. d - diameter, P - pressure difference between the two ends of the vessels. If radius is doubled, the increase in flow is 2 raise to 4th power = 16 ml/min If radius is quadrupled, the increase in flow is 4 raise to the ❗️ 4th power = 256 ml/min CLINICAL PEARL: Patient given with vasodilator, vessel diameter increased by 2x the flow would significantly increase. CASE SCENARIO Figure 13. Laminar Flow (A) Vs Turbulent Flow (B) You are a 25-year old healthy medical intern on duty at the ER today. Your first patient at the ER, Tatay Lito, came in with a complaint of severe left leg pain. After doing a doppler ultrasound, they found a blockage along his distal femoral artery. ❗High density, large diameter tubes, high velocity flow, low fluid viscosity predisposes to turbulent flow. Q3. From 2mm in radius, the radius of the clogged artery is now 1mm. Flow through the artery would decrease by how much? Reynolds number is dimensionless (unitless). → Sound of turbulence in vessels present as bruit A. 8x → Sound of turbulence seen in heart as murmurs B. 16x Answer: B. 16x POISEUILLE’S LAW To answer, identify which principle is applied for relationship of Applies to steady/nonpulsatile laminar flow of Newtonian fluids FLOW and RADIUS. Compute for Flow using Poiseuille’s Law. through rigid cylindrical tubes. Increase flow as radius and pressure gradient increases. Decrease flow as viscosity and length of tube increases. Relationship between pressure and flow → Flow is directly proportional to radius and pressure gradient → Flow is inversely proportional to viscosity and length of tube PHYSIOLOGY Hemodynamics and Venous Return PAGE 6 of 22 PHYSIOLOGY | LE1 Hemodynamics and Venous Return | Dr. June Cathleen C. Castillo, DPBA OHM’S LAW VASCULAR RESISTANCE Resistance = Voltage drop / Current Changes in vascular resistance can occur when there is a change Resistance per unit length of individual small blood vessel in caliber of vessels. Ohm’s Law in Physiology: Most important factor: contraction of circular smooth muscle cells → Arterioles → thick coat of circularly arranged smooth muscle fibers → can vary lumen radius WALL TENSION As blood flows through a vessel, it exerts a force on the vessel wall parallel to the wall. Transmural pressure the difference in pressure, in and outside the vessel. Resistance to flow depends only on dimension of a tube and The smaller the radius, the lower the tension on the wall ❗️ characteristics of fluid Radius as the principal determinant of resistance to blood flow ❗ necessary to balance the distending pressure ❗ Aorta → Tension = 170,000 dynes/cm Capillaries → 16 dynes/cm CLINICAL PEARL: Dilated Aorta T = Tensional stress on the wall ΔP = transmural pressure r = radius w = wall thickness SHEAR STRESS The tangential force of the flowing blood on the endothelial surface of the blood vessel Figure 15. Laminar Flow (Left) Vs Turbulent Flow (Right) Highest resistance is found in the individual capillary, but recall fundamental physics: Shear stress → nitric oxide release → vasodilation Shearing of vessel walls factors: → High velocity flow → Permeability of vessel walls → Biochemical activity ❗ → Blood coagulation Clinical Pearl: Hypertension → There would be subendothelial and endothelial changes that can predispose the vessel to tear → Uncontrolled hypertension leads to dissection of vessels (dissecting vessel aneurysm) RHEOLOGICAL PROPERTY OF BLOOD Blood ❗ ❗Individual Resistance Vessels = capillaries Total Resistance Vessels = arterioles → Non-Newtonian, viscosity may vary → “Apparent Viscosity” ▪ derived value of viscosity obtained under a particular → Although individual resistance is greatest in the capillary, more condition of measurement capillaries (billions of capillaries) are arranged in parallel than → Basically a suspension of formed elements (erythrocytes) in a arterioles homogeneous fluid (plasma); apparent viscosity varies as a → Total Resistance in capillaries is less than in arterioles function of hematocrit. In using the formula of getting the total resistance for vessels in Viscosity depends on HEMATOCRIT parallel, the Total R = resistance divided by the number of → whole blood is 3-4x as viscous as H2O resistors → In large vessels, increase in hematocrit cause increase in → Total resistance would significantly decrease → Why the arterioles are the resistance vessels ❗️ viscosity Fahraeus-Lindqvist effect: in small vessels, erythrocytes move to the center of the vessel, leaving cell free plasma at the vessel wall Space intentionally left blank → Less appreciable inc in viscosity. ▪ The erythrocytes are lined up in small vessels. ▪ Increase in velocity is less appreciable in small vessels. PHYSIOLOGY Hemodynamics and Venous Return PAGE 7 of 22 PHYSIOLOGY | LE1 Hemodynamics and Venous Return | Dr. June Cathleen C. Castillo, DPBA Hematocrit have little effect on TPR except when changes are CASE SCENARIO ❗ large CLINICAL PEARL: Polycythemia vs Anemia → Polycythemia: High hematocrit = High viscosity → Increases Your second patient, Michael, a 70 year-old male, came in at the ER with severe headache and nape pain. The ER consultant asked you to take the patient’s mean arterial pressure. TPR → Increases work of heart and BP The first Korotkoff sound came in at 180 mmHg. The last audible → Anemia: Low hematocrit = Low viscosity → Decreases TPR → Korotkoff sound disappeared at 120 mmHg. Decreased work of heart and BP Q4: What is the patient’s Mean Arterial pressure? III. BLOOD PRESSURE a. 140 mmHg A. BLOOD PRESSURE b. 150 mmHg Arterial Blood Pressure ANS: A. 140 mmHg → force of blood against the walls of the arteries Systolic NOTE TO ANSWER: → maximal arterial pressure within the cardiac cycle 1. Identify which is the given values Diastolic 2. Recall the formula for Mean Arterial Pressure: → minimal arterial pressure within the cardiac cycle MAP = (1 systolic + 2 diastolic) / 3 Pulse Pressure → difference between systolic and diastolic pressure DETERMINANTS OF ABP Physical Factors MEAN ARTERIAL PRESSURE → Fluid Volume and Arterial Compliance (static elastic 📖 Average force that drives blood flow into the blood vessels The average arterial pressure during a single cardiac cycle, ~80 characteristic of system) Physiologic Factors 💬 mmHg [Guyton & Hall] → Cardiac output (HR x SV) and Total Peripheral Resistance Considered a better indicator of perfusion to vital organs than SBP ( or Systemic Vascular Resistance) As blood is pumped out of the left ventricle into the aorta and distributing arteries, pressure is generated. ARTERIAL ELASTICITY 💬 → MAP = (CO x SVR) + CVP Aorta and Pulmonary arteries ▪ CVP: Central Venous Pressure → high elastin, highly distensible: 💬 → CVP is usually 0 → MAP ≈ CO x SVR ▪ Systole→ distends. ▪ SVR: Systemic Vascular Resistance ▪ Diastole → recoils and propel blood forwards. → CO = HR x SV If RIGID → Systole → no distension. → Diastole → cannot recoil. → Increased pressure needed for ventricles to pump blood vs. a large “afterload” ▪ Increased work of heart. → With age, decreased elastin, decrease arterial compliance ▪ Increase pulse pressure. Figure 16. Diagram of Mean Arterial Pressure with Cardiac Output and Systemic Vascular Resistance At normal resting heart rates, MAP can be approximated by the following equation. 💬 From here, the main determinants of the arterial blood pressure can be known. Space intentionally left blank Figure 17. Compliant arteries (A and B). Rigid arteries (C and D). Blood flows through the capillaries during systole (C), but ceases during diastole (D). PHYSIOLOGY Hemodynamics and Venous Return PAGE 8 of 22 PHYSIOLOGY | LE1 Hemodynamics and Venous Return | Dr. June Cathleen C. Castillo, DPBA → 💬 In a normal compliant aorta During systole, the heart contracts and pumps out a certain stroke volume (volume of blood). → Since the arterial compliance is normal, the aorta has distensibility (can stretch its walls). ▪ It can save a substantial fraction of stroke volume along its arterial walls. → 💬 ▪ there is an amount of blood not pumped out during systole During diastole (heart relaxation), the aorta recoils. ▪ There is an amount of blood not pumped out during systole. ▪ The volume of blood stored in the walls would be displaced during the recoil. ▪ This ensures that though the heart relaxed, the capillary flow 💬💬 would still be continuous along the tissues. In a rigid artery During systole, no blood (stroke volume) is stored or saved in 💬the walls since they are not elastic or distensible During diastole, no stroke volume will be pushed forward by the aorta to the capillaries → the flow to the capillaries would cease ARTERIAL COMPLIANCE Change in volume over a given change in pressure Units: ml/mmHg Compliance decrease with age because arteries become stiff Figure 19. Relation of Stroke Volume to Mean Blood Pressure CASE SCENARIO You took the BP again and it increased to 200/120. After taking the Xray, the result indicated that Michael has a rigid, atherosclerotic aorta. Q5: What is the patient’s Pulse pressure? a. 80 mmHg b. 120 mmHg ANS: A. 80 mmHg Know the Definition of Pulse Pressure PULSE PRESSURE Pulse Pressure = Systolic BP - Diastolic BP main determinants: Stroke Volume and Arterial Compliance (Physical determinants of arterial BP); → PP = SV / Ac Q6: If his aorta is RIGID, which of the following is TRUE? a. The rigid aortic wall will not allow it to distend during systole b. The rigid aortic wall will not allow it to distend during diastole ANS: A. Understand arterial compliance and how the aorta responds to the pumping action of the heart Figure 18. Change in Arterial Compliance in relation to age BLOOD PRESSURE MEASUREMENT STROKE VOLUME AND PULSE PRESSURE STROKE VOLUME Volume of blood pumped out of left ventricle during each systolic cardiac contraction SV = EDV - ESV Normal amount = 80 ml Normal Arterial compliance = 2ml/mmHg Thus, Normal Pulse Pressure = 40 mmHg A large stroke volume produces larger pulse pressure at any 💬 given compliance As the stroke volume increases → greater mean BP → the ❗ pulse pressure also increases Clinical Pearl: Hemorrhage → Hemorrhage → decreased SV → decreased pulse pressure → Age → decreased elastin in aorta → decreased arterial 💬 compliance → increased pulse pressure Widened pulse pressure: usually increase in systolic pressure and when there is a decrease in arterial compliance (e.g. rigid Figure 20. Schematic diagram of different non-invasive blood 💬 arteries) Narrow pulse pressure: occur with a decrease in SV (e.g. decreases in blood volume, decrease effectivity of pump) pressure measuring methods PHYSIOLOGY Hemodynamics and Venous Return PAGE 9 of 22 PHYSIOLOGY | LE1 Hemodynamics and Venous Return | Dr. June Cathleen C. Castillo, DPBA Non-invasive blood pressure measurement that can be intermittent KOROTKOFF SOUNDS or continuous Pulsatile sounds you can hear when taking blood pressure. → Intermittent BP measurement: use an inflatable cuff Due to the turbulence caused by brachial artery compression. ▪ Can be done manually (through auscultatory or palpatory method) or by automated method (e.g., oscillometry) → Continuous BP measurement: use volume clamp method and arterial applanation tonometry ▪ Arterial applanation tonometry can be automated (automated systems) and can be done manually (hand-held sensors) AUSCULTATORY BP MEASUREMENT Figure 22. Korotkoff Sound Volume in Between Systolic (Left) and Diastolic (Right) When the Blood pressure apparatus is pumped way above the systolic BP, the Korotkoff sound disappears. As you deflate the cuff, the Korotkoff sounds will reappear once it reaches the systolic BP (A) Sound is louder in between systolic and diastolic. Figure 21. Procedure for Auscultatory Blood Pressure Measurement Sound will be softer until it disappears, at the level of the diastolic pressure (B) Use a sphygmomanometer, which cuffs an artery, and a stethoscope to listen for the Korotkoff sounds. Steps: → Ask the patient to lose any tight clothing or to remove long sleeve garments to access their upper arm (do not use the arm that may have a medical problem). → Place the cuff in the upper arm and secure it. → Connect the cuff tubing to the sphygmomanometer and secure → Rest the patient’s arm on a surface that is leveled with their heart. → Place the stethoscope over the brachial artery in the bend of the elbow → Listen to the Korotkoff sounds → Pump up the cuff slowly → Listen when the pulse disappears (indication to stop inflating the cuff) Figure 23. Korotkoff Sound Volume Phases.How to Read an → Start to deflate the cuff very slowly while watching the level of Oscillometric Reading the gauge of the sphygmomanometer OSCILLOMETRIC MEASUREMENT → Note the sphygmomanometer reading when the pulse Used for self monitoring of blood pressure. reappears (record as the systolic pressure) Use of maximum volume change as an indication of the average → Deflate the cuff further until the pulse disappears (record as of systolic and diastolic blood pressure within the artery. the diastolic pressure) Uses a variety of algorithms and transducer microprocessors to → Record the two measurements: first indicate the systolic and detect changes in pressure. then the diastolic. Pulse detection by oscillometric machines depends on the ▪ Sample Reading: amount of change in the volume of the arm with each pulse. − 120/80 → With regular pulses and relatively smooth changing arm o 120 - Systolic reading. volume, it is much easier for the microprocessor to estimate the o 80 - Diastolic reading. systolic and diastolic Blood Pressure. → Tell the patient their blood pressure monitoring. → However if pulses are irregular and there are arm movements under the cuff, pressure changes in the cuff will not rise and fall smoothly, leading to difficulty in making precise calculations. Space intentionally left blank Space intentionally left blank PHYSIOLOGY Hemodynamics and Venous Return PAGE 10 of 22 PHYSIOLOGY | LE1 Hemodynamics and Venous Return | Dr. June Cathleen C. Castillo, DPBA Figure 26. Arterial Cannulation Technique Figure 24. How to Read an Oscillometric Reading OTHER NON-INVASIVE BP MONITORING Volume Clamp Method → Continuous non-invasive BP monitoring → obtained by applying pressure via the finger cuffs such that the blood volume flowing through the finger arteries is held constant → Cnap – the machine ▪ Detects blood volume changes in the finger, transforming plethysmographic signals into continuous blood pressure information Figure 27. How BP is Measured Using Arterial Cannulation IV. REGULATION OF ARTERIAL BLOOD PRESSURE A. INTRINSIC AND EXTRINSIC CONTROL OF VASCULAR TONE 💬 Intrinsic Important for local blood flow regulation → Myogenic mechanism → Endothelial factors: nitric oxide and endothelin → Local hormones and chemicals: arachidonic acid, histamine, bradykinin. → Tissue metabolites. Extrinsic 💬 → Tissue metabolites Primary function: regulation of arterial blood pressure by altering the systemic vascular resistance → Neural or Hormonal Figure 25. BP-monitoring Device and Reading ▪ Sympathetic nerves ▪ Angiotensin INVASIVE BLOOD PRESSURE MONITORING ▪ Atrial natriuretic peptide Continuous BP Monitoring Done through the cannulation of a peripheral artery Commonly utilized in the management of critically ill and perioperative patients Space intentionally left blank Figure 28. Factors That Affect Control of Vascular Tone at the Arterial Level PHYSIOLOGY Hemodynamics and Venous Return PAGE 11 of 22 PHYSIOLOGY | LE1 Hemodynamics and Venous Return | Dr. June Cathleen C. Castillo, DPBA Table 5. Summary of factors affecting the caliber of the arterioles → Immediate range of control of baroreceptors is around 100 to Vasoconstriction Vasodilation 180 mmHg → Inhibits vasoconstrictor area which leads to the increase in Local factors vagal stimulation and vasodilation Decreased local temperature Increased CO2 and decreased O2 Nucleus of the tractus solitarius (NTS) in the medulla Autoregulation Increase K+, adenosine, lactate → Site of the central projections of the chemoreceptors and Decreased local pH Increased local temperature 💬 baroreceptors 💬 Receives input from baroreceptors When stimulated, it sends inhibitory signals to the Rostral Endothelial products Endothelin-1 Nitric oxide 💬 Ventrolateral Medulla (RVLM) to inhibit vasoconstriction Sends excitatory signals to the cardiac vagal motor neurons in the nucleus ambiguous to increase parasympathetic Locally released platelet serotonin Kinins activity Thromboxane A₂ Prostacyclin → Stimulation of NTS would inhibit sympathetic nerve output flow Circulating neurohumoral agents of the peripheral blood vessel = depressor effect ▪ For patients with lesions at the NTS, they would have general Epinephrine (except in skeletal Epinephrine in skeletal muscle vasoconstriction which shows a pressor effect on the muscle and liver) and liver patient. Norepinephrine Calcitonin G-related protein ▪ Impulses that arise from aortic arch baroreceptors reach the Arginine vasopressin (AVP) Substance P NTS via the afferent fibers in the vagus nerve. Angiotensin II Histamine Endogenous digitalis-like Atrial natriuretic peptide (ANP) substance Neuropeptide Y Vasoactive intestinal polypeptide (VIP) Neural factors Increased sympathetic nerve Decreased sympathetic nerve activity activity These are factors affecting the caliber of the arterioles and thus, the vascular tone ARTERIAL PRESSURE REGULATION Under extrinsic control of blood pressure Immediate Control (control occurs over seconds) → ANS, Reflexes (Baroreceptor, Chemoreceptors, CNS ischemic response) Intermediate-Term Control (occurs from minutes to hours) → Renin-Angiotensin Aldosterone System (RAAS) → Stress relaxation of vasculature → Capillary Fluid Shift Figure 30. Carotid Sinus and Carotid Body and Their Innervations Long-Term (occurs days to weeks) → Renal-blood Volume Pressure Control C. NEURAL CONTROL ROSTRAL VENTROLATERAL MEDULLA (RVLM) Stimulating RVLM releases GLUTAMATE on preganglionic sympathetic neurons → excitatory input to sympathetic nerves → 💬 vasoconstriction. As RVLM is not inhibited, its effect on the nerves is always vasoconstriction However, an increase in BP would activate the Nucleus of the Tractus Solitarius (NTS) → NTS will send inhibitory signals to RVLM → vasodilation → decreased heart rate Figure 29. Chart for approximate potency of different control mechanisms at different time intervals after the onset of a disturbance to arterial blood pressure B. ARTERIAL BARORECEPTORS Arterial baroreceptors (or pressoreceptors) are stretch receptors 💬 located in the carotid sinuses and in the aortic arch Baroreceptors are activated when pressure in the carotid sinus and aortic arch increases Figure 31. Areas of the Brain and Their Roles in Nervous Regulation of Blood Circulation PHYSIOLOGY Hemodynamics and Venous Return PAGE 12 of 22 PHYSIOLOGY | LE1 Hemodynamics and Venous Return | Dr. June Cathleen C. Castillo, DPBA Table 6. Factors That Affect the Activity of RVLM Neurons 💬 Slower due to slow release of Norepinephrine and slow secondary messenger cAMP FACTORS AFFECTING ACTIVITY OF RVLM NEURONS DIRECT STIMULATION Parasympathetic → SA & AV Nodes, Atrial Myocardium Increase in CO2 Hypoxia (decrease in O2) EXCITATORY INPUT Cortex via hypothalamus Mesencephalic periaqueductal gray Brainstem Reticular Formation Pain Pathways Somatosympathetic reflex Carotid and aortic chemoreceptors INHIBITORY INPUT Cortex via hypothalamus Caudal ventrolateral medulla Caudal medullary raphe nuclei Lung inflation efferents Carotid, aortic, and cardiopulmonary baroreceptors Figure 32. Sympathetic Innervation of the Systemic Circulation RVLM can receive positive (excitatory) input from: → Cortex (via hypothalamus): explains why there are cardiac reactions in extreme emotions (e.g., stress, sexual excitement, anger) → Mesencephalic periaqueductal gray, brainstem reticular formation, pain pathways: explains why blood pressure increases in acute pain ▪ For prolong pain, there may already be vasodilation → Somatosympathetic reflex: activation of afferents from exercising muscles → Input from carotid and aortic chemoreceptors Inhibitory input can be received from: → Cortex via hypothalamus → Caudal medullary raphe nuclei → Lung inflation efferents → Activation of: ▪ Caudal ventrolateral medulla ▪ Carotid, aortic and cardiopulmonary baroreceptors CASE SCENARIO Your next patient at the ER is Carmine, a 20-year-old female who stepped on a nail. You took her BP and it is noted to be 140/80, which she said is unusually high for her. Q7: Which is true? a. Acute pain would lead to vasoconstriction of vessels b. Acute pain would lead to vasodilation of vessels Figure 33. Anatomy of Sympathetic Nervous Control of the ANS: A. Acute pain would usually be under your sympathetic system. Circulation Furthermore, it is important to understand what controls vasoconstriction and vasodilation of vessels. Note: as shown by the dashed red line, a vagus nerve that carries parasympathetic signals to the heart V. AUTONOMIC NERVOUS SYSTEM A. IMMEDIATE CONTROL 💬 Sympathetic 💬 All parts of the heart and blood vessels (except capillaries) Most parts of the circulatory system receive input from the 💬 sympathetic nerves Activation of which would release norepinephrine that acts on 💬 alpha 1 receptors mediating vasoconstriction Most arterioles constricted = increase in total peripheral 💬 resistance 💬 Most veins constricted = increase in venous return Release of Epinephrine = Beta activation of the heart = increase in heart rate, increase in rate of transmission of cardiac conductive tissue (dromotropy), and also increase in ventricular 💬 contraction (inotropy). Release of acetylcholine from postganglionic sympathetic nerves activates the muscarinic receptors in the heart resulting in decrease in heart rate, increase in rate of transmission of cardiac conductive tissue or dromotropy, and increase in ventricular 💬 contraction or inotropy. Alters heart rate and AV conduction slowly as compared to vagal stimulation. Figure 34. Effects of Increased BP PHYSIOLOGY Hemodynamics and Venous Return PAGE 13 of 22 PHYSIOLOGY | LE1 Hemodynamics and Venous Return | Dr. June Cathleen C. Castillo, DPBA If there is an increase in blood pressure: BAINBRIDGE REFLEX → The pressure in the carotid sinus and the aortic arch would increase → Would be detected by the baroreceptors Activated baroreceptors: → Afferent fibers in the glossopharyngeal and vagus nerve would release glutamate to the Nucleus Solitarius which will send inhibitory signals to your rostral ventrolateral medulla. Efferent fibers would be on the ANS Inhibition of the rostral ventrolateral medulla would result in: → Decrease in activity of the sympathetic nervous system, resulting in vasodilation and a decrease in systemic vascular Figure 36. Bainbridge Reflex resistance via alpha-1 receptors. Where blood volume changes would lead to increase in right → Decrease in inotropy via alpha-1 receptors atrial pressure, leading to atrial receptor stimulation and results to → Increase in parasympathetic nervous system Bainbridge Reflex = increase in heart rate → Decrease in heart rate via muscarinic receptors On the other hand, an increase in blood volume leads to an → All would lead to a decrease in blood pressure 💬For💬 example, increase in cardiac output would increase atrial pressure which a person is hurt or experiences pain: results in stimulation of Baroreceptor Reflex = decrease in heart BP will increase rate. ▪ This increase is a trigger sensed by the baroreceptors in the During transfusion/infusion is a result of the balance of Bainbridge 💬 carotid sinus and aortic arch. Reflex (increased HR) and Baroreceptor Reflex (decreased HR) Baroreceptor afferent fibers (glossopharyngeal nerve and RESPIRATORY SINUS ARRHYTHMIA 💬 vagus nerve) releases glutamate The glutamate released would activate the Nucleus Tractus Solitarius (NTS) More pronounced in children The heart rate increases during inspiration and decreases ▪ NTS: sends inhibitory signals to RVLM during expiration. 💬▪ RVLM: increases the sympathetic outflow → During inspiration: increase in HR because of activation of Therefore, activation of NTS would lead to: stretch receptors ▪ Decrease in sympathetic outflow → During expiration: decrease in HR If via alpha-1 receptors → vasodilation → decrease in Change in intrathoracic pressure would also lead to an increase SVR in venous return If via beta-1 receptors (affects the heart) → decreased → Leading to an increase in volume inotropy (force of contraction) → Bainbridge reflex would be activated → leads to decrease in ▪ Increase in vagal tone or parasympathetic tone HR Via muscarinic receptors → decreased HR Figure 35. Effects of Decreased Arterial Pressure 💬 Overall, a decrease in BP would occur: Figure 37. Respiratory Sinus Arrhythmia Diagram → Decrease in arterial pressure results in a decreased baroreceptor firing. → This result to increased sympathetic outflow and decreased vagal activity/parasympathetic activity → Baroreceptor firing exerts tonic inhibitory influence on the sympathetic outflow from the medulla. → Increase in sympathetic activity would increase the SVR. → Decrease in vagal activity would lead to increase in cardiac output. → (1) Increase in cardiac output + (2) Increase in Systemic Vascular Resistance + (3) Negative Feedback = decrease in arterial pressure 💬💬WithThea baroreceptors decreased BP, 💬 💬→RVLM will not be stimulated (no firing) NTS will not be activated would be disinhibited, leading to: Figure 38. Respiratory Sinus Arrhythmia OTHER REFLEXES increased sympathetic activity Atrial and Pulmonary Artery Reflex → increased SVR → Low pressure receptors in atria and pulmonary arteries → increase inotropy → increased cardiac output → Minimize arterial pressure changes in response to a change in → decreased vagal activity → increased HR blood volume PHYSIOLOGY Hemodynamics and Venous Return PAGE 14 of 22 PHYSIOLOGY | LE1 Hemodynamics and Venous Return | Dr. June Cathleen C. Castillo, DPBA Volume Reflex and ANP (Atrial Natriuretic Peptide) → Stretch of Atria → Decreased ADH release in Posterior Pituitary → Decreased afferent arteriolar resistance in kidneys → Increased GFR → Increased fluid filtration → Release of ANP from atria → vasodilator effects and potent natriuretic and diuretic on kidneys ANP: most important regulator of blood volume pressure → Ex. Needed by patients with congestive heart failure (CHF) Prevents vast retention of sodium chloride and water while reducing fluid retention and prevention of elevation of the central venous pressure. CHEMORECEPTOR REFLEX Primary Function: monitors blood PO2, PCO2, and pH & maintains these 3 factors within a narrow physiologic range PERIPHERAL CHEMORECEPTORS Detects increase in CO2 and H+ & decrease in O2 levels only if PaO2 < 80 mmHg Primary effect of activation: Excitation of Medullary Vagal Figure 40. Anterior View of the Aortic Arch Showing the Innervation → 📋 Center that leads to a slight decrease in HR. Found in 2 locations of the Aortic Bodies and Baroreceptors B. INTERMEDIATE TERM CONTROL ▪ Small Carotid Bodies (External Carotids) Stress-Relaxation of Vasculature − Afferent nerves join with the sinus nerve before entering → When the BP is too high, vessels are stretched until the glossopharyngeal nerve to synapse with the RTS in pressure normalizes the medulla. Capillary Fluid Shift − Increase in firing of signals with (↓PO2) hypoxemia, → Increased capillary pressure would lead to sipping of the fluid (↑PCO2) hypercapnia, (↑H+) and acidosis. into the tissues − Sensitive to changes in the PO2, PCO2 , and pH of → Done to reduce the volume the volume intravascularly arterial blood. Renin-Angiotensin System (RAAS) − Thresholds to activate peripheral chemoreceptors: Activated within 30 minutes to several hours o PO2 = 80 mmhg, PCO2=40 mmhg, pH=7.4 − Reduced carotid perfusion during hypotension increases RENIN-ANGIOTENSIN SYSTEM carotid body firing. ▪ Aortic Bodies (Aortic Arch) − Decrease in sympathetic outflow functions similar to carotid bodies chemoreceptors Detects increase in CO2 and H+ as well as decrease in O2 levels only if the PaO2 is less than 18 mmHg. Decrease in PaO2 → stimulation of chemoreceptors The increased activity in afferent nerve fibers → increased tone of resistance and capacitance vessels → Activation of peripheral chemoreceptors is the exhalation of the medullary vagal center which will lead to a slight decrease in heart rate. → The total response of the chemoreceptors also depends on a secondary response which is caused by your respiratory activity. Examples: → Hypocapnia → Increased lung stretch ▪ Both inhibit the medullary vagal center which will decrease HR Figure 41. Renin-Angiotensin-Aldosterone System Receptor that is responsible for the [RAAS] response: juxtaglomerular cells in the afferent arterioles proximal to your glomeruli These receptors detect a decrease in arterial blood pressure Upon detection there would be a release of renin from your kidney which occurs in 30 minutes to 1 hour. The renin will cleave the end terminal of your angiotensinogen leading to the formation of your angiotensin. Angiotensin 1 is already a vasoconstrictor although its effect is Figure 39. Chemoreceptor Reflex[Berne and Levy Physiology 7e] only mild PHYSIOLOGY Hemodynamics and Venous Return PAGE 15 of 22 PHYSIOLOGY | LE1 Hemodynamics and Venous Return | Dr. June Cathleen C. Castillo, DPBA ACE is found in high amounts as the endothelium of your lung VI. VENOUS RETURN vessels and this enzyme will convert angiotensin 1 to A. VENOUS SYSTEM angiotensin 2. Veins → high capacitance → large reservoir Angiotensin 2 is a powerful vasoconstrictor. The overall effect of your RAAS is vasoconstriction which is → Can hold up to 70% of blood mostly in the arterioles and less in the veins and this will lead Able to adjust the volume of blood returning to the heart (preload) into increase in your total peripheral resistance → increase Distensible and low-resistance in blood pressure but the effect will be only halfway to normal Control filtration and absorption by adjusting post-capillary and needs 20 minutes to be active. resistance Assist in CV adjustment accompanying the body position C. RENAL BLOOD VOLUME PRESSURE CONTROL Mechanism: Long-Term Regulation B. VENOUS COMPLIANCE Pressure Diuresis Change in venous volume (ΔV) related to a change in distending → An increase in blood volume without changes in vessel pressure capacitance will increase BP Varies with body position → The effect of the kidneys would be pressure diuresis LE veins are more compliant to veins near the heart → There would be an increase in urine output as BP increases Veins in lower extremities also thicker than veins in brain or upper Pressure Natriuresis extremities → Pressure natriuresis is an increased output of salt → BP With age, elastin replaced by collagen → decreased increases. compliance → For this to happen you need aldosterone to regulate the salt → Age is inversely proportional to venous compliance uptake. C. VENOUS RETURN Venous Return → Flow of blood from the periphery back to the right atrium (RA) → The rate of which blood returns from the thorax from the peripheral vascular beds and adjusts the rate at which the blood enters the central venous compartment Factors that affect changes in venous return: → Venomotor tone → Respiratory Activity → Orthostatic Stress or Gravity Preload: force that stretches the cardiac muscle prior to your contraction and is composed of volumes that fills the heart from venous return. Figure 42. Acute and Chronic Renal Output Curves An increase in venous return will also increase the preload and the diastolic volume. Figure 44. Venous Return D. FACTORS THAT CAN CAUSE TRANSIENT CHANGES IN VENOUS RETURN 1. SKELETAL MUSCLE PUMP (MUSCLE CONTRACTION) Figure 45. Skeletal Pump Rhythmical contraction of limb muscle during locomotor activity such as walking and running will promote venous return by muscle pump mechanism. Figure 43. Increase ECF volume to increase arterial pressure. An increase in blood volume without changes in vessel capacitance will increase BP → The effect of the kidneys would be pressure diuresis → Would be an increase in urine output as BP increases PHYSIOLOGY Hemodynamics and Venous Return PAGE 16 of 22 PHYSIOLOGY | LE1 Hemodynamics and Venous Return | Dr. June Cathleen C. Castillo, DPBA 2. DECREASED VENOUS COMPLIANCE 4. VENA CAVA COMPRESSION Figure 46. Decreased Venous Compliance Sympathetic activation of veins → decreased venous Figure 49. Vena Cava Compression compliance → increased CVP → Inc cardiac output through An increase in resistance of vena cava occurs when the thoracic the Frank-Starling mechanism. → increased VR vena cava is compressed Frank Starling mechanism Ex. Valsalva Maneuver → Increase in force of contraction would expel more blood from → Maximal force expired through a closed glottis the left ventricle so the CO will increase if the preload → Leading to an increase in intrathoracic pressure → vena increases. (Increase in preload = Increase in CO) cava compressed → increased in venous return. → Preload is generally expressed as the right atrial pressure 5. GRAVITY or the pressure which drives the filling of the heart 3. RESPIRATORY ACTIVITY Figure 47. Respiratory Activity Figure 50. Effect of Gravity in Venous Return, Supine and Standing Position There is distribution of arterial and venous pressure in upright and supine position. Zero reference point would be at the level of the right atrium In supine position: the arterial and venous pressure are evenly distributed along the horizontal axis Figure 48. Respiratory Inspiration and Expiration with Venous In standing position: the atrial pressure is increased by the Return weight of blood column below the heart and decreased by equal During respiratory inspiration: value above the heart thus the venous blood would pool upon → The venous return is transiently increased because of a standing in the lower part of your body. decrease in right atrial pressure and the opposite would Venous valves interrupt the fall of blood and lessen this hydrostatic occur in expiration. effect and negative pressure in the chest and inside the cranium will counteract the effect of gravity. PHYSIOLOGY Hemodynamics and Venous Return PAGE 17 of 22 PHYSIOLOGY | LE1 Hemodynamics and Venous Return | Dr. June Cathleen C. Castillo, DPBA E. VENOUS VALVES Increase in venous return would lead to an Gravity can cause venous distention pooling of blood in → Increase in end-diastolic volume 💬 dependent vessels → Venous distention. → Increase in stroke volume Because the venous system has a low pressure (compared to → Increase in cardiac output the arterial system which has high pressure), making it prone to F. CENTRAL VENOUS PRESSURE pooling of blood. Venous valves → one-way valves; prevents backflow for blood Venous system has 2 compartments: → The large and diverse peripheral venous compartment → A smaller intrathoracic sections (VCs and RA) which includes the vena cava and the right atrium CVP: filling pressure in thoracic vena cava and right atrium → Increased by either an increase in venous blood volume or by a decrease in venous compliance G. INFLUENCE OF CVP AND PVP