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Chapters 14 & 15
The Cardiovascular System
| Question | Answer |
|---|---|
| What are the functions of the Cardiovascular system? | Transport materials, nutrients, water, and gases to body tissues, materials from cell to cell in the body, waste products/ metabolizes that cells eliminate-- transport to the lungs and kidneys for excretion |
| The cardiovascular is a _____ transport | Vascular |
| The vascular transport needs a steady supply of _____ | Oxygen |
| If blood flow to the brain is stopped, consciousness is lost after _____ | 5-10 sec |
| Irreparable brain damage after ______ of no blood flow | 5-10 min |
| Low blood flow | Ischemia |
| Low oxygen | Hypoxia |
| Zero oxygen present | Anoxia |
| What constitutes the cardiovascular system? | Heart, blood--formed elements and plasma, vasculature (arteries, capillaries, veins) |
| Valves throughout the veins keep blood moving in ________ | One direction |
| Blood flowing into the heart is ______ | Deoxygenated |
| From the right side of the heart, pumped to the lungs via pulmonary circulation | Deoxygenated blood |
| Pumped from the left side of the heart to the rest of the body via systemic circulation | Oxygenated blood |
| The heart is located in the | Thoracic cavity |
| Bottom point of heart | Apex |
| The heart is surrounded by the | Pericardium |
| Pericarditis results in | Friction rub |
| The heart is divided by the ______-- prevents blood from mixing | Septum |
| Both atria contract at the same time followed by both ventricles. T or F | T |
| Ventricles will contract from | The bottom and upward |
| Connective tissue rings surrounding the 4 heart valves serve as insertion and origin for | Cardiac muscle |
| _________ will put the apex and base together | Ventricular contraction |
| Heart valves prevent | Backflow |
| Between the atria and ventricles | Antrioventricular (AV) valves |
| Between the right atrium and right ventricle | Tricuspid valve |
| Between left atrium and left ventricle | Bicuspid valve |
| Between the ventricles and the arteries leaving that particular ventricle | Semilunar valve |
| Between the right ventricle and pulmonary artery | Pulmonary valve |
| Between left ventricle and the aorta | Aortic valve |
| Thin flaps of tissue joined at their base to a ring of connective tissue | Atrioventricular valves |
| The flaps of AV connect to _________(ventricular side) | Chordae tendineae |
| Chordae tendineae attaches to _________ of the ventricle, that provide stability | papillary muscles |
| Has three cuplike leaflets that "snap" shut and do not need connective tendons | Semilunar Valves |
| Prevent blood that has entered the arteries from flowing back into the ventricles during ventricular relaxation | Semilunar valves |
| During ventricular contraction, the ______ remain closed to prevent blood flow backward into the atria | AV valves |
| Cardiac muscle cells (do/dont) need nerve innervation to contract | Dont |
| The signal is ______, comes from within the heart but can be influenced by nervous innervation (sympathetic and parasympathetic) | Myogenic |
| signal comes from _________(aka pacemaker).. smaller and contain fewer contractile fibers than other myocardial contractile cells--lack sacromeres- no contraction | autorhythmtic cells |
| Organized in sacromeres, smaller and have single nucleus per fiber, have intercalated disks (cell junctions between the cells), T-tubles are larger and branch within, sarcoplasmic reticulum is smaller, mitochondria occupy one third of cell volume | Contractile cardiac muscle cells |
| An action potential moves across the sarcolemma and into the t-tubule-- this opens voltage gated ______ on the cell membrane | L-type Ca++ (Calcium entry and excitation contracton (EC) coupling) |
| Ca++ enters the cell, causing RyR on the SR to open--Ca++ induced Ca++ release-- results in a Ca++ "spark" Several Ca++ sparks sum to create a _______ signal. Ca++ binds troponin and follows the same contractile mechanism as skeletal muscle | Ca++ (Calcium entry and excitation contraction (EC) coupling) |
| Ca++ is pumped back into the SR via action of the ____________ | Ca++ ATPase (Cardiac muscle relaxation) |
| Ca++ is also pumped out of the cell via _______ | Na+ Ca++ exchanger (Cardiac muscle relaxation) |
| Cardiac contraction can be graded. T or F | T |
| Each fiber has the ability to | Vary the amount of force it generates |
| Cardiac muscle contraction is proportional to: | The number of active crossbridges, dependent on the amount of Ca++ in the cytosol, more Ca++, more troponin bound, more actin and myosin cross bridges can form |
| Which heart valve is located between the left atrium and the left ventricle? | Bicuspid valve |
| Lack of blood flow to the brain can result in irreparable damage to neural tissue to the ischemia. What is the term given to the lack of oxygen that accompanies ischemia? | Hypoxia |
| T or F blood returning to the right atrium from the superior and inferior vena cava is free of oxygen | F |
| The tricuspid valve opens due to | Atrial contraction |
| Cardiac muscle cells have | a smaller SR |
| During cardiac muscle relaxation, Ca++ is pumped out of the cell via | Na+/K+ ATPase |
| After the cardiomyocyte membrane is depolarized, what channels open on the cell membrane? | L-type Ca++ |
| T or F the more Ca++ in the cytosil, the greater the generated force is in the cardiomyocyte | T |
| Myocardial action potentials | Contractile Cells: Phase 4: -resting potential (-90mV) Phase 0: depolarization voltage-gated Na+ channels open and Na+ enters (channels close at +20mV) Phase 1: initial repolarization K+ begins to leave via K+ channels |
| Myocardial action potentials (cont'd) | Phase 2: plateau slow voltage-gated Ca++ channels finally open after initial depolarization; some “fast” K+ will shut Phase 3: rapid repolarization slow voltage-gated K+ channels are open; resting potential is reestablished |
| The longer AP in cardiac muscle prevents | Tetanus |
| Myocardial action potentials-myocardial autorhythmic cells= | pacemaker potential |
| The pacemaker potential starts at _____ and slowly moves towards threshold | -60mV |
| Pacemaker potentials | At -60mV, I-f channels are open Permeable to both Na+ and K+ Na+ influx > K+ efflux, which causes a gradual depolarization As the membrane potential becomes more positive, If channels shut, and Ca++ channels open |
| Pacemaker potentials (cont'd) | Ca++ enters and causes the action potential Ca++ channels shut at the peak of the AP, while at the same time, slow K+ channels have finally opened K+ efflux leads to repolarization |
| Heart rate can be influenced by the | autonomic nervous system |
| _______ is determined by speed of pacemaker potential Changes ion permeability in the autorhythmic cells. Increased Na+ and Ca++ permeability…? Increased K+ permeability and decreased Ca++ permeability…? | Heart rate |
| Decrease parasympathetic, increase sympathetic (catechoamines acting on B1 adrenergic receptors) | To speed up rate of heart |
| Increase parasympathetic pathway, ACh acting on muscarinic receptors | To slow the heart |
| Catecholamines (NE/EPI), bind to B1 adrenergic receptors (w/ a cAMP second messenger), increases ion flow through both Ca++ and I-f channels, speeds up the PP | Sympathetic stimulation |
| ACh will bind to muscarinic cholinergic receptors, K+ permeability increases (hyperpolarizes the cell lowering the beginning of the pacemaker potential), Ca++ permeability decreases, slows PP | Parasympathetic stimulation |
| The typical starting membrane potential in autorhythmic cardiomyocytes is | -60mV |
| During the gradual depolarization to threshold in a pacemaker potential... | The membrane is permeable to Na+ and K+ and I-f channels are open |
| Ach binding to muscarinic cholinergic receptors does not increase heart rate T or F | T |
| After the cardiomyocyte membrane is depolarized, what channels open on the cell membrane? | L-type Ca++ |
| Contraction of the whole heart is coordinated by an _______(all individual cells need to depolarize in coordination) | Electrical signal |
| AP generated in the ______(right atrium) | Sinoatrial (SA) node |
| Wave of depolarization spreads over the internodal pathway and to the _______(found at the bottom of the right atrium) | atrioventricular (AV) node |
| Depolarization moves into the ventricles to the _______ via the Av bundle and left//right bundle branches | Purkinje fibers |
| What is the purpose of this internodal conducting system? | Allows for rapid transduction of the signal |
| ***The SA node will also spread the action potential to the adjacent contractile cells( they will depolarization and contract, but transduction is slower) | |
| Why is it necessary to direct the signal through the AV node and not the atria? | If the signal passed from the atria directly to the ventricles, the top of the ventricles would contract first This would prevent the blood from being pushed out the tops of the ventricles and into the arteries |
| The internodal system spreads the signal to the | apex ***the bottom of the ventricles to contract first |
| Transmission through the AV node is (slower/faster) than the rest of the internodal system--- this allows for the atria to complete contraction before ventricular contraction | slower |
| T or F upstream pacemakers set the rate | T |
| *** SA node--> AV node--> AV bundle--> Bundle branches | |
| Displays the hearts electrical activity | Electrocardiogram (ECG) |
| Electrodes placed on both arms and the left leg (creates a triangle around the heart). | Einthoven's Triangle |
| Pair of electrodes | Lead |
| ECG is recorded from one lead at a time to record a ______ | cardiac cycle-->series of waves and segments |
| Atrial depolarization | P wave |
| Ventricular depolarization | QRS complex |
| ventricular repolarization | T wave |
| *** Mechanical contraction is slightly logging behind the electrical conduction | |
| Atrial contraction | PQ segment |
| Ventricular contraction | ST segment |
| ST segment depression can indicate | myocardial ischemia |
| What is happening during the ST segment of a normal ECG | Ventricular contraction |
| Phase 1: The heart is at rest; Atrial and ventricular diastole Atria fill with blood AV valves open and blood will fill into the ventricles (gravity) | Cardiac cycle |
| Phase 2: Atrial systole Final 20% of ventricular filling is accomplished | Cardiac cycle |
| Phase 3: Early ventricular contraction Depolarization wave moves down the internodal conducting system towards apex Ventricles contract from the bottom | cardiac cycle phase 3 cont'd: AV valves shut - associated with the first heart sound (S1 – “lub”) Semilunar valves are also shut at this time, and therefore blood stays in the ventricle: known as isovolumic contraction |
| Phase 4: Ventricular ejection Ventricles continue to contract, forcing open the semilunar valves Blood is forced out of the ventricles and into the arteries | cardiac cycle |
| Phase 5: Ventricular relaxation Ventricular pressure decreases below that of arterial pressure The resulting backflow fills the “cups” of the semilunar valves (remember their structure) | cardiac cycle phase 5 cont'd: This will cause the semilunar valves to shut Second heart sound – S2 “dub” Isovolumic relaxation |
| X-axis | volume |
| Y-axis | Pressure |
| Blood flows from areas of high to low pressure T or F | T |
| The starting point is A Ventricle is relaxed Holding the least amount of blood that it will hold during the cycle | Looking at pressure and volume changes in depth... cont'd: As ventricles fill, the volume increases without the pressure increasing (expansion) (A→B) at this point - End Diastolic Volume (EDV) ≈135mL |
| Point B: Ventricle contracts with both mitral and aortic valve shut – therefore pressure increases as the volume remains constant (B→C) Isolvolumic Contraction | Looking at pressure and volume changes in depth |
| Point C: Ventricular pressure will exceed aortic pressure, aortic valves open Pressure continues to rise Volume in the ventricle decreases as blood is ejected into the aorta (C→D). | Looking at pressure and volume changes in depth |
| Point D: – ventricular contraction is complete; the amount of blood remaining in the ventricle at this point is referred to End Systolic Volume (ESV) ≈65mL | Looking at pressure and volume changes in depth |
| The ventricle relaxes (D→A); the aortic valve is shut, and therefore volume does not change Isovolumic relaxation | Looking at pressure and volume changes in depth |
| What causes s1 or the lub sound of the heart | shutting of the semilunar valve |
| Aortic pressure is greater than ventricular pressure during isovolumic contraction T or F | T |
| The centricles are empty at the end of the cardiac cycle T or F | F end systolic volume |
| Amount of blood pumped by one ventricle during a contraction | Stroke volume= EDV-ESV |
| EDV= | 135mL |
| ESV= | 65mL |
| What would happen during exercise? | 100mL-- due to increase in EDV increasing preload in heart |
| SV is directly related to the force of contraction affected by | length of muscle fiber prior to contraction (this is dependent on the amount of blood in the ventricle (EDV)) Contractility- intrinsic ability for the cardiac muscle to contract at any given length |
| Standard measure of cardiac performance.. blood volume pumped by one ventricle in a given period of time | cardiac output= HR x SV |
| What happens if cardiac output decreases in one ventricle? | it will result in a pooling of blood in the circulation behind the weaker side of the heart |
| After running on a treadmill for 15min, our subject’s HR is 155 BPMs. If LV EDV was determined to be 150mL, and ESV was 45mL, what is the CO for our subject? | 16.3L/min |
| If the stroke volume of the left ventricle is 250mL/beat and the stroke volume of the right ventricle is 251mL/beat, what happens to the blood distribution between the systemic and pulmonary circulation after 10 heart beats?? | The pulmonary circulation will have gained 10mL of blood while the systemic circulation will have lost 10mL… |
| ***Force proportional to sarcomere length-- the longer (optimum), the more force created | length-tension relationship |
| The ventricle wall stretches as it fills with more blood, which is called ________, the stronger the force of contraction | preload |
| stroke volume is proportional to EDV | Frank-Starling law |
| EDV is a good indicator of the amount of | preload/stretch |
| blood returning from systemic or pulmonary veins will ultimately end up in our ventricles..... therefore the EDV is determined by the | venous return(flow of blood back into heart) |
| Three factors affecting venous return | venous contraction/compression, abdominal and thoracic pressure changes (due to breathing), sympathetic nervous innervation |
| The veins are squeezed by our contracting skeletal muscles, "skeletal muscle pump this pushes the blood forward. EDV increases, and therefore, so will stroke volume (Frank-Starling law) | venous contraction/compression EX: compression socks |
| During inspiration, what happens to the pressure in the thoracic cavity? | increases...inferior vena cava (pressure changes) |
| More blood is drawn into the thoracic cavity, increasing venous return. this is known as | respiratory pump (pressure changes) |
| Sympathetic nervous innervation causes a _______. catecholamines (EPI, NE, DOPA) acting on ________. This squeezes more blood into the heart.. EDV increases as will SV | vasoconstriction (When blood vessels constrict, blood flood is slowed or blocked. adrenergic receptors |
| The intrinsic ability of a cardiac muscle fiber to contract at any given length | contractility |
| contractility is controlled by | nervous and endocrine |
| affect contractility | inotropic agents positive inotropic effects (norepinephrine on beta 1 receptors) will cause an increase in Ca++-- graded contraction! |
| ***EPI/NE--> adrenergic receptor--> cAMP messenger--> acts on Ca++ channels (increases the time they remain open) | contractility |
| The load that the ventricle has to overcome during contraction.. in order to eject the blood | afterload |
| afterload is determined by | arterial blood pressure and EDV |
| afterload is associated with many cardiovascular pathologies, such as | loss of aortic compliance(stretchability), systemic hypertension(increase in blood pressure), may result in left ventricular hypertrophy(enlargement of an organ) (LVH)-- loses elastance |
| A patient’s aortic valve has become constricted, creating a condition known as cardiac stenosis. Which ventricle is affected by this change, and what happens to the afterload on that ventricle? | Increased afterload on the left ventricle |
| What allows our blood to flow through our vasculature(blood vessels)? | A pressure gradient |
| The highest pressure occurs in the _____ due to LV contraction | aorta |
| pressure will continually decrease throughout the circulation--lowest in the | vena cava |
| The pressure of moving fluid (increases/decreases) as it travels a distance | decreases |
| Blood in our vessels exert two pressure components: | dynamic (hydraulic pressure) and lateral (hydrostatic pressure) |
| When a fluid moves through a system (blood moving through the vessels) it will | lose pressure this is due to energy lost at friction |
| ****Blood flows from areas of higher to lower pressure | |
| The larger the ______, flow will increase | pressure gradient |
| Flow is proportional to | ΔP (gradient) ***not dependent on the total pressure (absolute pressure) |
| Our cardiovascular system will ______ flow of blood | oppose--friction in our vessels |
| As resistance increases, flow will | decrease |
| Flow is proportional to | 1 ___ R Which equals ΔP / R |
| resistance is determined by three factors | vessel radius (r)-- smaller radius, higher resistance, tube length (L)--longer tube, higher resistance, and fluid viscosity (η)- thicker fluid, more resistance |
| Poiseuille's law | R=8Lη/πr4 = 1/r4 |
| Which of these variables has the most influence on resistance? | Vasoconstriction and vasodilation has a large effect on the resistance in that particular vessel |
| ______ is dependent on the flow rate and cross sectional area | velocity |
| the volume of blood that passes a given point per unit time (L/min)--how much | flow rate |
| how far a fixed amount of blood travels per unit time-- how fast | velocity |
| the relationship between flow rate and velocity is | v=Q/A V= velocity, Q= flow rate, A= cross sectional area of the vessel |
| What happens to velocity as a vessel constricts? | velocity increases and rate remains constant |
| arteries are referred to as the | pressure reservoir |
| total blood flow through the entire system is the same as the | cardiac output... 5L/min |
| veins are referred to as the | volume reservoir |
| multi layers; the inner most layer is a thin layer of endothelial cells | blood vessels |
| the endothelium... | secrete paracrines, regulate diameter (blood pressure regulation), vessel growth, absorption of materials |
| connective tissue and ______ surround the endothelial | smooth muscle Circular layer of vascular smooth muscle for vasoconstriction and vasodilation Maintain muscle tone (partial contraction at all times) Depends on Ca++ entry from extracellular fluid |
| arteries carry blood ____ from the heart | away |
| thick smooth muscle layer with a lot of connective tissue (fibrous and elastic) | arteries |
| flow of arteries is described as _______into smaller vessels | divergent (infinite sequence) |
| as the size of the vessels shrinks, the walls become (more/less) muscular and (more/less) elastic | more; less |
| site of exchange between the blood and the interstitial fluid | capillaries |
| lack smooth muscle and fibrous/elastic connective tissue--facilitates exchange | capillaries |
| single endothelial layer supported by a basement membrane | capillaries |
| cells surrounding the capillaries contributes to tightness characteristic of capillaries EX: blood brain barrier | pericytes |
| for veins, blood flow is | convergent (to come together) |
| when venules converge into veins, they become | larger in diameter |
| hold more than half of the blood in our bodies--volume reservoir | veins |
| walls are thinner w/ less elastic--readily expand with blood | veins |
| venous blood must flow... | against gravity internal one-way valves aid |
| varicose veins (enlarged veins)... | faulty valves, blood pools, may be hereditary, female, pregnancy, obesity, menopause |
| development of new blood vessels | angiogenesis |
| occurs during wound healing and uterine lining growth and in response to endurance training | angiogenesis |
| controlled by cytokines and growth factors released from the endothelium or surrounding tissues stimulate (mitogens): VEGF and FGF inhibit angiostatin and endostatin plays a role in the growth of malignant tumors | angiogenesis |
| the driving force for blood--generated by ventricular contraction | blood pressure |
| ****During ventricular diastole, the semilunar valves shut and the elastic arteriole walls will recoil | Driving pressure wave |
| blood pressure is (highest/lowest) in the arteries and (highest/lowest) in the veins | highest; lowest |
| aortic pressure = | 120 mmHg during systole and 80 mmHg during diastole |
| the pressure in vessel wall as blood is forced through during ventricular systole | pulse |
| pulse decreases over distance due to | resistance -- disappears at the capillaries |
| pulse pressure indicative of strength of the pressure wave. pulse pressure = | systolic-diastolic |
| single value to represent the driving pressure in our vessels | mean arterial pressure (MAP) |
| MAP= | diastolic pressure + (1/3)(systolic-diastolic)= 93.33 mmHg = _DP__+_______/3 |
| a balance between flow into the arteries and out of the arteries | MAP |
| flow into the arteries is the same as | cardiac output |
| flow out of the arteries is influenced by ______ of the arterioles | peripheral resistance |
| MAP is proportional to | CO x R |
| Describe what happens to MAP if CO remains the same, but arteriole resistance increases? | MAP increases hypertension |
| How do we regulate BP when blood volume change? | adjusting for small increase in blood volume is regulated by the kidneys -- will not affect long lasting changes in blood pressure |
| the renal and cardiovascular system work to restore a ___________ | loss of blood volume (dehydration, hemorrhage) kidneys can only conserve blood volume (prevent fluid loss) not restore it Cardiovascular compensation includes sympathetic nervous stimulation |
| distribution of blood between the arterial and venous sides also helps to | maintain arterial blood pressure If MAP drops, sympathetic stimulation cause venous constriction; this causes more blood to accumulate in the arterial side |
| blood pressure | sphygmomanometry |
| blood pressure: (a) Cuff pressure exceeds arterial pressure (b) cuff pressure is gradually released – blood flow is reestablished Korotkoff sound (systolic pressure) | (c) cuff pressure no longer is compressing the artery Korotkoff sound disappears (diastolic pressure) Normal <120/80 mmHg prehypertensive 120/80-139/89 mmHg hypertensive 139/89 mmHg |
| R is proportional to | 1/r4 |
| ***arterial resistance is influenced by: Local control – usually first level of control to meet the immediate metabolic needs of the tissue (i.e. paracrine control, NO, endothelin) | 2) Sympathetic control – regulate blood distribution for homeostasis (i.e. temperature regulation) 3) Hormonal control (i.e. angiotensin II, ANP) – act directly on arterioles or by influencing sympathetic control |
| vascular smooth muscle can respond to increased stretch in the vessel wall | myogenic autoregulation will cause constriction, resistance increases/flow decreases |
| mechanically gated Ca++ channels open, allowing for Ca++ to enter the cell | myogenic autoregulation |
| ______function in local control over vascular smooth muscle contraction | paracrines ex: oxygen, carbon dioxide, NO |
| aerobic metabolism (exercise)(increase)--> O2 (decrease)--> CO2 (increase)--> paracrine action--> vasodilation | active hyperemia (paracrines) |
| blood flow is blacked at a certain tissue decrease in O2 and increase in CO2 local hypoxia produces NO CO2 and NO act as vasodilators Blood flow is increased | re-active hyperemia (paracrines) |
| majority of vascular smooth muscle is controlled by | sympathetic innervation |
| myogenic tone of the arterioles is maintained by tonic release of | norepinephrine-- binds to α-adrenergic receptors to cause vasoconstriction |
| Where is epinephrine released from? | adrenal gland |
| ****NE--> α-adrenergic receptors-->vasoconstriction EPI--> B2 receptor--> vasodilation | sympathetic control |
| resting muscle receive ___% of CO | 20 |
| working muscle receive ____% of CO | 85 |
| blood flow through all the arterioles at the same time is equal to CO | parallel arrangement |
| arterioles have the ability to constrict: (increase/decrease) arteriole resistance, (increase/decrease) flow | increase;decrease allows blood to be rerouted |
| density is directly proportional to | metabolic activity (capillary exchange) |
| __________is only large enough for passage of 1 RBC at a time | capillary diameter |
| endothelial cells are connected to one another via “leaky” junctions Most common; found in muscle, connective tissue, neural tissue (i.e. blood brain barrier) | continuous capillaries |
| contain large pores, allowing passage of large volumes of fluid Kidneys and intestines | fenestrated capillaries |
| ***the smaller vessel area the higher flow velocity (if rate is constant) | |
| flow rate is low... therefore velocity rate is low | capillaries |
| Why is low velocity of flow through capillaries beneficial? | enhances gas exchange |
| exchange is accomplished via ______ and ________ | diffusion; transcytosis |
| ****exchange takes place either by movement between endothelial cells (paracellular) or through the cells (endothelial transport) | |
| *****small solutes or gases move either directly though or between the cell larger solutes and proteins require vesicles --- ex:transcytosis | |
| fluid is flowing out of the capillaries | filtration (bulk flow) |
| fluid is flowing into the capillaries | absorption (bulk flow) |
| bulk flow is dependent upon | hydrostatic pressure (exerted by fluid itself) and osmotic pressure (sucking pressure, dissolve solutes) |
| net filtration at the ______end | arteriole |
| net absorption at the ______ end | venous |
| 32 mmHg at the arteriole end and decreases (due to friction) to 15 mmHg at the venous end | capillary hydrostatic pressure |
| *****hydrostatic pressure of the interstitial fluid is very low filtration= hydrostatic | capillary hydrostatic pressure |
| determined by the solute concentration(proteins) | capillary osmotic pressure |
| 25 mmHg along the entire length of the capillary | capillary osmotic pressure absorption= osmotic pressure |
| ***Net flow is determined by the hydrostatic pressure gradient and the colloid gradient Net pressure = hydrostatic ΔP - colloid osmotic Δπ | |
| filtration is (greater/lesser) than absorption | greater |
| accumulation of fluid in the interstitial space--- result in swelling | edema |
| edema results from an alteration in | capillary exchange --- filtration>absorption |
| edema can also occur as a result of inadequate lymph drainage (obstruction) | elephantiasis (parasite) |
| increase in capillary hydrostatic pressure | filtration |
| decrease plamsa protein concentration | filtration |
| increased interstitial protein concentration | filtration |
| venous return decreases and CO falls from 5 to 3 L/min | orthostatic hypotension |
| orthostatic hypotension triggers the | baroreeceptor reflex |
| arterial BP drops | orthostatic hypotension |
| triggers baroreceptor reflex | heart rate increases, force of contraction increases, vessels constrict |
| ****normal BP and CO is returned to normal within 2 heart beats |
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mpuente14
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