Cardiovascular System Flashcards
1
Q
Main functions of circulatory system
A
- Transport and distribute essential substances to tissues
- Remove metabolic byproducts
- Adjustment of oxygen and nutrient supply in different physiologic states
- Regulation of body temperature
- Humoral communication
2
Q
Cardiovascular system anatomy
A
- Closed loop with two pumps working in series
- Works simutaneously to circulate blood throughout system, arteries take blood away from heart, veins carry blood back to the heart
3
Q
Pulmonary circuit
A
- Sends O2 from heart to lungs
- Right ventricle -> pulmonary trunk -> pulmonary arteries -> lungs pulmonary veins return O2 rich blood to left atrium
4
Q
Systemic circuit
A
- Left ventricle -> aorta carrying O2 rich blood from left ventricle -> branches with artery to each organ -> arteries divide to arterioles and capillaries which lead to venules
- Blood returns to right ventricle
- Once blood passes through tissue -> deoxygenated
- Picks up CO2 and waste products
- Oxygenated blood(left side), deoxygenated(right)
5
Q
Structure of heart
A
- Pericardium: contains pericardial fluid to protect heart
- Superior vena cava: Brings blood from upper body to heart
- Inferior vena cava: Brings blood from lower body to heart
- Aorta: carries blood from heart to rest of body
6
Q
Heart valves
A
- Heart has 4 valves to direct one way flow
- Semilunar valves:
- Cup like leaflets found at ventricular exit points
- Pulmonary valve: between RV and pulmonary trunk - Atrioventricular valves:
- Found between atria and ventricles
- Tricuspid valve on right AV junction
- Bicuspid(mitral) valve on left AV junction
- Valves reenforced by chordae tendinae attached to muscular projections within the ventricles
7
Q
Anatomy of heart: major vessels, input/output
A
- Deoxygenated blood enter through inferior/superior vena cava
- Pressure from blood closes tricuspid valve to force blood upwards -> move towards pulmonary semilunar valve -> blood become oxygenated
- Oxygenated blood enter through left pulmonary veins/arteries -> move through mitral valve up to aorta -> delivered to rest of body
- Chordae tendineae hold valves in and prevent backflow
8
Q
Passage of blood through heart
A
- Superior and inferior vena cava into heart -> right atrium -> tricuspid(AV) valve -> right ventricle -> pulmonary semilunar valve -> pulmonary trunks and arteries to lungs -> pulmonary veins leaving lungs -> left atrium -> bicuspid(mitral) valve -> left ventricle -> aortic semilunar valve -> aorta -> rest of body
- O2 rich blood to body
- O2 poor blood to lungs
9
Q
Cardiac muscle
A
- Myocardial muscle cells are branched, have a single nucleus, and are attached to each other by intercalated disks
- Syncytial network: branched myocyte connections(1 cell may be connected to several)
- Connected by intercalated disks containing desmosomes
- Mitochondria occupy 1/3 of cell volume
10
Q
Excitation-contraction coupling
A
- Action potential enters from adjacent cell
- Voltage gated Ca2+ channels open -> Ca2+ enters cell
- Ca2+ induced Ca2+ release through ryanodine receptor channels
- Release cause Ca2+ spark -> summed spark creates a signal
- Ca2+ ions bind to troponin to initiate contraction
- Relaxation occurs when Ca2+ unbinds from troponin
- Ca2+ pumped back into sarcoplasmic reticulum for storage
- Ca2+ exchanged with Na+ by NCX anti porter
- Na+ gradient maintained by Na+-K+ ATPase
11
Q
Action potential
A
- Upstroke phase: Na+ permeability increase as Na+ channels ope. Membrane potential approach action potential
- Downstroke phase: Na+ permeability decreases as Na+ channels inactivate. K permeability increases as K+ channels open. Membrane potential approaches resting potential
12
Q
Cardiac action potentials
A
- Differ from action potential found in neural and skeletal muscle cells. Extended refractory period
- Main difference is duration: nerves last about 1ms, skeletal muscle cell last about 2-5ms, cardiac last about 200-400ms
13
Q
Myocardial contractile cell action potential
A
- Na+ channels open
- Na+ channels close
- Ca2+ channels open; fast K+ channels close
- Ca2+ channels close; slow K+ channels open
- Resting potential
- Action potential finishes around same time as end of muscle contraction
- Refractory period lasts almost as long as entire muscle twitch
- Long refractory period prevents tetanus(where muscle cannot move)
14
Q
Skeletal muscle refractory period
A
- Refractory period very short compared to amount of time required for tension development
15
Q
Types of cardiac action potential
A
- Type 1: Non-pacemaker cell(myocyte): fast response action potentials, rapid depolarization in response to AP. contractile cells are “soldiers”, need instructions to fire. make up most of atrial and ventricular muscle wall
- Type 2: Pacemaker(autorhythmic) cells: unstable resting potential, spontaneous firing. Non-contractile cells, provide firing instructions to muscular soldiers. found in sinoatrial and atrioventricular nodes
16
Q
Funny Current Channels(If)
A
- Cause unstable resting potential, permeable to both K+ and Na+
- Open when polarized(K+ channels close)
- Some Ca2+ channels open, If channels close
17
Q
Roles of Na+ and Ca2+
A
- Role of Na+:
- Non-pacemaker cells: rapid depolarization phase caused by the opening of Na+ channels
- Pacemaker cells: Slowly depolarizing pacemaker potential(If opening results in net Na+ influx) for autorhythmic cells -> depolarization
- Role of Ca2+:
- Non-pacemaker cells: Ca2+ influx prolongs duration of action potential and produces plateau phase
- Pacemaker cells: Ca2+ ions involved in the initial depolarization phase of action potential
18
Q
Electrical conduction to myocardial cells
A
- Depolarization of autorhythmic cells rapidly spread to adjacent contractile cells through gap junctions
- All cells of intrinsic conduction system have ability to generate action potential. Made of autorhythmic cells
19
Q
Electrical conduction in heart
A
- SA node depolarizes(firing of action potential)
- Electrical activity goes rapidly to AV node via internodal pathways
- Depolarization spreads more slowly across atria. Conduction slows through AV node
- Depolarization moves rapidly through ventricular conducting system to apex of heart
- Depolarization wave spreads upward from apex
20
Q
Nodes
A
- SA Node: Sets pace of heartbeat at 70bpm. AV Node(50bpm) and Purkinje fibers(25-40bpm) can act as pacemakers under some conditions
- AV Node: Routes direction of electrical signals. Delays transmission of action potentials
21
Q
Conductive fibers
A
- Conductive fibers are sheathed(seperate from myocyte contractions)
- Atrial and ventricular myocyte syncytia also separated -> ensure ventricle do not beat too early
- Inert fibrous tissue barrier(no GAP junctions between them): AV pause allow complete contraction of atria before signal passes on. Atrium and ventricle do not compete
22
Q
Heart rate regulation
A
- SA Node action potential firing regulted by both sympathetic and parasympathetic fibers
- Sympathetic(increase cardiac function): Epinephrine and NE bind to beta-adrenergic receptor -> stimulate adenyl cyclase to produce cAMP -> activate PKA -> stimulate funny current channel and voltage gated Ca2+ channels -> faster heart rate
- Parasympathetic(decrease cardiact function): Acetylcholine bind to muscarinic receptor -> inhibit adenyl cyclase -> active GIRK -> rapid eflux of K+ to repolarize cel
23
Q
Parasympathetic control of heart rate
A
- Lowers heart rate
- Activates vagus nerve that innervates SA node
- Releases Ach to bind to M2R receptors in SA node cells
- At est, significant vagal tone on SA node -> resting heart rate between 60 and 80 bpm
- Atropine is a muscarinic receptor antagonist, leads to 20-40bm increase in heart rate -> inhibit vagal signal
24
Q
Control of heart rate
A
- To increase heart rate
- Need activation of sympathetic nerved innervating SA node that release NE that bind to beta-adrenergic receptors on SA node cells
- Can be stimulated by circulating catecholamines released from drenal gland during a sympathetic response
- Contraction strength: Parasympathetic nerved cannot change force of contraction because they only innervate SA node and AV node. Sympathetic fibers increase node rate and can increase force of contraction because they also innervate atria and ventricles
25
Electrocardiogram
- Three major waves: P wave, QRS complex, and T wave
- Measures electrical activity of heart
26
Electrical events of cardiac cycle
- P wave: atrial depolarization
- PQ/PR segment: conduction through AV node and A-V bundle. atria contract
- Q wave: depolarization signal travels down septum of heart
- R waves: signal reaches purkinje fibers and activate myocardium
- S wave: depolarization spread from apex to base, completion of R wave
- ST segment: ventricles contract
- T wave: repolarizing activity of ventricular myocardium. ventricular myocytes repolarize in an opposite sequence than depolarization
27
ECG analysis
- What is rate: look at the distance between R peak to calculate heart beat
- Is rhythm regular: are R intervals spaced identically
28
Abnormal ECGs
- Third degree block: normal P, wide QRS. top part of heart disconnected from bottom. complete block: alternate pacemaker in ventricle(purkinje fibers)
- Atrial fibrillation: no P, irregular QRS. normal conduction pathway through atria lost. fast heart rate
- Ventricular fibrillation: no P, no QRS. no blood flow, no rhythm
- Second degree block: normal P, normal QRS. P doesn't trigger QRS. extra P waves. partial disconnect between atria and ventricle.
29
Cardiac action potential to aortic flow
- Electrical signals originate in SA node and propagate through heart. Can be regulated by autonomic control
- Electrical signals are converted by contractile cells to generate force and pump blood
- Requires ordered electrical and contractile mechanism
- can monitor these signals and sounds to accurately assess cardiac function
- systems need to work at near 100% effectiveness
30
Cardiac cycle
- Sequence of events that occur when heart beats
- Two phases:
- diastole: ventricles relaxed
- systole: ventricles contract
- Three principles:
- heart is biological pump(contraction-relaxation cycle generates pressure gradients, directs orderly movement of blood through circulation)
- blood flows from high to low pressure
- Events on the right and left side of heart are same, but pressure are lower on right
31
Mechanical events of cardiac cycle
- Late diastole: both sets of chambers are relaxed and ventricles filled passively. Relaxation due to pressure in veins being higher than pressure in ventrioles
- Atrial systole: atrial contraction forces a small amount of additional blood into the ventricles. marks end of filling and ventricular diastole. marks beginning of ventricular systole
- Isovolumicc ventricular contraction: first phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves. ventricles contract, blood volume stays constant
- Ventricular ejection: as ventricular pressure rises and exceeds pressure in arteries, semilunar valves open and blood is ejected
- Isovoumic ventricular relaxation: as ventricles relax, pressure in ventricles fall, blood flows back into cusps of semilunar valve and closes them. Both valves close, volume remains same. Continues until pressure in ventricle drop belows vein-> AV valve opens for new cycle
32
Pressures in aorta, ventricle, atrium
- Atrial systole: left ventricular and atrial pressure aligned, atrium and ventricle are one large chamber. AV valve open
- Ventricular systole: AV valve close, ventricle contract. Aortic valve open. Left ventricular pressure similar to aortic pressure. Pressures interconnected until aorta close. decrease in pressure closes semilunar valve
- Ventricular diastole: AV valve open, aortic valve close. Left ventricular pressure drop back down to left atrial pressure. Due to blood exiting into large tissues during diastole
33
Ventricular pressure and volume
- Atrial systole: volume remain steady, isovolumic phase, mitral valve closed. Heart entering ventricular systole. Peak is end-diastolic volume(135 mL)
- Ventricular systole: Blood moves into aorta, volume drop.
- Ventricular diastole: End of isovolumic phase, open of AV valve. End systolic volume is minimum volume(65 mL).
- Highest volume at end of relaxation phase, lowest volume at end of contraction phase
34
Wiggers Diagram overview
1. Mitral valve closes
2. Aortic valve opens
3. End diastolic volume
4. Aortic valve closes
5. Mitral valve open
6. End systolic volume
35
Heart sounds
- Vibrations following closure of AV valve: "lub"
- Vibrations created by closing of semilunar valve: "dup"
36
Pressure volume loop
- Describes volume + pressure relationship in ventricle in one cardiac cycle
- Used to understand how heart physiology change over time
- 1. Begin of filling -> late diastole before atrial kick, volume increase, pressure constant
- 2. Max volume, slight pressure increase: end diastolic volume
- 3. Isovolumetric Contraction: Mitral valve close, ventricles contract. Volume stays same, pressure rise rapidly
- 4. Blood Ejection Phase: Pressure exceed aorta. Aortic valve opens, blood moves to aorta(volume decrease), pressure in ventricle lower than aorta. end systolic volume
- 5. Isovolumetric relaxation: Aortic and mitral valve close, pressure drop, isovolumetric relaxation
37
Preload
- Atrial filling pressure
- amount of blood filling heart chambers before contraction
38
Afterload
- Aortic pressure
- Resistance the heart must overcome to eject blood during contraction
39
ESPVR
- Contractility of heart at any given time
- Move left: stronger heart
- Move right: Weaker heart
40
EDPVR
- Capacity for ventricle to accept blood
- If ventricle more stiff, harder to fill
41
Cardiac Performance in Ventricles
- ESV = End systolic volume(65 mL)
- EDV = End diastolic volume(135 mL)
- Stroke volume: EDV - ESV, amount of blood pumped by 1 ventricle in 1 contraction
- increase preload, increase SV(increase EDV)
- increase afterload, decrease SV(increase ESV)
- increase inotropy, increase SV(decrease ESV)
- Cardiac output = heart rate x stroke volume
- amount of blood pumped in ventricle per unit time
- (70 beats/min x 70 mL/beat = 4.9L/min)
- normal blood volume is 5L
- Cardiac reserve: difference between resting and maximal CO. Cardiac output in an emergency situation
42
CV system as a series of bag with different compliance
- Arteries: 15% of blood, low compliance, low capacitance. stiff, not stretchy. capacitance for blood low because too stiff.
- Veins: 65-80% of blood. high compliance, high capacitance. can hold high volumes without change in pressure
- Veins -> arteries. Pumps blood from low to high pressure.
43
Stroke volume
- Frank-starling law states stroke volume increases as EDV increases
- Length-force relationship in intact heart
- More blood fed to the heart, more blood heart able to pump
44
How does increased EDV lead to increased SV
- Pressure in venus bag determines amount of blood that gets returned to heart, EDV affected by venus return
- Reach suboptimal state, fewer cross bridges and overstretching of sarcomeres
- Stretch increases number of crossbridges(increase force generation) and approach optimal sarcomere length(point where ventricular stretch optimizes amount of cross bridges that can form, optimize force generation)
45
Stroke volume
- In response to sympathetic activity, large veins constrict or squeeze. Activation of smooth muscle decreases compliance of large vein and increase pressure in system -> drive blood forward
- EDV affected by venous return
- Venous return is affected by:
- skeletal muscle pump: squeeze veins and help squeeze blood from lower compartments
- Respiratory pump: with each respiration, create vacuum within throacic cavity that draws blood upward passing it onto superior/inferior vena cava
- Sympathetic innervation
46
Extrinsic factors influencing stroke volume
- From autonomic nervous system
- Contractility is increase in contractile strength. Independent of stretch and EDV
- Increase in contractility comes from increased sympathetic stimuli, certain hormones, and Ca2+
47
Catecholamines modulate cardiact contraction
Epinephrine and NE -> activate cAMP secondary messenger -> phosphorylation of voltage gated Ca2+ channels, increase Ca2+ entry from ECF. cAMP also lead to the phosphorylation of phospholamban -> increase Ca2+-ATPase on sarcoplasmic reticulum -> increase Ca2+ release -> more forceful contraction -> Ca2+ remove from cytosol faster, shortening of Ca-troponin binding time -> shorter duration of contraction
48
Inotropic effect
- Effect of NE on contractility of heart lead to increase capacity to constrict harder
- Inotropy and frank-starling work together to produce an enhanced level of contraction and force generation
49
Altering inotropic state of heart changes slope of ESPVR
- Positive inotropic agent move ESPVR left
- Negative inotropic agent move heart right
50
Extrinsic regulation of heart rate
- Controlled by cardiovascular control center in medulla oblongata
- Cardio acceleratory positive signaling lead to release of sympathetic neurons -> increase heart rate
- Cardio inhibitory center lead to release of parasympathetic neurons -> decrease heart rate
51
Cardiac output
- Function of: heart rate(determined by rate of depolarization in autorhythmic cells) and stroke volume(determined by force of contraction in ventricular myocardium) -> influenced by contractility and EDV
52
Blood vessel anatomy
- Three layers: Tunic intimia(endothelium), tunic media(smooth muscle, controlled by sympathetic nervous system), tunic external(fibrous connective tissue)
53
Blood vessel structures
-From high to low pressure
- Artery
- Arteriole(most stiff to withstand high pressure during systole)
- Capillary(thin to allow for optimum exchange, exchange point for nutrients)
- Venule
- Vein
54
Windkessel effect
- large elastic arteries expand and store energy during ventricular ejection
- Arterial wall stretch during systole
- Ventricle contracts -> semilunar valve opens -> aorta and arteries expand and store pressure in elastic walls
55
Elastic recoil of arteries keep blood moving during ventricular relaxation
- Isovolumic ventricular relaxation
- Semilunar valve shuts, preventing flow back into ventricle
- Elastic recoil of arteries send blood forward into rest of the circulatory system
56
Veins and venous return system
- Venules drain blood from capillaries into larger veins
- Relatively less smooth muscle and connective tissue than arteries
- Valves prevent back flow, series of connected bags
- Veins carry about 70% of body's blood, act as reservoirs during hemorrhage -> prevent loss of blood
57
Capillary beds
- Interconnected system of capillary vessels that work through every tissue and bring blood source course
- Lie in between arterioles and venues
- Consist of two types of vessels
- Arteriovenous shunt: directly connected an arteriole to a venule, act as a bypass
- True capillaries: the nutrient exchange vessels, oxygen and nutrients diffuse to cells. carbon dioxide and metabolic waste products diffuse into blood
58
Precapillary sphincters
- Sphincters open: blood able to flow into true capillaries. in metabolically active tissue w/ lots of blood and nutrients
- Sphincters close: prevent blood flow into true capillaries
59
What determines blood flow in a system
- Flow is directly proportional to driving pressure gradient
- Flow is inversely proportional to resistance of the system
- Ohm's law
60
Fluid flow through a tube depends on pressure gradient
- Higher pressure gradient, greater fluid flow
- Fluid flows only if there is a positive pressure gradient
- Flow depends on pressure gradient NOT absolute pressure
61
Pressure gradient in CV system
- Blood pressure is greatest in aorta and decreases as you move through CV system, always maintaining positive driving force
- Heart generates high aortic pressures
- Return back to heart to generate higher pressure to feed arterial system
62
Resistance affects flow
- If resistance increases, flow decreases
- If resistance decreases, flow increases
63
Poisueille's Law
- Resistance is proportional to length of tube(increases as length increases)
- Resistance is proportional to viscosity/thickness of fluid(increases as viscosity increases)
- Resistance inversely proportional to tube radius to fourth power(decreases as radius increases)
64
Resistance: blood flow
- Small change in radius has enormous effect on resistance to blood flow
- Vasoconstriction: decrease in blood vessel radius and decrease in blood flow
- Vasodilation: increase in blood vessel radius and increase in blood flow
65
Factors that alter arteriolar resistance
- Myogenic auto regulation: effect of pressure on smooth muscle cell. Pressure gradient increases to drive higher flow -> constrict to reduce flow back to normal. Pressure drop -> smooth muscle cell vasodilate
- Paracrines(local): active hyperemia, reactive hyperemia
- Sympathetic control: SNS(norepinephrine) and adrenal medulla(epinephrine)
66
Active hyperemia
- Increase tissue metabolism -> increase metabolic vasodilators into ECF(adenosine, low O2, high CO2) -> arterioles dilate -> decrease resistance leads to increase blood flow -> O2 and nutrient supply to tissue increases as long as metabolism is increased
67
Reactive hyperemia
- Decrease tissue blood flow due to occlusion -> metabolic vasodilators accumulate in ECF -> arterioles dilate, occlusion prevents blood flow -> remove occlusion(produce temporary hyperemia) -> decrease resistance create increase blood flow -> as vasodilators wash away, arterioles constrict and blood flow back to normal
68
Sympathetic regulation: norepinephrine
- autonomic control of arteriolar diameter
- Increase norepinephrine constricts vessel
- Decrease norepinephrine -> blood vessel dilate
69
Contractile proteins in smooth muscle
- Actin: 43 kDa globular protein polymerizes into double-helix
- Myosins: 2 heavy and 2 light chains
- Heavy chain: actin binding site, ATPase activity
- Light chain: 1 regulatory(P site) and 1 other
- Phosphorylation of myosin chains facilitate cross bridge formation and vasoconstriction
- Calcium bind to calmodulin -> create calcium-calmodulin -> activate MLC kinase -> phosphorylate MLC2(regulatory light chain) -> increase cross-bridge formation, actin-myosin interaction, development of vasoconstriction
70
Pressure throughout systemic circulation
- Blood pressure is highest in arteries and decreases continuously as it flows through circulatory system
71
Measuring arterial blood pressure
- Brachial artery closed, pressure in cuff above 120, no sounds audible
- Pressure in cuff below 120, above 70, sounds audible
- Pressure in cuff below 70, no sound audible
72
Five Korotkoff sounds
- Snapping sund first heard at systolic pressure, clear tapping, repetitive sounds for at least two consecutive beats is considered systolic pressure
- Murmurs heard for most of area between systolic and diastolic pressure
- Loud, crisp tapping sound
- Sounds at pressures 10mmHg above diastolic described as thumping and muting
- Silence as cuff pressure drops below diastolic blood pressure
73
Pulse
- Pulse: pressure wave of circulating blood
- Monitored at pressure points where pulse is easily palpated
74
Blood pressure
- Pulse pressure = systolic P - diastolic P
- Mean arterial pressure(MAP) = diastolic P + 1/3(systolic P - diastolic P) = 2/3 diastolic + 1/3 systolic
- Heart spends more time in diastole than systole, used to understand medium/long term regulation of BP
75
Factor that affects pulse pressure
- Stroke volume
76
What controls pressure in aortic bag
- Mean arterial pressure is a function of cardiac output and resistance in arterioles. Both regulate aortic blood volume at entry and exit
- Increase cardiac output/increase resistance cause increase pressure
77
Total resistance influences mean arterial pressure
- Cardiac output proportional to pressure gradient between arteries in veins and total resistance of peripheral arteries and tissues
78
Resistance opposes flow
- Flow of blood in systemic circuit is directly proportional to pressure gradient, inversely proportional to resistance to flow
- increase TPR and cardiac output lead to increase MAP
79
Cardiac output influences MAP
- Cardiac output determined by heart rate and stroke volume
80
Blood volume influences MAP
- Blood volume determined by fluid intake and fluid loss
81
Renin-angiotensin aldosterone system
- Decrease pressure/blood flow -> juxtaglomerular apparatus in kidneys -> secrete renin to cleave angiotensinogen to angiotensin 1 -> cleave to angiotensin 2 -> act on adrenal cortex and vasoconstriction of arteries-> secrete aldosterone -> salt and water retention by kidneys -> increase blood volume and blood pressure
82
Aldosterone
- Adrenal cortex
- Reabsorption of salt and water by kidney
- Renin-angiotensin-aldosterone system
- Feedback loop: salt intake vs renin secretion
83
Blood pressure(fast vs. slow control mechanisms)
- Increase blood volume leads to increase blood pressure -> trigger
- Fast response: compensation by cardiovascular system
-> vasodilation -> decrease cardiac output -> decrease blood pressure back to normal
- Slow response: compensation by kidneys -> excretion of fluid in urine -> decrease blood volume -> decrease blood pressure to normal
84
Baroreceptor reflex(fast response)
- Detect how pressure changes over time
- Medullary cardiovascular control center
- Controls parasympathetic and sympathetic neurons -> affects SA node, ventricles, veins, arterioles
85
Response to increase BP
- increase blood pressure -> cardiovascular control center decreases sympathetic output and increase parasympathetic output -> decrease NE on beta1-receptors -> decrease force of contraction, decrease heart rate -> decrease cardiac output and peripheral resistance -> decrease blood pressure
86
Response to low BP
- Response to orthostatic hypotension(standing up too quickly, pulls venous blood away from heart decreasing cardiac output)
- decrease MAP -> cardiovascular control center -> increase sympathetic output and decrease parasympathetic output -> vasoconstriction, increase force of contraction, increase heart rate -> increase cardiac output and increase peripheral resistance -> increase blood pressure to normal
87
Cardiovascular response to exercise
- Increase in venous return and respiratory pump
- Increase in sympathetic activity, withdrawal of parasympathetic activity
- Neuromuscular junctions in skeletal muscle send signals to CCC
- Effects on HR + contractility, resistance arterioles in metabolically inactive tissues
- Local metabolites mediate profound vasodilation in skeletal muscle
88
Capillaries have slowest velocity of blood
- Velocity of flow depends on total cross-sectional area of all vessels at same level in CV system
- Capillaries have highest cross sectional area
89
Blood velocity is inversely proportional to cross-sectional area
- Velocity = Flow rate/Cross sectional area
90
Capillaries
- Exchange of materials occurs across very thin capillary wall
- Capillary density related to metabolic activity
- Over 10 billion capillaries with surface area of 500-700m^2 performing solute and fluid exchange
91
Continuous capillary
- Muscle and brain
- Must be transported by vesicular pathway
92
Fenestrated capillaries
- Leaky: high volumes
- Kidney, intestine
93
Capillary exchange
- Exchange between plasma and interstitial fluid can occur by paracellular pathways
- Larger solutes and proteins move by vesicular transport(transcellular through apical and basolateral membranes of cells)
- In most capillaries, large proteins are transported by transcytosis
- Small dissolved solutes, H2O and gases move by diffusion
94
Solute and fluid exchange across capillaries
- Most important means by which substances are transferred between plasma and interstitial fluid is by diffusion
- Lipid soluble substances diffuse directly through cell membrane of capillaries
- Lipid insoluble substances such as H2O, Na+, and Cl-, and glucose cross capillary walls via intercellular clefts
- Concentration differences across capillary enhances diffusion
95
Effect of molecular size on passage through capillary pores
- Width of capillary intercellular slit pores is 6 to 7 nanometers
- Permeability of capillary pores for different substances varies according to their molecular diameters
96
Final forces for transfer
- Bulk flow = mass movement of fluid as a result of hydrostatic or osmotic pressure gradients
- Absorption: fluid movement into capillaries
- Filtration: fluid movement out of capillaries(hydrostatic pressure, net filtration at arterial end)
97
Determinants of net fluid movement across capillaries
- Capillary hydrostatic pressure(Pc): forces fluid outward through capillary membrane
- Interstitial fluid pressure(Pif): opposes filtration when value is positive
- Plasma colloid osmotic pressure: opposes filtration causing osmosis of water inward through membrane
- Interstitial fluid colloid pressure: Promotes filtration by causing osmosis of fluid outward through membrane
- Overall net pressure: (Pc + Pif) + (pi p/c + pi if)
- Net inward, positive vectors
- Net outward, negative vector
98
Fluid exchange at a capillary
- Hydrostatic pressure and osmotic pressure regulate blood flow
- Net filtration: Pcap > colloid
- Net absorption: colloid > Pcap
99
Lymphatic system
- Returns fluid and proteins to circulatory system
- Picking up fat absorbed and transferring it to circulatory system
- Serving as filter for pathogens
- A route by which fluid and protein can flow from interstitial spaces to blood
- Prevent edema
- Lymph is derived from intersitial fluid
- Eventually drain into subclavian veins -> heart
100
Edema: fluid buildups/swelling
- Causes: Inadequate drainage of lymph
- Filtration > absorption
101
Elephantiasis
- Abnormal enlargement of any part of the body due to obstruction of lymphatic channels in area
- Don't allow proper fluid return to cardiovascular system -> built up fluid
- Transmitted by mosquito
102
Ascites
- Fluid in abdomen
- Don't have same high flowing plasma -> absorption of fluid to bloodstream is slowed -> capillary beds have high rate of filtration -> excess fluid buildup
103
Liver Cirrhosis
- Alcoholism, hepatitis, fatty liver disease, acetaminophen
- Decreased function of liver
