Circulation Flashcards

1
Q

Explain Poiseuille’s law and how it relates blood flow, pressure and resistance.

A

Flow=pressure/resistance. To change flow, have to either increase pressure (gradient) or decrease resistance. FLOW is directly related to r^4, while resistance is inversely related to r^4. Resistance also directly proportional to viscosity and length.

Pressure gradient tends to stay pretty constant, so changing r^4 (via arteriolar vasoconstriction or dilation) is most important determinant.

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2
Q

Define viscosity and how it changes with vessel diameter and hematocrit.

A

Shear stress/shear rate. It is internal frictional resistance of fluid in a column.

Hct: More hct=more more viscosity and slower flow
Diameter: Smaller diameter=smaller viscosity and faster flow (due to axial streaming and plasma skimming–RBCs tend to congregate in axial laminae, so this will be smaller in smaller vessels so you have more relative plasma and less viscosity).

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3
Q

Explain how hematocrit changes with vessel diameter.

A

Have more hct in larger vessels due to axial streaming.

Smaller vessels have fewer RBCs due to plasma skimming.

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4
Q

Define laminar and turbulent blood flow.

A

Laminar: Flows in individual columns that make a parabola.
Turbulent: Flows chaotically. Noisy.

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5
Q

Define Reynold’s number and how each of its parameters contributes to the development of turbulent blood flow.

A

Indicates propensity for turbulent flow. =densitydiametervelocity/viscosity.
Higher number=higher chance for turbulent flow.
The smaller the vessel, the faster the flow and the more likely you are to have turbulent flow (big increase in velocity for given diameter (r^4)).
Aorta a likely place for turbulent flow because it is both high in cross-sectional area and has high velocity.

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6
Q

Understand that turbulent blood flow contributes to heart sounds, murmurs and endothelial cell damage.

A

Also, bruits. Anything going through a stenosis could become turbulent and audible. Damages endothelium and can give you dissecting aneurysm.

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7
Q

Define Bernoulli’s principle and its application to the circulatory system.

A

Total nrg is conserved–potential+kinetic. In a stenotic system, PE (pressure) is converted to KE (flow). Faster flow=higher likelihood of turbulent flow. More important in sending flow down pressure gradient is sending flow down total nrg gradient.

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8
Q

Define the Laplace relationship and how wall tension affects the function of dilated hearts, capillaries, and aneurysms.

A

Wall tension=pressure*radius/wall thickness
So, small vessel=small wall tension (capillaries).
Dilated heart: Larger radius creates more wall tension. Shortening impeded, AL increased.
Aneurysm: Larger radius creates more wall tension, flow slowed down, more transmural pressure will eventually cause it to rupture.

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9
Q

Explain how wall tension and the anatomy of arterioles and precapillary sphincters (large wall thickness/lumen diameter ratio) operates in normal regulation of vascular resistance.

A

The higher the wall thickness/lumen diameter ratio, the more control over vessel diameter (and thus blood flow).

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10
Q

Define the relationships between velocity of blood flow and vessel cross sectional area.

A

Smaller area=faster flow (by factor of r^4)

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11
Q

Explain series and parallel resistances in the circulatory system.

A

Series: Resistances add up to total resistance. Tends to be in series until you get to viscera. Arterioles are in series, so change resistance in 1 change resistance of whole system.

Parallel: Total resistance is less than each individual resistance. Seen in capillary beds and viscera.

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12
Q

Define how velocity of blood flow, and pressures change throughout the circulatory system in relation to changes in total cross-section area.

A

Total cross-sectional area increase through capillaries, then decreases again in venules up through veins.
This means that Velocity decreases until you get into venues, where it starts going back up again.
Pressure continually goes down throughout the system

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13
Q

Explain the pulse pressure profiles throughout the circulatory system.

A

As you get further from heart in large arteries, systolic goes up and diastolic goes down, resulting in larger PP and lower mean arterial pressure (determined more by diastolic).
Due to decreases in arterial compliance the further you get.
Lose PP in arterioles and don’t get it back until atria.

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14
Q

Explain how elastin, smooth muscle and collagen function as structural components of
the vascular wall.

A

Elastin is the most elastic and responsible for most of arterial compliance. Within tunica intima (IEL) and media (EEL). NOT present in veins.

Smooth muscle: Somewhat compliant, in tunica media. Not as well developed in veins.

Collagen: Very uncompliant, in tunica medida. More pronounced in veins.

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15
Q

Define compliance.

A

Change in pressure for a given change in volume. C=dV/dP. Basically, how much the pressure in a vessel will go up with a given change in volume.

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16
Q

Explain how vessel wall compliance affects arterial pressures.

A

If you take away compliance (say by elastin becoming less elastic), then you will raise systolic pressure (aorta won’t distend when blood flows into it) and lower diastolic pressure (won’t recoil when blood leaves).

Put another way, to apply Bernoulli, in normal aorta, PE is converted to KE to move out walls of aorta when blood ejected into vessel. That pressure has nowhere to go in case of loss of elasticity, and will stay as PE (pressure) in artery.

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17
Q

Explain the windkessel (hydraulic filtering) properties of the aorta.

A

In normally compliant aorta, part of SV stored in artery as it is stretched during systole.
Once diastole hits, recoil of aorta forces that SV that was stored to leave, creating continuous flow (lower systolic pressure).
In non-compliant aorta, full SV must be ejected during systole (lower diastolic pressure because nothing in aorta at diastole).

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18
Q

Define the relationship between velocity, flow and vessel cross sectional area.

A

As cross sectional area increases, velocity decreases.

As cross sectional are a increases, flow increases.

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19
Q

Define the importance of wall/lumen diameter ratio to regulation of arterial pressure.

A

Higher ratio=more control over vessel flow. Biggest ratios are pre capillary sphincters and arterioles and thus these regulate flow the most.

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20
Q

Define the pressure pulse.

A

Pressure wave propagated down vessel wall. The less compliant, the faster the speed. Pressure strengths will feel different at different areas you take your pulse.

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21
Q

Define the physiological and physical factors that determine mean arterial pressure.

A

Physiological: CO (primarily regulated by ANS) and peripheral resistance (ANS that can be overridden by local control).

Physical: Blood volume (higher volume=more pressure) and arterial compliance (determined by age, location, volume,).

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22
Q

Define the primary determinants of systolic and diastolic pressures.

A

Systolic: CO, compliance, volume.
Diastolic: TPR, compliance (lowers it)

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23
Q

Explain how arterial compliance affects systolic and diastolic arterial pressures.

A

Increasing compliance increases systolic and decreases diastolic pressure.

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24
Q

Explain the factors that determine and regulate peripheral arterial resistance.

A

Blood viscosity: Only occurs in pathological conditions (blood doping, anemia).
Arteriolar radius: Determined by a bunch of stuff: Extrinsic control (hormones, baroreceptor, sympathetic) and local (EDRF, metabolites, myogenic response).

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25
Q

Explain how the autonomic nervous system regulates mean arterial pressure.

A

Increases HR and contractility, which increase SV and CO, and thus BP.

Increase venoconstriction to mediate more return to heart and increase SV

Increase arteriole constriction, which increases TPR to get blood to more vital organs

Para: Decrease HR (hyperpolarize MbP to and elongate refractory period).

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26
Q

Explain the cardiovascular adjustments and underlying mechanisms that operate during exercise.

A
  • Increased HR and contractility
  • Vasoconstriction to areas not being worked (kidney, splanchnics, etc)
  • Local metabolic vasodilation
  • Capillaries open
  • Enhanced O2 extraction in skeletal muscle but NOT in heart (dissociation curve shifts, O2 held less tightly by Hg)
  • Increase in venous return due to venoconstriction, respiratory pump, muscle pump.
  • Pulse pressure widens: Increase in systolic pressure due primarily to increase in SV, diastolic determined primarily by changes to TPR, which should remain relatively constant.
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27
Q

Explain the basic structural arrangement of the microcirculation including precapillary resistors, metaarterioloes, capillaries and postcapillary resistors.

A

Precapillary resistors: Arteriole, PCS, metarterioles (shunt)
Capillaries
Postcapillary resistors: Venules

28
Q

Explain the characteristic of capillary blood flow in terms of precapillary sphincter control, vasomotion and Rouleaux formation.

A

Flow is slow, not uniform. Sphincter controls if anything gets into capillaries–when more flow needed in that tissue, more sphincters open. Low pressure gradient within capillaries also slows flow down. Due to slow flow, blood can go retrograde.
Rouleaux formation: RBCs bigger than capillary diameter, so they stack in single-file line at angle to get through. Enhances gas exchange.

29
Q

Define and explain the determinants of transcapillary fluid (TCF) exchange in terms of interstitial and plasma hydrostatic and oncotic pressures.

A

HDSTP: Higher in capillaries than in tissue, pushes plasma and nutrients out when it exceeds capillary oncotic pressure.
Oncotic pressure: Higher osmolarity in capillary than in tissue, fluid/waste/nutrients comes back from tissue when it exceeds capillary HDSTP.

30
Q

Explain TCF exchange in different pathological conditions, i.e. hemorrhage, nephrosis, liver damage, portal hypertension, congestive heart failure, burns.

A

Hemorrhage: Lower volume, less HDSTP, pulls fluid from tissue to increase volume.
Nephrosis: Everything filtered out, lose proteins and thus oncotic pressure so no reabsorption
Liver damage: Albumin no longer made, oncotic pressure in capillaries reduced and get edema.
Portal HTN: Caused by either liver damage or CHF. Liver swells, constricts veins, causes backup into abdomen, higher HDSTP in abdomen causes ascites.
CHF: Increases HDSTP due to backup of venous system throughout entire body.
Burns: Make capillaries more permeable, fluid leaks out and edema.

31
Q

Define the importance of albumin in TCF exchange.

A

Albumin binds to Cl, which then binds to Na. So, albumin in the plasma also carries NaCl with it. This brings H20 and in and disproportionately contributes to higher oncotic pressure in capillaries and brings a lot of fluid into the capillaries from interstitium.

32
Q

Define pre/post capillary resistance and how it determines capillary hydrostatic pressure
under normal and abnormal conditions.

A

Precapillary resistance primarily determined by arterioles and pre capillary sphincters. High pre capillary pressure means that there is not a huge contribution from pre capillary resistance to HDSTP.
Postcapillary resistance determined by venous pressure,w which is lower and thus contributes significant amount to HDSTP in capillary.
Decreasing the pre/post capillary resistance ratio will increase HDSTP, while increasing the pre/post capillary resistance ratio will decrease HDSTP.

33
Q

Define the role of endothelial-derived mediators (prostacyclins, EDRF, NO, endothelin,
metabolites) in the regulation of resistance vessels, i.e. vasodilation or vasoconstriction.

A

Vasodilators: Prostacyclins, EDRF, NO, metabolites.
-All decrease actin/myosin interxns
Vasoconstrictor: Endothelin
-Increases IC Ca2+ release

34
Q

Explain the structure and function of the lymphatic system.

A

Returns interstitial fluid to circulation. Plasma and proteins expelled from tissues after they are used and higher rate of filtration than absorption means there is fluid in interstitum.
Structure similar to veins: Valvular unidirectional flow

35
Q

Define edema and the conditions that predispose edema.

A

Buildup of fluid in interstitial space. Can occur through CHF (increase HDSTP), liver failure (no albumin made, no oncotic pressure in capillaries), neprhosis (proteins all excreted), obstruction of venous return, burns, lymphatic obstruction.

36
Q

Define basal arterial tone and resting sympathetic tone.

A

Basal tone: Amount of vasoconstriction found under resting conditions without any input. Theoretcal.
Sympathetic tone: Resting vasoconstriction due to tonically released Nor.

37
Q

Define passive and active vasoconstriction or vasodilation.

A

Passive VC: Happens due to removal of ACh
Active VC: Addition of adrenergics
Passive VD: Removal of adrenergics
Active VD: Addition of ACh

Passive brings back to basal tone, active pulls it away from basal tone.

38
Q

Explain how alpha-1 and beta-2 adrenergic receptors mediate regulation of vascular tone.

A

A-1 receptors: On vascular smooth muscle and cause vasoconstriction. Not present in heart, lung or cerebral vessels.
B-2 receptors: On vascular smooth muscle in heart, skeletal muscle, bronchioles. Causes vasodilation. During sympathetic response, need more perfusion to heart, so sympathetics need to be able to dilate.

39
Q

Identify the anatomy of arterial baroreceptors.

A

Located in the carotid sinus (IX) and aortic arch (X). Fibers run to vasomotor center in medulla and are activated with sympathetic stimulation. Mechanoreceptors that are sensitive to stretch.

40
Q

Explain the arterial baroreceptor reflex.

A

A decrease in BP causes mechanoreceptors to decrease firing rate. This means fewer impulses get back to medulla, which induces a sympathetic response that increases vasoconstriction, BP and contractility via adrenergic stimulation. Firing increased by increase in arterial pressure in negative FB loop.

More sensitive to high pressures and more sensitive to changes than static pressures, but they adapt during HTN as threshold for firing is increased.

41
Q

Explain the anatomy and function of peripheral chemoreceptors.

A

Located in same area as baroreceptors and use same nerves. Respond to low O2 or high H+ or CO2 to stimulate respiration. Most sensitive to low O2 and high CO2. Activate parasyms to depress HR and sym to vasoconstrictor, but parasyms damped out by hypoxia and get an increase in HR, RR, BP.

42
Q

Explain the renin-angiotensin-aldosterone mechanism of blood volume regulation.

A

Primary system for long-term regulation of BP. Designed to mitigate dehydration. In response to low BP sensed by either afferent renal arterioles or baroreceptors, stimulates release of RENIN from JGA. This causes conversion of angiotensin to angiotensin I. ACE then converts I to angiotensis II. A-2 increases vasoconstriction, increases aldosterone release and Na reabsorption in kidney, and stimulates ADH and thirst for h20 retention. A2 is most potent vasodilator in body. In CHF, due to low BP, this is evoked, so give people ACE inhibitors and diuretics.

43
Q

Define the resistance vessels.

A

Arterioles, precapillary sphincters, metarterioles, veins (easily compressed and can thus be source of resistance).

44
Q

Explain the cellular mechanisms responsible for contraction of vascular smooth muscle.

A

Myogenic: Increased flow causes increase in stretch. Increased stretch on vascular smooth muscle causes a vasoconstriction.
Metabolic: Vasodilator metabolites that are a part of metabolically active tissue washed away with increase in flow due to increase in pressure. This causes vasoconstriction, which brings flow back down.

45
Q

Explain the myogenic, metabolic, endothelial and mechanical mechanisms that regulate blood flow.

A

Myogenic: Increased flow due to increased pressure causes stretching, which causes vascular smooth muscle contraction and reduction in flow.
Metabolic: Metabolically active tissue makes metabolites that are vasodilators. During AR these can be washed away, or if more flow is needed (as during exercise) AR is overcome by this to keep vasodilation.
Endothelial: EDRF released from endothelium in response to shear stress from increased flow. This vasodilates. Again, important in exercise.
Mechanical: Increase in tissue pressure compresses small vessels and alters flow. Ex: small vessels on endocardium can be constricted with high after load by strong ventricular contraction.

46
Q

Define the myogenic and metabolic mechanisms of autoregulation of blood flow.

A

Myogenic: Increased flow causes increase in stretch. Increased stretch on vascular smooth muscle causes a vasoconstriction.
Metabolic: Vasodilator metabolites (ADENOSINE, CO2, H) that are a part of metabolically active tissue washed away with increase in flow due to increase in pressure. This causes vasoconstriction, which brings flow back down.

47
Q

Compare/contrast autoregulation of blood flow to neural, metabolic and endothelial regulation of blood flow.

A

AR: In response to changes in flow due to pressure when there is no need for more O2 consumption. Ex: Standing up, will get more pressure due to gravity in feet but don’t need more perfusion in feet, so AR ensures that flow is constricted and maintains constant.
Neural is global and happens as a result of sympathetic or parasympathetic stimulation to send blood to where perfusion is needed.
Metabolic and endothelial are also in response to increased O2 demands, but they are local and cause vasodilation to increase perfusion.

48
Q

Define and explain active and reactive hyperemia.

A

Active: Increase in perfusion based on need of the tissue, as during exercise. Metabolically active tissues make more metabolites that are vasodilators.
Reactive: Transient increase in tissue perfusion in response to re-introduction of blood to tissue after brief arterial occlusion. Response to metabolic debt–lots of metabolites have built up so vessel is more dilated when blood reintroduced.

49
Q

Define the types of shock

A

Cardiogenic–heart can’t pump efficiently enough to keep up with body demand
Hypovolumic–Not enough blood to perfuse tissues. Baroreceptors can mask this to a point, then your BP crashes
Septic: Immune response causes massive vasodilation
Neurologic: Damage to spine that causes problems sympathetic control of vasoconstriction.
Anaphylactic: Low BP due to allergen.

50
Q

Describe the general anatomy of the coronary circulation.

A
Coronary arteries (dominance differs person to person) to capillaries (each cell in contact with 3-4 capillaries, which are not all opened all the time but open more with increased metabolic demands). 
Arteries start on the epicardial surface and go to endocardial, becoming smaller and they go endo.
51
Q

Describe how cardiac tissue pressure determines coronary blood flow.

A

Primary determinant of coronary blood flow is cardiac tissue pressure caused by aortic pressure. Highest pressure is in L coronary, and is highest at endocardial surface. Flow actually can go down in left coronary during early systole when pressure is maximum. Thus, the majority of L coronary perfusion of L myocardium occurs during diastole. With increased AL, pressure is more on endocardium, further reducing blood flow and producing ischemia.

52
Q

Explain the effects of left ventricular end-diastolic pressure on endocardial and epicardial coronary blood flow.

A

Diastolic pressure is higher at endocardium than epicardium. Thus, the vessels on the L endocardium are the most constricted by wall tension and the most at risk for ischemia because they are the most compressed. Therefore, anything that increases AL and changes EDP reduces flow to L endocardial surface. Epicardium normally has same flow as endocardium because it is more constricted.

53
Q

Describe the relative importance of neural versus metabolic regulation of coronary blood flow.

A

Metabolic control is central mode of regulation of coronary blood flow. B-1 receptors on pacemaker and myocardial cells and B-2 receptors on vascular smooth muscle cause vasodilation. As you increase O2 consumption (metabolism) of coronaries, get an increase in blood flow in linear relationship. Thus, more O2 consumption=less resistance=more flow. O2 supply must equal O2 demand, but heart is flow limited, so only way to increase supply is to increase flow.

54
Q

Explain the factors that determine myocardial oxygen supply and demand, and how the balance of these factors relates to the development of ischemia.

A

O2 demand is directly related to work done by heart. Work=MAP*systolic stroke volume. However, pressure work consumes much more O2 than volume work, meaning that HTN or any other increase in AL causes increased O2 demand. Thus, biggest determinants of O2 demand are AL, HR, contractility.

Biggest determinants of O2 supply are diastolic perfusion pressure and coronary vascular resistance, comprised of external compression and intrinsic regulation, and O2 carrying capacity.

Also, since heart consumes a lot of fatty acids, needs a lot of O2.

55
Q

Explain the concept of “coronary steal” and how it relates to the development of myocardial ischemia.

A

If you have a plaque in a coronary, it will be fully dilated when at rest and have similar amount of perfusion as a healthy, constricted artery. Once you start exercising, or inject a vasodilating agent, the dilation of healthy artery causes blood to flow into that one, causing decreased flow into area of plaque and ischemia.

56
Q

Understand the metabolic, mechanical and neurohumoral mechanisms that regulate the skeletal muscle circulation.

A

Metabolic: Muscle has large basal tone because it can hugely increase it’s blood flow during exercise via local metabolites. As with cardiac, metabolic is primary form of control in muscle.

Mechanical: Contraction squeezes vessels, resulting in O2 being cut off. This is big reason why isometric exercise can’t be sustained for very long. Squeeze veins during exercise and negative pressure in thorax.

Neuro: Alpha adrenergic receptors bind to Nor to cause vasoconstriction. Also have cholinergic receptors that cause vasodilation via NO release. Epi acts on B-2 receptors to cause vasodilation. Sympathetics also cause venoconstriction.

57
Q

Describe the anatomy and general characteristics of the cerebral circulation including the blood brain barrier.

A

Circle of willis connects vertebra-basilar arteries to internal carotids. BBB=prevents large molecules from getting through.

58
Q

Explain how autoregulation, tissue pressure (Monro-Kelli), metabolites, neural activity affect cerebral blood flow.

A

AR: Brain pretty dependent on AR, so decrease in pressure will cause vasodilation and increase in pressure will cause vasoconstriction. Flow does vary based on which parts of brain active. AR fails at very high or low pressures.

Tissue pressure: Brain volume+CSF volume+vascular volume=constant. Increasing 1 of these factors will decrease other 2. The increase of the other 2 cause pressure in cranium to go up.

Metabolites: Brain sensitive to CO2. CO2 gets into brain and causes a decrease in pH due to a rxn that makes H+, leading to vasodilation of cerebral arteries. Hyperventilate patients with high pressures to lower blood flow to cerebrum. Other vasodilators are adenosine, K+ and NO (uses cGMP)

Neural: Relatively weak. Cushing response: Elevated BP and lowered pulse due to high intracranial pressure.

59
Q

Define Cushing’s response and the underlying mechanisms.

A

Increased intracranial pressure leads to ischemia. This stimulates both sympathetic and parasympathetic nerves which will raise BP significantly and lower HR significantly.

60
Q

Describe the general anatomy and pressures within the pulmonary circulation.

A

Pulmonary circulation receives 100% of blood from circulation.
Pulmonary vessels are very compliant (thus lower pressures on R side of heart–about 14 mmHg (max is 25 mmHg) is mean arterial pressure. Such a low pressure system that backup is easy.
Capillaries are a major source of resistance in the lungs-tend to be located in the alveolar walls and are compressed with deep inspiration.
With increased perfusion pressure, new capillaries pop open.

61
Q

Describe the respiratory effects on the pulmonary circulatory pressures.

A

Inhalation compresses capillaries in alveoli and distends extra-alveolar vessels. Net effect is a slight increase or no change in resistance.
Exhalation distends capillaries in alveoli and compresses extra-alveolar vessels, causing slight decrease or no change in resistance.

62
Q

Describe the hydrostatic (gravitational) and “waterfall” effects on pulmonary blood flow, i.e.
zones 1, 2 and 3.

A

HDST: Higher pressures at lower parts of lung due to gravity means more perfusion. This is why pulmonary edema can be heard here best, and why those with pulmonary edema feel better supine. Above pulmonary artery, have to subtract 11 mmHg from pressure, and below have to add 11 mmHg.
Waterfall: Zone 1: PA>Pa>Pv, meaning that you won’t get any perfusion through here because alveolar pressure exceeds arterial/venous and vessels collapse.
Zone 2: Pa>PA>Pv. Get some flow through here, gradient dependent on difference between arteriolar and alveolar pressures and independent of venous. Corresponds to top 1/3 of lung.
Zone 3: Pa>Pv>PA. Bottom 2/3 or lung. Gradient depends on arterial-venous pressure difference.

63
Q

Explain the primary function of the cutaneous circulation.

A

To bring heat to periphery in order to get rid of it by convection. Main idea is to maintain constant body temp. Humans much better at heat loss than heat retention. Most important is NEURAL control, in response to core temp will get vasodilation (need to send more to skin to cool off) or vasoconstriction (less to skin to keep organs warm).

64
Q

Identify the characteristics of apical and non-apical skin in terms of blood flow and their
specific anatomical and functional differences.

A

Apical: At fingertips, lips, ears, nose, hands and feet. Don’t sweat much. Have glomus bodies that are good for heat loss. Have sympathetic adrenergics to produce active vasodilation.
Nonapical: No AV anastamoses and innervated by sympathetic cholinergics that produce vasodilation to get more blood to surface. Have both sympathetic adrenergics and sympathetic cholinergics to produce active vasodilation via bradykinin release from sweat gland.

65
Q

Describe the neural and thermal factors that regulate cutaneous blood flow.

A

Neural: Non-apical skin innervated by sympathetic cholinergics that produce active vasodilation via release of bradykinin from sweat glands. Apical skin innervated by sympathetic adrenergics causing active vasoconstriction.

Thermal: Hypothalamus regulates core temp. In response to high internal temp, will cause vasodilation via removal of sympathetics. Low internal temp, vasoconstriction.

BP not normally regulated heavily by flow to skin, except in cases of heat stress, where you have large amount of CO going to skin. Decreases BP and causes baroreceptor response.

66
Q

Describe the general anatomical features of the splanchnic circulation including the hepatic
portal system.

A
  • Arterial blood delivers O2 and metabolic substrates
  • Venous blood removes CO2 and nutrients that have been digested
  • Countercurrent flow=within intestinal villus, arterioles and venuoles run parallel. This allows Na and other solutes to diffuse from veins to arteries, increasing oncotic pressure in which stimulates further blood flow.
  • Portal circulation removes blood from intestinal capillary beds and brings to liver. Has pressure not much higher than IVC, so backup in IVC leads to backup of entire system and edema.
67
Q

Describe the neural and local regulatory mechanisms governing splanchnic blood flow.

A

Neural: Mostly sympathetic adrenergic vasoconstriction caused by nor binding to alpha receptors. During sympathetic response such as exercise or hemorrhage, blood shunted away from splanchnics. Also have Beta receptors for vasodilation, and parasympathetics that INDIRECTLY stimulates intestinal blood flow by stimulating intestinal motility and secretions, increasing metabolism.

Local: Increase in metabolism=decreased O2 and increased adenosine, CO2, H+. This all conspires to vasodilator, and the opposite happens with decrease in metabolism. Majority of intestinal blood flow from rate of active transports (countercurrent flow). A little AR too.