12/16 - Special Circulations

Front 1

Gravity affects the _____ pressure of blood vessels

Back 1

Transmural

Front 2

Effect of standing vs laying flat on pressure gradient?

Back 2

Pressure gradient (what determines flow between arterial and venous pressure) is still the same whether the person is laying or standing

Front 3

Arterial + venous pressure as we lay down vs stand up

Back 3

Arterial transmural pressure laying down = 95 mm Hg

Venous transmural pressure laying down = 5 mm Hg

(pressure gradient = 90 mm Hg); this applies at both head and feet

Arterial transmural pressure standing up = 95 + 80 mm Hg (pressure added from heart down) = 175 mm Hg in lower half of body; 95 mm Hg - 34 mm Hg in upper half of body = 61 mm Hg

Venous transmural pressure standing up = 85 mm Hg (5+80) in lower half of body and -29 in upper half of body (5-34)

Pressure gradient is still 90 mm Hg no matter where you are in standing body

Front 4

What senses changes in our posture?

Back 4

Baroreceptors in aortic arch + carotid body - sense a difference in pressure when we stand up

Front 5

Mechanisms to prevent venous pooling

Back 5

1) Sympathetic stimulation of alpha-adrenergic receptors increases venous tone

2) Skeletal muscle pump (very important)

3) Respiratory pump

Front 6

What does stimulation of alpha-adrenergic receptors on veins accomplish?

Back 6

Increased venous tone --> this stimulation changes compliance of the veins --> shifts the volume vs pressure curve to a more constricted setting

Front 7

Skeletal muscle pump for venous return

Back 7

Probably the mechanism we use most

Before muscle contraction, blood enters vein

When muscle contracts (ex in our calves when we walk around), the upper valve opens further but the lower valve closes so contracting muscle pushes the blood back up toward the heart

When muscle relaxes, upper valve closes to prevent backflow and lower valve opens to allow vein to flow

Front 8

Respiratory pump

Back 8

When we inspire, create negative pressure that sucks blood into the great veins (SVC/IVC) - most important during heavy breathing during exercise

Front 9

Coronary circulation + O2 extraction

Back 9

• Extraction is always maximal (~70%) and O2 is a flow limited substance (the only way we can increase delivery for heart metabolism is by increasing flow)
• Changes in coronary blood flow must be matched to metabolism needs

Front 10

Arrangement of coronary arteries

Back 10

Perpendicular with respect to muscle fibers

Heart contracts and squeezes all of the arteries basically shut during systole

Most of the blood flow through coronary circulation occurs during diastole

Front 11

Left and right coronary blood flow during diastole and systole

Back 11

• Coronary blood flow is maximized during diastole - as soon as isovolumetric relaxation occurs - huge upswing in coronary artery flow
• During isovolumetric contraction - coronary blood flow is almost down to 0
• Similar events occur in R and L ventricles, but in R ventricle there is less of an increase/decrease in blood flow b/c R ventricular pressures are not as extreme

Front 12

Equations for coronary blood flow

Back 12

CBF = Pressure gradient/CVR

CBF = P(aortic diastolic) - P(coronary sinus)/CVR

CVR = coronary vascular resistance

CBF = 225 ml/min (~5% of CO) under resting conditions

Front 13

How do we regulate coronary blood flow?

Back 13

• Adenosine hypothesis is most prevalent - vasodilatory metabolite
• Increase in adenosine decreases vascular resistance (vasodilation)
• Even though coronary vessels are sympathetically innervated, not a huge effect (metabolic >> sympathetic) - even during fight/flight we can have vasodilation to maximize coronary blood flow
• Coronary blood flow is very efficiently autoregulated - very stable flow over a wide range of pressures

Front 14

Metabolism in the heart?

Back 14

-At rest: mostly utilizes free fatty acids, some carbohydrates, a little bit of lactate from RBC metabolism

-During exercise: most carbons from lactate > FFAs > glucose

Aerobic metabolism

Front 15

Pulmonary circulation

Back 15

• Very low pressure circulation - lungs are all about gas exchange
• 100% of cardiac output is going here - obtain high cardiac output at a much lower pressure than systemic circulation; don't have to have this as a pressure reservoir - not worried about distributing blood flow according to metabolic demands of different tissues/different parts of the lung
• Arterioles in the lungs are not nearly as robust/high resistance as rest of the body
• High compliance - another volume reservoir
• Pressure is approx 15 mm Hg in pulmonary artery and 5 mm Hg in the pulmonary vein

Front 16

Partial pressures of inspired gas/blood coming to and from lungs

Back 16

Inspired air: PO2 = 150 mm Hg, PCO2 = 0 mm Hg

Alveolar pressures: PO2 = 100 mm Hg, PCO2 = 40 mm Hg

Incoming blood in pulmonary arteries: PO2 = 40 mm Hg, PCO2 = 45 mm Hg (remember, this is part of venous circulation)

Outgoing blood in pulmonary veins: PO2 = 100 mm Hg, PCO2 = 40 mm Hg (remember this is part of arterial circulation)

Front 17

Pressures in pulmonary artery vs other systemic arteries

Back 17

Pressures in pulmonary artery are a lot lower (both systolic and diastolic) than other systemic arteries - this favors reabsorption and prevents edema

Pulmonary HTN: if capillary pressure increases, this favors filtration and the interstitial space starts to fill with fluid --> pulmonary edema

Front 18

Zones of blood flow in the lung

Back 18

• Blood flow in base of lung >> blood flow in top of the lung
  
• Zone 1: top of lung - alveolar pressure is > both PA and PV pressure (no flow)
• Zone 2: PA pressure > alveolar pressure > PV pressure (pressure gradient really due to difference between PA and alveolar pressure)
• Zone 3: toward bottom of lung - when both PA/PV is greater than gas pressure
• Zone 4: very bottom of the lung (exception) - constriction of extra-alveolar vessels b/c lung is squished on top of diaphragm
• Even when you lay down these gradients exist - just from posterior to anterior instead of inferior to superior)

Front 19

How do we regulate pulmonary blood flow?

Back 19

1) O2 tension

2) Neural control: sparse innervation

3) Inflammatory substances

Front 20

O2 tension influence on pulmonary blood flow

Back 20

Decreased oxygen tension inside of an alveolus --> constriction of capillary in response --> increase in resistance --> decrease in blood flow through this capillary

This usually happens with constriction of airway when we are not getting good ventilation into a certain part of the lung -- shunt blood away from poorly ventilated arteries of the lung to better ventilated alveoli

Front 21

Neural control of pulmonary blood flow

Back 21

Sparsely innervated by sympathetic nerves (not a lot of muscular arterioles)

Activation of alpha-adrenergic receptors leads to increased sympathetic tone --> small inc in resistance --> small decrease in flow

Front 22

Inflammatory substance control of pulmonary blood flow

Back 22

Causes dilation in the periphery but constriction in the lung

Ex: Histamine, prostaglandins: increase R, decrease Q

This also helps divert blood from damaged areas of the lung

Front 23

Regulation of cerebral circulation

Back 23

1) Autoregulation: very efficient

2) Metabolic regulation

3) Cerebral ischemic reflex

4) Cushing reflex

5) Neural regulation

Front 24

Autoregulation of cerebral circulation

Back 24

Constant flow over range of pressures (60-150 mm Hg)

Very efficient

Front 25

Metabolic regulation of cerebral circulation

Back 25

• Increased CO2, H+, adenosine, or decreased O2 --> vasodilation --> inc flow
• CO2 response is mediated by H+ : Increased CO2 + H2O --> H2CO3 --> HCO3- + Increased H+ (correlated with respiration - more CO2 = hypoventilation)

Front 26

Cerebral circulation control by PO2 vs PCO2

Back 26

• Under normal circumstances, our lungs do a good job at keeping our arterial PO2 at 100 mm Hg and arterial PCO2 at 40 mm Hg
• Cerebral blood flow is controlled mostly by arterial PCO2 - within normal ranges, it is very sensitive to changes in PCO2
• In normal ranges, PO2 does not have a very strong influence on cerebral blood flow - however, if PO2 < ~60 mm Hg -- then PO2 becomes a very powerful regulator (ex - this happens at high altitudes)

Front 27

Cerebral ischemic reflex

Back 27

• Decrease in pressure = decrease in flow = increased systemic sympathetic tone = increase HR + SV, increase TPR --> increased pressure
• This diverts blood away from periphery and toward brain
• Mediated by brain chemoreceptors that sense increased CO2 or increased H+
• Sympathetic system does not have a strong effect on cerebral cirulation due to sparse innervation of cerebral blood vessels

Front 28

Cushing reflex

Back 28

Increased intracranial pressure leads to a compression of blood vessels --> increased systemic sympathetic response --> leads to an increase in pressure even further to attempt to increase flow through the compressed vessels

Front 29

Neural regulation of cerebral blood flow

Back 29

• Sympathetic: constrictor
• Parasympathetic fibers: dilator
• Sparse innervation -- overall effect is minor

Front 30

Blood brain barrier characteristics

Back 30

• Endothelial tight junctions - low permeability
• Reduced capillary exchange
• Separates blood from CSF
• Protects brain from ionic disturbances
• Consideration for drugs

Front 31

Control in cutaneous circulation

Back 31

Used for temperature regulation

-Sympathetic control >> local/metabolic control

-Vasoconstriction leads to decreased blood flow = decreased heat loss

-Skin can be a very good radiator of heat or insulator depending on high vs low perfusion

Front 32

Cutaneous circulation regulation in apical vs non-apical skin

Back 32

• Apical: (ex - palms/soles) - only innervated by sympathetic nerves - have high basal tone {mediated by NE}
• 1) Utilize glomus bodies - arterial-venous connection innervated by CNS - blood flow that does not go through capillaries (non nutrient providing)
• 2) Under cold stress - increase sympathetic tone to vasoconstrict
• 3) Under head stress - decrease sympathetic tone to increase flow
• Nonapical skin: (ex - chest/legs) - sympathetic constrictor nerves have a little tone (low resting activity) {mediated NE}; but also have sympathetic vasodilator nerves (appear to be cholinergic)
• 1) Under cold stress -- activate sympathetic constrictor nerves -- dec blood flow to nonapical skin
• 2) Under heat stress -- activate sympathetic vasodilator nerves (vasodilator effect actually mediated by bradykinin)

Front 33

Relationship between CO and TPR

Back 33

• Vasculature changes in resistance allows/causes changes in CO
• Heart needs to keep up with what vasculature does -- can only pump what is returned from the venous system
• If you suddenly decrease TPR - CO will go up as much as it can to maintain peripheral pressures

Front 34

Effects of epi vs norepi on CO, peripheral vascular resistance, and blood pressure

Back 34

• Physiologic/low dose epi: causes peripheral vasodilaiton (decreased peripheral vascular resistance) which allows for a sustained increase in CO to maintain mean arterial pressure (preferential binding to beta receptors - increase contractility, HR, vasodilation in skeletal muscle)
• Norepi/high dose epi: causes peripheral vasoconstriction (increased peripheral vascular resistance) - no sustained increase in CO, peripheral pressures increase (NE binds to both alpha and beta receptors, alpha receptors cause peripheral vasoconstriction and there are usually more alpha than beta on blood vessels so high dose epi will saturate all available receptors)

Front 35

Arterial pressure, TPR, CO in chronic diseases

Back 35

Arterial pressure remains stable despite changes in TPR - we are able to accomodate with CO

Reminder: pregnancy decreases TPR --> adding a whole new organ for blood to perfuse

Front 36

Changes as we move from prone --> erect (via tilt table) --> walking

Back 36

1) When we go from laying down to vertical, HR increases, RA pressure drops, SV decreases, central blood volume decreases --> increase in HR and CO trying to keep BP up but just barely keeping BP stable

2) When we start walking - we are engaging our auxilliary muscule pump -- everything goes back to normal - sympathetic nervous system allowed to turn off (no need with skeletal muscle pump) -- don't need to be overactivating SNS to inc HR/contractility to maintain BP

Front 37

What happens to CO during exercise?

Back 37

Vasodilation permits (causes) increase in CO

Inc HR can then increase CO even further

Blood is diverted away from nonessential organs to exercising skeletal muscle (B2 receptors - vasodilators on skeletal muscle)

Front 38

Pressure gradients in the pulmonary system

Back 38

1) Pressure gradients for flow (arterial-venous gradient) do not change from top to bottom

2) Transmural gradient can become very low and even negative at the top of the lungs due to gravity; this will cause capillaries to narrow/collapse - increased resistance so decreased flow; greater transmural pressure at the bottom of the lung will cause capillaries to enlarge - increased radius - increased flow

Front 39

Why do lungs have unique pressure gradients?

Back 39

1) Have a very low blood pressure compared to systemic circulation

2) Capillaries are essentially suspended in air - are able to collapse

Front 40

Most of the resistance in the pulmonary circulation is accounted for by _____ vs the systemic circulation _____

Back 40

capillaries vs arterioles