Arterial Blood Pressure

Front 1

Flow equation

Back 1

Q = ΔP/ R
or Q = π (ΔP) r4 / 8ηl

Front 2

Poseilles Law

Back 2

Resistance (mmhg/ml/min)
= 8ηl / r4 π

Front 3

Flow and vessel length?

Back 3

inversely prop to L
increased l = more R = > surface area for particles to rub against

Front 4

Viscosity

Back 4

Friection developed btwn molecules of fluid as they slide over eachother during flow= increases as hematocrit rises

Front 5

Reynolds number

Back 5

Nr= pDv/η
(p=density, D= diamter)
<2000 laminar flow, > 3000 turbulent, 2000-3000 = transition

Front 6

Turbulent Flow

Back 6

fluid doesn’t flow in definite laminae (layers), but rapid mixing occurs (like in blood). ΔP ~ proport to square of Q, vs 1st order in laminar Q
i.e., a heart will have to pump harder if turbulent flow develops

Front 7

Series resistance found

Back 7

BVs in specific organ (each organ supplied by netrowkr of large/small aa’s, arterioles, capillaries, etc)

Front 8

Benefits to parallel resistance

Back 8

oTotal R < R of any one resisotor → 1/ Rt = 1/ R1 + 1/ R2 + 1/ R3 +……
impact of changes in R of a few vascular beds on BP is minimized
Can use individual organ R to control blood distribution (flow) throughout the body
optimizes gas and substrate distribution dynamics

Front 9

Velocotiy- how does it relate to flow?

Back 9

V=Q/A

v ↓ as cross sectional area ↑

Front 10

wehre is largest drop in pressure?

Back 10

btwn arteries & arterioloes --- capillares in contrast have far > caps arranged in parallel, thus total R is less

Front 11

How does KE (dynamic pressure) respond to narrowing aorta

Back 11

↓ radius ↓ A, which ↑ velocity; v ↑ KE (sig in aorta where already high flow v) - lateral P must ↓ (for constant total P), or ↓ P pushing blood from coranary arteries to heart

Front 12

Arteries as P Reservoir - Systole

Back 12

ventricular contract: e- used to 1) distend arteries 2)expel blood into aorta
oArteries elasticity enables them to expand to temp hold excess ejected blood V storing some of the P e- imparted by cardiac contraction in their stretched walls (like balloon expands to accom extra V of air)

Front 13

Arteries as P Reservior- Diastole

Back 13

oWhen heart relaxes (stops pumping blood into arteries), stretched arterial walls passively recoil- pushes excess blood contained in arteries into downstream vessels- ensuring continuted blood flow to organs when heart relaxing

Front 14

Reason for dicrotic notch?

Back 14

– aortic valve closure produces a brief period of retrograde flow from aorta back to valve, there is a slight decrease in aortic P- creates extra hump.

Front 15

what happens when arteries lose elasticitiy

Back 15

when arteries rigid - no SV can be stored in artieres during systole and during diastole - flow through caps stopis since aa cant recoil, no constant Q - intermittent flow

Front 16

energy consequences of arterial loss of elasticity

Back 16

more energy (measure by 02) required in rigid system

Front 17

Elastance

Back 17

tendency of arterial walls to recoil (how rigid), inverse of compliance
-ΔP/ (ΔD/D)
-as age elastance increases - diameter changes less for given change in pressure

Front 18

which blood vessels are most compliant

Back 18

Veins - can hold largest V of blood at low P. arteries much < C - hold < blood. Recall compliance is a measure of "how stretchy" vessel is- how much V you can hold at given P

Front 19

compliance and age

Back 19

oCompliance of arteries ↓ as age↑: walls get stiffer, < distensible, < C, hold < blood at any given arterial P.

Front 20

which blood vessels have greatest elastance

Back 20

greatest in arteries, smallest in veins.

Front 21

blood flow through heart

Back 21

venae cavae → RA → (tricusp V) → RV → (SL valve)→ pulm artery → lungs → pulm vein → LA → (mitral valve) → LV →(sl valve) → aorta →body → vena cava

Front 22

When are semilunar valves open? closed?

Back 22

oOpen: ventricle P > aorta or pulm artery P (ventricle contraction & emptying)
oClose: ventricles relax; ventricular P < aorta or pulm artery

Front 23

back flow in semilunar valve prevented by:

Back 23

its anatomy- leakproof seam

Front 24

chordea tendinae

Back 24

o Edges of AV valve leaflets fastened by tough, thin fibrous cords of tendinous-type tissue, chordae tendinae, which prevent AV vavles from being everted (open in direction into atria).

Front 25

papillary muscles

Back 25

Chords extend from edges of each cusp; attach to papillary muscles (small) which protrude from inner surface of ventricular walls. When ventricles contract, papillary muscles also contract, pulling downward on chordea tendineae (closing AV valve cusps).

Front 26

Diastole

Back 26

elaxation and filling of the heart (Repoloarziation)

Front 27

Systole

Back 27

contraction and emptying of the heart (Spread of excitation)

Front 28

early ventricular diastole

Back 28

Atrium is still also in diastole; TP interval on ECG, (after VEN repolarization & before another atrial depol)
-Bc continuous inflow of blood from venous sys to atrium, atrial P slightly > VEN P (both are relaxed) (1). P differential: AV valve open, blood flows from atrium into VEN throughout VEN diastole (heart A).
-Passive filling causes VEN V to slowly rise even before atrial contraction takes places (2).

Front 29

late ventricular diastole

Back 29

SA node reaches threshold and fires. Impulse spreads throughout aorta, (P wave, 3). Atrial depolarization causes atrial contraction, raising atrial P curve (4) and squeezing more blood into VEN. Corresponding rise in VEN P (5) that occurs simultaneous to rise in arterial P is due to additional V of blood added to VEN by atrial contraction (6 ,heart B). Throughout atrial contraction, atrial P still slightly > VEN P, AV valve open.

Front 30

end of ventricular diastole

Back 30

Ends at onset of VEN contraction- atrial contraction and VEN filling complete. The V of blood in ventricle at end of diastole (7) is end-diastolic V (avg ~135 ml) No > blood will be added to VEN during this cycle.

Front 31

end diastolic volume

Back 31

max amount of blood that the ventricle will contain during given cardiac cycle

Front 32

what keeps AV valve closed

Back 32

As VEN contraction begins, VEN P immediately > arterial P. This backward P differential forces AV valve closed

Front 33

ventricular excitation and onset of ventricular sysole

Back 33

After atrial excitation, impulse travels through AV node and specialized conduction system to excite VEN. Simult, atria are contracting. When VEN activation complete, atrial contraction is already over. The QRS complex = VEN excitiation (8), which induces VEN contraction. The VEN P curve sharply increases shortly after QRS complex, signaling onset of VEN systole

Front 34

isovolumetric contraction

Back 34

After VEN P > atrial P and AV valve closed, to open aortic valve, VEN P must increase until > aortic P. So, AV valve closes and before aortic valve opens= is brief period when VEN = closed chamber (10). Bc all valves closed, no blood can enter or leave VEN (IVC – heart C). BC no blood enters or leaves, VEN at constant V and muscle fibers at constant length. IVC is similar to isometric contraction in skeletal muscle. During IVC, ventricular pressure continues to increase as the volume remains constant (11)

Front 35

systolic versus diastolic pressure

Back 35

sys: max P exerted into arteries when blood ejected into them (~120)
dys: min P within arteries when blood draining off into rest of vessels during diastole (~80 mmhg

Front 36

mean arterial pressure

Back 36

Pa = Pd + 1/3 pulse pressure
where pulse pressure = Systolic P- diastolic P

Front 37

physiological factors affecting artieral BP

Back 37

Cardiac output (HR x SV)
peripheral resistance
Physiological factors modify physical ones (arterial blood volume and arterial compliance)

Front 38

how does cardiac output affect BP

Back 38

increase in CO increases BP- MAP must rise to level where arterial outflow = CO (increase Q by increasing aterial P)

Front 39

TPR and Arterial BP

Back 39

o If ↑R in arterioles (by↓ diameter), initial response is to ↓ flow, but build up of blood in system, cause ↑BP to push > blood through arteries & maintain constant Q (↑P)

Front 40

arterial compliance and BP

Back 40

with ΔCO, compliance determines rate at which new equilibrium value of MAP will be approached. ΔP much faster in an older person with small C -- can cause vessel rupture

Front 41

Arterial Pulse P (sys-dys) mostly affected by...

Back 41

Stroke volume (changes arterial volume), but also by compliance

Front 42

anemia

Back 42

decreased hemocrit (b/c decreas mass of RBC)- get turbulent flow, causes fxnl murmers.

Front 43

MAP other equation

Back 43

MAP = cardiac output x TPR

Front 44

Reactive Hyperemia

Back 44

Increased blood flow after period of inadequate blood flow (after excersie or ischemic event).
-As flow decreases O2 supply decreases and CO2 levels increase - causing release of vasodilator metabolites --> extra compensatory flow

Front 45

vasodialator metabolites include

Back 45

lactate, adenosine, potassium (accumulate as increase metabolic activity)

Front 46

Endothelial vasodialators

Back 46

Nitric Oxide
prostaglandins (prostacyclin, PGE2)

Front 47

endothelial vasoconstrictors

Back 47

prostaglandins (thromboxane)
endothelin

Front 48

Prostaglandins and vasodilation

Back 48

prostacyclin and PGE2 - respond to shear stress (anatognize thromboxane)

Front 49

prostaglandins and vasoconstriction

Back 49

thromboxan, primarily platlet - but some endothelial; antagonizes prostacyclin

Front 50

endothelin

Back 50

responds to autocrine- paracrine molecules (NO, adenosine) for vasoconstriction

Front 51

Nitric oxide

Back 51

Cross endothelial cells to relax smooth muscle; responds to shear stress, NT/autocrine-paracrine moelcules (Ach, bradyknin, histamine, adenosine).

Front 52

Effect of metabolites on upstream arteries

Back 52

-Metabolites may propagate upstream
-Upstream vasodilation results in shearing stress in arterioles, causing even more metabolite release
-Diffuse through walls (especially NO)
-May act through surface receptors

Front 53

importance of arteriolar resistance

Back 53

converts pulsatile S-D P swings into arteries into non-flucuating pressure in capillaries
-high degree of resistance cuases marked drop in mean pressure as blood flows through - helps establish p diff to encourage Q from heart to downstream organs

Front 54

composition of arterioles

Back 54

thick latyer of smooth muscle richly innervated by sympathetic nerve fibers
-very little elastic connective tissue

Front 55

arterioles and vascular tone

Back 55

normally displays particial constriction - vascular tone- that establishes baselien arteriolar R. baseline from myogenic activity and sym supply continually releaseing NE (further enhancing tone)

Front 56

phases of systole

Back 56

isovolumentric ventricular contraction, ventricular ejection

Front 57

phases of diastole

Back 57

isovolumetric ventricular relaxation, atrial contraction

Front 58

conducting zone

Back 58

generations 0-16 --- airawys involved in gas transport
-trachea to terminal bronchioles

Front 59

respiratory zone

Back 59

16-23 where alveoli develop and gas exchange occurs--> respiratory bronchioles to alveolar sacs

Front 60

First air expired

Back 60

air from atomic dead space (air that reminas in the conduction airways - does not contribute to alveolar ventilation and not invovled in exhcnag eof o2 and Co2)

Front 61

First gas to enter lungs during inspiration

Back 61

alvolar air from the previous inspriation (so only 350/500ml of fresh air enters alveoli during inspiration)

Front 62

minute ventilation

Back 62

amt of air ventilated each minute;
Ve = TV * Respiratory freq OR
ve = atomic dead space + Alveolar TV

Front 63

alveolar ventiation

Back 63

Vt- Vd
or Ve (minute vent) - Vd
*part of inspired air entering alvolar/minute

Front 64

alveolar dead space

Back 64

2) Alveolar: Variable; Inspired air that gets into the alveoli that is in relative excess compared to the blood flowing through the alveolar capillaries (↑V/Q). This part of the alveolar gas is also considered “wasted” in terms of its lack of contribution to gas exchange and CO2 elimination. Increases in disease.

Front 65

physiological dead space

Back 65

VD/VT : Ratio of dead space to tidal volume-- Relative measure of Physiologic Dead Space.
Normally, VD/VT = 25- 35% of tidal volume or minutte ventilation is “wasted” dead
space-- increases with disease.

Front 66

Bohr Equation of calc physiological dead space

Back 66

VD/VT = PACO2- PECO2/PACO2

Front 67

Regional differences of ventilation

Back 67

lower regions of lung ventilate better than the upper zones. Diff disappears with subject in supine position (but posterior lung > anterior lung)

Front 68

CO2 content in arterial blood?

Back 68

27 mmhg - once gets into periphery CO2 added to blood (as product of metabolism)- why the pvCo2 goes up to 47

Front 69

Lung Recoil...

Back 69

lungs tend to recoil inward (deflation, or expiratory) with its resting V < residual V (trying to collapse to < RV)
-50% VC recoil P increased
-at TLC recoil pressure maximal ~30 cm h20 (amt h2o need to keep lungs inflated)

Front 70

Chest wall Recoil?

Back 70

recoils outward (inflation) with resting volume being at 70% TLC

Front 71

When is chest wall recoil positive?

Back 71

Expiratory (tries to recoil inward) when expanded to > 60% VC to TLC. Below 60% tries to recoild outward to resting position (creating negative pressure)

Front 72

Total recoil pressure at TLC

Back 72

add CW (10) and lung (40) positive inspiratory recoils

Front 73

Total Recoil Pressure at FRC

Back 73

zero -- respiratory system at rest due to balance of inward postive lung recoil and outward negative CW recoil

Front 74

what eventually limits inspiration

Back 74

eventaully limited by ability of inspiratory muscles to generate pressure to overcome both lung and CW recoil - max inspiration or TLC reached.

Front 75

Passive expiration

Back 75

from TLC to FRC (Rs resting level). first assisted by lung and CW recoi, then just lung recil to FRC. Beyound FRC requires expiratory muscles to generate P to overcome outward CW recoil 1

Front 76

Passive inspiration

Back 76

from RV to FRC, ie RS recoil is outward (inspiratory) due to CW elastic recoil

Front 77

Alveoli and Laplace's Law

Back 77

P = 2T/r --> in lungs alveoili at top of lung bigger than bottom -- if surface tension were the same smaller alveoli would empty into larger (lower Pressure alveoli)

Front 78

Lung surface tension dependant on...

Back 78

Relative area (actually volume); tension reduced at low volumes - imp for maintaining alveolar stability and lung integrity with varying degrees of alveolar inflation (alveoli > inflated at top of lung bc of gravity)

Front 79

role of surfactant

Back 79

lowers T of alveolar walls at low long volumes, so recoil pressure (P) of large and small communicating air spaces is the same.

Front 80

composition of surfactant

Back 80

phosphatidylcholine (70-80%)
DPPC (60-70%)

Front 81

surfactant synthesis

Back 81

in alveolar type 2 cells - begins in ER --> golgi --> multivesicular bodies --> lamellar bodies (whirls of surfactant). when lamellar bodies secreted, 1st tubular myelin & then surfactant film formed.

Front 82

Role of DPPC in surfactant

Back 82

when alveolar SA ↓ at low lung V, DPPC forms monolayer w/ hydrophilic polar head at liquid interface & hydrophobic fatty-a tail extending into air space. b/c fatty tail sturated - arranged in straight line, get close packing which causes mutual repulsion of DPPC, ↓ surface T, prevents alveolar collapse

Front 83

sufactant produced in fetus at

Back 83

at begining of 3rd trimester - increases radidly before term at 36 weeks. if baby born premature may have insufficent surfactant

Front 84

infantile respiratory distress syndrome

Back 84

insuff sufactant production --> loss of volume dependance of surface T and high T at low volumes, (ie increase minimal ST); resulting recoil P mediates widespread alveolar collapse, pulmonary edma and acute resp failure

Front 85

normal pleura pressure

Back 85

intathoracic pressure measured by esophageal catheter reflects pleural pressure (btwn 2 pleura) normally sub atm at -5 cmh20 due to opposing,but balanced recoil forces of lung and chest wall

Front 86

what happens to intrapleural pressure during inspiration

Back 86

insp muscles expand thorax- ipp and alveolar p becomes > negative (-30 at full inspiration)

Front 87

what happens to intraplueral pressure during expiration?

Back 87

if relaxed passive returns from > neg insp values to -5 ... if forced/rapid expiration (exp muscles of chest and ab recruited) ipp becomes +

Front 88

Transpulmonary pressure

Back 88

lung recoil pressure - can be obtained from measurements of esophogeal pressure recorded via esoph catheter manometer

Front 89

Elasticity of lungs

Back 89

compliance (normal ~.2 L/cmH20)
-highly compliant lungs distensible and easily inflated
-plot lung V (spirometer) vs transpulm P (esoph catheter)

Front 90

Lung ventilation and compliance

Back 90

distribution of inspired air dep on lung compliance - due to gravity get gradient of pleural pressure (> negative at top than bottom). Result = alveoli at top of lung assume larger V than bottom and lie at diff points along P-v cuve

Front 91

Varying compliance in the lungs

Back 91

-get compliance decrease closer to TLC
-at FRC - base lung at steeper, > compliant part of P-V curve than apex so get pref venilation of lung base and these alveoi inflate or expand to a greater degree than alveoli at apex; at RV- pref filling of apex, now at > compliant part of PV cruve

Front 92

basis of pulm fibrosis

Back 92

increased collagen deposition in lung resulting in increased lung elastic recoil and decreased lung compliance

Front 93

basis of emphysema

Back 93

destruction of alveolar septa--> decreased elastic recoil and increased compliance.

Front 94

shift of PV curve in emphysema

Back 94

shifts to left (loss of elastic recoil) and upward (long V increased) with steeper slope (compliance increase)
-at any lung volume recoil P decreased compared to normal

Front 95

shift of PV curve in pulm fibrosis

Back 95

right, downard with flatter sloep; more recoil P for given V (inreased recoil); lung compliance decreased (stiff lungs) and lung volume reduced

Front 96

emphesyma and lung volume

Back 96

Hyperinlation: loss of elastic recoil-- normal recoil of chest wall pulls "flabby" lungs outward to new resting V (FRC) > normal

Front 97

pulm fibrosis and lung volume

Back 97

increased recoil of lung overpowers that of chest wall - get restriction, or reduced lung volume

Front 98

arteriole tone at rest

Back 98

normal arteiole tone is somewhat contracted; this basal tone (being always contracted) is what allows arteriole to dialate. Tone maintained by sympathetic input and myogenic activity

Front 99

Sympathetic nervous system and contractility

Back 99

-catecholamines act on β1 Receptors coupled via Gs protein to adenyl cyclase →↑cAMP levels →activate kinases (ie: PKA) to P-late enzymes (2)
1) Sacrolemma Ca Channels: ↑ inward Ca current during plateu→↑ trigger Ca, ↑ Ca released from SR
2) Phospholambam: ↑ SR Ca pump activity; p-lation stimulate Ca-ATPase→↑ Ca uptake & storage

Front 100

Glycosides (digitalis

Back 100

-↑force of contraction by inhibiting the Na+/K+ ATPase in myocardial cell membrane.
-With Na/K inhibited, ↓ Na pumped out of cell, ↑ intracellular Na+ -- alters Na gradient across cell membrane
-Altered gradient affects Ca-Na exchanger; 1 Ca pumped out (uphill) for 3 Na in (downhill- maint by Na/K)
-no Na gradients = ↓ Ca leaves the cell → ↑ intracellular [Ca2+] good for contractility!