Concentration of RBCs, WBCs, Platelets
5 million RBC/microL
5000 WBC/microL
200,000 Platelets/microL
Normal Hematocrit %
45%
Concentration of Ionic Constituents of Plasma (Na, K, Ca, H, Cl)
Na: 145 mM
K: 4 mM
Ca: 2 mM
H: ~7.4 pH
Cl: ~98 mM (main anion)
Protein & Non-protein Constituents of Plasma (Albumin, Total globulin, Cholesterol, Glucose)
Albumin & total globulin are major proteins
Cholesterol: <200 mg/dl
Glucose: ~90 mg/dl
Ohm's Law
The current (I) passing through a conductor between two points is directly proportional to the voltage difference (deltaV) across the two points and inversely related to the resistance (R) of the conductor to current flow:
i) I = deltaV/R (volts sometimes
Fick's Law (variation of Ohm's)
J = -D
A
dc/dx
J=flux
D=diffusion coefficient (how readily it moves)
A=surface area (D*A is equivalent to conductance)
dc/dx=concentration gradient (outside-inside)
Resting Membrane Potential (RMP) due to?
Negative inside the cell mainly due to the relatively high permeability of the resting membrane to K
Nerst Equation and Ek, Ena, Eca
E=-61.5/z*log[Xi]/[Xo]
Ek=-95 mV
Ena=+70 mV
Eca=+120 mV
RMP in most working cells ~-80
PNa/PK
PNa/PK ~0.01-0.02 (resting membrane is 50-100xs more permeable to K than Na)
For NODAL cells (AV, SA node), PNa/PK ~ 0.1 (large) and therefore they have a less negative RMP ~-60 mV due to lower Pk rather than increase in Pna
Phase 0 of Ionic Current in Working Ventricular Cell
Depolarization due to rapid influx of Na+ (activation) so phase 0 is due to inward Na+ current (Ina)
HOWEVER, in the SAN and AVN, phase 0 due mainly to activation of Ca current (Ica)
Phase 1
Due to activation of transient outward K+ current (Ito) and rapid inactivation of Ina
Phase 2
Plateau due to decrease in gk (Ik1) and increased gCa
Ik1 is the inward (anomalous) rectifier
Gradual inactivation of Ica and gradual activation of Ik leads to phase 3 repolarization
Phase 3
Repolarization due to inactivation of Ica and delayed activation of Ik (delayed rectifier)
Phase 4
Resting membrane potential
Fast Response and Slow Response action potentials of cardiac cells
Fast
i. High RMP (very negative)
ii. Phase 0 due to influx of Na+
iii. Fast conduction
iv. Short RRP
Short
i. Low RMP (less negative)
ii. Phase 0 due to Ica
iii. Slow conduction
iv. Long RRP
Refractoriness
Time required for inward excitatory channels (na and ca) to recover from inactivation (voltage- and time-dependent)
Ca has a longer RRP
Mechanism of Pacemaker Potential of SAN
Pacemaker potential for SAN is -60 to -40 mV (less negative than for working fibers; na channels inactivated) and is due to 3 ionic conductances:
Decrease in gK
Increase in gf (funny Na channels)
Increase in gca (main one)
Effect of Autonomic NT's ACh & NE
ACh (vagal stimulation) > muscarinic (M2) receptor > increase gK, decrease gf, decrease gca > decrease slope of pacemaker potential > decrease HR
NE (sympathetic stimulation) > Beta-receptor > increase adenyl-cyclase > increase cAMPi > increase PKA > incr
Intercalated discs & Gap jxns
Intercalated discs are the connection between cardiac cells that involve physical coupling by desmosomes and fascia adherents.
The gap junctions (nexus) allow electrical coupling (intracellular current spread) by hemichannel connexins
Source-sink relationship
Source- provides charge (Ina, Ica); major measures of intensity of the current SOURCE are the upstroke velocity of phase 0 (Vmax or dV/dtmax) and AP amplitude
Sink - absorbs charge (internal (Ri) and membrane resistance (Rm)); Ri is the resistance of the
Factors affecting the Sink
Increases in [Ca] and [H] increase Ri (gap jxn) = decrease in CV (buildup)
Increases in [cAMP] decreases Ri = increase in CV
ECG Basics
a. SAN/AVN is slow response (CV ~ 0.05 - 0.1 m/sec) because gap jxns are not as prevalent
b. Working atrial myocardium is fast response (CV ~ 1 m/sec) containing 3 internodal (SAN to AVN) tracts (anterior, middle, posterior)
c. AVN is by coronary sinus on
ECG Time/Voltage Calibrations
i) Time: 1 cm = 0.4 sec (2 big squares, 10 little squares, 0.04 sec/mm)
ii) Voltage: 1 cm = 1 mV (0.1 mV/mm)
P Wave
Atrial depolarization
Baseline (Isopotential) after P wave
Time of activation of specialized tissues (AV node)
QRS Complex
Ventricular depolarization (larger than P because of greater mass; less duration than P because of quick His-Purkinje fibers
Baseline (isopotential) after QRS
Both ventricles are in a depolarized state
T Wave
Ventricular repolarization; longer in duration than QRS because of less synchronized repolarization process compared to rapid depolarization process by His-Purkinje network
PR Interval
Measure of time taken by impulse to pass from atria to ventricles (0.12-0.20sec; 3-5 small boxes)
QRS duration
Measure of time taken by impulse to pass through both ventricles (0.06-0.12; 1.5-3 small boxes)
ST Segment
Time when both ventricles are in depolarized state (Phase 2 plateau of ventricular AP)
QT Interval
Measure of duration of ventricular activity (correlates with AP duration; 0.30-0.40 sec); Decrease HR = Increase RT; Increase HR = Decrease QT
Heart Dipole
When heart is completely at rest there is no dipole
When heart is completely activated there is no dipole
Extracellular electrodes detect potential differences at cell surface (Resting toward positive electrode, depolarized toward negative electrode)
The
Volume Conductor
Conducting medium which transmits electrical potentials to the body surface (lungs, other tissues)
Leads I, II, III
Lead I: LA(+) - RA(-)
Lead II: RA(-) - LL(+)
Lead III: LL(+) - LA(-)
Form equilateral EINTHOVEN'S triangle
Three phases of ventricular activation
Septum activation
Activation of apex
Activation of base
Endo- to epicardium activation
Normal HR
60-100 bpm
Bradycardia
HR < 60 bpm (more than 5 boxes)
Tachycardia
HR > 100 bpm (less than 3 boxes)
Atrial Fibrillation
Marked by an undulating baseline; atrial rates can be 500-800 bpm
1st Degree AV Block
Prolonged PR interval (>0.20 sec) but each P wave IS followed by a QRS wave (successful delayed conduction)
2nd Degree AV Block
Prolonged PR interval (sometimes variable) and failure of some but not all atrial impulses to traverse the AVN (some P waves not followed by QRS)
3rd Degree AV Block
Complete AV block; no relationship between P & QRS waves; atria and ventricles (slow) beat independently
PVC
Premature ventricular contraction - Earlier than normal QRS complex not preceded by a p wave
Ventricular Tachycardia
Rapid, regular beats of ventricular origin (no p wave)
Broad QRS complexes due to slow conduction in working ventricular muscle
Ventricular Fibrillation
Bag of worms"; asynchronous activity leads to sudden cardiac death
Reentry
Reentry requires unidirectional block and relatively slow conduction
Frequency of tachycardia is related to size of circuit (smaller circuit = rapid; larger circuit = slower)
Calcium Distribution
Extracellular (2mM) 20,000 fold difference
Intracellular (0.1 microM)
Sarcoplasmic Reticulum (150 microM) 1500 fold difference
L-Type Calcium Channels
Voltage-gated" Ca channels in sarcolemma; control influx of Ca from ECF (long lasting)
Ryanodine Receptor
RyR2" Ca release channel from SR; for skeletal muscle
SERCA
Sarco-endoplasmic reticulum ca-ATPase for pumping Ca from the cytoplasm back into the SR; Negatively regulated by phospholamban (PLB)
Plasma membrane Ca-ATPase (PMCA)
ATP-dependent Ca pump that extrudes Ca from cytoplasm to extracellular space
NCX
Na/Ca exchanger extrudes one Ca ion to ECF in exchange for 3 Na ions that enter down conc. gradient
Na/K-ATPase
3 sodiums out, 2 potassiums in; not direct Ca handling protein but maintains Na gradient for NCX
Trigger Ca
Enters through sarcolemma via voltage-gated Ca channels; does not directly participate in actin/myosin cross-bridge formation but triggers release of Ca from SR
Activator Ca
Release by SR via RyR2 channels and combines with troponin allowing actin/myosin binding
Frank-Starling Law of the Heart
Length-force relationship; States that within limits, the heart pumps all the blood that comes to it via venous return without allowing excessive damming of blood in the veins; Increase venous return > increased stretch of muscle > enhanced inter-digitati
Preload and Afterload
Preload: degree of muscle stretch prior to contraction; volume of blood in ventricles at end diastole; represented by end diastolic pressure
Afterload: load against which muscle contracts; represented by arterial pressure (larger afterload = slower muscle
Valve opening
Semilunar valves are rapid opening and closure compared to AV valves which are slower and softer opening and closing
Isovolumic Contraction
When ventricles contract but there is no emptying (Must overcome aortic/pulmonic pressure)
Period of Ejection
Rapid ejection for first 1/3 of ejection phase, slow for last 2/3
Isovolumic Relaxation
Ventricular relaxation but no filling; Begins when aortic valve closes and ends when the AV valve opens
Rapid Inflow
Filling of the ventricles; Begins as soon as AV valves open; lasts ~first 1/3 of diastole
Diastasis
When inflow of blood is at near standstill; ventricles are relaxed and almost full
Valve Closure Timing
The mitral valve closes before tricuspid
The aortic valve opens after pulmonic
The pulmonic valve closes after aortic
Atrial Pressure Waves
A Wave: atrial contraction
C Wave: closure of AV valve; beginning of ventricular contraction causing bulging of AV valves back toward atria
V Wave: Opening of AV valve; during systole blood accumulated in the atria so atrial pressure had increased; when A
4 Heart Sounds
S1: AV valves close (Lub)
S2: Semilunar valves close (Dub)
S3: Inrush of blood during diastole (normal finding in children and young adults; disease in middle-old)
S4: Atrial contraction in late diastole; usually indicates presence of disease (stiff ventr
Calculating SV
SV = EDV - ESV
~ SV = 150 mL - 50 mL = 100 mL
Ejection Fraction (Normal value?)
EF = SV/EDV = 100/150 = 0.67 (~70%)
Measurement of CO
CO = SV x HR
Fick Principle to determine CO
CO = O2 Consumption (mL/min)/A-V O2 Difference (mL/L)
Blood taken from pulmonary artery and vein
Indicator Dilution Technique to determine CO
CO = I/(C x t)
CO = A/(C x (t2-t1))
A or I: Amount of indicator injected (mg)
C: Average indicator concentration (mg/L)
t: duration of first circulation in MIN (sec/60)
Thermodilution Technique to determine CO
Ice-cold dextrose solution ejected into RA; thermistor positioned in PA; a time-temp curve is generated (to determine circulation problems)
Chrono-tropic
Rate or change in frequency
Ino-tropic
Contraction
Lusi-tropic
Relaxation
Dromo-tropic
Conduction
Intrinsic HR
HR without neural or hormonal control is ~100bpm
Normal Resting HR
~60-70
PNS Fiber Regulation of HR and AV conduction
PNS fibers originate in the medulla oblongata with cells lying in the dorsal motor nucleus or nucleus ambiguous
Medulla > vagal nerves > ACh > M2 receptors > increase gk, decrease gf > decrease HR
PNS Activation Results In...
Negative chronotropic (SAN) and dromotropic (AVN) and inotropic (Atria) effects
Vagal Nerve Effects
Strongly innervate the SAN (right) and AVN (left)
SNS Regulation
Sympathetic preganglionic fibers arise from the interomediolateral cell column of C7-T6 and for sympathetic chains; Postganglionic nerve endings release NE to beta-receptors which increases gCa in cardiac cells
SNS Activation Results In...
Positive chronotropic (SAN) dromotropic (AVN) inotropic (working muscle) and lusitropic (working muscle) effects
Accentuated Antagonism (vagal)
Alone, vagal efferents do not modulate contractility of the ventricles to the degree that sympathetics do, but in the presence of adrenergic activity, vagal effects can be large
Intracellular vs. extracellular negative modulation of SNS by PNS
Extracellular: vagal efferents presynaptically inhibit release of NE from postganglionic sympathetic fibers
Intracellular: Muscarinic receptors directly inhibit cAMP formation by adenylyl cyclase
Baroreceptor Reflex
Stretch receptors in arch of aorta and carotid sinus
Increase pressure > increase stretch > increase baroreceptor firing rate > increase PNS (vagal) output, decrease SNS > decrease HR and P
Chemoreceptor Reflex
Aortic & carotid bodies
Decrease blood flow > decrease O2 > increase carotid body firing > decrease PNS, increase SNS > increase blood flow and HR
*Sleep apnea, intermittent hypoxia
Henry-Gauer Reflex
Stretch receptors in the ATRIA controlling blood volume; Increase in atrial pressure (vol.) results in decrease in secretion of vasopressin (anti-diuretic hormone ADH) and increase in excretion of water and decreases blood volume
Bezold-Jarisch Reflex
Stretch receptors in the ventricles that decrease HR in response to stretch
Respiratory Arrhythmia
Oscillations in HR coupled to respiratory cycle
Inspiration increases HR; Expiration decreases HR
Due to reflex changes in baroreceptors
Heterometric (changing length) Autoregulation
Frank-Starling mechanism involving ventricular function curve; changes in preload are most important; Ventricular performance increases with increase in fiber length
Homeometric (intracellular ca availability) Autoregulation
SNS activation & circulating catecholamines from adrenal gland (NE, Ep) increase [Ca] which increases contractility
Staircase Phenomenon
Increase in stimulation rate increases developed force due to rate-induced [Ca] that cannot be sequestered back into the SR fast enough
Asymmetric SNS Effects
Left stellate ganglion causes greater contractile response of ventricles than right stellate ganglion (more HR)
Major Factor Affecting CO
HR to a lesser extent because of ventricular filling time; SV affects it most with contractile strength
Assessment of Contractility in Humans (CO)
EF ~0.7
+dP/dt is measure of rate of contraction
-dP/dt is a measure of rate of relaxation (difficult because preload and afterload can change)
SNS has positive effect on both
Velocity, Flow and Area Relationship of blood
Q = v/(pi)r^2
Capillaries ~ 1 mm/sec
Aorta ~ 500 mm/sec
Capillary velocity is slow enough to allow for effective diffusion of CO2, O2, and other molecules
Total Pressure of Blood
Ptotal = Pstatic + Pdynamic
Pstatic is the main component; not moving
Pdynamic is due to movement of fluid (kinetic)
As vessel diameter increases, flow...
Increases; according to Poiseuille's Law
Q = deltaP(pi)r^4 / 8nl
Assumptions of Poiseuille's Law
i) l (length) is long compared to radius
ii) the tube is rigid (not in CV system)
iii) there is steady flow, no pulsations (not in CV)
iv) the tube is "wetted": there exists a boundary layer of fluid with zero velocity
v) fluid behaves as a Newtonian flui
Changes in viscosity of blood due to...
Hematocrit, flow (shear rate), and tube diameter
Measuring resistance (equation)
Only indirectly calculated; R = deltaP/Q
Pressure at inflow minus pressure at outflow
*Inverse of resistance is conductance
Measuring Resistance in Series
Rt = R1 + R2 + R3...
Measuring Resistance in Parallel
Rt = 1/(1/R1 + 1/R2 + 1/R3)
Laminar Flow
Velocity of blood is zero at vessel wall and is greatest at the center of the vessel
Reynold's Number (Re) describing laminar flow becoming disordered or turbulent
Re = vdp/n
v = velocity
d = diameter
p = density of fluid
n = viscosity
Re < 2000 is considered laminar
Re > 3000 is considered turbulent
Shear Stress on vessels is caused by...
the flow of viscous fluid causing pulling of the endothelium; may stimulate release of vasodilator molecules
Viscosity of Water vs. Blood
Water 1
Plasma 1.5
Fahraeus-Lindqvist Effect describes...
the decrease in blood viscosity in vessels with smaller radius and is the result of redistribution of RBCs during blood flow
RBCs flow toward center of vessel (faster) while plasma flows toward vessel walls
Blood thins as it flows toward the capillaries (
Steps in Hemostasis (6)
1) Subendothelial exposure (damage) - collagen is exposed > thromboxane A2 released > vasoconstriction
2) Platelet adhesion- von Willebrand factor + ADP + Ca2+
3) Platelet Activation- Pseudopods, Ca2+, degranulation > serotonin > vasoconstriction and hist
Compliance Relationship Between Vol. & Pres.
C = delta V/ delta P
Inverse of elastance (1/elastance)
Arteries have low compliance (increase in volume equals large increase in pressure)
Veins have high compliance (increase in volume with minimal increase in pressure)
Psf
Mean Circulatory Filling Pressure; Degree of filling of the entire CV system (arterial compliance and venous compliance) ~ 7 mmHg; Major factor determining the rate at which blood flows from the vascular tree into the right atrium
SNS dramatically affects
Pulse Pressure
Difference between systolic (Ps) and diastolic (Pd) ~ 40 mmHg
Increasing SV will increase Ps but Pd stays the same
Decreasing compliance will increase Ps and minor Pd
Mean Arterial Pressure (MAP) equation
MAP = Pd + 1/3(Ps - Pd)
MAP = CO x TPR (P = Q x R)
TPR increase in arterioles increases MAP
Hypertension
MAP > 110 mmHg
Ps > 140 mmHg and/or Pd > 90 mmHg
2 Mechanisms Leading to HTN
1) Volume-loading
Impaired kidney fxn > increased volume > increased Psf > increased VR > increased CO > increased MAP
2) Vasoconstrictor substances increase vascular resistance (Ang II, NE, E)
Treatment of HTN
1) Diuretics
2) Sympathetic (anti-SNS) agents - Beta-blockers, systemic alpha1-adrenergic antagonists
3) Ca2+ channel blockers - blocked channels in SMCs thereby decreasing SMC contraction (decr. TPR)
4) Direct Peripheral Vasodilators
5) ACE Inhibitors
6)
Pressure Pulse Dampened at...
Arterioles; due to combined effects of vascular distensibility and resistance; pressure pulse encounters greater and greater resistances to deformation
Microcirculation Pathway
Arterioles > metarterioles (have intermittent muscular coat) > precapillary sphincters > capillaries (no smooth muscle, don't vasodilate/constrict) > venules
Metarterioles and pre-capillary sphincters respond strongly to local tissue factors
Capillary pores are called...
intercellular clefts or tight junctions (major route of transcapillary exchange)
Fenestrae are...
specialized intercellular clefts found in more porous capillary beds, i.e. kidney, liver (wider)
Law of Laplace
Explains why capillaries don't burst at high pressures
T = P*r
T = tension of vessel wall
P = transmural pressure
r = radius
Must account for wall thickness (w)
T = P*r/w
Radius is 3000 times less than arteries
Fick's Law of Diffusion for Transcapillary Exchange
J = -(D
A)
dc/dx
D = diffusion coefficient; inversely proportional to sqrt of MW: D = 1/(sqrtMW); As MW decreases, D increases
A = surface area
dc/dx = concentration difference (Co-Ci)
(4) Starling Forces (Pressures)
1) Capillary Hydrostatic Pressure (Pc) - causes bulk flow of fluid from capillaries to interstitium; Pc drops from arteriolar end to venule end; Mean Pc ~ 17mmHg
2) Interstitial Fluid Hydrostatic Pressure (Pi) - (+) indicates water moving INTO the capilla
Pre/Post-Capillary Resistance Affects on Pc
Increased PRE-capillary resistance = decreased Pc, net absorption; Increase POST-capillary resistance = increased Pc, net water filtration
Edema can occur when...
Pregnancy (pressure on abdominal veins)
Venous Obstruction
Blocked Lymphatics
Low blood protein
Nephrosis
Increased Capillary Porosity
Differences between vascular smooth muscle and cardiac or skeletal muscle...
Smaller (spindle shaped), less organized, poorly developed SR, more actin than myosin, exhibit slow prolonged contractions (tone), do not exhibit APs
Sources of Ca2+ for VSM cell contraction...
Mainly from extracellular Ca2+ through slow channels (positive inotropic effect, target for anti-HTN medicine), also from SR (by neural or humoral agents, pharmacy-mechanical coupling causes release from SR w/o membrane potential change)
Top 2 Organs that get the most blood flow per unit weight
Kidneys and adrenal glands
Local tissue factors causing arteriole/metarteriole response
decr O2, incr CO2, incr H+, incr Lactic Acid, incr Adenosine = vasodilation (Nitric oxide release)
Path for NO production and effect
Agonist (ACh, Serotonin, Histamine) release > Nitric Oxide Synthase catalyzes L-arginine + O2 to Nitric Oxide + L-Citruline > NO release to VSM cells > NO causes G-Cyclase to catalyze GTP to cGMP which causes relaxation
*Phosphodiesterases break down cGMP
2 Mechanisms Explaining Local Blood Flow Control
1) Vasodilator mechanism- Incr metabolic rate > incr vasodilator agents (CO2, lactic acid, etc.) > vasodilation > incr blood flow
2) O2 Demand mechanism- Decr O2 > decr VSM tone > vasodilation > incr blood flow
Reactive vs. Active Hyperemia (blood flow above normal)
Reactive: Tissue blood flow greater than control upon release of vessel occlusion; Duration and degree of hyperemia is a fxn of the duration of the occlusion
Active: Occurs during increased activity of the tissue which causes enhanced blood flow (increase
Metabolic Mechanism of Autoregulation by Arterial vessels
Increased arterial pressure > transient increase in blood flow > washout of vasodilator substances > vasoconstriction
Decreased arterial pressure > transient decrease in blood flow > buildup of metabolites > vasodilation
Myogenic Mechanism of Autoregulation by Arterial Vessels
Stretch-induced; increased pressure > increased stretch > vasoconstriction
*May be protective mechanism against very high blood pressure
Q = PR
Maintenance of blood flow despite pressure changes
Vasomotor Center Control of PNS & SNS
Baroreceptors, Chemoreceptors, or Hypothalamus send signals to the sensory area to regulate the pressor (SNS), depressor, or cardioinhibitory (PNS) regions; Depressor modulates the pressor; Cardioinhibitory regulates the depressor
Vasomotor Tone (tonic)
Tonic vasomotor efferent tone by SNS; vasodilation occurs by inhibiting this tonic output (arteries & veins (lesser extent))
PNS Effect on blood vessels vs. HR
Minor factor in regulation of blood vessels (via ACh release) but a major factor in regulation of HR
Baroreceptor, Cardiopulmonary Receptor, Peripheral Chemoreceptor (aortic/carotid body) Reflexes
Baroreceptor - increased stretch > vasomotor center > reflex inhibition of pressor region > vasodilation, decr HR (MAJOR reflex)
Cardiopulmonary Receptor - in atria, ventricles and pulmonary vessels; increased stretch > vasomotor center > vasodilation
Che
Hormones controlling circulation:
Catecholamines (E, NE)
Angiotensin II
Vasopressin (ADH)
Bradykinin
Histamine
Prostaglandins
Catecholamine effects (E, NE)
Alpha receptors - blood vessels (vasoconstriction)
Beta receptors - heart (+ino, dromo, chrono)
Angiotensin II Pathway and Effect
Angiotensinogen (produced in liver) is catalyzed by Renin (produced in kidney) to angiotensin I; Angiotensin I is catalyzed to Angiotensin II by ACE (produced in the lungs)
Vasopressin (ADH) Effect and Produced from What?
Produced from posterior pituitary; Vasoconstricting agent
*Important in control of water reabsorption in kidney by the Henry-Gauer Reflex (stretch in atria > decr ADH > incr diuresis
Bradykinin and what effects its levels
Small polypeptide that regulates vessel diameter
It is digested by carboxypeptidase and ACE
ACE inhibition leads to increased bradykinin which causes coughing?
It is a vasodilator that stimulates production of NO
Histamine
Powerful vasodilator and increases capillary permeability (liberated in response to cell damage) by release from mast cells
Prostaglandins
Generated via metabolism of AA;
Mostly vasodilators
Extrinsic vs. Intrinsic Use Preferences by Tissues
Brain, heart - intrinsic
Skin - extrinsic
Skeletal muscle (at rest) - extrinisic
Skeletal muscle (at exercise) - intrinsic
Major factor determining CO; Normal value CO
Venous Return!
CO ~ 5L/min
Permissive level in NON-stimulated heart ~10-13L/min
Venous Return is determined by what 2 factors...
MAP and TPR
VR = (MAP-RAP)/TPR (Q=P/R)
RAP is normally 0
Metabolic Rate mostly affects
TPR
Incr metabolic rate > decr TPR > incr VR & CO
Pressure Gradient for VR is ____ - _____?
Psf-RAP
Normal Psf is ____mmHg
~7mmHg given that TPR is constant