CVPR 03-24-14 09-10am Hemodynamics - Proenza Flashcards Preview

CVPR Unit 1 > CVPR 03-24-14 09-10am Hemodynamics - Proenza > Flashcards

Flashcards in CVPR 03-24-14 09-10am Hemodynamics - Proenza Deck (80):


Basic physics of blood flow; Movement of blood is driven by differences in pressure throughout the CV system; Basic physics of flow through a tube predicts many properties of CV system.


Effect of Pressure differences

Pressure differences (deltaP) drive blood flow through vessels; the difference between arterial & venous pressure is drives blood flow through organs.


Transmural pressure

Difference in pressure between inside & outside of a vessel (across the vessel wall)


Gravitational pressure

Also affects blood flow (positional changes)


Pressure in different vessels

Highest pressure in the aorta… Elastic walls of vessels dampen pulsatile pressure but offer very little resistance to flow, so there is not much drop in BP through arteries….Big drop in pressure in arterioles (aka resistance vessels)…..Very low pressure in capillaries & in the venous system.


Pressure in systemic vs. pulmonary circulation

Pressure in systemic circulation >>> pulmonary circulation


Cardiac output, resistance, and pressure in Left vs. Right sides of Heart

CO equal between sides; Resistance & Pressure different (much lower in pulmonary circulation)


Total Blood Volume & it is mostly found

About 5L; Greatest blood volume in venous system (veins = “capacitance vessels”)


Blood volume in arterial vs. venous sides

Varies a lot depending on blood volume & pressure


Flow (Q)

CONSTANT through system; the cardiovascular system is a closed loop, so flow through the capillaries MUST be the same as flow through the aorta (on average)


Flow (Q) and Cardiac output (CO)

CO = Total flow in the cardiovascular system = volume of blood pumped per minute by the heart


Velocity (v)

Distance per unit time (cm/sec) [as opposed to flow, which is volume per unit time]; v = Q/A


Velocity (v) and Cross-sectional area (A)

Velocity depends inversely on cross-sectional area (A)…..slowest through biggest cross-sectional area, like a river…total cross-sectional area is smallest in the aorta (--> fastest flow) and greatest in capillary beds and pulmonary circulation (--> slowest flow in these areas of exchange)


Flow equation

Q = deltaP / R…..where, Q = flow (volume/time), deltaP = pressure difference, R = resistance


Cardiac output version of the Flow equation

CO = (mean arterial pressure – venous pressure) / total peripheral resistance (TPR)


Flow equation & Ohm’s law

Flow eq. is analogous to Ohm’s law for electricity (V = IR, I = V/R), where blood flow is like current, pressure is like voltage, resistance is like…resistance.


Flow equation – characteristics

Require pressure difference; Flow In MUST equal Flow Out; Flow is directly proportional to pressure, inversely proportional to resistance.


Assumptions of flow equation that are not really valid for cardiovascular system:

Constant pressure, Constant resistance, Straight rigid tube..…Nonetheless, pressure & flow through the system as a whole can be approximated fairly well with the flow equation.


Poiseuille’s Equation

An extended version of the flow equation: Q = ΔP x (π x r^4) / 8ηl ……… Q = flow, r = radius, l = length, ΔP = pressure difference, η = viscosity of blood…… (π x r^4) / 8ηl is the inverse of resistance in the flow equation….. For the exam, you do not have to memorize the equation per se, but you need to understand how each variable affects flow, and that the FLOW VARIES WITH THE 4TH POWER OF THE RADIUS


Effect of Increased vessel size (radius) on resistance & flow (Poiseuille’s Law)

Increased radius = Decreased resistance, Increased flow.


Vessel radius and flow

Increase size of vessel (radius) = decrease resistance, increase flow….. Radius has huge effect on flow (flow varies with 4th power), so doubling the radius increases flow by 16-fold (24)….. In CV system, vessel diameter is the major mechanism by which flow is controlled (vasoconstriction & vasodilation).


Effect of Increased length of vessel on resistance & flow (Poiseuille’s Law)

Increased length = increase resistance, decrease flow


Effect of increased viscosity on resistance & flow (Poiseuille’s Law)

Increased viscosity = increase resistance, decrease flow


Viscosity of blood...what it depends on, gender differences

Mostly depends on hematocrit (proportion of RBCs, normally 38-46% in women, 42-54% in men)


Assumptions of Poiseuille’s Law that are not valid for cardiovascular system:

Constant pressure, Constant resistance, Constant radius, Single length, Constant viscosity, Laminar flow….Only valid for single vessels


Resistance in parallel vs. in series

Poiseuille’s law is only valid for single vessels…..Parallel vessels (most of systemic circulation) decreases total vascular resistance.…. Series vessels increases total vascular resistance.


Resistance in parallel – calculation & significance

1/ total R = sum of 1 / individual resistances…….Therefore: 1. Total resistance of a network of parallel vessels (capillary bed) is lower than the resistance of single lowest resistance vessel in the system (single capillary), 2. Changing the resistance of a single vessel in a parallel system has little effect on the total resistance of the system


Resistance vs. Blood flow in parallel circulations

Pressure is the same in each parallel vessel, but the blood flow through each can be different…..EX: Capillaries are highest resistance of all vessels (smallest diameter), yet total resistance of capillary beds is quite low & is independent of individual capillaries because there are many parallel vessels.


Resistance in series – calculation

Resistances in series are additive: total R = sum of individual Rs (i.e., R in artery + R in arteriole + R in capillaries)…..Therefore: Total resistance of a series of vessels is higher than the resistance of any individual vessel.


Resistance in series – location of most resistance

Largest proportion of total resistance is in arterioles, the major resistance vessels that regulate flow to tissues.


Resistance & Blood flow in series circulations

Blood flow through vessels in series is constant, but the pressure decreases through the series of vessels (e.g.,, pressure drops through the systemic circulation)


Laminar flow

Smooth, streamlined, most efficient type of flow; Velocity slowest at edge of tube, fastest in center; Assumed type of flow in the flow equation (non-pulsatile laminar flow); Not completely the case in the CV system.


Turbulent flow

Irregular type of flow, with eddies & vortices; Requires more pressure for same average velocity compared with laminar flow; Produces shear force


Factors that increase turbulent flow

Large diameter, high velocity, low viscosity, abrupt changes in diameter, irregularities on tube walls (things that promote turbulence promote damage to endothelial lining through the shear force created)


Shear force - how created, what it is, what it causes

Produced by turbulent flow; Viscous drag of fluid flowing through tube, which exerts force on the walls; Can damage vascular endothelium, promoting development of thrombi, emboli, & atherosclerotic plaques


Pulsatile flow

Heart pumps intermittently, creating pulsatile flow in the aorta = arterial pressure in not constant.....Pulsatile flow requires more work (stop & go driving at rush hour uses up more gas)…pulsatile flow is dampened from aorta to capillaries (where it becomes constant rather than pulsatile)


Systolic pressure

Peak aortic (~arterial) pressure; Systole = contraction phase of cardiac cycle


Diastolic pressure

Minimum aortic pressure: Diastole = relaxation phase of cardiac cycle


Normal blood pressure value

Systolic / diastolic = <120/80mmHg (range: 90-120 / 60-80)


Pulse pressure – how to calculate & normal value

Systolic – Diastolic = 120 – 80 = 40 mmHg


Pulse variation, pressure, & velocity in different vessels

In capillary beds, no pulse variation, pressure & thus flow is continuous…..Pulse pressure, mean pressure & velocity all decrease from aorta to capillaries


Mean Arterial Pressure (MAP) - calculation

At resting HRs, MAP= ~Diastolic pressure + 1/3(systolic – diastolic)… resting HRs, NOT the arithmetic average of systolic & diastolic pressure b/c diastole is longer than systole


Mean Arterial Pressure (MAP) – what it depends on

Depends on HR. At rate higher than resting HRs, diastole is relatively shorter, so MAP approaches the average between systolic & diastolic pressures


Compliance equation

C = ΔV/ΔP….. C= compliance in ml/mmHg, ΔV = change in volume in ml, ΔP = change in pressure in mmHg… how much change in volume is elicited by a change in pressure


Compliance represents…

…the elastic properties of vessels (or chambers of the heart)


Relative compliance in veins vs. arteries

Veins are more compliant than arteries – more V per P


Relative compliance in different arteries & what it contributes to

More compliance in aorta = lower pulse pressure…. Degree of compliance in the major arteries contributes to transformation of pulsatile flow from heart into continuous flow in microcirculation.


Compliance is determined by…

… relative proportion of elastin fibers vs, smooth muscle & collagen in vessel walls



NOT the same as atherosclerosis…. Rather, a general term for loss of compliance caused by thickening & hardening of arteries….SOME IS NORMAL W/ AGE (pulse pressure 40 mmHg in young adults, ~60+ mmHg in elderly people…younger people have more compliant arteries than older people)


LaPlace’s Law - equation

T = ΔP x r / µ…..T = tension (wall stress), ΔP = transmural pressure, r = radius, µ = wall thickness


LaPlace’s Law describes...

The relationship between tension in a vessel wall and the transmural pressure


Relationship in LaPlace’s Law

Tension in the vessel increases as pressure & radius increase. (Thus, HTN increases stress on vessel [and chamber] walls.)


Aneurysms & LaPlace’s Law

Weakened vessel wall bulges outward, increasing radius, thus increasing tension that cells in the wall have to withstand to prevent the vessel from splitting open….Over time cells become weaker, allowing wall to bulge more so that tension increases further, until aneurysm ruptures.


Two major processes of cardiovascular transport:

1. Bulk transport, 2. Transcapillary transport (movement of cargo between capillaries and tissue)


Bulk transport

Movement of substances through the CV system (cargo from point A to point B in whole CV system)…Can be applied also to consumption of a substance


Bulk transport - Transport rate (x)

x = Q[x]……..x is amount of substance x, Q is flow, [x] is concentration of substance x……..EX: How much O2 is carried to a muscle in 1 minute? O2/min = CO[O2] …..where where O2/min = transport rate (ml O2/min), CO = cardiac output (ml blood/min), and [O2] = concentration of O2 (ml O2/ml blood)


Fick’s Principle – what it explains

An expansion of the bulk transport idea to consider how much of a substance is used by a tissue….basically, the amount used is equal to the amount that enters the tissue minus the amount that leaves, which can be determined as the flow times the concentration (as with bulk transport)


Fick’s Principle – equation

X used = Xi – Xo = (Q[x]i) – (Q[x]o) = Q([x]I – [x]o)…..where Xused is the amount of a substance used by the tissue, Xi is the initial amount, Xo is the final amount, and Q is flow (constant through system)


Fick’s Equation & Cardiac output

To measure CO based on myocardial oxygen consumption…. mVO2 = CO ([O2]a – [O2]v)…where, mVO2 is myocardial oxygen consumption (X is general Fick’s equation), CO is cardiac output (like flow, Q), [O2]a & [O2]v are arterial & venous oxygen concentrations (same as Xi and Xo)


Oxygen consumption in the whole body

Can be determined by looking at the difference between oxygen levels in the pulmonary vein minus the pulmonary artery, which is opposite from the expression used for with myocardial oxygen consumption & CO (which was arterial minus venous concentration) b/c blood in the pulmonary vein is oxygenated and blood in the pulmonary artery is deoxygenated.


Fractional O2 Extraction (EO2) from blood

= amount of oxygen used by a tissue expressed as a fraction of the original (arterial) oxygen concentration…. EO2 = (absolute value of arterial O2 – abs. value of venous O2) / abs. value of arterial O2


Transcapillary transport – forces determining solvent movement

Two opposing forces determine solvent movement – hydrostatic pressure and oncotic pressure


Hydrostatic Pressure (P) definition

= simply fluid pressure (blood pressure in this case)


Net hydrostatic pressure in a capillary bed

= difference between capillary pressure & interstitial pressure


Hydrostatic pressure (P) and Solvent movement

Solvents move from high pressure to low pressure…..BP in capillaries ~ 25 mm Hg, while P in interstitial space ~ 0 mm Hg….Hydrostatic pressure promotes FILTRATION (movement of fluid out of capillaries)


Oncotic pressure (π) definition

= aka colloid osmotic pressure; the osmotic force created by proteins in the blood & interstitial fluid


Major determinants of oncotic pressure

α Globulin and albumin


Oncotic pressure (π) and Solvent movement

Solutes move from high concentration to low concentration…Solvents move toward high concentration of solutes…..Oncotic pressure of blood in capillaries (πc) is higher than oncotic pressure of interstitial fluid (πi)….Capillary oncotic pressure promotes REABSORPTION of fluid (movement of fluid into capillaries)


Starling Equation for transcapillary transport (AKA Starling’s law of the capillary)

Flux = k[(Pc – Pi) – (πc- πi)]….where Flux = net movement across capillary wall, k = constant, Pc = capillary hydrostatic pressure, Pi = interstitial hydrostatic pressure, c = capillary oncotic pressure, i = interstitial oncotic pressure


(Pc - Pi) in Starling Equation

= net hydrostatic pressure….tends to be outward (filtration)


(πc – πi) in Starling Equation

= net oncotic pressure…..tends to be inward (reabsorption)


Net movement of water in and out of a capillary

= simply the outward force minus inward force, or the balance between filtration & reabsorption


Factors promoting filtration & the effect of excess filtration

Factors that increase blood pressure (HTN) or reduce oncotic pressure (liver disease)…..Excess filtration causes edema (swelling) in tissues.


Net flux from arterial to venous end of capillaries

= not constant….Pc is higher on arterial side & lower on venous side….c is lower on arterial side & higher on venous side…..Thus, there is a tendency toward filtration on the arterial side and reabsorption on the venous side.


Net flux in different capillary beds

Net flux is different in different capillary beds…e.g., capillaries in kidney favor filtration, capillaries in gut favor reabsorption


Regulation of Net flux

regulated primarily by control of capillary hydrostatic pressure (via vasoconstriction/vasodilation of arterioles)


Diffusion – what molecules CAN diffuse across cell membranes

Gases are lipid soluble & diffuse freely across cell membranes (CO2, O2, NO, etc.); Other lipid soluble molecules also diffuse freely (e.g., some vitamins); Small lipid-INSOLUBLE molecules can also diffuse, through inter-endothelial junctions between capillary endothelial cells (salts, water, glucose, etc.).


Rate of diffusion of O2

Rate of diffusion from capillary to tissue depends on…1. Distance between capillary & tissue, 2. Amount of O2 carried in blood (free and bound to hemoglobin).


Interendothelial junction

Allow small lipid-insoluble molecules (e.g.: water, salts, glucose) to diffuse across vascular cell membranes; Vary in size, density, & permeability in different tissues.


Diffusion – what molecules CANNOT diffuse across cell membranes

Large molecules (e.g., albumin, other proteins) cannot cross most capillary walls (except in some cases by endo- or exocytosis, or in lymphatic capillaries, in which the junctions are quite permeable) including through interendothelial junctions.

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