Hemodynamics & Instrumentation - Video Notes (Vocabulary flashcards)
Hemodynamics: Overview
Definition: The study of the movements of blood and the forces concerned therein; describes the set of forces or mechanisms involved in regulation of blood flow within the body.
Energy concepts: Energy is the capacity to do work and overcome resistance; energy cannot be created or destroyed; Energy Conservation – net energy never changes, just changes form.
Types of hemodynamic energy:
Potential energy (Pressure) – Systolic Pressure
Kinetic energy (Velocity) – movement of blood
Total Fluid energy = Potential energy + Kinetic energy
In the vascular system, most energy is dissipated as heat due to friction.
Flow basics: Q = V × A (Flow = Velocity × Area). The vascular system attempts to maintain flow.
If Velocity increases, Vessel Area has decreased (diameter reduced).
If Area increases, Velocity decreases.
Flow directions follow pressure gradients: Flow goes from higher pressure to lower pressure.
Pressure hierarchy (typical): Left ventricle = highest pressure; Right atrium = lowest pressure.
Summary concept: Energy conservation with friction leads to dissipation, while the system maintains overall flow through adjustments in velocity and cross-sectional area.
Bernoulli Principle, Continuity, and Flow Relationships
Bernoulli Principle (applied to vessels): Relationship between energy, velocity, and pressure assuming (approximately) frictionless, constant flow along a streamline.
As pressure decreases, velocity increases.
As pressure increases, velocity decreases.
Interpretations: Pressure is potential energy; Velocity is kinetic energy.
Along a narrowing (decreased area): velocity increases and pressure decreases.
Along an expanding section: velocity decreases and pressure can rise.
Mathematical intuition: Along a streamline, P + rac{1}{2}
ho v^{2} = ext{constant} (ideal, inviscid flow).
Continuity Equation (flow conservation):
Q = vA or equivalently, velocity and area trade off to conserve flow.
Higher velocity implies smaller cross-sectional area; larger area implies lower velocity.
Practical interpretation: In real vessels, energy is lost to friction/heating, so the equality is an approximation; the net energy is conserved in form, not in magnitude.
Poiseuille’s Law and Flow Determinants
Poiseuille’s Law (laminar flow in a cylindrical vessel):
Q = rac{(P1 - P2)\pi
^4}{8\,
u\,L}Corrected standard form: Q = rac{(P1 - P2)\pi
^4}{8\,
u\,L} where$P1 - P2$ = pressure gradient (gradient driving flow)
$
$ = radius of vessel$
u$ = dynamic viscosity of blood$L$ = vessel length
Assumptions (as listed): constant flow rate, constant viscosity, straight rigid vessel.
Derived relationships:
Flow is directly proportional to pressure gradient: larger gradient → more flow.
Flow is directly proportional to radius to the fourth power: Q \propto r^4
Resistance $R$ in Poiseuille’s context is R = \frac{8\nu L}{\,\pi r^4}, so $R$ is inversely proportional to $r^4$.
Practical example: Halving the radius results in a 16-fold decrease in flow, illustrating the sensitivity of flow to small radius changes.
Parameter Effects on Flow and Vascular Resistance
Pressure gradient: directly proportional to flow.
Velocity: directly proportional to flow.
Area (cross-sectional area): directly proportional to flow when considering velocity; inversely related to velocity through the Continuity equation.
Resistance: inversely proportional to flow; in physiological terms, resistance decreases as radius increases.
Ways to decrease resistance (while keeping other factors constant):
Increase radius (dilate vessel)
Decrease vessel length (shorter path)
Decrease viscosity (e.g., hematocrit changes vary over time; generally, viscosity effects are maintained)
Parallel vessels reduce overall resistance vs. series arrangements
Vessels in series vs parallel:
Series arrangement yields higher resistance than parallel arrangements.
Overall flow distribution depends on network geometry.
Summary: Increases in friction/resistance reduce flow; factors that reduce resistance or increase driving gradient promote flow.
Arterial Hemodynamics
Arterial system characteristics:
High-pressure system with mean arterial pressure roughly MAP \approx 70-100 \,mmHg (classic clinical range).
Blood flow pattern depends on location, size, and course of vessels.
Flow patterns in arteries:
Laminar flow: most common
Plug flow: seen in larger arteries at certain phases of systole
Turbulent flow: can occur distal to stenosis or in large vessels; contributes to pressure drop after a stenosis
Flow patterns quick recap:
Laminar: parabolic velocity profile; fastest in the center; slower near walls due to friction; boundary layer is the thin, slow-moving layer near intima.
Plug: layers accelerate at similar rates in large arteries during systole.
Turbulent: swirling flow, some reverse components; more likely distal to stenosis; contributes to large pressure drops.
Reynolds number (Re) to predict turbulence:
Re = \frac{\rho v D}{\mu} where $\rho$ = density, $v$ = velocity, $D$ = diameter, $\mu$ = viscosity.
In most physiological conditions, density and viscosity are relatively constant; turbulence mainly from velocity changes and vessel size.
Rule of thumb: Re < 2000 → laminar; Re > 2000 → turbulence.
Waveforms and Arterial Flow Characteristics
Arterial Doppler waveform characteristics depend on distal arteriolar beds, not the name of the artery.
High-resistance waveforms:
Multiphasic with potential flow reversal due to reflections.
Common in peripheral vessels.
Low-resistance waveforms:
Monophasic with one predominant direction of flow during the cardiac cycle.
Example: Internal carotid artery (proximal cerebral circulation).
Systole vs diastole differences:
Greater difference implies increased pulsatility or resistance distally.
Distal beds: High resistance distally; Low resistance distally in certain vascular beds.
Post-stenotic consequences:
Post-stenotic turbulence occurs at the exit and just distal to a significant stenosis; can have elevated velocity.
Post-stenotic flow patterns: dampened (parvus tardus) waveform distal to severe disease; delayed upstroke with reduced velocity.
Velocity graphs: example visual cues include upstroke, peak systole, diastolic troughs, and post-stenotic changes.
Venous Hemodynamics and Transmural Pressure
Venous system: lower pressure (mean ~5-15 \,mmHg); shape determined by transmural pressure (intraluminal minus interstitial).
Hydrostatic effects:
Hydrostatic pressure (HP) = \rho g h; acts on both arteries and veins; increases with standing.
Transmural pressure:
P{tm} = P{intraluminal} - P_{interstitial}
High transmural pressure expands the vessel; low transmural pressure collapses the vessel.
Respiratory influence on venous pressure:
Pressure in chest changes with respiration:
Inspiration: chest pressure decreases; abdominal pressure increases; diaphragm descent partly collapses the inferior vena cava (IVC), impeding venous return from the legs; pulmonary venous pooling increases.
Expiration: chest pressure increases; abdominal pressure decreases; venous return from legs to heart increases; venous return to thorax decreases.
Calf muscle pump:
Contraction of calf muscles propels venous blood toward the heart; considered the “heart of the venous system” in terms of propulsion.
Venous valves:
Valves throughout the venous system prevent backflow due to gravity; create a holding chamber during venous return.
Venous waveforms and phasicity:
Venous waveforms are phasic with respiration; veins near the heart can be pulsatile.
Veins distant from the heart show phasic variations with respiration.
Abnormal: lack of phasicity can indicate proximal obstruction.
Hemodynamics: Summary of Key Concepts
Bernoulli principle ties together pressure and velocity; higher velocity associates with lower pressure, and vice versa, under ideal conditions.
Poiseuille’s Law links flow to pressure gradient, radius, viscosity, and vessel length; flow is extremely sensitive to radius (fourth power).
Arterial flow patterns reflect downstream vascular beds and are assessed via waveforms and Doppler velocities.
Reynolds number predicts laminar vs turbulent flow; turbulence contributes to energy losses and is commonly linked to stenosis.
Venous hemodynamics are governed by low pressures, hydrostatics, and mechanical aids to return (respiration, calf pump, valves).
Transmural pressure and hydrostatic effects critically influence venous return and vessel caliber.
Instrumentation and artifacts in Doppler imaging can affect interpretation and require understanding of controls and common artifacts.
Instrumentation and Doppler Principles
Doppler shift basics:
Doppler shift is the change in frequency due to moving reflectors (RBCs) observed by a stationary transducer.
Difference between transmitted frequency and received frequency is the Doppler shift.
Positive shift: flow toward the transducer; Negative shift: flow away from the transducer.
Most accurate when angle = 0°; Doppler shift is zero at 90°; never exceed 60° in practice.
The Doppler shift equation (simplified form):\Delta f = \frac{2 f_0 v \cos\theta}{c} where
$f_0$ = transmitted frequency,
$v$ = blood velocity,
$\theta$ = angle between flow direction and ultrasound beam,
$c$ = speed of sound in tissue.
Pulse-wave Doppler (PW):
A pulse is transmitted and returns; provides depth-specific information.
Pulse Repetition Frequency (PRF) controls the sampling rate; depth selection introduces trade-offs.
Common artifact: aliasing when Doppler shift exceeds \frac{PRF}{2} (Nyquist limit).
Aliasing elimination strategies: increase PRF, decrease Doppler shift, or adjust baseline.
Controls and typical settings:
PW Doppler: PRF/Scale, Gate and Sample Volume, Spectral Gain, Baseline, Angle Correction.
Color Doppler: PRF/Scale, Gate and Sample Volume, Color Gain, Packet Size, Persistence, Priority.
Color Doppler concepts:
Displays velocities with color pixels; colors (blue/red) show direction relative to transducer.
Aliasing can occur with color Doppler in stenotic regions.
Artifacts (common categories):
Reverberation (spurious echoes)
Shadowing (from bone, calcifications, or acoustic impedance)
Partial volume artifact (slice-thickness issues): echoes/doppler signals from part of the slice thickness can be misattributed; explains why some signals appear in or near anechoic structures.
Clutter/Wall motion artifacts
Motion artifacts
Color Bleeding/Blooming (color spill-over)
Mirror Image artifacts (phantom duplication across strong reflectors)
Clinical Flow Patterns: Lab vs Clinical Application
In lab-like analysis (idealized): velocity and pressure may appear constant or simplified; clinical vascular imaging emphasizes the impact of area changes, pulsatility, and complex flow paths.
Post-Stenotic and Waveform Changes with Disease
Post-stenotic turbulence: turbulence downstream of a stenosis; can have elevated velocities and disturbed flow patterns.
Dampened (Tardus-Parvus) waveform: monophasic, delayed upstroke, reduced peak velocity distal to a significant stenosis.
Quick Reference: Numerical and Conceptual Notes
Flow and energy:
Q = vA
P + \frac{1}{2}\rho v^{2} = \text{constant} (Bernoulli, ideal case)
E = P + \frac{1}{2}\rho v^{2} (total fluid energy per unit volume)
HP = \rho g h (Hydrostatic pressure)
Vascular resistance and flow:
Q = \dfrac{(P1 - P2)\pi r^{4}}{8\eta L}
R = \dfrac{8\eta L}{\pi r^{4}}; radius has a fourth-power effect on flow
Q \propto r^{4}; halving $r$ → flow reduces by factor 16
Reynolds number:
Re = \dfrac{\rho v D}{\mu} (or using $v$ and $D$)
$Re < 2000$ laminar; $Re > 2000$ turbulence
Transmural pressure:
P{tm} = P{intraluminal} - P_{interstitial}
Doppler physics:
\Delta f = \dfrac{2 f_0 v \cos\theta}{c}
Angle considerations: best near 0°, zero at 90°, never > ~60° in practice
Aliasing: occurs when Doppler shift exceeds \frac{PRF}{2}; mitigated by higher PRF, lower Doppler shift, or baseline adjustments
Course Logistics (Context from Transcript)
Course structure: 30% quizzes (based on reading and class lecture; quizzes at the beginning of most classes)
60% exams: midterm and final
10% presentation assignment
Instructor: Adam Olsen MS RVT RDMS; Director of Radiology – Capital Health; Course Instructor at TJU since 2017; TJU graduate 2009; SIU graduate 2025
Student count (as per transcript): 17 students
Summary and Practical Implications
Understanding the interplay between pressure, velocity, and cross-sectional area is essential to interpret Doppler signals and waveforms.
Poiseuille’s law emphasizes how small changes in radius dramatically affect flow, making stenosis a critical determinant of downstream hemodynamics.
Recognition of flow patterns and waveforms helps differentiate normal physiology from pathology (high vs low resistance beds, post-stenotic changes, tardus-parvus, and dampened flows).
Venous hemodynamics require integrating hydrostatic effects, respiration, calf pump function, and valves to understand venous return.
Mastery of Doppler physics and artifacts is essential for accurate image interpretation and avoiding misdiagnosis.