Download Physiologic Concepts of Hemodynamic Monitoring

Physiologic Concepts of
Hemodynamic Monitoring
Edward Hamaty D.O. FACCP, FACOI
Simplified Concept of the Circulatory System
Blood Volume
• Normal Blood Volume
– Female: 4.0 – 4.5 liters or 67 ml/kg
– Male: 5.0 – 5.5 liters or 75 ml/kg
• Normal control of blood volume
– Plasma refill
– ADH
– Aldosterone
– Erythropoietin
Distribution of Blood Volume
Blood Volume and Pressure-Systemic
Flow Resistance Map
Functional Correlates of PV Structure
Structural Characteristics of PV System
Blood Vessel Types
Vascular Resistance Control Points
Distribution of Cardiac Output
Poiseuille’s Law (pwä-zwēēz]
Vascular Resistance in Series/Parallel
Components of Vascular Resistance
• R = nL/r4.
• It is seen that n, the viscosity, is the
fluid resistance factor.
• L/r4 the blood vessel resistance factor.
• The radius is the most important factor
in determining vascular resistance.
• The viscosity is the second most
important.
• The fourth power effect on flow is
profound.
Effect of Radius on Flow
• Q = ∆Pr4∏/8L‫ח‬
• Assuming that pressure remains
constant, decreasing the radius of a
tube by ½ reduces flow to 1/16 of its
original value.
• Decreasing the RADIUS of a tube by
16% decreases flow to ½ of its original
rate.
• Decreasing the RADIUS of a tube by
16% increases the pressure needed to
maintain flow to twice the original
value.
Effect of Radius on Flow
• Rewritten as simple proportionalities:
• Q = Pr4
• P = Q/r4
• Based on the proportionality for flow, it can
be stated that because flow varies directly
with r4, if pressure remains constant as radius
decreases, flow decreases.
• Stated another way, if the radius decreases,
pressure must increase to maintain flow.
Viscosity
• In a homogeneous liquid such as water,
in an artificial system, viscosity is a
constant.
• In the case of a two-phase medium such
as blood flowing in an in vivo circulatory
system, viscosity is NOT constant, but
depends on several factors– The concentration of the suspended
medium (the cells)
– The velocity of flow
– The radius of the vessel
Viscosity
• The relative viscosity of PLASMA is about 1.3
x water.
• The relative viscosity of whole blood depends
mainly on the cell concentration or
hematocrit.
• At a normal Hct of 42 to 45, the relative
viscosity of blood is about 3.6 x water.
• However, because the relationship is
exponential, an increase in 10 in the Hct from
the level of 40 will increase the viscosity
about 25% and an increase of 20 to the level
of 60 will increase viscosity about 60%.
Viscosity
• Viscosity is related to:
– Hematocrit
– Blood Flow
– Vessel Diameter
• The hematocrit is the most important factor
governing blood viscosity.
• Viscosity of whole blood is about 3.5 times
that of water.
• A decrease in hematocrit to half normal
causes the viscosity of blood to decrease to 2
times that of water.
Viscosity
•Anemia, therefore, improves the rheologic
properties of blood.
•Polycythemic states have an adverse effect on
blood flow. When the Hct is raised to 70%
above normal, the viscosity of blood increases
to 20 times normal.
Viscosity
Viscosity
• In low Hct states, such as anemia,
viscosity and therefore vascular
resistance both fall, resulting in
increased cardiac output.
• In high Hct states, such as polycythemia
and leukemia, with Hct of 60-70%, a
profound increase in systemic and
pulmonary vascular resistance occurs
with a resultant elevation of BP.
Viscosity
• Vessel bore and flow rate are two
additional factors affecting blood flow in
a two-phase medium.
• In tubes less than 200 micrometers in
diameter-which would include
arterioles, capillaries, and venules- the
relative viscosity of the blood decreases
and offers less resistance to flow.
• This phenomenon, for which there is no
satisfactory explanation, is sometimes
called the Fahraeus-Lindqvist effect.
Viscosity
• At low flow rates the apparent viscosity
increases (anomalous viscosity).
• This phenomenon has been attributed to the
disposition of red cells in the flowing stream.
– At higher velocities the cells accumulate in the
axial part of the stream.
– At low velocities that have a more even distribution
and hence offer greater flow resistance.
– At low velocities rouleaux formation may occur.
– This effect is exaggerated in low flow states such
as burns or shock, causing pronounced cell
clumping or sludge in the microcirculation with
severe hindrance to flow and resultant tissue
ischemia.
Viscosity
• Therefore, in different parts of the
circulation there will be significant
variations in blood vessel diameter, flow
velocity, and Hct and that the net effect
on viscosity is not always predictable.
• Present evidence suggests that the Hct
effect is the most important and
predominate one.
• Under special circumstances
temperature may affect viscosity.
– 2% rise in viscosity/1oC fall in temp.
Viscosity
• During prolonged exposure to cold and
high wind the extremities will become
chilled, and the reduced flow effect of
vasoconstriction will be enhanced by
the increased vascular resistance
resulting from the heightened viscosity.
• This can intensify ischemia.
Viscosity and O2 Delivery
Viscosity and Cardiac Output
Flow Velocity and Turbulence
•Linear velocity varies inversely with the cross
sectional area of the circulation.
Flow Velocity and Turbulence
•Poiseuille’s Law assumes laminar flow.
•At high velocities flow becomes turbulent.
–In this case, flow is approximately proportional to
the square root of the pressure gradient rather than
the pressure itself; the turbulent stream now offers a
considerable increase in resistance.
Reynolds Number
•Reynolds has defined the factors affecting this
phenomenon and stated that turbulence is likely
to occur in a moving stream when the Reynolds
ratio (Re) exceeds a value of about 1000 for
blood or 2000 for homogeneous fluids.
Cell Function and Ion Concentrations
• In general, cell function is stimulated or
depressed by ionic concentrations.
• This ionic influence may be described
qualitatively in terms of the capacity to
increase or depress irritability of nerve
and striated muscle cells.
• A coefficient of irritability, K, has been
related to EFC or plasma cationic
concentrations by the following
formula:
Cell Function and Ion Concentrations
• K = [Na+][K+][OH-]
[Ca++][Mg++][H+]
The ions in the numerator are “irritability
ions”, because increases in their
concentrations heighten cell irritability
and decreased concentrations depress
it.
In contrast, the “paralysis ions” of the
denominator depress cell irritability
with increasing concentrations and
intensify it with decreased
concentrations.
Cell Function and Ion Concentrations
• Cardiac muscle is an exception to this
general rule. For this tissue:
• K = [Na+][Ca++][OH-]
[K+][Mg++][H+]
Increased Ca++ causes vasoconstriction,
increased K+ causes vasodilatation,
increases in Mg++ cause powerful
vasodilatation. Increased H+ also
causes vasodilatation.
The only anions with significant effects
include acetate and citrate, both of
which cause mild vasodilatation.
Total Peripheral Resistance
Pulmonary Vascular Resistance/Pcap
Pulmonary Vascular Resistance/Pcap
Coronary Circulation
Venous Return Curves
• The main changes in cardiac output are
determined by the metabolic
requirements of the body, it is evident
that the body sets the pace, not the
pump!
• The heart, from a flow standpoint, plays
a “permissive” role and does not
regulate its own output.
• In human circulation, the heart
functions as a “demand” pump and will
eject only the minimum volume
demanded of it.
Venous Return Curves
• The output of the heart, therefore, represents
a balance between the VENOUS RETURN-the
demand-and the ability of the heart to meet
that demand.
• For these reasons, it is necessary to consider
the regulation of cardiac output from two
different standpoints:
– The role of systemic factors in determining cardiac
output (i.e. what influences the return flow of
blood to the heart)
– The role of cardiac factors in determining cardiac
output (i.e. what influences the ability of the heart
to pump out the blood returned to it.)
Venous Return Curves
• “Mean circulatory filling pressure” is the
average of the pressures in all segments of
the vascular system when each one is
weighted in proportion to the compliance of
its respective segment.
• This average pressure would be a single,
integrated, hydrostatic measurement of the
degree of filling of the circulation and would
represent the force tending to propel blood
toward the right atrium
• The mean circulatory pressure for the
systemic system (PSF) is about 7 mm Hg.
• The mean circulatory pressure for the
pulmonary circulation (PPF) is about 5 mm Hg.
Venous Return Curve
Venous Return Curve
Venous Return Curve
Venous Return Curve
Venous Return Curve
Ventricular Function Curve
Ventricular Function Curve
Ventricular Function Curve
• Hypereffective Heart—normally only 2 factors:
– Nervous stimulation
• Sympathetic stimulation
• Parasympathetic inhibition
– Hypertrophy of the cardiac muscle
• Hypoeffective Heart
– Inhibition of nervous excitation of the heart
– Pathologic factors that cause abnormal heart
rhythm or rate of heartbeat
– Valvular heart disease
– Increased arterial pressure
– Congenital Heart Disease
– Myocarditis
– Cardiac anoxia
– Myocardial damage/toxicity
Cardiac Output
Cardiac Output
Cardiac Output
Cardiac Output
Pressure Volume Curves
Summary Slide
Determinants of Cardiac Output
Transmural Pressure
Compliance or Distensibility
Compliance or Distensibility
Compliance or Distensibility
Pressure-Volume Compliance Relationship
Physiology of the Wedge Pressure (PAOP)
Physiology of the Wedge Pressure (PAOP)
Physiology of the Wedge Pressure (PAOP)
Physiology of the Wedge Pressure (PAOP)
Intravascular Pressure
PAOP/Wedge Pressure
Ventricular
Compliance
LV Volume
Juxtacardiac
Pressure
Physiology of the Wedge Pressure (PAOP)
Physiology of the Wedge Pressure (PAOP)
Physiology of the Wedge Pressure (PAOP)
Physiology of the Wedge Pressure (PAOP)
Therefore, ONCE AND FOR ALL, THE
WEDGE PRESSURE IS NOT directly
equal to PRELOAD (LEFT
VENTRICULAR END DIASTOLIC
VOLUME)!
It IS and always WAS the intravascular
pressure resulting from the interplay
of:
PCWP = LVEDVolume + JCP
Compliance
Pressure-Volume Compliance Relationship
Pressure-Volume Compliance Relationship
Right vs Left Heart Properties
Afterload
•Resistance to
forward blood
flow caused by
aortic pressure
and total
peripheral
vascular
resistance:
Myocardial Oxygen Consumption
Laplace and Wall Tension
CO and Oxygen Delivery
Oxygen Content
Oxygen Consumption
Oxygen Consumption
Normal Oxygen Values
Dynamics of Oxygen Supply and Demand
• Compensatory Mechanisms
– When the balance between oxygen supply
and demand is threatened, the body
mobilizes its compensatory mechanisms to
ensure adequate oxygen delivery.
– The two most important ones are an
increase in cardiac output and an increase
in oxygen extraction.
Dynamics of Oxygen Supply and Demand
Oxygen Dissociation Curve
Oxygen Extraction
Oxygen Extraction
Specific Threats to Oxygen Balance
Specific Threats to Oxygen Balance
Specific Threats to Oxygen Balance
Specific Threats to Oxygen Balance
Specific Threats to Oxygen Balance
Specific Threats to Oxygen Balance
Specific Threats to Oxygen Balance
Specific Threats to Oxygen Balance
SvO2
Relationship between SVO2 and Components
Oxygen Flow-Consumption Diagram
SvO2 Decision Tree
SvO2 and CvO2
SvO2 and CvO2
Pulmonary Physiology – V/Q Mismatching
Pulmonary Physiology – V/Q Mismatching
Pulmonary Physiology – V/Q Mismatching
Pulmonary Physiology – Transit Time
Biphasic VO2-DO2 Model
Biphasic VO2-DO2 in Health and Disease
Slope of the Extraction-SvO2 Curve
Slope of the Extraction-SvO2 Curve
Oxygen Flux Test
Tissue Oxygenation Process