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Physiology of
HEMODYNAMICS-1
DR. GHALEB ALMEKHLAFI
OBJECTIVES
TO DESCRIBE THE BASIC HEMIDYNAMIC DIAGRAMS
•vascular function diagram
•cardiac function diagram
•Ventricular pressure-volume loops
Introduction-why physiology?
• The biologic system is complex
• the organs cross-talk
• disease disrupt function and interaction of organs
• The organ interaction try to compensate-physiologic reserve
• Derangement of function indicate failure of compensation
• critically illness indicate organ failure
• Knowing Physiology and pathophysiology Can help directing the
management of complex situations
Anatomy of the circulation
arterial vs venous circulations
Arterial circulation
• function is to distribute blood
• 10%of blood volume
• maintaining high pressure is a
guarantee of perfusion-MAP
• governed by laws of pressure
difference
Venous circulation
• function is to collect blood-reservoir
• contain ∼70% of blood volume
Capacitance = volume / transmural pressure mmHg
• low pressure 0-10 mmhg
• The volume is primarily regulated ,not
tone
• BF is governed laws of pressure
difference
MAP-RAP = CO x SVR
The circulation dynamics
The cardiac output
Vascular function
diagram
“Obviously, except under momentary
conditions the venous return and the
cardiac output must be equal.” — Arthur
Guyton
Arthur Clifton Guyton
(September 8, 1919 – April 3, 2003)
The experiment
• The invention of extracorporeal pumps allowed Guyton to
control the heart function via the speed of a mechanical pump
and separate pump effects from the vascular tree as the circuit.
• He achieved maximum venous return with zero RAP.
• Further increases in flow via increases in pump function were
limited by collapse of the intrathoracic vessels.
• When he increased RAP above zero (i.e., above atmospheric
pressure), pump flow and therefore venous return would decline
until flow ceased completely.
• He termed the pressure at zero flow mean circulatory filling
pressure (MCFP).
• By influencing MCFP via volume expansion or epinephrine, he
could increase venous return without changes in pump function
(7,8,10).
• From this, Guyton reasoned that in the steady state circulation,
venous return (and therefore cardiac output in conclusion) was
driven by the venous return driving pressure
• (VRdP = MCFP minus RAP) divided by the resistance to venous
return (RVR):
Venous Return
• rate at which blood is
returned to the heart (in
L.min-1).
• driven by the pressure
difference between MSFP
and RAP
• At steady state, venous
return is equal to cardiac
output
VR=MSFP−RAP/RVR
MSFP
• In a circulatory standstill,
pressure and volume
equilibrate in the whole
system at MCFP
• Volume is distributed
according to each segments
compliances
• The equilibrating pressure is
related to blood volume and
is independent of the hearts’
function.
mean systemic filling pressure [Pmsf]
•The Pmsf is determined
by
1. venous blood volume
• Filling volume
• Stretching volume
2-venous compliance
2 volumes-Stressed and unstressed
Stressed and unstressed vascular volume
unstressed volume :
fills the system without
exerting tension in the
vessel wall. P=0
stressed volume:
blood volume that creates
positive transmural
pressure via the elastic
recoil of the vessel wall
below –4 mm Hg,the veins collapse preventing any further
increase in flow. Vascular waterfall= maximal flow
independent of downstream pressure
Venous return-normal
Vascular
waterfall
VR=MSFP−RAP/RVR
•MSFP
• Volume
e.g. Haemorrhage, resuscitation.
• Compliance
•RAP
• Respiratory pump
(Negative intrathoracic pressure reduces RAP, improving
venous return.)
• Positive pressure ventilation
• Pericardial compliance
• Constriction
• Tamponade
•Resistance to Venous Return
• Posture
• Vascular compression
• Obesity
• Pregnancy
• Laparoscopy
• Ascites, edema,ACS
•Other factors affecting venous return
• Skeletal muscle pump
Contraction of leg muscles in combination with an intact
venous system propels blood back towards the heart.
• Venous valves
Factors Affecting Venous Return
MSFP-relevance to critical care practitioners
VR=MSFP−RAP/RVR
•MSFP
• Volume
e.g. Haemorrhage,
resuscitation.
• Compliance
Factors Affecting Venous
Return
Change in msfp
Change in resistance to VR
VR can only be zero if Pms – PRA is
zero
resistance becomes infinite below –4 mm Hg, preventing any
increase in flow above that present at –4 mm Hg.
SELECTIVITY OF VASO ACTIVE DRUGS
Predominant venous vasodilators like
nitroglycerin reduce preload .
Arterial vasodilators like hydralazine reduce
afterload
norepinephrine
augment Pmsf,
increase cardiac function,
increasing the resistance to venous
return and afterload
leading to decreased VR and rt and
down-shifting the cardiac function
curve
vasopressor
CARDIAC FUNCTION DIAGRAM
STARLING’S LAW
By raising or lowering an artificial venous reservoir
Starling showed that increased RAP resulted in increased SV
STARLING’S LAW
The curve status is defined by the existing
conditions of
• afterload
• inotropy and
• diastolic compliance
Vascular function curve
Dependant or independent-RAP,CO,VR
Do the cardiac output and venous return
depend on RAP?
Does RAP depend on the cardiac output and
venous return?
The answer to both is yes!
They all depend on each other.
Both curves can be equal only at the single
point where the two curves intersect.
Only transient and small deviations in these two
curves are possible unless either or both of the
function curves change in shape.
Momentary changes
• CO and VR are equal (at 5 L/min) only
when the CVP is 2 mm Hg.
• If CVP decrease to 0 for any reason, CO
would fall (to 2 L/min) but VR would
increase (to 7 L/min).
• Increase VR will return CVP back to the
original level (2 mm Hg) in a very short
time.
• Conversely, in the same logic the similar
thing would happen when CVP were to
increase.
• conclusion: CVS automatically adjusts to
operate at the point where the cardiac
and venous function curve intersect.
Dynamics of the curves-matching
Dynamics of the curves-matching
Eh is the slope of the
Frank-Starling curve
Eh=pmsf-pra
Both curves increase
or decrease by the
msfp and RAP
difference
high cardiac performance [Eh] low cardiac performance
Starling did not consider the MSFP
Function curves-clinical relevance
Cardiac Cycle
SAGAWA
Ventricular pressure-
volume loops
clinical implications of
vascular and cardiac
function curves=part2
Thank you

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Hd physiology part1

  • 2. OBJECTIVES TO DESCRIBE THE BASIC HEMIDYNAMIC DIAGRAMS •vascular function diagram •cardiac function diagram •Ventricular pressure-volume loops
  • 3. Introduction-why physiology? • The biologic system is complex • the organs cross-talk • disease disrupt function and interaction of organs • The organ interaction try to compensate-physiologic reserve • Derangement of function indicate failure of compensation • critically illness indicate organ failure • Knowing Physiology and pathophysiology Can help directing the management of complex situations
  • 4. Anatomy of the circulation
  • 5.
  • 6. arterial vs venous circulations Arterial circulation • function is to distribute blood • 10%of blood volume • maintaining high pressure is a guarantee of perfusion-MAP • governed by laws of pressure difference Venous circulation • function is to collect blood-reservoir • contain ∼70% of blood volume Capacitance = volume / transmural pressure mmHg • low pressure 0-10 mmhg • The volume is primarily regulated ,not tone • BF is governed laws of pressure difference MAP-RAP = CO x SVR
  • 10. “Obviously, except under momentary conditions the venous return and the cardiac output must be equal.” — Arthur Guyton Arthur Clifton Guyton (September 8, 1919 – April 3, 2003)
  • 11. The experiment • The invention of extracorporeal pumps allowed Guyton to control the heart function via the speed of a mechanical pump and separate pump effects from the vascular tree as the circuit. • He achieved maximum venous return with zero RAP. • Further increases in flow via increases in pump function were limited by collapse of the intrathoracic vessels. • When he increased RAP above zero (i.e., above atmospheric pressure), pump flow and therefore venous return would decline until flow ceased completely. • He termed the pressure at zero flow mean circulatory filling pressure (MCFP). • By influencing MCFP via volume expansion or epinephrine, he could increase venous return without changes in pump function (7,8,10). • From this, Guyton reasoned that in the steady state circulation, venous return (and therefore cardiac output in conclusion) was driven by the venous return driving pressure • (VRdP = MCFP minus RAP) divided by the resistance to venous return (RVR):
  • 12.
  • 13. Venous Return • rate at which blood is returned to the heart (in L.min-1). • driven by the pressure difference between MSFP and RAP • At steady state, venous return is equal to cardiac output VR=MSFP−RAP/RVR
  • 14. MSFP • In a circulatory standstill, pressure and volume equilibrate in the whole system at MCFP • Volume is distributed according to each segments compliances • The equilibrating pressure is related to blood volume and is independent of the hearts’ function.
  • 15. mean systemic filling pressure [Pmsf] •The Pmsf is determined by 1. venous blood volume • Filling volume • Stretching volume 2-venous compliance
  • 17. Stressed and unstressed vascular volume unstressed volume : fills the system without exerting tension in the vessel wall. P=0 stressed volume: blood volume that creates positive transmural pressure via the elastic recoil of the vessel wall
  • 18. below –4 mm Hg,the veins collapse preventing any further increase in flow. Vascular waterfall= maximal flow independent of downstream pressure
  • 19.
  • 21. VR=MSFP−RAP/RVR •MSFP • Volume e.g. Haemorrhage, resuscitation. • Compliance •RAP • Respiratory pump (Negative intrathoracic pressure reduces RAP, improving venous return.) • Positive pressure ventilation • Pericardial compliance • Constriction • Tamponade •Resistance to Venous Return • Posture • Vascular compression • Obesity • Pregnancy • Laparoscopy • Ascites, edema,ACS •Other factors affecting venous return • Skeletal muscle pump Contraction of leg muscles in combination with an intact venous system propels blood back towards the heart. • Venous valves Factors Affecting Venous Return
  • 22. MSFP-relevance to critical care practitioners
  • 23.
  • 24. VR=MSFP−RAP/RVR •MSFP • Volume e.g. Haemorrhage, resuscitation. • Compliance Factors Affecting Venous Return Change in msfp Change in resistance to VR VR can only be zero if Pms – PRA is zero resistance becomes infinite below –4 mm Hg, preventing any increase in flow above that present at –4 mm Hg.
  • 25.
  • 26. SELECTIVITY OF VASO ACTIVE DRUGS Predominant venous vasodilators like nitroglycerin reduce preload . Arterial vasodilators like hydralazine reduce afterload norepinephrine augment Pmsf, increase cardiac function, increasing the resistance to venous return and afterload leading to decreased VR and rt and down-shifting the cardiac function curve
  • 28.
  • 29.
  • 31. STARLING’S LAW By raising or lowering an artificial venous reservoir Starling showed that increased RAP resulted in increased SV
  • 32.
  • 33. STARLING’S LAW The curve status is defined by the existing conditions of • afterload • inotropy and • diastolic compliance
  • 35. Dependant or independent-RAP,CO,VR Do the cardiac output and venous return depend on RAP? Does RAP depend on the cardiac output and venous return? The answer to both is yes! They all depend on each other. Both curves can be equal only at the single point where the two curves intersect. Only transient and small deviations in these two curves are possible unless either or both of the function curves change in shape.
  • 36. Momentary changes • CO and VR are equal (at 5 L/min) only when the CVP is 2 mm Hg. • If CVP decrease to 0 for any reason, CO would fall (to 2 L/min) but VR would increase (to 7 L/min). • Increase VR will return CVP back to the original level (2 mm Hg) in a very short time. • Conversely, in the same logic the similar thing would happen when CVP were to increase. • conclusion: CVS automatically adjusts to operate at the point where the cardiac and venous function curve intersect.
  • 37.
  • 38. Dynamics of the curves-matching
  • 39. Dynamics of the curves-matching Eh is the slope of the Frank-Starling curve Eh=pmsf-pra Both curves increase or decrease by the msfp and RAP difference high cardiac performance [Eh] low cardiac performance Starling did not consider the MSFP
  • 41.
  • 45.
  • 46.
  • 47. clinical implications of vascular and cardiac function curves=part2

Editor's Notes

  1. The experiment showed that VR is derived by pressure gradient
  2. What is MSFP?
  3. the key factor is the msfp
  4. WHAT CREATS THE MSFP
  5. bb