applied physiology ii. circulation, haemodynamic support

Applied physiology II.Circulation, haemodynamic

support

Rudas László

University of Szeged

Department of Anaesthesiology and Intensive Care

Medical ICU

The cardiovascular system provides appropriate oxygen and energy supply, via appropriate local circulation to the tissues.

Circulation consists of macrocirculation and microcirculation

Normal circulation requires:a pump, blood vessels, and normal blood volume

The „Pump”

Say kids!What does theheart generate?

Pressure?

Both !

Stroke volume

Pre

ssu

re

Contractility

contractility

The role of contractility

contraktility elastance

Stroke volume

Art

eria

l pre

ssu

re

Arterial elastance

Stroke volume

Art

eria

l pre

ssu

re

elastance

Heart - circulation coupling

Stroke volume

Art

eria

l pre

ssu

re contractility

elastance

HeartCirculation

Coupling Systems

A different view,

(a different representation)

of the „Pump”

Lef

t ven

tric

ular

pre

ssur

e

Left ventricular volume

End-systolicPressure-volume relationship

End-diastolicPressure-volume relationship

Isometriccontraction

Isometricrelaxation

Ejection

Ventricular filling

Lef

t ven

tric

ular

pre

ssur

e





Isometricrelaxation

Ejection

Ventricular filling

Sympathetic activation

Dyastolic function is dependent on both

normal active relaxation, and passive

distensibility.

Lef

t ven

tric

ular

pre

ssur

e





Isometricrelaxation

Ejection

Ventricular filling

Systolic dysfunction

Lef

t ven

tric

ular

pre

ssur

e



End-diastolicPressure-volume

relationshipIsometriccontraction

Isometricrelaxation

Ejection

Ventricular filling

Diastolic dysfunction

The „Pump” and theconcept of „preload”

contractility

elastance

Stroke volume

Art

eria

l pre

ssu

re

The role of the end-diastolic volume

12840

5

10

15

20C

ard

iac

ou

tpu

l (l/m

in)

Right atrial pressure (mmHg)

Cardiac function curve

the good old Starling curve

The preload of a muscle strip

Length increase (mm)

0 2 4

Act

ive

ten

sion

(g)

0

4

8

For thick walled spheres=PR/2w

w=wall thicknessP=pressureR=radius

LaPlace formula

The preload is the wall stress of the ventricle prior to ejection.

Clinically it is characterized by the ventricular end-diastolic volume, and/or ventricular end-diastolic pressure.

Lef

t ven

tric

ular

pre

ssur

e


End-systolicPressure-volume

relationship

End-diastolicPressure-volume

relationship


Isometricrelaxation

Ejection

Ventricular filling

The role of the end-diastolic volume

Lef

t ven

tric

ular

pre

ssur

eThe markers of the preload

End-diastolic pressures

End-diastolic volume

Lef

t ven

tric

ular

pre

ssur

eThe markers of the preload



Which marker is more reliable ??



Factors to be considered:

1. The end-diastolic pressure-volume relationship is curvilinear.above a certain point monimal volum cshange is mirrored by considerable pressure elevation. The slope of the relatiomship changes from subject to subject

2. The left vantricular diastolic function is very sensitive to ischemia, and injury.Thus end-diastolic pressure may rise without volume change.

Lichtwarck-Aschoff et al. Intensive Care Med1992; 18:142-147




1. The end-diastolic pressure-volume relationship is curvilinear.above a certain point monimal volum cshange is mirrored by considerable pressure elevation. The slope of the relatiomship changes from subject to subject

2. The left vantricular diastolic function is very sensitive to ischemia, and injury.Thus end-diastolic pressure may rise without volume change.

3. End-diastolic pressure may be influenced by the fact, that left and right heart share location within the pericardial space. Dilation of the right ventricle, or pericardial fluid accumulation may also increases EDP.

Watch out for that kitty !!!

The vasculature

P V

pressure

Vol

um

e

Vascular compliance

3202401608000

1

2

3

4

Rel

atív

e vo

lum

e

241680

pressure (cm water)

AORTA VENA CAVA

Compliance

Intravascular

pressures


1. Vessels could be considered as conduits, connecting the heartto the periphery.

2 Vessels, however are also elastic „containers”, and their capacity to blood is determined by their distending pressure.

3 Pressure could be generated by blood flowing through the tubes.

4 Certain amount of pressure could be also generated by „overstretching” the vessels,

5 The distensibility and the resistance characteristics of the vessels differ tremendously at different sites of the circulation

Arterial pressure generation

Cardiac output

Arterial pressure

The „Ohmic” resistance

Cardiac output 1

300

Cardiac output 2

P1 P2

Generated flow = cardial output (CO)

Generated pressure = mean art. pressure (MAP)– right atrial pressure (RAP)

Systemic Vascular Resistance (SVR = (MAP-RAP)/CO dimension: Hgmm/l/min

SVR index (SVRI) = (MAP-RAP)/CI dimension: Hgmm/l/min/m2

The „overstretching” of the vessels:

I. With „arrested circulation”

During circulatory arrest theblood volume

distrbute according to the distensibility of

the various vascular compartments, and

will exert a steady pressure on the walls.

That pressure is the mean vascular filling

pressure

Pms0 5 10 15 20

BloodVolume

% of control

0

100

Rothe et al. Arch Intern Med 146:977-82, 1986

3.5 l (50 ml/kg) „unstressed volume”

Venous Capacity

Pms0 5 10 15 20

BloodVolume

% of control

0

100


Sympathetic blockade

Noradrenalin

Venous Capacity

Pms0 5 10 15 20

BloodVolume

% of control

0

100


Sympathetic blockad

Noradrenalin

Reflex compensation range:15-20 ml/kg 1-1.5 l blood

Venous Capacity

Mean systemic filling pressure

During circulatory arrest theblood volume

distrbute according to the distensibility of

the various vascular compartments, and

will exert a steady pressure on the walls.

That pressure is the mean vascular filling

pressure

Circulatory arrest

During circulatory arrest the heart itself will distend as well. (The heart ismuch more compliant, than the arterial system).

The distension of the heart however is not proportional, (The right heart is much more complient than the left)

Intact circulation

Chamberlain D et al. Resuscitation 2008;77:10-15

Cardiac arrest: MRI series

Changes in ventricular volumes following arrest

Mean systemic filling pressure is the

prevailing pressure at the venus

capillary end, in normal basline

conditions it is around 8 mmHg.

The „overstretching” of the vessels:

II. With increasing cardiac output

„compliant ér”

„noncompliant ér”

How this applies

to the total circulation ?

Circulatory arrest Increasing CO

When generating cardiac output, the heart

Translocate blood from the venous compartment

To the arterial compartment

Questions of venous return

- Peripheral passive regulation

Effect of Sympathetic Tone on Auto-Transfusion Splanchnic Regionfrom


Time (seconds)

Spl

anc

n i B

lood

Flo

w (m

/mi n

)

0 10 20

100

200

300

Arterial Inflow

Venous Outflow

Arterial Outflow Restriction

45 ml


- Peripheral active regulation

Effect of Sympathetic Tone on Auto-Transfusion Splanchnic Regionfrom


Time (seconds)

Sp

lan

cni

Bl o

od F

l ow

(m

/ mi n

)

0 10 20 0 10

100

200

300

Arterial Inflow

Venous Outflow

Arterial Outflow Restriction Splanchnic Nerve Stimulation

45 ml 71 ml


- Return to the heart

Venous return

Right atrial pressure

Venous return curve

100

Virolainen J. Eur Heart J 1995;16:1293-1299.

Influence of negative intrathoracic pressure on right atrial

and systemic venous drainage

DSA image „Müller manoeuvre” -40 Hgmm

DSA imagenormal inspiration


Ven

ou

s re

turn

(l/

min

)

Car

dia

c o

utp

ut

(L/m

in)


Apart from temporary fluctuations,

cardiac output and

venous return should be equal.


Ven

ous

retu

rn (

l/min

)

/Car

dia

c ou

tpu

t (L

/min

)

The Guyton diagram

Cardiac function

- systolic function

contractility

preaload

afterload

heart rate

- diastolic function

structure of the myocardium


-Does the pump function

Influence venous return?

Cardiac output and right atrial pressure in pacemaker dependent dogs

Sheriff DD és Mendoza JR. Exerc Sport Sci Rev 2004;32:31-35

Pacemaker dependens alanyok perctérfogat és RAP összefüggései

Sheriff DD és Mendoza JR. Exerc Sport Sci Rev 2004;32:31-35

Questions

of the „afterload”

The afterload is the wall stress of the ejecting ventricle.

Clinically it is characterized by the ventricular pressure generated during ejection. (it is certainly an oversimplification).

myocardial wall stress during systolic ejection

afterload

ventricular ventricular myocardial

systolic radius systolic pressure wall thickness

end diastolic radius output impedance normal growth, hypertrophy

systemic arterial pressure outflow tract resistance

diastolic pressure systolic pressure vascular resistance

obstructive CMP

blood volume pulse pressure

total peripheral resistance stroke volume

arterial complianceNorton, Advances in Physiology Education 2001;25:53-61

The abnormal distensibility of ther

conductance vessels (i.e. increased

stiffness), contributes to the

increased central arterial pressure

during ejection.

„Afterload mismatch”: a relative term

Lef

t ven

tric

ular

pre

ssur

e


Lef

t ven

tric

ular

pre

ssur

e


Everybody in the room

who knows 3 ways to increase

Cardiac output raise hand !!

Types of circulatory failure

- a szív csökkent pumpafunkciója - cardiogenic shock

- reduced venous return - hypovolaemic shock

- csökkent artériás tónus a véráramlás abnormális eloszlásával - distributive shock

- outflow obstruction - obstructive shock

Let’s put the puzzle together

(start with normal parameters)

In order to put the puzzle together, I had to

change

the directions of the axes

of certain traditional diagrams.

Do not panick!

Cardiac output

Arterial pressure

Systemic vascular resistance

Cardiac output 1

300

Cardiac output 2

Venous return

Right atrial pressure

Venous return curve

10

Cardiac output / Venous return

Right atrial pressureArterial pressure


Cardiac output 1

300

Venous return curve

Cardiac output 2

10

Apart from temporary fluctuations, cardiac output and venous return should be equal.

Arterial pressure

Arterialvolume

300

Arterial compliance curve

Pressure in the great veins

Venousvolume

Venous compliance curve

10



Arterialvolume

Venousvolume

2. Systemic vascular resistance

Cardiac output 1

300

artériás

3. Arterial compliance curve

vénás

4. Venous compliance curve

1. Venous return curve

Cardiac output 2

10

Mechanisms of failure


Low cardiac output



Arterialvolume

Venousvolume


300

artériás


vénás


Venous return curve

Cardiac output

10

Therapy ?

Limitations of the therapy ?


Decreased venous return- hypovolemia



Arterialvolume

Venousvolume


300


vénás


Venous return curve

Cardiac output 2

10



Arterialvolume

Venousvolume


300


vénás


Venous return curve

Cardiac output 2

10

Secunder systolic dysfunction

Therapy ?

Limitations of the therapy ?


Loss of vascular resistance



Arterialvolume

Venousvolume


300

artériás


vénás


. Venous return curve

10

Therapy ?

Diastolic heart failure is suspected in cases

where clinical signs of decompensation are

present, in spite of preserved systolic

function (EF≥50%).

(The diagnosis could be further confirmed by

echocardiography).

myocardial end-diastolic wall stress

preload

end-diastolic end-diastolic myocardial wallradius filling pressure thickness

compliance of total blood volume normal growthventricle and blood volume distribution hypertrophypericardium venous compliance

venous return

Norton, Advances in Physiology Education 2001;25:53-61

applied physiology ii. circulation, haemodynamic support

Documents

volume change

vantricular diastolic

appropriate local circulation

different representationof

wall thicknessp

appropriate oxygen

wall stress

blood vessels