20459323 Pulmonary Circulation

7/28/2019 20459323 Pulmonary Circulation

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The Pulmonary Circulation


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Importance

Separate pulmonary and systemic circulationsare optimal for facilitating gas exchange

The anatomy and physiology of the pulmonarycirculation are markedly different from thesystemic circulation

Abnormalities in pulmonary blood flow affect theoxygenating function of the lung

Anaesthesia and surgery may have importanteffects on the pulmonary circulation, especially indisease states

The pulmonary circulation may be alteredtherapeutically to improve V/Q ratios


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Overview

Functional anatomy

Determinants of: Pulmonary blood flow

Pulmonary blood volume Pulmonary haemodynamics

pressures

vascular resistance

Measurement of pulmonary blood flow


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Pulmonary Vascular Anatomy

Arteries Pulmonary blood flow ~ systemic

PVR only 1 / 6 SVR

Media thickness ~ 1/2 systemic

Lie close to corresponding air passages Arterioles

Transition at 100 (ID)

Virtually no muscular tissue*

Thin media of elastic tissue

Structurally similar to venules


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pulmonary vascular anatomy

Pulmonary endothelial cells Exposed to entire cardiac output

Link pulmonary and systemic circulations

Regulate vascular smooth muscle tone

Capillaries Dense network over alveolar walls

More than one alveolus per capillary network

Cross- sectional area influenced by alveolar inflation

Venules and veins Venules ~ arterioles (gas exchange possible with reverse flow)

Veins do not accompany arteries (via intersegmental septae)


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The Bronchial Circulation

Arises from arch of aorta

1% of cardiac output

Nutrient down to terminal bronchioles

Humidifies / warms inspired air Some flow returns to systemic circulation (azygos

to SVC)

~ normal systemic flow

Some flow returns to pulmonary veins

= venous admixture


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Pulmonary Blood Flow

Slightly less than systemic flow Bronchial and thebesian venous admixture

From 5 l/m at rest to 25 l/m with exercise

Increased PBF minimally affects PVR

Limited ability to control flow distribution PBF is markedly affected by gravity:

dependent perfusion > nondependent

Maldistribution of pulmonary flow affects gasexchange


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Pulmonary Blood Volume

Influenced by:

Posture Falls by 27% on standing from lying (due to systemic pooling)

Drugs Due to greater vasomotor activity of systemic circulation

Increased by vasopressors / MAST suit

Decreased by vasodilators / lumbar sympathectomy

Left heart failure


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Pulmonary Vascular Pressures

Small pressure drop cf. systemic circulation PAP = 25/10mmHg

Concept ofdriving pressure rather than simpleintravascular pressure (cf atmospheric) is useful..

Pulmonary driving pressure = mPAP - mLAP

Driving pressure is unaffected by IPPV as PAP and PVPare both increased

PBF = driving pressure / PVR


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Effect of gravity on alveolar andvascular pressures

ZONE 1

pA >pa >pV

ZONE 2Pa >pA >pV

ZONE 3

Pa >pV >pA

No flow

Flow Pa -pA

Flow Pa -pV


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pulmonary vascular pressure

Transmural pressure = pressure gradientfrom inside to outside of vessel

For larger vessels, extravascular pressure

= intrathoracic pressure Transmural pressure gradients are

highest in dependent parts of lung Site of pulmonary oedema


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Effect of changes in intra-alveolarpressure on intrathoracic and pulmonaryvascular pressures

Intrathoracic P = alveolar P - alveolar transmural P

Alveolar transmural pressure depends on lungvolume

IPPV: Intrathoracic pressure increases by lessthan 1/2 the inflating pressure

Less if poor lung compliance

Increased intra-alveolar pressure directlyincreases SAP (early valsalva) and PAP

spont.vent.produces higher PAP with expiration


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Pulmonary Vascular Resistance

Pulmonary driving pressure

PVR = Cardiac output

But: Assumes laminar blood flow PVR falls as flow increases due to low vasomotor

tone Blood is a non - Newtonian fluid (viscosity varies

with linear velocity) Units: usually 50-150 dyne.s.cm-5


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Factors Affecting PVR -passive

Cardiac output

Increased CO produces minimal impact on PAPdue to dilation / recruitment of collapsed vessels

Recruitment mainly in non-dependent lung Usually all of lung is perfused during spont.vent

Distension occurs in all pulmonary vessels Especially with pneumonectomy / ASD / VSD

Lung inflation

Minimum at FRC...


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Relationship Between PVR and LungVolume

Pulmonaryvasc

ularresistance

Lung Volume

RV FRC TLC

compression of alveolar vessels

compression of corner vessels*

/ HPV of collapsed lung units

*lie at junctions between 3 or more alveoli


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Active Control of PulmonaryVascular Resistance

Usual state = active vasodilatation

Many receptors / agonists implicated in vitro,relative importance in humans is unknown

Many of the basic control mechanisms probably

act directly on smooth muscle Endothelium acts to modulate the smooth muscle

response


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...active control of pulmonary vascularresistance

Endothelial / smooth muscle receptors... Many types Agonists:

from nerve endings (eg. Noradrenaline / Ach)

Produced locally (eicosanoids) Via blood (peptides)

Some similar / identical agonists may produceopposite effects at different receptors

Eg. Noradrenaline at 1and

2receptors


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Role of the endothelium and NO

Many pulmonary vasodilators (eg. Ach /vasopressin) are endothelium-dependent

Common pathway mainly via NO

Basal production of NO helps maintain a low

PVR


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Activation and Action of NO in the Pulmonary Vasculature

Vascular endothelium

Receptor activation

L-arginine L-citrulline

Ca++

NO synthase

Guanylate cyclase

GTP

Cyclic GMP G Kinase

Ca++ RELAXATION

Vascular muscle

NO


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Respiratory effects on PVR

Hypoxia

Induces HPV Unique to pulmonary vasculature

Mediated by both mixed venous (20%) and alveolar

hypoxaemia (80%) Overall response is nonlinear

HPV diverts blood from poorly perfused areas Optimises V/Q

Diverts blood from foetal lungs

If chronic: produces pulmonary hypertension


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Mechanism of HPV

Mediated via small arterioles (30-30m)Distal to lobar arteries, proximal to capillaries

Non-neural (occurs in transplanted lung)

Biphasic responseInitial phase:

Seconds - maximal at 5-10 minutes

Returns almost to baseline

Second phase:

Slow, sustained vasoconstriction, plateau at ~ 40 min.

Mechanism Inhibition of O

2sensitive K+ channels

Inhibits K+ efflux, producing depolarisation and Ca++ entry through

voltage -dependent Ca++

channels


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100

80

60

40

20

0

0 20 40 60 80

Alveolar PO2

Pressor

response(% max.)

The Effect of Changes in Mixed Venous and Alveolar PO2 on

Pulmonary Vasoconstriction

10mmHg

20mmHg

30mmHg

40mmHg

60mmHg

Mixed venous PO2


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Effect of pCO2 and pH on HPV

Hypercapnia and acidosis Both respiratory and metabolic acidosis augment HPV

Slight vasoconstriction

Hypocapnia and alkalosis Metabolic and respiratory alkalosis both inhibit / abolish

HPV

Vasodilation


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Anaesthesia and PVR

Intravenous Minimal effect on HPV, vascualar tone or oxygenation

Exceptketamine (increases PVR)

Volatile anaesthetics Minimal effect on PVR, decrease PAP

PAP effect: sevoflurane > isoflurane

Effect on PBF due to negative inotropy Halothane reduces PBF, no effect on PVR

Isoflurane

No effect on HPV at 1-1.2 MAC

N20 increases PVR / attenuates HPV

Reduced / no effect if chronically elevated PVR


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Neural Control of PulmonaryBlood Flow

1. Adrenergic Thoracic sympathetic fibers

Smooth muscle of pulmonary arteries / arterioles

Both constrictor (1-norad.) and dilator (

2-circulating adren.)

2- vasodilatation

Presynaptic: inhibition of NA release Postsynaptic: increase NO production in endothelium

Dominant effect is 1:

sympathetic stimulation PVR


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neural control of pulmonaryblood flow

2. Cholinergic Vagal stimulation produces vasodilatation

ACh release stimulates M3receptors

Endothelium and NO dependent

AChis constrictor if no endothelium

? Significance of cholinergic control in humans

3. Non- adrenergic / non- cholinergic (NANC) Anatomically related to ANS

Different neurotransmitters

Mostly inhibitory in lung, vasodilatation via NO release

? Functional significance


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Humoral Control of PulmonaryBlood Flow

*Probably minimal role in control ofnormalPBF Involved in pulmonary vascular diseases

Catecholamines Adrenaline / dopamine:

and effects

Mainly vasoconstrictor Eicosonoids

Pulmonary vessels metabolise arachadonic acid to PGs/TXA2

Mainly constrictor except PGI2

May be involved in pulmonary hypertension in sepsis / CHD /

reperfusion injury


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humoral control of pulmonaryblood flow

Amines Histamine: variable, constricts resting smooth muscle

5-HT (serotonin): released from activated platelets

Constrictor

May aggravate pulmonary hypertension due to PE

Peptides Diverse responses

Mainly vasodilatation via endothelial receptors

Mainly vasoconstriction via direct smooth muscle action

Purine nucleosides Variable responses

Adenosine is a vasodilator

Receptors and agonists involved in active control of pulmonary vascular tone


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Receptor Subtypes Principle Responses Endothelium

Group agonists dependent?

Adrenergic 1 noradrenaline constriction No

2 noradrenaline constriction Yes 2 adrenaline dilatation Yes

Cholinergic M3 acetylcholine dilatation Yes

Amines H1 histamine variable Yes

H2 histamine dilatation No

5-HT1 5-HT variable variable

Purines P2x ATP constriction No

P2y ATP dilatation Yes

A1 adenosine constriction No

A2 adenosine dilatation No

Eicosanoids TP thromboxane A2 constriction No

? Prostacyclin (PGI2) dilatation ?

Peptides NK1 Substance P dilatation Yes

NK2 Neurokinin A constriction NoAT angiotensinogen constriction No

ANP ANP dilatation No

B2 bradykinin dilatation Yes

ETA, ETB endothelin const.A, dil.B NoA, YesBV1 vaso ressin dilatation Yes


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Measurement of the pulmonarycirculation

Pulmonary blood volume Dye - dilution: PA to PV or LA

Usually 10-20% of blood volume

Pulmonary vascular pressure

PAP: Swan - Ganz catheter / echocardiography PVP: PCWP / LA catheter

Pulmonary blood flow... Fick principle

Dye / thermal dilution

2-D ultrasound of PA + Doppler flow velocity


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pulmonary blood flow

Fick principleO2 extraction = amount added to blood flowing though lungs

VO2 = Q (Ca O2- CvO2)

Q =

Ca O2- CvO2

Limitations:

Does not include extrapulmonary shunt flow

Does not include oxygen consumption by the lung

May be large if lungs are infected

VO2


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Modified Fick Method

Soluble, inert tracer gas (15% N2O,freon / argon)

Short sampling period (single breath) Mixed venous concentration ~ 0

tracer gas uptakeQ = art. tracer gas concentration*

* ~ PET. ALVtracer gas X blood solubility coefficient Noninvasive Limited if large alveolar dead space or shunt


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Thermodilution Measurement of Cardiac Output

SVC

PA

injectate at

known T

thermistor

temp

time

Higher blood flow lower temperature rise in PA


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Echocardiographic Measurement ofPulmonary Blood Flow

Diameter of PA measured PA cross -sectional area calculated

Mean flow in PA measured / beat Velocity. time integral (VTI)

Stroke volume = PA area X VTI

Cardiac output = SV X HR

DPaVel.

time

VTI

= area under curve


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Summary

The pulmonary circulation differs markedly inanatomy and function to the systemic circulation

Large changes in cardiac output produce littlechange in PAP due to distension and recruitment

Pulmonary arteries are low pressure and lessinfluenced by neural control than are systemic

The pulmonary circulation has limited ability tocontrol blood flow distribution through the lung


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summary

Pulmonary vascular resistance is influencedpassively by factors such as cardiac output,posture and lung volume

Pulmonary vascular resistance is actively

influenced by cellular, respiratory, neural andhumeral factors

Documents

20459323 Pulmonary Circulation