Respiratory PhysiologyLecture 6

Pulmonary circulation and pulmonary prefusion

Zuheir A Hasan

Professor of physiology

Department of Basic Medical Sciences

School of Medicine

HU

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Lecture objectives

• Compare and contrast the bronchial circulation and the pulmonary circulation.

• Describe the physiological anatomy of the pulmonary circulation, and explain its physiologic consequences.

• Compare and contrast the pulmonary circulation and the systemic circulation. ( blood flow pressure and resistance )

• Describe and explain the effects of lung volume on pulmonary vascular resistance.

• Describe and explain the effects of elevated intravascular pressures on pulmonary vascular resistance.

• List the neural and humoral factors that influence pulmonary vascular resistance.

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Lecture objectives

• Describe the interrelationships of alveolar pressure, pulmonary arterial pressure, and pulmonary venous pressure and their effects on the regional distribution of pulmonary blood flow.

• Predict the effects of alterations in alveolar pressure, pulmonary arterial and venous pressures, and body position on the regional distribution of pulmonary blood flow.

• Describe hypoxic pulmonary vasoconstriction and discuss its role in localized and widespread alveolar hypoxia.

• Review pulmonary capillary dynamic ( starling forces, filtration and reabsorption)

• Describe the causes and consequences of pulmonary edema.

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Anatomic relationship between the pulmonary artery, the bronchial artery, the airways, and the lymphatics. A, alveoli; AD, alveolar ducts; RB, respiratory bronchioles; TB, terminal bronchioles.

The pulmonary vasculature is innervated by both sympatheticand parasympathetic fibers of the autonomic nervoussystem. The innervation of pulmonary vessels is relatively sparse in comparison with that of systemic vessels, and the autonomic nervous system has much less influence on the pulmonaryvessels.

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Schematic diagram of bronchial and pulmonary circulation

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Blood supply to the conducting zoneThe bronchial circulation

• The bronchial circulation is a systemic vascular bed that supplies blood to the, to supporting tissues of the lungs (connective tissue, septa, and large and small bronchi

• originates from Bronchial arteries arise from the descending aorta and feed capillaries that drain either via bronchial veins or via anastomoses with pulmonary capillaries into pulmonary veins

• These connections allow small amounts of deoxygenated blood to bypass the blood–gas interface and reenter the systemic circulation without being oxygenated.

• This venous admixture represents a physiologic shunt that decreases pulmonary vein O2 saturation by 1%–2%.

• Receive 2 percent of cardiac output of the left ventricle.

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The Pulmonary and systemic Circulation

Characteristics of pulmonary Circulation

• The pulmonary artery is thin, with a wall thickness about one-third that of the aorta.

• Pulmonary arteries have larger diameters and thinner wall thickness than their counterpart systemic arteries

• The pulmonary arterial branches are very short.

• Thin walled vessels at all levels.( pulmonary arteries, and even the smaller arteries and arterioles )

• .The distensibility of pulmonary veins is similar to that of systemic circulation.

• Consequences of this anatomy - the vessels are:

• Distensible (have higher compliance).

• Compressible.

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Blood Volume of the Lungs

• The blood volume of the lungs is about 450 milliliters, about 9 percent of the total blood volume of the entire circulatory system. .

• 70 ml in the pulmonary capillaries. The remainder is divided about equally between the pulmonary arteries and the veins.

• Lungs serve as a blood reservoir due to distensible (high compliance).

• Accommodate increase in cardiac output for (During exercise )

• Cardiac pathology may shift blood from the systemic circulation to the pulmonary circulation.

a. Failure of the left side of the heartb. Mitral stenosis or regurgitation

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Pulmonary and systemic Circulation Pressures

• low pressure circulation and low resistance (one-tenth the resistance of the systemic circulation)

• a systolic pressure of about 20-25 mmHg and a diastolic pressure of 8 mmHg in the pulmonary artery

• The mean arterial pulmonary• pressure is about 15 mmHg.• Right ventricle Pressure

25/0The blood volume in the which perfuse through pulmonary capillary approximately equal to the stroke volume of the right ventricle.

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Pulmonary circulation pressure

• Pulmonary Pressures• Pulmonary artery pressure

• systolic 25 mmHg

• diastolic 8 mmHg

• mean 15 mmHg

• capillary 7 mmHg

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Pressure in the pulmonary systemPulmonary wedge pressure

• The mean pressure in the left atrium is 2 mmHg (1-5 mmHg).

• Pulmonary wedge pressure is a good estimate of left atrial pressure (just 2-3 mmHghigher).

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PULMONARY RESISTANCE TO FLOW

• Pressure drop of 12-10 mmHg

• Flow of 5l/min

• Resistance 1/10 systemic circulation

• Length of Time Blood Stays in the Pulmonary

Capillaries about 0.8 sec

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▪ Pulmonary Blood Flow (PBF) = Cardiac Output (5 L/min).

▪ PBF = ∆P / Pulmonary vascular resistance (PVR)

PBF = (MPAP – MLAP) / PVR

where:

MPAP: mean pulmonary artery pressure

MLAP: mean left atrial pressure

PVR = (MPAP – MLAP) / PBF

= 1/10 of systemic VR

▪ Pulmonary vessel constriction PVR

▪ Pulmonary vessel dilation PVR4/3/2021

Blood Flow to the Lungs / PVR

14

Pulmonary Vascular Resistance

PVR = k • mean PA pressure - left atrial pressure

cardiac output

mean PA pressure - left atrial pressure = 10 mmHg

mean aorta pressure - right atrial pressure = 98 mmHg

Therefore PVR is 1/10 of SVR

Vascular Resistance =input pressure - output pressure

blood flow

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MEASUREMENT OF PULMONARYBLOOD FLOW

Fick Principle

VO2 = Oxygen Consumption CaO2= Arterial Content

CvO2= Venous Content

VO2=Q(CaO2-CvO2

)

Q = Blood flow

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Calculation of pulmonary blood flow

VO2 = 250 ml/min

CaO2= 20 ml O2/100 ml blood

CvO2= 15 ml O2/100 ml blood

VO2=Q(CaO2-CvO2

)

Q = 250 ml O2/min = 250 ml O2 * 100 ml blood

(20-15) ml O2/100 ml blood min 5 ml O2

Q = 5000 ml blood /min

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Influences on Pulmonary Vascular Resistance

Pulmonary vessels have:

-Little vascular smooth muscle.

-Low intravascular pressure.

-High distensibility and compressibility.

Vessel diameter influenced by extravascular forces:

-Gravity

-Body position

-Lung volume

-Alveolar pressures/intrapleural pressures

-Intravascular pressures

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•Transmural pressure = Pressure Inside – Pressure Outside.

–Increased transmural pressure-increases vessel diameter.

–Decreased transmural pressure-decreased vessel diameter (increase in PVR).

–Negative transmural pressure-vessel collapse.

•Different effects of lung volume on alveolar and extra alveolar vessels.

PiP outside

Influences of Pulmonary Vascular Resistance

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Illustration of alveolar and extra-alveolar pulmonary vessels during an inspiration

The alveolar vessels(pulmonary capillaries) are exposed to the expanding alveoli andelongated. The extra-alveolar vessels, here shown exposed to the intrapleural pressure, expand as the intrapleural pressure becomes more negative and as radial traction increases during the inspiration.

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Schematic representation of the effects of changes in vital capacity on total pulmonary vascular resistance and the

contributions to the total afforded by alveolar and extra alveolar vessels.

During inflation from residual

volume (RV) to total lung

capacity (TLC), resistance to

blood flow through alveolar

vessels increases, whereas

resistance through extra

alveolar vessels decreases.

Thus, changes in total

pulmonary vascular resistance

form a U-shaped curve during

lung inflation,

PVR is Lowest at FRC.

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Schematic representation of the effects of changes in Lung volume on total pulmonary

vascular resistance

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The effect of cardiac output pulmonary blood pressure and blood flow on pulmonary vascular

resistance

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Recruitment and Distention in Response to Increased Pulmonary Artery Pressure and blood flow

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Recruitment and Distention in Response to Increased Pulmonary Artery Pressure and blood flow

vascular resistance decreases in response to increase blood pressure The upper figure shows a group of pulmonary capillaries, some of which are perfused. At left, the previously unperfumedcapillaries are recruited (opened) by the increased perfusion pressure. At right, the increased perfusion pressure has distended those vessels already open.

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Control of Pulmonary Vascular Resistance

• Summary of passive Influences on PVR:

Lung Volume (above

FRC)Increase

Lengthening and

Compression

Lung Volume (below

FRC)Increase

Compression of

Extraalveolar Vessels

Flow, Pressure DecreaseRecruitment and

Distension

GravityDecrease in Dependent

Regions

Recruitment and

Distension

Interstitial Pressure Increase Compression

Positive Pressure

VentilationIncrease

Compression and

Derecruitment

Influence Effect on PVR Mechanism

T. Sisson4/3/2021 26

Control of Pulmonary Vascular Resistance

** Sympathetic Innervation

-Adrenergic agonists

Thromboxane/PGE2

Endothelin

Angiotensin

Histamine

adenosine,

Ach

prostacyclin (PG I2),

Alveolar hypercapnia

Low pH of mixed venous blood

**Alveolar Hypoxia

Increase

Parasympathetic Innervation

Acetylcholine

-Adrenergic Agents

PGE1

Prostacycline

Nitric oxide increases the synthesis of cyclic GMP that subsequently inhibits

calcium channels and promotesvasodilation

Bradykinin

Decrease

• Active Influences on PVR: Effects on extra-alveolar

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O2=100

CO2 =40

O2=100

CO2 =40

O2= 40

CO2 =45

O2= 150

CO2 =0

A) normal

↓O2

↑CO2

↓O2

↑CO2

B) hypoxic

↓O2

↑CO2

↓O2

↑CO2C) hypoxic vasoconstriction

O2=100

CO2 =40

Hypoxic vasoconstrictionIllustration of the physiologic function of hypoxic

pulmonary vasoconstriction

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Illustration of the physiologic function of hypoxic pulmonary vasoconstriction (HPV).

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hypoxic pulmonary vasoconstriction• Alveolar hypoxia constricts small pulmonary arteries.

• Probably a direct effect of the low PO2 on vascular smooth muscle

• When PAO2 < 73 mm Hg.

• Increase in PVR as a result of low alveolar O2 concentrations.

• Automatic distribution of blood to areas of increased ventilation

• Important for distribution of blood flow to the lung regions according to their alveolar PO2.

• Directs blood flow away from poorly ventilated areas of the diseased lung in the adult

• Functions to reduce the mismatching of ventilation and perfusion

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Hypoxic Pulmonary Vasoconstriction

Regional hypoxia (e.g. bronchial obstruction) → divert blood away from a poorly ventilated region

Generalized hypoxia (e.g. in high altitude or chronic hypoxia as in asthma) cause vasoconstriction in both lungs can lead to increased pulmonary artery pressure (pulmonary hypertension and right ventricle hypertrophy

Generalized hypoxia plays an important non-pathophysiological before birth Its release is critical at birth in the transition from placental to air breathing.

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Mechanism Hypoxic Pulmonary Vasoconstriction

• Mechanism is not completely understood:• Response occurs locally and does not require

innervation.• Mediators have not been identified.

• Some studies suggest that hypoxia may directly induce vasoconstriction by inhibition of oxygen-sensitive potassium ion channels in pulmonary vascular smooth muscle cell membranes.

• With low partial pressures of oxygen, these channels are blocked, leading to depolarization of the cell membrane and activation of calcium channels, causing influx of calcium ions.

• The rise of calcium concentration then causes constriction of small arteries and arterioles

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Starling forces

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Dynamics of capillary fluid exchange: Pulmonary circulation

• The pulmonary capillary hydrostatic pressure is low chance of capillary filtration Thus low filtration

• The interstitial fluid hydrostatic pressure in the lung is more negative (-8 mmHg) than that in the peripheral subcutaneous tissue (-5 mmHg) enhances absorb fluid from the alveoli.

• The pulmonary capillaries are relatively leaky to protein molecules , therefore , greater extravascular colloid osmotic pressure.

• In the pulmonary circulation, two additional forces play arole in fluid transfer surface tension (pulls inwardly) and alveolar pressure (tends to raise interstitial pressure .

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Pulmonary Capillary Dynamics

• Outward Forces

• Pulmonary capillary pressure 7 mmHg

• Interstitial osmotic pressure 14 mmHg

• Negative interstitial pressure 8 mmHg

• Total 29 mmHg

• Inward Forces

• Plasma osmotic pressure 28 mmHg

• Net filtration pressure 1 mmHg

• Negative interstitial pressure keeps alveoli dry

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Pulmonary Capillary Dynamics

Forces Outward

Pcap + πint – Pint

7 + 14 + 8= 29

Forces Inward

28

Net movement

+1 outward

Outward fluid movement is

transferred to

lymphatics….similar to

systemic circulation.

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Pulmonary Edema

• Causes of pulmonary edema• left heart failure

• damage to pulmonary membrane

• Safety factor• negative interstitial pressure

• lymphatic pumping

• decreased interstitial osmotic pressure

• Safety factors in chronic conditions : expansion of lymphatics

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Cardiogenic Increase in pulmonary venous and capillary pressure (left sided heart failure, mitral valve stenosis)

None cardiogenic • Increased capillary membrane permeability due to damage

capillary membrane to associated with infections • pneumonia • noxious gases (chlorine, sulfur dioxide).

• Large decrease in intrapleural pressure (inspiring heavily against a closed airway, i.e. severe laryngeal spasm. Negative pleural pressure is transmitted to interstitial and alveolar spaces, favoring fluid movement out of pulmonary capillaries

• Increased surface tension as in acute respiratory distress syndrome (ARDS),

• Living at high elevations (part of mountain sickness or high-altitude pulmonary edema) especially when exercising in the first few days

Pulmonary Edema - fluid accumulation in pulmonary interstitial space Causes of pulmonary edema

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Safety Factor against edema in Chronic Conditions.

• Safety Factor in Chronic Conditions. When the pulmonary

• capillary pressure remains elevated chronically (for at least 2 weeks), the lungs become even more resistant to pulmonary edema because the lymph vessels expand greatly, increasing their capability of carrying fluid away from the interstitial spaces perhaps as much as 10-fold.

• Therefore, in patients with chronic mitral stenosis, pulmonary capillary pressures of 40 to 45 mm Hg have been measured without the development of lethal pulmonary edema

• Pulmonary edema safety factor: protection against edema until pulmonary capillary pressure equals capillary osmotic pressure.

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Heart Failure and Pulmonary Edema

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Pulmonary edema safety factor: protection against edema until pulmonary capillary pressure equals capillary osmotic pressure.

Fluid in Pleural Cavity and lymphatics

•A thin layer of mucoid fluid lies between parietal

and visceral pleurae to reduce friction between

lung/pleural/chest wall during ventilation.

Because net Starling Force is +1, fluid slowly,

but continuously, filters out of pulmonary

capillaries.

•Lymphatic system helps to maintain a negative

pressure of pleural fluid/space and keeps lungs

from collapsing

•Pleural Effusion-collection of fluid in pleural

space. Caused by lymphatic obstruction (tumor),

heart failure, reduced plasma osmotic pressure,

infection/inflammation of capillary membranes

causing increased permeability. fluid

production>drainage•Pulmonary lymphatics drain into the right lymphatic

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CLINICAL CORRELATION

• A 60-year-old man who had a left ventricular myocardial infarction 3 months ago returns to the cardiologist because of dyspnea on exertion but not at rest, a cough productive of frothy fluid after exercise, and orthopnea (easier breathing in the upright than recumbent position).

• At rest, his heart rate is 105/min, blood pressure is 120/90 mm Hg, and his respiratory rate is increased at 20/min. His chest radiograph shows evidence of edema in gravity-dependent lung regions.

• The patient does not have dyspnea (the feeling of difficult breathing or “shortness of breath”) at rest and his blood pressure is within the normal range. His heart rate at rest is slightly above the normal range (50–100/min; tachycardia) and his respiratory rate is high (normally 12–15/min; tachypnea) He does have orthopnea.

CLINICAL CORRELATION

• He had a left ventricular myocardial infarction 3 months ago and the damaged heart muscle has been replaced with scar tissue that cannot contract. Although his left ventricle can generate a sufficient stroke volume at rest, it cannot match the increased right ventricular output during exercise, leading to increased left atrial pressure.

• Because there are no valves between the left atrium and the pulmonary veins and capillaries, pulmonary capillary hydrostatic pressure increases. Filtration of fluid from the capillaries into the pulmonary interstitiumincreases sufficiently to exceed the ability of the pulmonary lymphatic drainage to remove it, resulting in interstitial edema and then alveolar edema.

CLINICAL CORRELATION

• The dyspnea results from several factors. Pulmonary vascular congestion (excess blood in the pulmonary blood vessels) decreases the compliance of the lungs. Interstitial and alveolar edema increases the alveolar– capillary barrier for gas diffusion. This is particularly a problem for oxygen diffusion, as will be discussed in the

• next chapter. Stretch receptors in the pulmonary circulation respond to pulmonary vascular congestion and the

• arterial chemoreceptors respond to low arterial Po2, both contributing to the sensation of dyspnea, as will be discussed in Chapter 38. He breathes more easily in the

• upright position because the edema fluid collects in lower

• regions of the lungs, allowing better gas exchange in upper

• parts of the lungs.