Pulmonary Circulation and Fluid Balance

functions of pulmonary circulation

reoxygenate the blood and eliminate CO2

aid in fluid balance in the lung

distribute metabolic products to and from the lung

pulmonary circulation direction of travel

1. deoxygenated blood from right atrium→right ventricle→pulmonary trunk, which branches into right and left main pulmonary arteries→arterioles→capillaries→gas exchange

2. oxygenated blood from exiting capillaries→pulmonary venules→pulmonary veins→left atrium

how much blood is present in alveolar-capillary network at any time?

about 75 mL, but this can increase to 150-200mL during exercise, due to recruitment of new capillaries

which structures closely follow branching airways?

pulmonary arteries, arterioles, capillaries

which structures are more distant to branching airways?

venules and veins

bronchial circulation

arises from aorta and provides nourishment to the lung parenchyma

almost the entire cardiac output is

directed into the pulmonary circulation

in other words, at any one time, there is as much blood flowing through the lungs as all the other organs and tissues combined

what is needed for gas exchange to work well?

needs a very thin membrane separating blood and air, so pressure in pulmonary circulation needs to be much lower than in systemic

what would happen if the pressure in pulmonary circulation was higher than in systemic?

pressure would force fluid to leak from pulmonary capillaries into the alveoli

how much blood flows through right and left ventricles at rest?

5L

left ventricle

thick, muscular wall→systemic circulation, high resistance, high pressure system

if cardiac output increases (e.g. exercise) pressure increases so strong muscular wall needed to generate high pressures

right ventricle

much thinner wall, about 1/3rd thickness of other→pulmonary circulation, low resistance, low pressure system

if cardiac output increases, pulmonary arterial pressure does not increase much

pulmonary circulation

high flow, high compliance, low pressure system

arteries are thin walled, little smooth muscle

easily distensible, more compliant than systemic vessels

what is the mean pressure in main pulmonary artery?

about 14mmHg

what are mean systolic and diastolic pressures?

24 and 9 mmHg

what is the mean pressure in aorta?

90mmHg

driving pressure in systemic circulation much ______ than in pulmonary circulation

higher

pulmonary capillaries

almost entirely surrounded by gas

very thin layer of epithelial cells lining the alveoli, but these provide little support

liable to collapse or distend, depending upon the pressures within them and surrounding them

pressure within is close to alveolar pressure

if alveolar pressure rises, these will collapse

transmural pressure

pressure difference between inside and outside capillaries

alveolar vessels (pulmonary circulation)

exposed to alveolar pressure and are largely the capillaries

caliber is determined by the relationship between alveolar pressure and pressure within them

extra-alveolar vessels

arteries, arterioles, veins, and venules running throughout the surrounding lung

caliber greatly affected by lung volume as this determines the “pull” (radial traction) on the tissue around them

as lung expands, vessels are pulled open—effective pressure around them is low

pulmonary vascular resistance

= (input pressure - output pressure)/blood flow

= (PPulm artery - Pleft atrium)/Qt

given that blood flows are equal, this is only 1/10 that of the systemic circulation

the high resistance of the systemic circulation is the result of

very muscular arterioles that allow the regulation of blood flow to the various organs of the body

the pulmonary circulation has no muscular vessels and has as low a resistance as is compatible with

distributing the blood in a thin film over the vast area within the alveolar walls

decreased PVR

can fall even lower if either arterial or venous pressure increase

mechanisms: recruitment or distension (likely both often occur together)

decreased PVR- recruitment

normally, some capillaries are closed or open with no blood flow

as pressure increases, these vessels begin to conduct blood

this is the main mechanism for this as pulmonary arterial pressure starts to rise

decreased PVR- distension

at even higher pressure, widening of individual capillaries occurs

capillaries likely change from near-flattened to more circular

this occurs at high pressures

what happens to PVR when lung volume increases and alveoli fill?

air-filled alveoli will start to compress alveolar capillaries- PVR increases

what happens to PVR when lung volume increases?

the larger extra-alveolar vessels increase in diameter because of radial traction and being pulled open more—PVR decreases

what happens to PVR during expiration when deflated alveoli apply least resistance to alveolar capillaries?

decreases

what happens to PVR during expiration as volumes decrease?

smooth muscles in extra-alveolar capillaries resists distension and tends to collapse down—PVR increases

distribution of blood flow in upright human lung

can be measured using modified version of radioactive Xe method

Xe is dissolved in saline and injected into peripheral vein

when it moves into pulmonary capillaries it moves into alveolar gas space because of low solubility

distribution of radioactivity can be measured by counters over the chest

decreases from bottom to top

uneven distribution of pulmonary blood flow

low pressure/low resistance system, so influenced by gravity more than systemic circulation: less blood flow at apex, more at base

upright subject: every 1cm above/below the heart, there is a corresponding 0.74 mmHg change in hydrostatic pressure

lung divided into

3 functional zones defined by relationship between arterial, venous, and alveolar pressures

lung zone 1

capillaries collapse because of higher PA

normally does not exist, but can occur with positive pressure ventilation or decrease in Pa (blood loss)

lung zone 2

PA > Pv, so partial collapse

lung zone 3

PA < Pa and Pv: capillaries fully distended, low resistance, high blood flow

major factor regulating pulmonary blood flow

PAO2

when this falls, smooth muscle in the walls of the small arterioles constricts

hypoxic vasoconstriction

occurs in small arterial vessels when PAO2 falls

occurs in isolated lung, so not dependent on CNS

excised segments of pulmonary artery demonstrate effect

non-linear curve, marked effect when PAO2 is less than 70mmHg—marked vasoconstriction

adaptive mechanism to reduce blood flow to poorly ventilated area where blood flow would be wasted

blood flow redirected towards well-ventilated areas to increase efficiency of gas exchange

mechanism of oxygen-sensing unclear (modulation of K+ channels? ROS production? cellular energy state?)

pulmonary blood flow is primarily regulated by

passive mechanisms dependent on gravity, but active mechanisms do occur

pulmonary vasoconstrictors and vasodilators

can influence vessel caliber, but effects are usually local and short-lived

e.g. nitric oxide- derived from endothelium and relaxes blood vessels

• NO→guanylate cyclase→cGMP→relaxation

• inhaled NO decreases hypoxic pulmonary vasoconstriction

potent vasoconstrictor examples

endothelin-1 (ET-1) and thromboxane A2 (TXA2)

from vascular endothelial cells

fluid balance in lung

essential to keep alveoli free of fluid

water movement is governed by two forces

hydrostatic pressure and oncotic pressure

what forces water out?

hydrostatic pressure results from the pumping of the heart and effect of gravity on the column of blood in the vessel

what tends to pull water in?

oncotic pressure results from osmotic pressure exerted by plasma proteins, mainly albumin

what does balance between hydrostatic and oncotic pressure result in?

small net movement of fluid out of the vessels and into the interstitial space

how is fluid removed from the lung interstitium?

draining into lymphatics, then entering the circulation via the vena cava

approx 30mL fluid/hr returned to the circulation via this route

starling’s law

net fluid out= K[(Pc-Pi) - σ(πc - πi)]

Pc - Pi= hydrostatic pressure

πc - πi= oncotic pressure (colloid osmotic pressure)

σ= reflection coefficient

K= filtration coefficient, constant

reflection coefficient

σ

reflects how effective the capillary wall is in preventing the passage of proteins

what is normal oncotic pressure in capillaries?

approx 28 mmHg

pulmonary edema

abnormal accumulation of fluid in the extravascular spaces and tissues of the lung

normal flow in lung (compared to pulmonary edema)

normally a small flow from lung into the lymph

any factor that increases fluid filtration out of capillaries or that impedes pulmonary lymphatic function causing the pulmonary interstitial pressure to rise will result in excessive fluid movement

interstitial edema

first stage, here there is increased flow with engorgement of perivascular and peribronchial interstitial spaces called cuffing

widened lymphatics

little effect on pulmonary function at this stage

alveolar edema

second stage, fluid moves into the alveoli, which fill up, impeding gas exchange

ventilation is prevented, shunting of blood away from edematous areas occurs

hypoxemia inevitable

edema fluid may move into airway and be coughed up as frothy sputum

pulmonary edema causes

increased capillary hydrostatic pressure

increased capillary permeability

reduced lymph drainage

decreased colloidal osmotic pressure

uncertain

pulmonary edema causes- increased capillary hydrostatic pressure

most common cause, almost always results from cardiac disease: acute myocardial infarction, mitral valve disease

left atrial pressure rises, causing increase in pulmonary venous and capillary pressures

rate of rise in pressure important: if slow, caliber of lymphatics may accommodate for many years; if rapid (e.g. infarction) then onset rapid. also, non-cardiac, e.g. excessive IV fluids

pulmonary edema causes- increased capillary permeability

inhaled toxins (chlorine, sulphur dioxide) or ingested toxins (endotoxin)

radiation treatment, ARDS

edema fluid has high protein concentration and contains many blood cells

pulmonary edema causes- reduced lymph drainage

can be an exaggerating factor, if another cause is present

increased central venous pressure in ARDS, heart failure

also obstruction of lymphatics as in cancer

pulmonary edema causes- decreased colloidal osmotic pressure

rarely factor alone, be can exaggerate if another cause is present

over-transfusion with plasma

hypoproteinimia of nephotic syndrome

pulmonary edema causes- uncertain

high altitude pulmonary edema, neurogenic seen after CNS damage, e.g. head trauma, heroin overdose

metabolic function of lung

endothelial cells lining pulmonary circulation are exposed to entire cardiac output, so they provide a good place to modify biologically active substances

angiotensin I

only example of biological activation in lungs

converted to angiotensin II by ACE