Pulmonary Circulation

•The pulmonary circulation originates from the right ventricle. The main pulmonary arteries branch into lobar arteries and enter the lungs with the lobar bronchi.

 

  •The arteries branch in tandem with the airways and additionally feature right-angle bifurcations in order to reach peribronchiolar alveoli.

  •The amount of blood ejected by heart into pulmonary circulation is same as the amount ejected into systemic circulation.

 

   •Pulmonary vascular bed handles cardiac output in such a way that pressure is not high for the same volume.

   •Systemic circulation is a high pressure circulation due to greater resistance offered by the blood vessels ( mainly arterioles ) of the systemic vascular bed.

  •The pulmonary circulation on the other hand is a low pressure circulation due to less resistance offered by the pulmonary vessels.

  •The total resistance in pulmonary circulation is about one tenth of systemic circulation.

FUNCTIONAL ORGANISATION

   •Branch of pulmonary arteries and airway branch run parallel to each other.

 

  •Pulmonary capillaries are large in diameter and have multiple anastomoses.

 

  •Each alveolus is surrounded by a capillary basket.

  •Pulmonary artery branch divides to form arterioles making an extensive capillary lattice around a single alveolus.

 

  •Drains into pulmonary veins.

 

  •Pulmonary vessels are having blood which is about 40% of total weight of lungs.

FUNCTIONS OF PULMONARY CIRCULATION 

•Gas exchange – brings venous blood from various parts of body in contact with alveoli for exchange of gases.

 

•Filter – filter thrombi and emboli that originate from venous compartment and right side of the heart.

•Endothelial cells of pulmonary vessels release fibrinolytic agents that lyse blood clots(thrombi) and thus prevent the entry of these thrombi and emboli into coronary, cerebral and other important vessels.

 

•Metabolic functions-  vasoactive hormones are metabolized.

•Angiotensin I is converted to Angiotensin II in the lungs by ANGIOTENSIN CONVERTING ENZYME (ACE).

 

•Serves as blood reservoir - 500 ml of circulating blood is present in pulmonary circulation.

SPECIAL FEATURES OF PULMONARY CIRCULATION 

    •Pulmonary circulation is a low pressure and low resistance system.Pulmonary artery has thin walls and more compliant.

 

   •Due to their high compliance pulmonary vessels can accommodate a relatively large amount of blood.

  •Pulmonary arterioles are thin walled and contain less smooth muscle. Hence the ability to constrict is less and are highly compliant.

 

  •Capillaries form lattice in the alveolar wall and they collapse if local alveolar pressure exceeds capillary pressure.

 

  •Change in pulmonary venous and left atrial pressures profoundly affects gas exchange.

Wedge pressure reflects left atrial pressure

 

PULMONARY VASCULAR RESISTANCE (PVR)– 

Its very low, 1/10th of systemic vascular resistance.

•Reasons- 

A) Pulmonary resistance vessels (arterioles) are thin, short and wide with high compliance.

B) Resting vasoconstrictor tone is very low and arterioles are mostly dilated.

PVR falls with increased pulmonary arterial pressure and increased cardiac output 

•Mechanisms  -

1.Capillary recruitment – when blood flow increases , the collapsed vessels in lungs are opened. This decreases the overall PVR.

 

2. Capillary distension in response to increased pressure. This occurs due to thin and highly compliant pulmonary capillaries.

PHYSIOLOGICAL SIGNIFICANCE OF LOW PVR

   •When the flow rate is high, decreased PVR decreases velocity. This gives more time for capillary blood to take up O2 and remove CO2.

 

  •Capillary distension decreases PVR, increases capillary surface area. This facilitates diffusion of gases along the alveolar capillary membrane.

 

  •The decrease in PVR decreases the load on Right ventricle and decreases the capillary pressure that prevents pulmonary edema.

PULMONARY BLOOD FLOW 

•10% of circulating blood volume – 500 mL.

 

     •In pulmonary arteries- 150 mL

     •In pulmonary veins – 270 mL

     •In pulmonary capillaries – 80mL

FACTORS AFFECTING PULMONARY BLOOD FLOW 

•Pulmonary vascular resistance (PVR)

 •Gravity

 •Alveolar pressure

 •Arterial to venous pressure gradient

PULMONARY VASCULAR RESISTANCE 

PVR is affected by lung volumes, hormones and oxygen tension.

1.Lung volumes - 

pulmonary vessels are of two types-

 

Alveolar vessels (arterioles, capillaries , venules) subjected to alveolar pressure and

Extra-alveolar vessels( pulmonary arteries and veins) subjected to pleural pressure.

•High lung volumes –pleural pressure is more negative. Alveolar vessels are compressed and pulmonary vascular resistance is increased.

 

•Low lung volumes – pleural pressure is positive. It increases PVR. PVR is lowest at functional residual capacity and increases at both higher and lower lung volumes.

 

2.Hormones – 

Vasoconstrictors increase PVR. Vasodilators decrease PVR

 

3. Oxygen tension – 

low O2 tension decreases PVR by causing vasoconstriction.

4. Effects of gravity

•Upright posture pulmonary blood flow increases from apex to base of the lungs.

 

•Physiologically , lung is divided into three zones with perfusion changes.

•Alveolar pressure – depends on lung volumes and changes pulmonary blood flow

 

•Arterio venous pressure gradient – affected by alveolar pressure and determines rate of blood flow.

REGULATION OF PULMONARY BLOOD FLOW

•Regulated by active and passive factors.

 

•Active factors are neural , hormonal and chemical.

Neural regulation

•Richly innervated by sympathetic nerves.

•Resting sympathetic tone of pulmonary circulation is  almost absent.

•Unaffected by ANS in normal conditions.

Hormonal regulation

Vasoconstrictors decreases pulmonary blood flow , some of them include

   •Serotonin

   •Norepinephrine

   •Endothelin

   •Angiotensin

   •Thromboxane A2

   •Leukotrienes

 

Vasodilators increases pulmonary blood flow, some of them include

•Adenosine

•Acetylcholine

•Prostacyclin

•Bradykinin

•Nitric oxide

•Increase pulmonary blood flow

CHEMICAL REGULATION 

•Hypoxemia or alveolar hypoxia causes vasoconstriction of small pulmonary arteries.

 

•Hypoxia directly causes contraction of pulmonary vascular smooth muscles.

 

•High CO2 and low blood pH – vasoconstriction.

 

•Hypoxia inhibits K+ channels and opens the voltage gated Ca+2 channels .

 

• Influx of Ca+2 causes vasoconstriction.

 

Passive factors

•Cardiac output – higher Cardiac output increases pulmonary circulation

 •Gravity

 •Lung volumes

FILTRATION ACROSS PULMONARY CAPILLARIES

•Starling forces governs filtration of fluid across capillary walls in pulmonary circulation.

 

•Surface tension favors filtration  and alveolar pressure opposes filtration

 

1.Hydrostatic and osmotic pressure gradients- hydrostatic pressure lesser than osmotic pressure favors net absorption of fluid from interstitial space into capillary blood.

2.Alveolar surface tension favors filtration.

 

3.The extensive and well developed in lungs.

 

• The lymphatics in terminal bronchioles drain the excess fluid from peribronchial space.

APPLIED PHYSIOLOGY 

PULMOMARY EDEMA 

•Develops when excess of free fluid accumulates in interstitial spaces and alveoli.

 

•Causes – 

   1. Increased capillary hydrostatic pressure

   2.Increased alveolar surface tension.

   3.Decreased oncotic pressure.

   4. Increased capillary permeability.

Effects of pulmonary edema

•Decreases gas exchange resulting in hypoxemia, hypercapnia.

 

•Obstructs small airways and it increases airway resistance.

 

•Lung compliance decreases due to interstitial swelling and increased alveolar surface tension.

 

•Work of breathing increases due to decreased compliance and airway obstruction.

Physiological basis of treatment of pulmonary edema

•Aim of treatment is to reduce pulmonary capillary hydrostatic pressure.

 

•1. Diuretics – decrease blood volume.

•2. Digitalis – increases left ventricular function.

•3. Vasodilators – relaxation of systemic blood vessels

DROWNING

•Fresh - water drowning : Aspiration of water occurs into the lungs, death doesn’t occur due to pulmonary edema.

 

•Death is due to ventricular fibrillation.

 

•Entry of water into blood causes hypotonicity and hemolysis.

 

•Hemolysis  causes hyperkalemia and hyponatremia.

 

•Ventricular fibrillation occurs due to hyperkalemia and hypoxemia.

Salt water drowning

•Aspirated water is hypertonic due to high sodium and chloride content of sea water.

 

•Hypertonic fluid in alveoli produces pulmonary edema.

 

•Cause of death is asphyxia.