Pressures shown in the above figure are in mmHg.

The Pulmonary versus Systemic Circulation

The atria of the left and right side of the heart are thin-walled, low pressure chambers.  Note, the pulmonary arterial pressure is much lower than in the aorta (systemic arterial pressure).  The pulmonary circulation is, overall, a much lower pressure system than is the systemic circulation.  The systemic circulation has to work against gravity, especially when a person is standing, and the system needs more pressure to do this!  Remember that the pulmonary circulation is only as tall as the lungs!  The systemic circulation must also redirect blood according to the needs of the body using smooth muscle; in order to accomplish this task, the systemic circulation must be capable of generating significant resistance with smooth muscle.  Remember, too, that systemic resistance generated primarily by arterioles is necessary to generate the high pressures required to drive blood through the high volume, long distance systemic circulation!  The pulmonary circulation, on the other hand, only needs to get blood from the top to the bottom of the lungs which are perfused by constant low pressure; there is very little redirection of blood within the pulmonary circulation, other than from locally hypoxic pockets in the lung!  Pulmonary arterioles have much less smooth muscle than systemic arterioles and, thus, pulmonary arterioles generate much less resistance than systemic arterioles.

Similarly, there is very little smooth muscle in the pulmonary veins, which run freely in the lung parenchyma with no firm structures around them.  If the lungs are expanded, the lungs pull on the walls of the large vessels (veins) to dilate them (ie. lung expansion causes tension of the parenchyma and outward expansion of the vessel walls = vasodilation, and the pressure within the vessel drops).  Recall that as the chest expands during inspiration, central venous return is also increased, leading to an increase in heart rate during the inspiratory phase of respiration.

Transmural pressure = the pressure difference between alveolar pressure and pressure within the capillaries (across the capillary wall).  Transmural pressure affects pulmonary capillary pressure.  Eg. if pressure increases in the alveolar spaces (eg. sneezing) that pressure can collapse the capillaries (no blood flow due to increased alveolar pressure).

Wedge Pressure = pulmonary arterial pressure.

The lungs respond to drugs:

For example, norepinephrine causes vasoconstriction in the pulmonary circulation while at the same time increasing respiration rate and causing bronchodilation.  The net effect of sympathetic activity on blood pressure, which is to increase blood pressure, overwhelms the effect of vasoconstriction in the low resistance vessels of the pulmonary circuit.  Thus, the net effect of sympathetic activity is to increase ventilation and perfusion of the lungs.  Isoproterenol blocks norepinephrine receptors.

Figure: Pulmonary Vascular Resistance: As lung volume increases, vascular resistance initially drops and then rises.

When lung volume is low (or collapsed), pressure on the vessels increases vascular resistance.  At moderate lung volumes, vascular resistance is low.  When lung volume is increased above the normal operating range, vascular resistance increases to extremes as stretching of the lungs causes stretching of capillaries to the point that blood cannot get through the capillaries.  This means that pulmonary vascular resistance is lowest in the normal operating range... that is when there is about 2.5 L to 3.0 L of air in the lungs (ie. the actual volume of air in the lungs between end expiratory and end inspiratory volume).

The critical capillary opening pressure of a pulmonary capillary is considerable less than that of a systemic capillary.  This is because the metarterioles and precapillary sphincters in the pulmonary circuit have less smooth muscle, and are therefore less resistant to blood flow, than their counterparts in the systemic circulation!  Notice that recruitment (opening) of pulmonary capillaries begins in the 3-5 mmHg pressure range while recruitment of systemic capillaries begins in the 8 mmHg range.

Calculation of Vascular Resistance: You may wish to return to the cardiovascular physiology section to review the calculations of pulmonary and systemic vascular resistance.  If not, recall that mean arterial pressure in the systemic circulation is approximately 7 times greater than in the pulmonary circuit and that systemic vascular resistance is approximately 10 times greater than pulmonary vascular resistance!

Figure: Pulmonary Vascular Pressure versus Resistance

Local Hypoxic Vasoconstriction

Recall that local vasoconstriction occurs in response to lowering of O₂ tension in the alveolar gas.  Essentially, the smooth muscle in the arterioles supplying alveoli with low O₂ constrict.  This is a local myogenic effect in response to hypoxia; this effect occurs even if you cut the autonomic nerves.  Once again, ask yourself, where is the logic of constricting arterioles to areas of low pO₂ in the lung?  Blood perfusing areas of low pO₂ will not be maximally oxygenated.  Constriction of blood vessels in the area of low pO₂ diverts blood away from the alveoli supplied by (for instance) an obstructed bronchiole to prevent a lowering of the pO₂ in the blood returning to the heart.  This can also happen in a generalized manner - eg. in fetal circulation.

Fetal circulation: The lung of the fetus receives only 15% of cardiac output.  Active pulmonary arteriolar vasoconstriction maintains a high resistance to pulmonary circulation.  At baby's first breath, alveolar pO₂ increases and pulmonary vascular resistance dramatically decreases as the pO₂ approaches normal levels and the lung receives 100% of cardiac output rather than 15%.  A text figure depicting fetal circulation may be of some use!  Recall that the foramen ovale allows oxygenated blood returning from the placenta to the right side of the heart via the vena cava to pass directly into the left side of the heart for dispersal to the body.  In addition, the ductus arteriosus allows the majority of blood entering the pulmonary trunk to be transferred to the aorta, in order to bypass the lungs.

Brisket Disease in Cattle = High Altitude Disease = Cor Pulmonale

Cattle have well-developed smooth muscle in the pulmonary circulation and it is highly reactive to altitude.  Brisket disease is also known as cor pulmonale (right heart failure due to pulmonary vascular hypertension).  Take a cow to 7000 feet above sea level or higher (ie. where there will be a decrease in ambient O₂) and there will be generalized vasoconstriction of the vessels but mainly the arteries and arterioles to the lung, giving increased pulmonary vascular resistance.  Normal, mean arterial pressure in the pulmonary circuit is approximately 15 mmHg.  In a cow with brisket disease, the pulmonary arterial pressure may approach 100 mmHg (yes, that's right, we're talking about pressure in the PULMONARY circuit!).  The right heart must work very hard to pump against such high resistance and pressure, which results in right heart failure causing systemic edema (in cattle, leading to edema in the brisket and abdominal region - ie. in regions of the systemic circulation close to the ground).  Fortunately, the condition is reversible if you get the cow down to a lower elevation soon enough to allow the vascular resistance to decrease.  Recall that in the cardiovascular section, we noted that cor pulmonale also occurs in humans (right heart failure associated with increased pulmonary vascular resistance, as might be seen in emphysema or COPD).