Pulmonary circulation Flashcards
The bronchial arteries:
Supply the blood to the tracheobronchial tree as far as the terminal bronchioles
Originate from the thoracic aorta
Have the characteristics of systemic arteries
Bronchial veins return blood into:
The right atrium via the azygos veins
The left atrium via the pulmonary veins
The return of desaturated bronchial blood into the left heart causes venous admixture into the arterialised blood, so contributes to physiologic shunt. It also accounts for the slightly greater cardiac output of the left side of the heart compared to the right side of the heart
In diseased states with increased bronchial artery flow, what happens to arterial oxygen saturation?
Arterial oxygen desaturation occurs, e.g. in longstanding pulmonary hypertension.
Pulmonary vascular resistance definition and equation:
Even though it is a simplification, pulmonary vascular resistance (PVR) is generally expressed in a similar way to Ohm’s law in electrical circuits:
PVR = driving pressure/ cardiac output
Because the compliance of the pulmonary vasculature is high, PVR is only about 1/10 of the systemic vascular resistance (SVR).
The pressure drop between the pulmonary artery and the left atrium is about 10 mmHg and cardiac output is about 5 L/min, so, PVR = 10/5 = 2mmHg/L-1/min
Or if multiple by 80 to convert units = 160 dyn/sec/cm
What happens to the pulmonary vascular resistance during exercise?
During exercise cardiac output increases by 4-7 times.
To keep the pulmonary pressure constant with these large changes of pulmonary blood flow, the PVR decreases as the blood flow increases.
Two mechanisms are known:
1) Recruitment. Previously unperfused pulmonary capillaries are opened, mainly in the upper part of the lung (low capillary pressure)
2) Distension. With higher vascular pressure, widening of the thin-walled pulmonary vessels occurs
These mechanisms control pulmonary artery pressure, protect the right ventricle and prevent development of pulmonary oedema.
What is the effect of lung volume on pulmonary vascular resistance?
The influence of lung volume on pulmonary vascular resistance is complex and not yet fully understood.
Animal experiments have shown that small lung volumes as well as high lung volumes are associated with increased PVR.
Fig 1 illustrates how extra-alveolar vessels are pulled open by the surrounding lung parenchyma in the inflated lung.
At low lung volumes these vessels are narrow because of the smooth muscle tone, which causes increased PVR
At high lung volumes the alveolar capillaries stretch within the thinning alveolar wall which also increases PVR
What affects the distribution of blood flow in the lungs?
The distribution of blood flow within the lung is affected by gravity because of the low pressure and the distensibility of the pulmonary vasculature. Blood flow and pulmonary artery pressure are influenced by hydrostatic pressure differences within the lung.
Describe zone 1 of the lung:
At the top of the lung the intravascular pressures are reduced compared to the main pulmonary artery according to the hydrostatic level. Alveolar pressure exceeds venous and arterial pressure and results in no blood flow, so PA > Pa > Pv
Describe zone 2 of the lung:
In the middle zone, at the same hydrostatic level as the main pulmonary artery, the blood pressure might fall below alveolar pressure only during diastole and result in intermittent blood flow, so that Pa > PA > Pv
Describe zone 3 of the lung:
In the lower part of the lung, arterial pressure is augmented by the hydrostatic pressure and exceeds alveolar pressure during the entire cardiac cycle, which produces continuous blood flow, so Pa > Pv > PA
Describe hypoxic pulmonary vasoconstriction:
Besides the described passive, physical effects on pulmonary vascular resistance and blood flow, there are active control mechanisms.
The most important effect on blood flow distribution is hypoxic pulmonary vasoconstriction. With falling oxygen-concentration in the alveoli, vasoconstriction of the adjacent blood vessels occurs. Diverting blood flow to better aerated areas of the lung optimizes the ventilation-perfusion ratio. The mechanism is still unclear but it is present in isolated pulmonary vessels and smooth muscle cells. Chronic hypoxia causes proliferation of vascular smooth muscle cells and can lead to pulmonary hypertension.
Hypoxic pulmonary vasoconstriction is opposite to the effect of hypoxia on systemic vessels.
Maximal hypoxic vasoconstriction occurs during the fetal period to limit pulmonal blood flow to less than 15% of cardiac output