Respiratory Physiology FRCA – Dead Space and Shunt – Flashcards

Volume of gas in conducting airways without any possibility of participating in gas exchange ~1500mls per tidal breath

Volume of alveoli that are ventilated but not perfused

Anatomical dead space + Alveolar dead space

Fowler's method: Patient takes a breath of 100% O2 and then exhales through a nitrogen analyser Phase 1: Anatomical dead space gas = 100% O2 Phase 2: Mixed anatomical and alveolar dead space gas = rising N2 concentration Phase 3: Pure alveolar gas = plateau of N2 concentration Upstroke of phase 2 curve is divided equally in half to give areas A and B. Anatomical dead space = 0 up to and including B

Bohr's Equation: Used to determine the volume of lung that does not excrete CO2 The concentration of CO2 in air is minimal All expired CO2 must come from alveolar ventilation Vd/Vt = (PaCO2 - PeCO2) / PaCO2

Increasing body size Increasing age Bronchodilatation Lung disease e.g. emphysema Jaw thrust

Supine posture Bronchoconstriction e.g. asthma Lung disease e.g. obstructing tumours ET tubes

Increasing age Anaesthetic gases (unknown mechanism) Reduced pulmonary artery pressure (e.g. hypotension) Reduced perfusion to apices of lung IPPV due to exaggerated hydrostatic failure of perfusion and reduced pulmonary blood flow Lung distension e.g ARDS Oxygen resulting in hyperopic vasodilatation

Hypoxic vasoconstriction

Deoxygenated blood enters left side of the heart for anatomical reasons: Thebesian veins Bronchial circulation Right to left shunt

Sum of anatomical shunt and functional shunt

Alveolar perfusion without adequate ventilation resulting in V/Q mismatch E.g. Odema Infection ARDS Atelectasis

Alveolar ventilation = 4.5L/min Pulmonary arterial blood flow = 5L/min Normal V/Q ratio = 0.9

Qs/Qt = (CcO2 - CaO2)/(CcO2 - CvO2)

4%

Shunt does not normally case increased PaCO2 because higher concentrations of carbon dioxide are sensed by central chemoreceptors increasing ventilatory rate. PaCO2 will therefore only increase when the shunt fraction increases beyond 50%.

The alveolar-arterial pO2 difference increases with alveolar pO2 in a non-linear manner governed by the oxygen dissociation curve. At high alveolar pO2, a plateau of alveolar/arterial pO2 difference is reached, but the alveolar pO2 at which the plateau is reached is higher with larger shunts. Due to the nature of the ODC, on the flat upper part, increasing FiO2 will only slightly increase sO2 as Hb is fully saturated In the presence of high pAO2 a huge gradient will be present between the predicted arterial pO2 and the actual. This would otherwise be much smaller.

Bases of lungs

Bases of lungs

Top of the lungs Decreased pACO2 and increased pAO2

Bottom of the lungs Increased pACO2 and decreased pAO2

2/3 of the way up (approx rib number 3)

Not normally seen in healthy lungs: PA > pa > pv Only seen at apex of lungs in haemorrhage or PPV Normally pulmonary arterial pressure is sufficient to pump blood to the top of the lungs, however, in this situation, pa pressure is less than PA pressure compressing blood vessels and preventing flow The lung is ventilated but not perfused Alveolar dead space created

Optimal V/Q matching: pa > PA > pv Arterial pressure exceeds alveolar pressure in systole, however alveolar pressure is still greater than venous pressure creating a "waterfall effect"

Represents the majority of the lungs in health: pa > pv > PA No external resistance to blood flow Flow is determined by the pa-pv pressure difference Capillaries open independent of respiratory cycle increasing perfusion at bases and resulting in a low V/Q

Seen in upright posture/atelectasis: pa > pi > pv > PA Weight of lung tissues causes increased interstitial pressure which compresses extra-alveolar capillaries thus reducing blood flow. The pa-pi pressure difference determines whether there is blood flow. pi affects pa and pv equally so the pa>pv pressure difference remains the same.

Blood flow to posterior regions of lungs will become greater than to the anterior portions of the lungs. The difference between the apex and base of the lung will diminish in the supine patient.

Dependent lung: Increased ventilation compared to top lung (more compressed = greater compliance = better ventilation) Increased perfusion compared to top lung (effect of gravity) V/Q will be lower in comparison to top lung

Due to mediastinal weight increase in relaxed anaesthetised patient, the lungs move down the compliance curve. Dependent lung: Poorly compliant Poor ventilation Increased perfusion initially until hypoxic vasoconstriction occurs V/Q low (lower than upper lung)

Radioactive xenon can be dissolved in normal saline and injected into a peripheral vein. It has a very low solubility so when it reaches the pulmonary capillaries it will quickly move from the blood into the alveolar gas.

High V/Q units e.g. apices there is high PAO2 and low PACO2 but they are less well perfused and therefore contribute less to overall gas exchange. These units are on the upper part of the ODC where small changes have little effect on sO2. In low V/Q units e.g. bases there is a low PAO2 and higher PACO2 and are better perfused so contribute more to overall gas exchange. These units are on the steep upslope of the ODC where small changes have a big effect on the degree of sO2. The net result is often a reduction in pO2. The same does not apply for CO2 as this is a more linear curve so high V/Q units compensate for low V/Q units.

Gives a ratio of physiological dead space volume to tidal volume. VD/VT = (PaCO2 - PECO2)/PaCO2 VD: Physiological dead space VT: Tidal volume PECO2: Expired CO2 concentration PaCO2 = Surrogate for PACO2

30%