Pulmonary shunt

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A pulmonary shunt is the passage of deoxygenated blood from the right side of the heart to the left without participation in gas exchange in the pulmonary capillaries. It is a pathological condition that results when the alveoli of parts of the lungs are perfused with blood as normal, but ventilation (the supply of air) fails to supply the perfused region. In other words, the ventilation/perfusion ratio (the ratio of air reaching the alveoli to blood perfusing them) of those areas is zero. [1] [ clarification needed ]

Contents

A pulmonary shunt often occurs when the alveoli fill with fluid, causing parts of the lung to be unventilated although they are still perfused. [2]

Intrapulmonary shunting is the main cause of hypoxemia (inadequate blood oxygen) in pulmonary edema and conditions such as pneumonia in which the lungs become consolidated. [2] The shunt fraction is the percentage of cardiac output that is not completely oxygenated.[ clarification needed ]

In pathological conditions such as pulmonary contusion, the shunt fraction is significantly greater[ clarification needed ] and even breathing 100% oxygen does not fully oxygenate the blood. [1]

Intrapulmonary shunt is specifically shunting where some of the blood flow through the lungs is not properly oxygenated. Other shunts may occur where venous and arterial blood mix but completely bypass the lungs (extrapulmonary shunt). [3]

Anatomical shunt

If every alveolus was perfectly ventilated and all blood from the right ventricle were to pass through fully functional pulmonary capillaries, and there was unimpeded diffusion across the alveolar and capillary membrane, there would be a theoretical maximum blood gas exchange, and the alveolar PO2 and arterial PO2 would be the same. The formula for shunt describes the deviation from this ideal. [4]

A normal lung is imperfectly ventilated and perfused, and a small degree of intrapulmonary shunting is normal. Anatomical shunting occurs when blood supply to the lungs via the pulmonary arteries is returned via the pulmonary veins without passing through the pulmonary capillaries, thereby bypassing alveolar gas exchange. Capillary shunting is blood that passes through capillaries of unventilated alveoli [4] or deoxygenated blood flowing directly from pulmonary arterioles to nearby pulmonary veins through anastomoses, bypassing the alveolar capillaries. [5] In addition, some of the smallest cardiac veins drain directly into the left ventricle of the human heart. This drainage of deoxygenated blood straight into the systemic circulation is why the arterial PO2 is normally slightly lower than the alveolar PO2, known as the alveolar–arterial gradient, a useful clinical sign in determining the cause of hypoxemia. [6]

The alveolar-arterial (A-a) gradient measures the difference between oxygen concentrations in the alveoli and the arterial system. This is an important clinical method of narrowing the differential diagnosis for hypoxemia. [7] The gradient calculation is as follows:

Where PAO2 represents the alveolar oxygen pressure and PaO2 represents the arterial oxygen pressure.

The alveolar oxygen pressure is not easily measured directly and is therefor estimated using the alveolar gas equation. [7]

Where PAO2 represents alveolar oxygen pressure, Patm represents atmospheric pressure (at sea level 760 mm Hg), PH2O represents partial pressure of water (approximately 45 mm Hg), FiO2 represents the fraction of inspired oxygen (for room air, 0.21), PaCO2 represents the partial pressure of carbon dioxide in the alveoli (in normal physiological conditions around 40 to 45 mmHg), and where RQ represents the respiratory quotient, which is generally assumed to be 0.8. The arterial oxygen pressure (PaO2) and arterial carbon dioxide pressure (PaCO2) can be directly measured using an arterial blood gas test (ABG) or estimated via the venous blood gas test (VBG), and since carbon dioxide rapidly diffuses in and out of the lungs, arterial carbon dioxide pressure and alveolar carbon dioxide pressure are effectively equal. [8]

The A-a gradient should theoretically be zero in a healthy person, but almost never is. A normal person will have an A-a gradient estimated by: Normal Gradient = (Age in years/4) + 4. If the A-a gradient is significantly higher than the result of this equation, the person likely has a disorder of the alveoli, causing oxygen to be unable to diffuse into the blood. If the person has a normal A-a gradient but still has hypoxemia, then there is probably a cause unrelated to the alveoli, such as hypoventilation, obstructive lung disease, or shunting.

Pathophysiology

An irregular distribution of ventilation can occur in asthma, bronchiolitis, atelectasis, and other conditions, [9] which have the effect of reducing the amount of oxygen present in some alveoli relative to others. If the normal perfusion of these alveoli were to persist, the blood in those regions would be less oxygenated than blood in the normally ventilated alveioli, and the combined blood oxygenation after mixing would be lower than normal. A pulmonary shunt occurs when this imbalance is undercompensated. The normal response of pulmonary blood vessels sensing a low oxygen saturation is to constrict, slowing the flow through the underoxygenated areas, thereby giving it time to increase saturation and increasing relative flow through those areas with more effective oxygenation, resulting in a higher combined oxygenation. [10] [11] If there is no oxygen available in the alveoli, the blood cannot be oxygenated and any blood flowing through such areas of the lung is considered an intrapulmonary shunt.

While in a pulmonary shunt, the ventilation/perfusion ratio is zero, lung units with a V/Q (where V = ventilation, and Q = perfusion) ratio of less than 0.005 are indistinguishable from shunt from a gas exchange perspective.[ citation needed ]

When alveoli fill with fluid, they are unable to participate in gas exchange with blood, causing local or regional hypoxia, thus triggering vasoconstriction. This vasoconstriction is triggered by a smooth muscle reflex, as a consequence of the low oxygen concentration itself. Blood is then redirected away from this area, which poorly matches ventilation and perfusion, to areas which are being ventilated.

A decrease in perfusion relative to ventilation (as occurs in pulmonary embolism, for example) is an example of increased dead space. [12] Dead space is a space where gas exchange does not take place, such as the trachea; it is ventilation without perfusion. A pathological example of dead zone would be a capillary blocked by an embolus. Although ventilation at that area is unaffected, blood will not be able to flow through that capillary; therefore, at that zone there will be no gas exchange. Dead zones may be corrected by supplying 100% inspired oxygen; when a capillary is blocked, the blood inside of it does not flow and upstream blood distributes between other capillaries that are exchanging gases effectively. The resulting blood that flows through them will not be 100% saturated, as it contains some unoxygenated blood (the one that came from the blocked capillary). For this reason, blood will actually be able to obtain the extra oxygen supplied to the patient.[ clarification needed ]

Pulmonary shunting causes the blood supply leaving a shunted area of the lung to have lower levels of oxygen and higher levels of carbon dioxide (i.e., the normal gas exchange does not occur).

A pulmonary shunt occurs as a result of blood flowing right-to-left through cardiac openings or in pulmonary arteriovenous malformations.[ clarification needed ] The shunt which means V/Q = 0 for that particular part of the lung field under consideration results in de-oxygenated blood going to the heart from the lungs via the pulmonary veins.

If giving 100% oxygen for five to ten minutes doesn't raise the arterial tension of oxygen more than it does the alveolar pressure of oxygen then the defect in the lung is because of a pulmonary shunt. This is because although the oxygen partial pressure of alveolar gas has been changed by giving pure supplemental oxygen, the arterial gas oxygen concentration will not increase that much because the V/Q mismatch still exists and it will still add some de-oxygenated blood to the arterial system via the shunt. [13]

See also

Related Research Articles

<span class="mw-page-title-main">Hypoxia (medicine)</span> Medical condition of lack of oxygen in the tissues

Hypoxia is a condition in which the body or a region of the body is deprived of adequate oxygen supply at the tissue level. Hypoxia may be classified as either generalized, affecting the whole body, or local, affecting a region of the body. Although hypoxia is often a pathological condition, variations in arterial oxygen concentrations can be part of the normal physiology, for example, during strenuous physical exercise.

<span class="mw-page-title-main">Respiratory system</span> Biological system in animals and plants for gas exchange

The respiratory system is a biological system which consists of specific organs and structures used for gas exchange in animals and plants. The anatomy and physiology that make this happen varies greatly, depending on the size of the organism, the environment in which it lives and its evolutionary history. In land animals, the respiratory surface is internalized as linings of the lungs. Gas exchange in the lungs occurs in millions of small air sacs; in mammals and reptiles, these are called alveoli, and in birds, they are known as atria. These microscopic air sacs have a very rich blood supply, thus bringing the air into close contact with the blood. These air sacs communicate with the external environment via a system of airways, or hollow tubes, of which the largest is the trachea, which branches in the middle of the chest into the two main bronchi. These enter the lungs where they branch into progressively narrower secondary and tertiary bronchi that branch into numerous smaller tubes, the bronchioles. In birds, the bronchioles are termed parabronchi. It is the bronchioles, or parabronchi that generally open into the microscopic alveoli in mammals and atria in birds. Air has to be pumped from the environment into the alveoli or atria by the process of breathing which involves the muscles of respiration.

<span class="mw-page-title-main">Respiratory failure</span> Inadequate gas exchange by the respiratory system

Respiratory failure results from inadequate gas exchange by the respiratory system, meaning that the arterial oxygen, carbon dioxide, or both cannot be kept at normal levels. A drop in the oxygen carried in the blood is known as hypoxemia; a rise in arterial carbon dioxide levels is called hypercapnia. Respiratory failure is classified as either Type 1 or Type 2, based on whether there is a high carbon dioxide level, and can be acute or chronic. In clinical trials, the definition of respiratory failure usually includes increased respiratory rate, abnormal blood gases, and evidence of increased work of breathing. Respiratory failure causes an altered state of consciousness due to ischemia in the brain.

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Dead space is the volume of air that is inhaled that does not take part in the gas exchange, because it either remains in the conducting airways or reaches alveoli that are not perfused or poorly perfused. It means that not all the air in each breath is available for the exchange of oxygen and carbon dioxide. Mammals breathe in and out of their lungs, wasting that part of the inhalation which remains in the conducting airways where no gas exchange can occur.

<span class="mw-page-title-main">Gas exchange</span> Process by which gases diffuse through a biological membrane

Gas exchange is the physical process by which gases move passively by diffusion across a surface. For example, this surface might be the air/water interface of a water body, the surface of a gas bubble in a liquid, a gas-permeable membrane, or a biological membrane that forms the boundary between an organism and its extracellular environment.

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<span class="mw-page-title-main">Generalized hypoxia</span> Medical condition of oxygen deprivation

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<span class="mw-page-title-main">Hypoxemia</span> Abnormally low level of oxygen in the blood

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The factors that determine the values for alveolar pO2 and pCO2 are:

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<span class="mw-page-title-main">Breathing</span> Process of moving air in and out of the lungs

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Fraction of inspired oxygen (FIO2), correctly denoted with a capital I, is the molar or volumetric fraction of oxygen in the inhaled gas. Medical patients experiencing difficulty breathing are provided with oxygen-enriched air, which means a higher-than-atmospheric FIO2. Natural air includes 21% oxygen, which is equivalent to FIO2 of 0.21. Oxygen-enriched air has a higher FIO2 than 0.21; up to 1.00 which means 100% oxygen. FIO2 is typically maintained below 0.5 even with mechanical ventilation, to avoid oxygen toxicity, but there are applications when up to 100% is routinely used.

In the respiratory system, ventilation/perfusion (V/Q) mismatch refers to the pathological discrepancy between ventilation (V) and perfusion (Q) resulting in an abnormal ventilation/perfusion (V/Q) ratio. Ventilation is a measure of the amount of inhaled air that reaches the alveoli, while perfusion is a measure of the amount of deoxygenated blood that reaches the alveoli through the capillary beds. Under normal conditions, ventilation-perfusion coupling keeps ventilation (V) at approximately 4 L/min and normal perfusion (Q) at approximately 5 L/min. Thus, at rest, a normal V/Q ratio is 0.8. Any deviation from this value is considered a V/Q mismatch. Maintenance of the V/Q ratio is crucial for preservation of effective pulmonary gas exchange and maintenance of oxygenation levels. A mismatch can contribute to hypoxemia and often signifies the presence or worsening of an underlying pulmonary condition.

<span class="mw-page-title-main">Pathophysiology of acute respiratory distress syndrome</span>

The pathophysiology of acute respiratory distress syndrome involves fluid accumulation in the lungs not explained by heart failure. It is typically provoked by an acute injury to the lungs that results in flooding of the lungs' microscopic air sacs responsible for the exchange of gases such as oxygen and carbon dioxide with capillaries in the lungs. Additional common findings in ARDS include partial collapse of the lungs (atelectasis) and low levels of oxygen in the blood (hypoxemia). The clinical syndrome is associated with pathological findings including pneumonia, eosinophilic pneumonia, cryptogenic organizing pneumonia, acute fibrinous organizing pneumonia, and diffuse alveolar damage (DAD). Of these, the pathology most commonly associated with ARDS is DAD, which is characterized by a diffuse inflammation of lung tissue. The triggering insult to the tissue usually results in an initial release of chemical signals and other inflammatory mediators secreted by local epithelial and endothelial cells.

<span class="mw-page-title-main">Ventilation–perfusion coupling</span> Relationship between respiratory and cardiovascular processes

Ventilation–perfusion coupling is the relationship between ventilation and perfusion processes, which take place in the respiratory system and the cardiovascular system. Ventilation is the movement of gas during breathing, and perfusion is the process of pulmonary blood circulation, which delivers oxygen to body tissues. Anatomically, the lung structure, alveolar organization, and alveolar capillaries contribute to the physiological mechanism of ventilation and perfusion. Ventilation–perfusion coupling maintains a constant ventilation/perfusion ratio near 0.8 on average, while the regional variation exists within the lungs due to gravity. When the ratio gets above or below 0.8, it is considered abnormal ventilation-perfusion coupling, also known as a ventilation–perfusion mismatch. Lung diseases, cardiac shunts, and smoking can cause a ventilation-perfusion mismatch that results in significant symptoms and diseases, which can be treated through treatments like bronchodilators and oxygen therapy.

References

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  2. 1 2 Fraser, Robert (1988). Diagnosis of Diseases of the Chest . Philadelphia: Saunders. p. 139. ISBN   0-7216-3870-8.
  3. ↑ "Intracardiac and Intrapulmonary Shunting". cmrc.com. 23 March 2022. Retrieved 25 December 2022.
  4. 1 2 Peruzzi, William T.; Gould, Robert W. (April 2004). "Setting the record straight on shunt". acutecaretesting.org. Retrieved 17 September 2019.
  5. ↑ Rishi Desai. "Pulmonary shunts: Transcript for Pulmonary shunts". osmosis.org. Retrieved 17 September 2019.
  6. ↑ Hantzidiamantis, Paris J.; Amaro, Eric (2023), "Physiology, Alveolar to Arterial Oxygen Gradient", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   31424737 , retrieved 2023-11-02
  7. 1 2 Hantzidiamantis, Paris J.; Amaro, Eric (2023), "Physiology, Alveolar to Arterial Oxygen Gradient", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   31424737 , retrieved 2023-07-20
  8. ↑ Sharma, Sandeep; Hashmi, Muhammad F.; Burns, Bracken (2023), "Alveolar Gas Equation", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   29489223 , retrieved 2023-07-20
  9. ↑ Wilmott, Robert W.; Becker, Bradley A. (2011). "Pulmonology". Pediatric Secrets. pp. 648–678. doi:10.1016/B978-0-323-06561-0.00017-3. ISBN   9780323065610.
  10. ↑ Silverthorn, D.U. (2016). "Chapter 14-15". Human physiology (7th ed.). New York: Pearson Education. p. 544.
  11. ↑ Sylvester, J. T.; Shimoda, Larissa A.; Aaronson, Philip I.; Ward, Jeremy P. T. (2012-01-01). "Hypoxic pulmonary vasoconstriction". Physiological Reviews. 92 (1): 367–520. doi:10.1152/physrev.00041.2010. ISSN   1522-1210. PMC   9469196 . PMID   22298659. S2CID   78887723.
  12. ↑ Prentice D, Ahrens T (August 1994). "Pulmonary complications of trauma". Critical Care Nursing Quarterly. 17 (2): 24–33. doi:10.1097/00002727-199408000-00004. PMID   8055358. S2CID   29662985.
  13. ↑ Egan's Fundamentals of Respiratory Care, p. 951
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