29b: Gas Exchange and Ventilation (VA) & Perfusion (Q) Relationships
Two Modes of Regional Distribution of V/Q in Chronic Bronchitis
ØNormal at ~1 ØLow V/Q region with high perfusion/decreased ventilation ØLung unit behind diseased airways (obstructed/narrow/inflamed) ØVery limited gas exchange; dependent of collateral ventilation.
Two Modes of Regional Distribution of V/Q in Severe Emphysema
ØNormal at ~1 and 2nd mode, high V/Q ~10 with low perfusion ØDestroyed regions of lung where the capillaries are ablated secondary to alveolar wall deterioration. ØVentilated but not perfused; affects CO2 accumulation in blood.
What does an increase in AaDO2 indicate?
Efficient or abnormal gas exchange.
Failure of lung regeneration
independent of continuing SARS-CoV-2 replication, microvascular thrombosis/endothelial dysfunction and deleterious inflammation, may embody the mechanisms for tenacious lung dysfunction in COVID-19.
Regional Distribution of Ventilation and Perfusion Varies with Age
1. In A: V/Q ration close to 1.0; the curves are symmetric on a log scale with no areas of high or low V/Q ratios and there is no shunt. 2. In B: there are areas where perfusion exceeds ventilation and the V/Q <1 and regions where ventilation exceeds perfusion, and the V/Q is >1 but there are no shunts. Shunts: V/Q = 0
BENEFITS OF AWAKE PRONING
1.Maintains optimal respiratory rate/enhances gas exchange 2.Ventilation is homogeneous throughout lung parenchyma; redistribution of blood flow improves V/Q ratio. 3.Intrapulmonary shunts are reduced with proning/lung compression is reduced and oxygen levels improve. 4.Lying on stomach directs fluid to ventral region where there is comparatively less perfusion. 5.No invasive specialized equipment required in emergency situations.
MICROVASCULAR THROMBOSIS & V/Q MISMATCH
1.Microvascular thrombosis near ventilated alveoli produces dead space and prevents gas exchange; V/Q mismatch. 2.Common in COVID-19 pneumonia patients 3.Alveolar-capillary microthrombosis
Awake Proning to Improve Gas Exchange in COVID-19 Pneumonia Patients
1.Patients normally rest in supine position and fluid accumulates in dorsal regions of the lungs. (increased perfusion pressure) 2.Fluid accumulation causes increased pressure over alveoli, atelectasis and limited gas exchange. 3.Prone positioning redistributes fluid towards ventral regions to allow improved gas exchange/reduced lung collapse. 4.Recruitment of alveoli previously collapsed into the dorsal surfaces of the chest cavity.
COVID-19 Recovery Process
1.Re-epithelialization and removal of hyaline membrane, regression of stroma and leukocyte cell accumulations around the alveolar-capillary gas exchange zone. 2.Alveolar epithelium will regenerate; residual Type II cells will proliferate/differentiate into Type I cells used for gas exchange.
Thebesian vessels
2-3% of the cardiac output is shunted in this manner via Thebesian vessels that supply the left ventricle drain directly into the arterial circulation, rather than the coronary sinus in the right atrium.
The normal alveolar-arterial difference increases ? mmHg every decade of life.
3 mmHg
What is the upper limit of normal AaDO2?
< 25 mmHg
Hallmark of hypoventilation
A normal AaDO2, because PAO2 and PaO2 decrease with low ventilation
Pulmonary Tuberculosis
High PO2 environment at apex of the lung affects the distribution of pulmonary tuberculosis (tuberculosis bacillus thrives in O2-rich environment).
V/Q Mismatch Most Common Cause of Hypoxemia
Alveolar ventilation is abnormal in one of the parallel units; complete block causes a reduction in PaO2. A portion of the cardiac output passes the un- ventilated lung. The most common cause is atelectasis, a condition resulting from loss of ventilation to a gas-exchange unit (mucus plug, airway edema, foreign boy, tumor in the airway).
Simplified model of two normal parallel lung units
Alveolar ventilation is normal, and a portion of the cardiac output bypasses the lung. Deoxygenated blood mixes with oxygenated blood. Depending upon the size of the shunt, the PaO2 will vary accordingly. Perfusion is equally distributed between both units and this physiological shunt has V/Q=0. Conditions: Both units receive comparable quantities of ventilation (fresh air) and blood flow (perfusion) for their size. ØPaO2 and PaCO2 in arterial blood ØPAO2 and PACO2 in the alveoli ØPIO2 and PICO2 of the inspired air ØPpvO2 and PpvCO2 in the pulmonary venous blood
Regional Distribution of Perfusion in the Upright Lung
At the apex of the lung is a high V/Q, low perfusion due to gravity. So, there is higher alveolar oxygen and lower carbon dioxide. Overall V/Q in the normal lung is 0.8, it is composed of a wide range of localized ventilation- perfusion rations. At the base of the lungs, perfusion is greater than ventilation, so V/Q <1 and there is lower alveolar oxygen and higher alveolar CO2 at the lung bases.
ALTERNATIVE TREATMENTS TO IMPROVE GAS EXCHANGE
High doses of supplemental oxygen, either through a continuous positive airway pressure (CPAP) machine, the same machine used to treat sleep apnea, or through a supercharged oxygen system known as a high-flow nasal cannula (HFNC). Intervention increases driving force for oxygen diffusion into the capillary blood.
Lung Mechanisms of Arterial Hypoxemia
Diffusion deficits Shunt Ventilation/Perfusion Mismatch Alveolar hypoventilation
COVID-19 & "HAPPY HYPOXIA" Silent Hypoxemia
ER patients with drastically low oxygen levels. X-rays reveal severe pneumonia. (patients are still able to talk). Chief complaint is dyspnea, "some shortness of breath". Vital signs indicate need for ventilator support.
What can cause hypoventilation?
Encephalitis, drugs, dislocation of C-spine, poliomyelitis, Guillian-Barre syndrome, muscle atrophy, trauma, or cancer obstructing airway. To treat, fix the underlying cause to restore gas exchange since the lung is normal.
Ventilation-Perfusion Ratio
Figure A: Normal with lung adequate ventilation and perfusion; normal values for gases. Figure B: Alveoli have a "decreasing" V/Q relationship. The V/Q = 0 (zero) secondary to absent ventilation. Values mimic mixed venous blood. Figure C alveoli have a V/Q = to infinity secondary to absent perfusion. In these alveolar units, the O2 and CO2 levels are near the values for ambient air. No perfusion to bring CO2.
Regional Distribution of Perfusion
Gravitational forces are equal on arteries and veins (but not on alveoli) and there is an increase in flow at the base of the lungs. Results in distension of the blood vessels and lowering resistance. Zone 1 does not exist normally; but, can be reached when a subject is mechanically ventilated. Hemorrhage is a physiological condition that reduces arterial pressure. Under conditions of decreased arterial pressure, blood flow rises only to the point where arterial pressure equalized PA; above this there is no flow. Zone 2 has blood existing that is most reflective of PaO2. Zone 3 has the best blood; follows a pressure gradient; no collapsed capillaries.
Alveolar-arterial Difference (AaDO2)
In normal patients, there is little to no difference between alveolar O2 and arterial O2. In normal subjects, AaDO2 < 15 mmHg. However, a small difference comes from a small number of veins (bronchial and mediastinal veins carrying deoxygenated blood) that empty directly into the arterial circulation, bypassing the lungs. Oxygenated and deoxygenated blood mixing causes a reduction in the PaO2
SARS-CoV-2 ALVEOLAR Invasion
Infected (viral replication) alveolar epithelium detached leaving behind a porous alveolar capillary barrier (gas exchange surface). Loss of pulmonary epithelium results in plasma exudation and hemorrhage, formation of hyaline membranes containing fibrin, Factor VIII (coagulation factor) and cytokeratins—diffuse alveolar damage (DAD) and ARDS. Hyaline membrane that develops in alveoli during ARDS and impedes normal gas exchange.
Tetralogy of Fallot
Most common cyanotic congenital heart disease which is characterized by pulmonary valve stenosis, ventricular septal defect (hole between right and left ventricles) and overriding aorta. Commonly seen in DiGeorge syndrome.
Guillain-Barre syndrome
Muscle weakness (neuromuscular disease) diaphragm doesn't generate great force for bulk air flow, results in decreased minute ventilation, PaO2, and PaCO2 increases. Hypoxia and hypoxemia result.
Where V/Q mismatch exists
NO gas exchange occurs
What is most common cause of arterial hypoxemia?
Patients with cardiopulmonary disease and old age, mismatching of ventilation and perfusion.
Emphysema
The lung parenchyma is damaged and regions of lung where capillaries are ablated. Patients have high V/Q ~10 with low perfusion, this affects CO2 accumulation in the blood, because the lung is ventilated but not perfused.
Va/Q in a single alveolus
The ratio is equal to alveolar ventilation (VA) divided by the capillary blood flow (Qc).
What is the major determinant of normal gas exchange in the pulmonary system?
The ratio of ventilation to perfusion (defined as V/Q)
Va/Q in the entire lung
The total alveolar ventilation divided by the cardiac output.
Does a V/Q relationship always mean a normal lung?
There are compensatory mechanisms for maintenance of a normal V/Q relationship, but a normal value doesn't always mean a normal lung. If a patient is experiencing decreased ventilation with normal perfusion, the V/Q is less than 1. So, the reduced ventilation results in hypoxic vasoconstriction at an attempt to reduce perfusion and normalize V/Q.
