BLDE University Journal of Health Sciences

: 2021  |  Volume : 6  |  Issue : 2  |  Page : 111--114

PhyGeometry: ORGANizing physiology

Hwee-Ming Cheng, See-Ziau Hoe 
 Department of Physiology, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia

Correspondence Address:
Prof Hwee-Ming Cheng
Department of Physiology, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur


PhyGeometry is a visual learning and teaching aid, combining physiological information into and part of geometric triangles. PhyGeometry is a useful summary picture of key factors that affect or are part of a physiological event or mechanism. PhyGeometry helps to “ORGANize,” bring order, beauty, and symmetry into learning and teaching physiology.

How to cite this article:
Cheng HM, Hoe SZ. PhyGeometry: ORGANizing physiology.BLDE Univ J Health Sci 2021;6:111-114

How to cite this URL:
Cheng HM, Hoe SZ. PhyGeometry: ORGANizing physiology. BLDE Univ J Health Sci [serial online] 2021 [cited 2022 Jan 26 ];6:111-114
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 Tidal Volume, Frequency of Breathing, and Alveolar Ventilation

Students are taught to summarize, synthesize what they read and learn into organized, for example, mental maps and flow diagrams. The exercise of gathering essential information into systematic, directional categories, and subclasses of contributing factors is a good revision in itself. One can only simplify when one has understood and grasp the qualitative and quantitative aspects of a physiological process.[1]

In this article, we share a useful approach for students to collect key physiological factors into triangular geometric figures. We have called this learning and teaching visual aid “PhyGeometry.” We illustrate PhyGeometry by giving examples from Respiratory Physiology.

The diagram [Figure 1]a shows an inverted triangle with Alveolar ventilation (VA) at the bottom corner. The two determinants of VA are the Tidal volume (TV) and the Frequency of breathing (Fq). In the triangle, between the TV and the Fq is the Anatomical dead space (anat dspace). Visually, this easily reminds the student that VA is calculated from (TV– anat dspace) multiply by the Fq.{Figure 1}

VA replenishes the alveoli with fresh TV air. In pulmonary patients with restrictive problems, the TV is shallow and this is compensated by a higher breathing rate. On the other hand, in obstructive pulmonary disease, the patients breathe slowly due to the elevated airway resistance. Breathing is slow and labored to increase the TV.

 Lung Recoil, Elasticity and Surface Tension

The collapsed fetal lungs in utero are expanded from birth. In vivo, the tendency of the lung to recoil to its natural state is balanced by the opposing outward recoil of the chest wall. The lung recoil, placed at the apex of the triangle, is due to two factors [Figure 1]b. The elasticity of the lung tissues produces the elastic recoil. Elasticity is defined physiologically as the recoil force that opposes distention or stretch. Lung elasticity is thus also inversely related to lung compliance. The second factor is the alveolar surface tension generated by the air-liquid lining interface in the alveoli. The direction of the alveolar surface tension is an inward collapsing force. Alveolar stability is achieved by the function of pulmonary surfactant which decreases the alveolar surface tension.[2]

 Pulmonary Vascular Resistance, Distention, and Recruitment

Compared to systemic blood vessels, the pulmonary vasculature is relatively compliant. As such, the pulmonary vascular resistance (pvr) is decreased when the blood pressure in the pulmonary artery increases. Pressure or mechanical vasodilation occurs with distention and recruitment of less patent pulmonary blood vessels. These pulmonary hemodynamics accounts for the fact that the larger right ventricular output during physical activity does not raise the pulmonary arterial pressure too much. The initial increased blood pressure stretches the compliant pulmonary vessels and lowers the pvr, counteracting a large increase in pulmonary arterial pressure. The open bottom corner of pvr in the triangle is to indicate the vasodilation of a reduced pvr by the vascular distention and recruitment [Figure 1]c.

 Oxygenation, Partial Pressure of Oxygen in Alveolar and Pulmonary Capillary

The rate of oxygenation at the alveolar-capillary membrane is described and included in the term Diffusion capacity of oxygen (O2) in the Lungs or DLO2.

There are three factors in this DLO2. The O2 Diffusion per time (VO2) is given as the apex of the triangle, and this is the numerator in the equation [Figure 2]a.{Figure 2}

The denominator is the difference of the partial pressure of O2 (PO2) in the Alveolar air (PAO2) and in the pulmonary capillary (PcO2). Hence, the unit for the Lung DLO2 is mL O2/min/mmHg.

Not that that the pulmonary capillary PO2 rises rapidly to equilibrate with the alveolar air PO2 and equilibration is achieved in half the pulmonary transit time. At this point, no further passive diffusion or transfer or oxygenation of the blood occurs.

Further oxygenation can be achieved in the pulmonary blood flow is increase brining a greater blood volume/min of deoxygenated blood to be re-oxygenated. This is the reason why normal lung oxygenation is described as perfusion or flow-limited.

The other major factor that affects oxygenation is the total available surface area of the alveolar-capillary membrane for O2 diffusion.

 Blood Oxygen Content, Dissolved Oxygen, and Hemoglobin-Bound Oxygen

The blood O2 content (CaO2) in arterial or venous blood is predominantly associated with hemoglobin. Arterial blood is around 98% saturated with O2 and in venous blood, the term de-oxygenated is somewhat misleading as hemoglobin is still 75% saturated with O2 in venous blood.

The PO2 that represents the dissolved O2 is in equilibrium with the hemoglobin-bound O2. In fact, the hemoglobin-O2 saturation is determined by the PO2 in blood. This is represented graphically in the hemoglobin dissociation (association) sigmoid curve. The much smaller amount of dissolved oxygen could also be indicated in the triangle PhyGeometry with a smaller font size “dissolved” [Figure 2]b.

However, O2 that is bound to hemoglobin does not contribute to the value of the mmHg of dissolved O2 in blood plasma. This explains why in anemic hypoxia due to carbon monoxide competitive displacement of hemoglobin-bound O2, the PO2 remains unchanged. The peripheral chemoreceptors are unstimulated giving no conscious awareness to the victim of the gas toxicity. The total CaO2 is drastically reduced with unchanged PO2.

 Cardio-Respiratory Delivery of Oxygen to the Cells

The normal arterial CaO2 is about 20 ml O2 per 100 mL of blood. For cells to receive adequate oxygenation, blood flow must be optimal. A poor cardiac output (CO) leads to a stagnant hypoxia as cells are receiving insufficient O2 for their metabolic needs.

The rate of O2 delivery to the cells in mL O2/time is then the product of the arterial CaO2 and the CO [Figure 2]c. For a 70 kg male adult, this will be 20 mL O2/100 mL multiply by 50 since the CO is 5000 mL/min. This gives a value of around 1000 mL O2/min.

At rest, the tissue O2 extraction or consumption rate is about 25% or 250 mL O2/min.

During exercise, the greater demand of O2 is met primary by the increased CO.[3] The arterial CaO2 is not greatly increased since at normal resting arterial PO2 of about 100 mmHg, the hemoglobin-saturation is already close to 99%.

 Blood Carbon Dioxide Content, Bicarbonate, and Carbaminohemoglobin

The blood CO2 content (CaCO2) is a combination of three forms of CO2. The dissolved CO2 gives the partial pressure of CO2 (PCO2) in the blood. Two thirds of the total CO2 are carried as bicarbonate (HCO3−) [Figure 3]a, generated by red cell carbonic anhydrase. Some CO2 is bound to hemoglobin as carbaminohemoglobin.{Figure 3}

The hydration of CO2 to carbonic acid inside erythrocytes and subsequent production of HCO3− and hydrogen ions occur inside the red cells where the carbonic anhydrase is localized. Hemoglobin also buffers the hydrogen ions and this prevents venous blood from becoming acidic.

In addition, the buffering of hydrogen ions shifts and promotes the dissociation reaction of carbonic acid and generation of HCO3−, the major form of CO2 in blood.

So at any one time, besides O2, hemoglobin has two other “passengers,” the associated CO2 and the buffered protons (H + HbCO2).

Protonated hemoglobin also has less affinity for O2 and this enhances unloading of O2 to the tissues (Bohr's effect).

 Alveolar Air PCO2, Alveolar Ventilation, and Cellular CO2 Production

One primary objective of VA is to maintain a constant PCO2 in alveolar air. The partial pressure gradient for CO2 diffusion is only 6 mmHg (alveolar air, 40 mmHg and mixed venous blood, 46 mmHg). Thus, small changes in alveolar air PCO2 will affect the removal and expiration of metabolic CO2. The accumulation of CO2 or hypercapnia will acidify the blood and neuronal functions in particular are easily depressed by acidosis.

Specifically, the value of alveolar air PCO2 is determined by the balance of two factors.[4] The ratio of cellular CO2 production and the VA [Figure 3]b. At rest, if a person voluntarily hyperventilates, the alveolar PCO2 will be decreased giving a respiratory alkalosis.

In a patient with poor VA, the normal resting CO2 tissue production will lead to an increase in alveolar PCO2 above 40 mmHg. The arterial blood PCO2 will then also be increased in parallel after equilibration at the alveolar–capillary membrane.

During exercise, the alveolar air PCO2 is little changed as the increased metabolic CO2 generation is balance by exercise hyperventilation.

Besides the ratio of CO2 production and VA, another pulmonary functional ratio affects the alveolar air PCO2. This is related to the ventilation/perfusion (V/Q) matching. At the apex of the upright lungs, a higher V/Q ratio gives a lower PCO2 while at the basal alveoli, with a lower V/Q ratio, the alveolar PCO2 is slightly higher than 40 mmHg.

In learning respiratory physiology, it is essential to think beyond or outside the “thoracic box.” The ultimate consumer need is at the cells and cardiovascular and pulmonary blood flow is crucial to meet the end-user tissue metabolic requirements. Mixed venous blood in pulmonary artery needs to be re-oxygenated and recirculated to the periphery. Think Cardio-Respiratory physiology!

 Peripheral Chemoreceptors, Hypoxia, Hypercapnia, and Acidosis

The chemical control of ventilation involves chemosensors, central and peripheral chemoreceptors. The central chemosensors are located in the brainstem close to the respiratory control neurons.

The peripheral chemoreceptors are found in the carotid and aortic bodies (the O2 in the word “bO2dies” is to help students distinguish between the carotid sinus baroreceptors that monitor blood volume/pressure) [Figure 4]a.{Figure 4}

These arterial chemosensors are sensitive and stimulated by to three parameters and afferent sensory impulses are transmitted to the respiratory regulatory neurons. They are hypoxic hypoxia (reduced arterial PO2), reduced arterial blood pH below 7.4 and an increased arterial PCO2 above 40 mmHg.

CO2 can transverse the blood brain barrier and stimulate also the central chemoreceptors. Decreased PO2 does not stimulate the central chemoreceptors. CO2 and not O2 is the primary chemical regulator of pulmonary ventilation.

Noncarbonic acids that lower blood pH like lactic acid does not cross the blood–brain barrier to act on the central chemoreceptors.[5]

 Respi-Renal Regulation of Extracellular pH

In pH regulation, the lungs and the kidneys function in concert to handle respectively the carbonic and the noncarbonic acid loads added daily to the body on a normal diet [Figure 4]b. Think Respi-Renal physiology!{Figure 4}

The pH of the extracellular fluid is reflected and associated with the respective ratios of the base/acid pairs of all the chemical buffers. Quantitatively, the bicarbonate/carbonic buffer is the most important. The carbonate/carbonic acid buffer is an open system,[6] meaning the two components are linked to two major organ functions. Renal function targets the HCO3− concentration. Respiratory function, through regulating partial pressure of CO2 affects the carbonic acid.

The normal ratio of this bicarbonate/carbonic acid at pH 7.4 is 20:1. A higher ratio occurs in alkalosis and a ratio <20 indicates acidosis. If the cause of the acid base disturbance is due to respiratory function, it is either respiratory acidosis or respiratory alkalosis. Any cause of pH imbalance that alters the HCO3− concentration is termed metabolic, whether it is nonrenal or renal reasons, for example, metabolic acidosis in diarrhea and renal tubular acidosis, respectively.

The immediate compensation for acid base fluctuation is to restore the ratio as close to 20:1 as possible. Complete normalization of both the HCO3− and carbonic (PCO2) values take place eventually.


By using Triangle PhyGeometry, we can create visual summaries of essential mechanisms and concepts in Physiology. The upright triangle can be rotated with the apex pointing right or even an inverted triangle, combined with key factors at the corners and words in the triangle to concisely present a PhyGeometric icon that highlights a specific area of physiology. Besides triangles, it is possible to also creatively use the geometric Square for more complex Physiology. Hopefully, this introduction to triangle PhyGeometry will provide a fresh, fun approach, a good right angle and perspective to enjoy learning and teaching Physiology.

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Conflicts of interest

There are no conflicts of interest.


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