Hypertension, Biomechanics, and Your Lungs: The Silent Changes Happening Inside

Much of the headline science in medicine concerns our underlying biochemistry, be it signaling between cells, our metabolism, what we share with our biome, our immune responses, or the risk factors underlying coronary artery disease. Biomechanical changes are mentioned in passing, such as how proteins fold when created or the loss of response in blood vessels in the face of hypertension. 

When I trained as a vascular surgeon, we knew far more about the biomechanics of blood vessels than their biochemical machinations. Perhaps that is why I am fascinated with how Newtonian physics's simple rules can impart so much to our physiologic responses. A new study provides an example. 

Hypertension, high blood pressure, remains the single most common chronic, non-communicable disease (NCD) afflicting our population. It is often included in the #1 listed NCD, cardiovascular disease, followed by cancer, chronic respiratory disease, and diabetes. It would not be surprising then that individuals with hypertension go on to develop others in the top three. The study in Advances in Respiratory Medicine looked at the association of hypertension with changes in lung biomechanics. The researchers enlisted 461 individuals aged 60 or greater who were nonsmokers with no documented chronic diseases other than hypertension. They categorized based on the presence of hypertension and the degree of physical activity (inactive or active). The cohort had a mean age of 69.88 with a BMI of 28 – not too heavy or thin. 

They performed a series of standard lung function tests and measured the mechanical characteristics of the lungs using impulse oscillometry [1]. The lungs have two entwined biomechanical functions -  to exchange air and to exchange the CO₂ and O₂ in the air and circulation. The research focused on the exchange of air, the biomechanics of breathing. Briefly, we actively expand our respiratory muscles, the diaphragm and muscles between our ribs, the intercostals, to inhale air. Exhalation is more of a passive process as the muscles relax, and the elastic tissue in the walls of the lung returns the lungs to the prior size. 

The researchers found:

• The pulmonary function and mechanics of adults with hypertension were impaired in relation to the non-hypertensive cohort. 
• Forced vital capacity (FVC) measures the maximum amount of air a person can forcefully exhale after breathing in as deeply as possible. A lower-than-normal FVC reading indicates restricted breathing. The reduced FVC was seen in those with hypertension.
• FEV₁ is the forced expiratory volume in the first second of exhalation. The FEV1 % was also reduced in those with hypertension.
• Oscillometry measured pulmonary impedance, a measure of the resistance to flow by the airways as their size diminishes, and pulmonary reactance, a measure of the elastic recoil associated with exhalation. While there was no difference in pulmonary impedance between those with and without hypertension, the hypertensive patients all demonstrated increased resistance. From a physiologic point of view, the increased resistance in the airways was compensated for by increased elasticity. 
• As you might expect, inactivity worsened these changes, and activity provided some mitigation. 
• The researchers employed a standard questionnaire about symptoms and physical functioning associated with quality of life issues, the SF-36. Interestingly, but unsurprisingly, activity was the discriminator, with those more active having better physical functioning, less bodily pain, better general health, vitality, and social functioning. 

Dyspnea is the subjective feeling of shortness of breath. The researchers point out that roughly 30% of adults over 60 have “difficulty to breath while walking at a horizontal level or on a slope.” However, none of these patients, with or without hypertension, expressed dyspnea – even though hypertension resulted in measurable changes in lung function. It would be fair to argue that the biomechanical compensation, where increased resistance was balanced by increased elastic recoil, is why none of these patients demonstrate pulmonary disease symptoms. Another compensatory mechanism to overcome inhalation resistance would be increasing the respiratory rate and inhaling fewer volumes. This is a known pulmonary response to aging. 

The Why

“The present study showed for the first time that SAH, beyond lung function, also impairs lung mechanics in older adults and that a physically active lifestyle is associated with attenuation of such impairments, while no differences were found regarding the levels of dyspnea.” 

The lung is highly vascular, and because of its role in gas exchange, which can only occur over exceedingly small distances, there is an “intimate anatomical coupling of vascular parenchymal elements.” Increasing blood pressure increases the stiffness in the vessels, just as increasing the amount of air in a balloon will increase its stiffness. That vessel stiffness, in turn, stiffens the surrounding tissue, which we can measure with oscillometry FVC and FEV₁. These are all biomechanical changes; we need not posit any tissue destruction as is seen in chronic obstructive pulmonary disease associated with loss of the lung’s elasticity or recoil. 

From a biomechanical perspective, hypertension and COPD can be a two-way street, although with the significant decline in smoking, more traffic runs from hypertension to COPD. COPD can result in hypertension because the lowered level of oxygen, due to the loss of alveolar surface area where gases are exchanged, puts more work on the heart, and one of its compensations is increased blood pressure to increase flow and oxygen delivery. 

In patients with the later stages of COPD, there is an increasing incidence of hypertension. While it remains difficult, if not impossible, to separate this chicken-egg dilemma, subtle anatomic alterations of our tissue biomechanical changes are clearly implicated – we can conjecture that significant hypertension’s effect on lung tissue is a tipping point for those who develop COPD. 

[1] Impulse oscillometry (IOS) generates pressure oscillations at the mouth, propagating through the airways and causing the lung tissues to stretch and recoil. Low-frequency signals penetrate deep into the lungs, while high-frequency signals remain in the proximal airways. 

Source: Physically Active Lifestyle Attenuates Impairments on Lung Function and Mechanics in Hypertensive Older Adults Advances in Respiratory Medicine DOI: 10.3390/arm92040027