This chapter is not relevant to any specific Section from the 2023 CICM Primary Syllabus, because there is no specific entry for obesity in the Respiratory section. However, the examiner's foreword feels it is Important to note that all trainees are expected to have, "for all sections of the Syllabus an understanding of normal physiology, and physiology at the extremes of age, obesity," etc., etc. Thus, this chapter deals with the extremes of obesity. It would have been omitted completely if not for Question 5(p.2) from the second paper of 2008, which asked the candidates to "describe the respiratory changes that occur in morbid obesity". Of course, as the college examiners point out, "obesity is an increasing problem in the broader community" and this topic was bound to make its way into an Intensive Care career pathway physiology exam, as our units often become the default destination for people in the over-200kg range with whatever trivial medical problems, because OSA.
Respiratory Changes that Occur in Morbid Obesity
Obesity-related changes Effect of these changes
Airway function and structure
- Decreased pharyngeal diameter
- Increased tendency to collapse during sleep and sedation
Structural properties of the chest wall and lung volumes
- Decreased chest wall compliance
- Decreased FRC (mainly due to decreased ERV)
- Decreased lung compliance due to decreased lung volume (FRC)
- Slightly decreased total lung capacity (TLC)
- Increased airway resistance due to decreased lung volumes
- Specific airway conductance remains the same.
Function of respiratory muscles
- Increased total respiratory muscle mass
- Increased respiratory effort and increased oxygen use by respiratory muscles
- Lower PaO2 chronically (in some studies)
- Increased V/Q mismatch due to decreased FRC
Control of ventilation
- Obesity hypoventilation syndrome:
- Resting increased PaCO2 even when awake
- Decreased reactivity of respiratory control reflexes
Demands on the respiratory system
- Increased body mass = increased total body oxygen demand and increased ventilatory requirements for the clearance of the excess CO2
Instead of this unprofessional summary, one may wish to avail themselves of various legitimate peer-reviewed resources. Stephen Littleton's article (2012) makes an excellent starting point, and would be enough to prepare for the written paper all on its own. Other great reviews include Sood (2009) and Parameswaran et al (2006). They all overlap significantly, with a few unique elements in each publication. Alternatively, if "legitimate" and "peer-reviewed" aren't your thing, locally a series of articles responses to other obesity-associated questions in the CICM first and second paper exams:
"Morbid" obesity, though a term which is in wide circulation, is often misused colloquially in medical corridor conversation, perhaps as a substitute for more pejorative adjectives. Bray (1992) spells this out pretty clearly:
"Several terms have been used to describe this top 0.1% of the weight group. The surgeons have frequently used the term morbid obesity to define a group of people in whom medical complications justify surgical intervention. This group has also been called corpulent, jumbo, extreme, massive, malignant, gross, or super obese."
"Jumbo" and "corpulent" being unacceptable in these delicate times, the term "morbid" remains a safely medical-sounding label which separates obese people who don't need an ICU consult before surgery from those who do. It was originally coined by surgeons in the 1960s, as a means of manufacturing an indication for yet more surgery (Payne & DeWind, 1969). These patients, their obesity is "refractory to conservative management", they argued, and therefore aggressive surgical management "seemed justified". The original definition also consisted of weight-based criteria ("100%, or more than 100 lb, above average body weight") but the real definition clearly was "large enough and desperate enough to be referred to my rooms for a jejunocolic bypass". Considering that chronic diarrhoea and hideous electrolyte derangements were the normal course of recovery, the risk of death from obesity-related complications must have been quite great.
In the modern day, the definition for morbid obesity remains surgical. The American Society for Bariatric Surgery instead defines morbid obesity as "a lifelong, progressive, life-threatening, genetically related, costly, multifactorial disease of excess fat storage with multiple comorbidities", defined by objective criteria as being at least 100 lb heavier than ideal body weight, or a body mass index (BMI) of 40. A BMI of over 35 can still score you this label if you have been "experiencing obesity-related health conditions, such as high blood pressure or diabetes".
Publications often abjure the use of this terminology in favour of other, more scientific definitions (i.e. those which are based on some sort of epidemiological progression of increased risk from obesity-related disease). For example, Jonathan Purnell (2018) instead uses terms like "generalized obesity" (BMI > 30 kg/m2) and "extreme obesity" (BMI > 40 kg/m2), following the WHO classifications which are BMI-based and mainly relevant to the specific disease risk patterns of the white man. The CDC divides obesity into classes, as does the WHO, and the now-rescinded 2013 NHMRC guidelines, on the basis of BMI, as seen below:
So in short, there is no standard definition for "morbid" obesity, nor can anybody really agree on how "morbid" you need to be. Why go on this tangent? Well. In their model answer to Question 5(p.2) from the second paper of 2008, the college examiners mentioned that a definition of morbid obesity was expected from a good answer. They chose ">200% ideal body weight or body mass index > 35" as the official definition for that answer. One can only assume that these are people who are too busy to revise their answer grading rubrics. If this question ever appears again, one can safely assume that this is the definition they will expect to see, even though it may not match any contemporary society guidelines.
The college examiners list "fat infiltration of pharyngeal soft tissues" as one of the physiological processes associated with obesity, which makes morbidly obese patients prone to airway obstruction. Nishimura et al (2003), by means of dynamic MRI and endoscopy, were able to clearly demonstrate the effect this crowding has on upper airway obstruction in obese patients. In short, it's hideous:
"Difficult intubation" is not a physiological consequence of morbid obesity, insofar as intubation is not a physiological phenomenon. However, it was included as one of the factors by the examiners, and therefore may score some marks.
The lungs are an organ which is fortunately spared the deposition of fat in obesity, but unfortunately they are surrounded on all sides by other structures which gladly overgrow with adipose tissue. This results in the decrease in lung volume (see below), and the decrease in lung volume leads to decreased lung compliance (as the lung slips further down the steep volume-compliance relationship). The chest wall and abdomen also contribute to decreasing the compliance of the total respiratory system (Pelosi et al, 1996)
Obese subjects routinely have an increase in airway resistance reported, while their specific airway conductance remains the same. Without revisiting the definition of these terms, it will suffice to say that all of this apparent change in resistance is due to the decreased FRC. With partially collapsed lungs, the weight of the tissue surrounding each little bronchus is greater, and therefore the resistance to airflow increases. As one can see from these data from Rubenstein et al (1990), when the resistance is indexed to lung volume, one notices that the difference is minimal:
The effect of obesity on the total body oxygen demand is actually less straightforward than a direct upscaling of the metabolic demands. Specifically, fatty tissue (which is what there is the greatest preponderance of here) has a relatively low metabolic rate. Ergo, the morbidly obese individual will consume less metabolic substrate than a non-obese individual of the same mass (eg. comparing a 200cm tall person with a weight of 100kg to a 140cm person with a weight of 100kg). That amount of oxygen consumption will be slightly greater than what one might expect from a calculation based on ideal body weight, because a morbidly obese patient will usually have somewhat more muscle tissue than a lean person of a similar height. Moreover, breathing itself requires more effort and therefore consumes more energy.
In short, morbidly obese patients consume more oxygen and produce more carbon dioxide per minute than do lean patients, and it is more than would be expected from their ideal body weight, but less than would be expected from their actual body weight. Ravussin et al (1982) locked a bunch of people in airtight chambers and then measured their energy consumption form a 24-hr period; RMR was 7592 ± 351 kJ/day in the obese, 6652 ± 242 kJ/day in the moderately obese, and 6118 ± 405 kJ/day in the controls. For the record, the controls weren't exactly tiny (103kg on average), but the obese were properly obese (~170kg).
For the morbidly obese, the mundane act of breathing requires more energy. Because of their increased abdominal and chest wall mass, morbidly obese patients "dedicate a disproportionately high percentage of total VO2 to conduct respiratory work, even during quiet breathing" (Kress et al, 1999). The amount of additional O2 / CO2 flux to be expected is something like 150% of the normal values.
Obese subjects have a tendency of keeping a higher resting PaCO2, a phenomenon known as "obesity hypoventilation syndrome". That feature of the CO2 being elevated while awake is what separates this from simple obstructive sleep apnoea. Olson & Zwillich (2005) describe this thing very well. Hypoxia is not a part of the definition but is very often a part of the presentation. These subjects, when forced to do so in a laboratory, may hyperventilate themselves to a normal CO2 level (Leech et al, 1991), which suggests there's nothing intrinsically wrong with their respiratory muscles- rather, the involuntary background control of respiration is what is broken. The pathophysiology of this is thought to be related to the blunting of the aforementioned reflexes which occurs during sleep (where the patient is exposed chronically to hypercapnia and hypoxia)
The chapter on lung volumes and capacities goes into more detail about this, and so here, it will suffice to say that:
These data can be represented diagrammatically by borrowing some data from Jones et al (2006):
This is reflected in some changes in the spirometry results of obese subjects. The FEV1/FVC ratio is usually well preserved unless the subject is of truly gargantuan proportions, but both FEV1 and FVC tend to decrease with increasing body mass. The central distribution of fat is of greater importance in this, as the ERV and FRC are mainly being decreased by the weight of the fatty tissue as it envelops the trunk).
Obese patients tend to have a lower PaO2 than lean patients. This is not always possible to demonstrate in published papers; for example, Vaughan et al (1981) reported essentially normal PaO2 values in a group of patients with an average BMI around 50. However, when people are actually able to demonstrate poor oxygenation in this group, they usually attribute it to V/Q mismatch in the collapsed lung bases. "The lung bases are relatively overperfused and underventilated when obese patients are studied in the sitting position", complains Littleton (2012). This is consistent with the finding of decreased FRC and ERV.