Question

Todd is a 44-year-old electrical engineer who works 50–60 hours per week. He is 5’9”, 233 pounds, with total cholesterol of 192 mg · dL–1, low-density lipoprotein (LDL) of 138 mg · dL–1, high-density lipoprotein (HDL) of 41 mg · dL–1, triglycerides of 200 mg · dL and blood glucose of 120 mg dL. Todd’s resting heart rate is 81 bpm and blood pressure is 144/86 mmHg. His waist and hip circumference measures are 42 inches and 40 inches, respectively.

Todd has never smoked, but usually has one to two glasses of wine with dinner. He reports no leisure-time physical activity and does not exercise on a regular basis (less than two sessions per month).

Todd denies all complaints of chest discomfort and shortness of breath at rest or with exertion; however, he has gained 20 pounds over the last 2 years. Todd’s wife reports he snores frequently and has difficulty waking up in the mornings. Further testing reveals that Todd has obstructive sleep apnea and is being treated with continuous positive airway pressure (CPAP).

A review of his family history reveals that Todd’s father had double-bypass surgery at age 53 and suffered a fatal myocardial infarction at age 62. Todd’s brother (42 years old) also is hypertensive and was recently diagnosed with type 2 diabetes, which is being treated with diet and physical activity recommendations.

Questions:

Known CV, metabolic or renal disease?

Absolute or relative contraindications to exercise testing?

Signs or symptoms suggestive of disease?

Moderate or vigorous intensity? Why?

Medical clearance needed? Why or why not?

Should they get medical clearance before progressing to higher intensities? Why or why not?

ACSM CVD Risk Factors? How many?

Answer 1

Greetings of the day!

Answer:

INTRODUCTION

Obstructive sleep apnea (OSA) is characterized by recurring episodes of cessation (apnea) or reduction (hypopnea) in airflow during sleep caused by obstruction of the upper airway. In recent population-based studies, the estimated prevalence of moderate to severe sleep-disordered breathing ranges from 3% to nearly 50% depending on age group and sex

• Obstructive sleep apnea (OSA) is likely underdiagnosed ,however, lack of appropriate treatment puts many at risk of poor quality of life, comorbidity, motor vehicle crashes and increased health care utilization.

• Obstructive sleep apnea should be considered in symptomatic patients with suggestive craniofacial features or comorbidities, even in the absence of classic risk factors such as older age, male sex or obesity.

• Polysomnography is the gold standard for diagnosis; however, home sleep apnea testing may be used to confirm the diagnosis in symptomatic patients with a high pretest probability of OSA and without clinically important cardiopulmonary comorbidity.

• Good evidence supports treatment of OSA with targeted therapies including continuous positive airway pressure or oral appliances, as well as promotion of weight loss and moderate exercise for those who are overweight (alternative treatments may be tried for those who do not tolerate usual therapies).

Risk factors for developing OSA

Modifiable Risk Factors for OSA

Obesity

Drugs – opiates, benzodiazepines, and alcohol intake

Smoking (active and passive)

Supine body position during sleep

* Nasal congestion or obstruction

Non-modifiable Risk Factors for OSA

Gender: men more than women

Genetic predisposition

Race

Aging

Menopause

* Craniofacial anatomy (retrognathia and micrognathia)

^*potentially corrected by surgery

Known CV, metabolic or renal disease?

KNOWN EVIDENCES FOR:

Cardiovascular and cerebrovascular diseases

Many studies have examined the role of OSA as a pathogenetic factor in cardiovascular and cerebrovascular diseases, as well as the potential protective effects of CPAP treatment. OSA may increase cardiovascular risk through multiple intermediate mechanisms, such as intermittent hypoxia, high sympathetic nervous activity, systemic hypertension, endothelial cell dysfunction, oxidative stress, inflammation, and accelerated atherosclerosis . On the other hand, chronic intermittent hypoxia could also activate some protective mechanisms, for example through the development of coronary vessel collaterals in patients with ischemic heart disease.

Systemic hypertension

The best studied cardiovascular comorbidity in OSA is systemic hypertension . Respiratory events during sleep are associated with hypertensive peaks occurring at the end of apneas and hypopneas, increased mean nocturnal blood pressure, and increased variability of blood pressure. A dose-response relationship has been shown between OSA severity and blood pressure . OSA patients may show elevated blood pressure values during sleep only, or during sleep and wakefulness, making 24-hour monitoring of blood pressure highly advisable in the OSA population . Resistant hypertension, i.e. incomplete blood pressure control on three antihypertensive drugs, is also frequent in OSA patients.

Several studies assessed the potential benefit of CPAP treatment on blood pressure values, and meta-analyses demonstrated that on average blood pressure decreased by only a small amount during CPAP treatment. However, the therapeutic effect of CPAP on hypertension varied according to OSA severity, compliance to CPAP treatment, and baseline blood pressure values . OSA patients with resistant hypertension showed a quite large decrease in blood pressure during CPAP . Antihypertensive drugs, and diuretics in particular, may slightly decrease AHI in OSA . In general, pharmacological treatment to control hypertension is necessary in hypertensive OSA patients, given the small effects of CPAP on blood pressure.

Cardiovascular events and/or death

Several studies have addressed the question of OSA and cardiovascular morbidity and mortality. The prospective cohort study by Marin and coworkers reported a high cardiovascular risk in patients with severe OSA, which was normalized by CPAP treatment. The results of observational studies confirmed the association of untreated OSA with overall and cardiovascular mortality. In patients undergoing percutaneous coronary intervention, OSA was associated with occurrence of cardiovascular events during follow up.

Randomized controlled trials (RCTs) in OSA patients with known coronary artery or cerebrovascular disease were then designed to verify whether treatment of OSA in patients at high cardiovascular risk might exert a protective role. However, RCTs on the effects of CPAP in patients with known coronary or cerebrovascular disease failed to show any protective effect of CPAP treatment on cardiovascular risk . Current uncertainty is due to the discrepancy between data obtained from observational studies and RCTs . Different patients’ characteristics according to the type of study may explain the different results. In particular, only patients without excessive daytime sleepiness were included in long-term RCTs, since it would be unethical to withdraw treatment in symptomatic patients. It is known that compliance to CPAP treatment in non-sleepy patients is low, as underlined in a recent pro-con debate . Good compliance to CPAP, i.e. mean nightly use ≥ 4 hours, was associated with some protection, especially for occurrence of stroke.

Another area of current interest is whether OSA may modify the outcomes of acute coronary syndromes (ACS). OSA prevalence is high in patients with ACS, and severe OSA occurs in 25% of the patients . The ongoing ISAACC trial (Impact of Continuous Positive Airway Pressure on Patients with ACS and Nonsleepy OSA) will provide long-term data on the effects of treating OSA in this population.

Arrhythmias

Arrhythmias are frequent in OSA patients, especially atrial fibrillation (AF). A permissive role of OSA towards the arrhythmogenic mechanism of AF is suggested by the higher risk of recurrence of AF in patients with OSA compared to non-OSA subjects and by the protective effect of CPAP treatment. Conversely, the literature on ventricular arrhythmias is relatively scarce and heterogeneous, as pointed out by a recent review . Incidence of sudden cardiac death is increased at night in OSA according to some reports . while other studies found a uniform distribution over 24 hours . Studies in patients with implantable cardioverter-defibrillator devices (ICD) have reported a high frequency of nocturnal discharge in OSA compared to non-OSA patients or patients with chronic heart failure and central apneas .

Cerebrovascular disease

Several studies reported an increased risk of stroke in snorers and OSA patients . CPAP treatment may reduce the risk of stroke , but most studies have used a composite cardiovascular outcome including stroke, rather than reporting data for each type of events. Available RCTs on the effects of CPAP in patients with stroke and OSA are usually short-term, and the low acceptance of CPAP treatment in patients with OSA and previous stroke is an additional difficulty to be considered. A recent meta-analysis on RCTs in the latter population reported improvement in neurological function in CPAP users . More studies are necessary to evaluate the possible protective effects of CPAP on survival after stroke.

Metabolic diseases

The relationship between OSA and metabolism is highly complex. On one hand, OSA is often associated with obesity, which by itself is characterized by disturbed energy metabolism and adipose tissue inflammation. On the other hand, nocturnal intermittent hypoxia has been shown to affect glucose metabolism, and OSA could independently contribute to the pathogenesis of metabolic disorders . The bidirectional relationships between OSA and disturbed energy metabolism or type 2 diabetes are current topics of interest, given the obesity epidemics and the increasing prevalence of type 2 diabetes worldwide.

OSA and the Metabolic Syndrome

The metabolic syndrome (MetS), a pre-diabetic state associated with central obesity and increased cardiovascular risk , is highly prevalent in OSA patients and, according to some authors, OSA should be considered as an additional manifestation of MetS . OSA may play a role in the pathogenesis of insulin resistance, the main feature of MetS, through intermittent hypoxia and sleep loss or fragmentation . A fascinating recent research area is represented by the role of gut microbiota in metabolic derangements induced by intermittent hypoxia or sleep fragmentation . Readers interested in the complex mechanisms of the interaction between OSA/intermittent hypoxia, adipocyte dysfunction, and inflammatory activation in adipose tissue, are referred to extensive reviews on these topics .

Although a positive effect of OSA treatment on metabolic disturbances might be expected based on the pathophysiological links described above, CPAP treatment does not modify visceral fat or metabolic variables unless concurrent weight loss occurs. Nevertheless, short-term CPAP treatment for 8 hours/night improves insulin resistance, suggesting that prolonged nightly treatment with CPAP may be needed to modify glucose metabolism in OSA, possibly through decreased sympathetic activation. Activity of insulin in the carotid body, and a common pathway involving both intermittent hypoxia and metabolism, is an interesting recent pathogenetic hypothesis possibly explaining the intertwining effects of OSA and glucose dysmetabolism.

OSA and diabetes

The bidirectional relationship between OSA and diabetes is especially interesting from a clinical point of view. Treatment of OSA may help to prevent severe consequences of diabetes. This might indeed be the case, since although glycemic control does not improve during CPAP treatment according to meta-analyses , untreated OSA in diabetic patients is associated with increased prevalence of neuropathy, peripheral arterial disease, diabetic retinopathy and diabetic nephropathy. Data on the effects of CPAP on diabetic complications are scarce. Compared to poorly compliant patients, optic nerve function improved in severe OSA patients with good compliance to CPAP treatment . A recent post-hoc analysis of data from the SAVE study highlighted a higher risk of adverse outcomes in diabetic compared to non-diabetic patients, and a protective effect of CPAP on recurrent cardiovascular events only in diabetic patients with OSA showing a good adherence to CPAP treatment, i.e. at least 4 h/night, in the first 2 years of the study.

In summary, OSA may worsen metabolic abnormalities, and OSA treatment with sufficient adherence could play a protective role, especially when concomitant lifestyle interventions and weight loss are implemented. Screening for OSA in diabetic patients should be systematically done, since CPAP treatment for at least 4 h/night may be protective, especially when diabetic complications are also present [88].

Renal disease

Renal diseases and OSA share common risk factors, like arterial hypertension, diabetes mellitus, obesity and advanced age. Each of such factors may give some independent contribution to the onset and progression of the other one . OSA may endanger the kidney through several interacting mechanisms, including nocturnal intermittent hypoxemia, recurrent nocturnal blood pressure peaks, sympathetic hyperactivity, hyperactivation of intrarenal renin-angiotensin system, oxidative stress and systemic inflammation, endothelial dysfunction. A relationship between nocturnal hypoxemia and hyperactivation of the intrarenal renin-angiotensin system has been experimentally demonstrated.

Cross-sectional epidemiological studies have not consistently reported an association between OSA and either albumin excretion or eGFR. When an association was found, either severity of nocturnal hypoxemia or the apnea/hypopnea index were reported to correlate to renal alterations. These studies highly differed in design, sample size, recruitment criteria (patients referred to sleep laboratories, general population, diabetes as an inclusion or an exclusion criterion), so that it is difficult to draw firm conclusions from them.

More interesting and consistent results were obtained from longitudinal investigations. In a large study on US veterans, the annual rate of decline of eGFR was higher among patients diagnosed with sleep apnea than among controls [93]. Three retrospective cohort studies in Taiwan found a higher incidence of chronic kidney disease (any stage) among OSA than control subjects. However, all these studies lacked polysomnographic information about OSA severity. Another longitudinal study on patients recruited in a sleep laboratory found that an accelerated decline in eGFR was more common among subjects who spent >12% of sleep time with oxygen saturation <90% than in less hypoxic subjects. By contrast, a long-term study on the population-based Wisconsin Sleep Cohort did not find any difference in the rate of decline of eGFR between subjects initially showing an AHI>15 and other subjects . However, the less severe nocturnal hypoxemia in sleep apnea subjects from the general population may at least partly explain the different results obtained in the Wisconsin cohort and in studies on OSA patients.

Most papers on the effects of OSA treatment on kidney function showed positive effects of CPAP. Two small studies on subjects with a high baseline GFR found a reduction of filtration fraction due to decrease in glomerular hyperfiltration . Two other small studies on subjects with mildly or severely impaired renal function observed an increase in eGFR or a decrease in eGFR decline . More recently, a RCT could not demonstrate a difference in the rate of eGFR decline between subjects with OSA and cardiovascular diseases treated by CPAP or under “usual care”; however, the power of the study could be insufficient to demonstrate a difference between the two groups . In a study with a larger number of patients recruited in different sleep laboratories, therapy with fixed CPAP, but not with autoadjusting CPAP, could blunt the spontaneous trend of eGFR to decline over time.

In summary, there is some evidence that OSA may worsen kidney function through several mechanisms, and CPAP may exert beneficial effects.

Absolute or relative contraindications to exercise testing?

Signs or symptoms suggestive of disease?

Obstructive sleep apnea is when something blocks part or all of your upper airway while you sleep. Your diaphragm and chest muscles have to work harder to open your airway and pull air into your lungs. Your breath can become very shallow, or you may even stop breathing briefly. You usually start to breathe again with a loud gasp, snort, or body jerk. You may not sleep well, but you probably won't know that it’s happening.

The condition can also lower the flow of oxygen to your organs and cause uneven heart rhythms.

Obstructive Sleep Apnea Symptoms

Common obstructive sleep apnea warning signs include:

• Daytime sleepiness or fatigue
• Dry mouth or sore throat when you wake up
• Headaches in the morning
• Trouble concentrating, forgetfulness, depression, or crankiness
• Night sweats
• Restlessness during sleep
• Problems with sex, like a low sex drive
• Snoring
• Waking up suddenly and feeling like you're gasping or choking
• Trouble getting up in the mornings
• Waking up often in the middle of the night to pee
• High blood pressure
• Gastroesophageal reflux disease (GERD)

If you share a bed with someone, they'll probably notice your sleep apnea before you do.

Symptoms in children may not be as clear. They may include:

• Bed-wetting
• Choking or drooling
• Sweating a lot at night
• Ribcage moves inward when they breathe out
• Learning and behavior problems
• Problems at school
• Sluggishness or sleepiness (often seen as laziness)
• Snoring
• Teeth grinding
• Restlessness in bed
• Breathing that pauses or stops
• Unusual sleeping positions, such as sleeping on their hands and knees, or with their neck bent far back

Many other medical conditions can also cause these symptoms. Talk to your doctor to rule them out.

Obstructive Sleep Apnea Causes

Obstructive sleep apnea usually happens when the muscles that control your airway relax too much, narrowing your throat. You wake up for a moment to reopen your airway, but you probably won’t remember doing it. This might happen dozens of times each hour.  

Other things that block your throat can cause obstructive sleep apnea, like obesity, swollen tonsils, and health problems like endocrine disorders or heart failure.

Moderate or vigorous intensity? Why?

Exercise experts measure activity in metabolic equivalents, or METs. One MET is defined as the energy it takes to sit quietly. For the average adult, this is about one calorie per every 2.2 pounds of body weight per hour; someone who weighs 160 pounds would burn approximately 70 calories an hour while sitting or sleeping.

Moderate-intensity activities are those that get you moving fast enough or strenuously enough to burn off three to six times as much energy per minute as you do when you are sitting quietly, or exercises that clock in at 3 to 6 METs. Vigorous-intensity activities burn more than 6 METs.

One limitation to this way of measuring exercise intensity is that it does not consider the fact that some people have a higher level of fitness than others. Thus, walking at 3 to 4 miles-per-hour is considered to require 4 METs and to be a moderate-intensity activity, regardless of who is doing the activitya young marathon runner or a 90-year-old grandmother. As you might imagine, a brisk walk would likely be an easy activity for the marathon runner, but a very hard activity for the grandmother.

As per the researches,

Increasing physical activity may lower the risk of obstructive sleep apnea (OSA), according to results of a new study.

“The rates of sleep apnea in children and adults are continuing to rise. Therefore, understanding the role of modifiable protective factors for sleep apnea is important,” senior author Lyle Palmer, PhD, said in a press release. “Exercise is one such protective factor and has many other positive effects on general health. Sleep health care professionals should be trying to get their patients to exercise more.”

To reach their conclusion, the researchers assessed the lifestyle, medical, sociodemographic, and sleep health data that had been collected from 155,448 adults participating in the Ontario Health Study.

Of these adults, 39.8% were men and 60.2% were women. Overall, 6.9% of the respondents had been diagnosed with OSA. Those with OSA were more sedentary than their counterparts without OSA, sitting for a median 4.4 hours more per week.²

After adjusting for potential confounding factors, total physical activity (metabolic equivalent of task hours per week), vigorous-intensity activity, and walking were all associated with decreased prevalence of OSA.

In fact, based on the physical activity of participants with and without OSA, the researchers determined that a modest increase in physical activity is associated with a 10% reduction in OSA risk. And this reduction in OSA risk can be achieved by adding 20 minutes to a daily walk or increasing vigorous daily activity by 8 minutes.

According to the researchers, the findings are independent of other known OSA risk factors, such as gender, age, ethnicity, and obesity.

“Our results highlight the importance of physical activity as a preventive measure against developing sleep apnea,” Dr Palmer said in the press release. “One surprising finding was that not only vigorous physical activity, but also just walking alone was associated with a decreased risk of sleep apnea.”

Moderate-intensity activity was not associated with OSA risk, according to the researchers.

Medical clearance needed? Why or why not?

Yes, medical clearance is needed for OSA because it causes many life threatening complications.

a medical clearance is defined as an “official authorization for something to proceed or take place.” An example of this is when one healthcare provider requests a clearance (usually a signed form) from another healthcare provider prior to providing treatment or having the patient involved in an activity.

A medical clearance is used to determine whether a proposed treatment or activity could affect the patient’s condition or, conversely, if the patient’s condition could affect a proposed treatment or activity.

The Problem

The problem at issue is that providing a medical clearance denotes that the patient is free of (all) risks. However, there are always risks involved when treatment is rendered.

Therefore, a physician who signs off that a patient is cleared to undergo a particular treatment or activity is at risk of being brought into a claim should an unexpected outcome arise – either related or unrelated to which the clearance referred.

Potential Solutions

Collaborative dialogue between providers is paramount for treatment planning and patient care. The more information the doctor requesting the consult has, the better they are able to plan for and mitigate potential complications and determine the recovery period.

A solution for mitigating exposure when asking for or providing medical information is to request and/or provide a medical consultation or assessment.

This way, as the physician providing the consultation or assessment, you are confirming the treatment, therapies and findings provided by you to the patient. You are not certifying patients are free of risk. In this case, the ultimate decision to proceed with a treatment or activity in light of the consult or assessment belongs to the patient.

Pathophysiology of OSA:

Screening for OSA:

MEDICAL CLEARANCE MAY BE OBTAINED AFTER STARTING THE TREATMENT:

Should they get medical clearance before progressing to higher intensities? Why or why not?

NO, NOT ONLY BEFORE PROGRESSION, BUT AFTER PROGRESSION ALSO.

Medical clearance and risk assessment should be repeated in case of progressions and after any surgeries. A medical clearance is valid until the end of a tour or home leave , whichever is shorter,or until the work period in case of job, unless there is a significant change in the individual's medical condition.So, it should be done in both cases before, and after progression of OSA , because whatever may be the condition during the screening .

ACSM CVD Risk Factors? How many?