“Given the acute cardiopulmonary stressors consequent to repetitive upper airway collapse, as well as evidence for cardiovascular homeostatic dysregulation in subjects with apnea, there is ample biologic plausibility that OSA imparts increased cardiovascular risk, independent of comorbid disease” (ATS, 2008).
Obstructive sleep apnea is characterized by the partial or full collapse of the upper airway and which causes interruption of ventilation. This causes multiple to several abrupt awakenings during the sleep cycle per hour. These mild to severe awakenings are caused by the upper airway collapse and the body responds to the lack of oxygen by stimulating the Central Nervous System (CNS) thereby sending a nerve impulse to say to the body “Hey I can’t breathe here!” This fragmented sleep, caused by these episodes of apnea (no airflow) and/or hypopnea (partial airflow), are due to the airway obstruction. This is the true danger of obstructive sleep apnea. The detrimental cardiopulmonary effects due to that lack of oxygen are the real danger of OSA.
There are many ways to diagnose or confirm Obstructive Sleep Apnea (OSA). There are cardinal signs and symptoms that are important to know. The most common clinical sign is snoring, due to the relaxation and loss of sympathetic tone in the oral airway during sleep. This is causing the tongue to fall back and occlude the airway or the tissue in the airway itself is decreasing the diameter. Also keep in mind that not everyone who snores has OSA, there are anatomical features that can cause snoring to. The biggest sign is “daytime sleepiness,” this shows that they are either not sleeping well due to the apnea/hypopnea or that they are hypoventilating due to the airway collapse/obstruction. This is also causing headaches due to the carbon dioxide retention caused by the hypoventilation. Due to the increase in work to fight against that airway obstruction, the body increases its intrathoracic pressure. This can cause many cardiac problems such as “acute leftward intraventricular septal shift,” “alterations in transmural cardiac pressures,” “impedance of Left Ventricular filling,” and “an increase in myocardial oxygen demand,” due to the increased venous return to the heart and from the taxing nature of the disease process itself. There is also a major concern with the Oxygen Desaturation, which is can be monitored via Oximetry.
The most important test is the “sleep study.” This involves the patient spending the night at the Sleep Lab, and monitoring the patient for apnic or hypopnic episodes. There are many types of monitors and wires placed on the patient as they sleep. This data is collected and compiled into the patients results trended through the night. The results are based on Apnea-Hypopnea Index, either mild, moderate, or severe. A patient with a more mild form of OSA has an AHI of >5, < 15 episodes per hour. The moderate level includes an AHI of > or equal to 15, but no more than 30 episodes an hour. Lastly, the severe level is an AHI > or equal to 30 episodes an hour. In some of the more severe cases of OSA, it has been noted that a patient has had more than 100 episodes of apnea in an hour and they lasted from 20-40 seconds for each one. This is why monitoring and diagnosing of OSA is so important. Of course, further physician assessment and treatment is needed throughout and after testing.
Obstructive Sleep Apnea is a multifaceted disease and the body varies in response for every person it affects. These individuals may also have different factors or comorbidities that will worsen their disease more than others. There are two types of factors that can affect OSA separate from its own disease process. One is the genetic factor, and the other is the “self-induced” comorbidities. These can both occur at the same time or can appear separate in their own forms.
The genetic factor is still being researched even now, 30 years later. As everyone knows the anatomy of every person is different, some more different than others. The biggest concern is any enlargement of the tissues or tongue that would affect the patency of the patient’s airway. A smaller airway is a predisposing factor in and of itself for OSA. A family history or close relatives that have or had OSA will increase your risk of acquiring it. Just being the make gender increases your risk. Understanding these factors, and the many others not listed, could help with diagnosing appropriately and getting early treatment for those who don’t actually know they have OSA. This could potentially, if caught early, decrease the severity of their symptoms in the future and help with a better quality of life for them.
The “self-induced” comorbidities that affect OSA are great in number. Obesity is one of the biggest comorbidities but is not a predisposing factor. Having the extra weight and strain on the body causes the symptoms to be worse due to the detrimental effects that extreme weight does to the patient. Smoking is not only a problem and risk factor for smoking but it’s also a risk for getting COPD, see the “Overlap Syndrome” for more details. The airway trauma caused by the heat of smoking, and the toxins in the cigarettes themselves can cause such severe cardiopulmonary effects that this one comorbidity can end your life via heart dysfunction/failure. These effects of trauma and inflammation the body has a tremendous effect. There are many things like diet and bad habits that we do to ourselves on a daily basis that if we fought to get rid of those things are body would only be fighting the disease and not fighting itself too.
The main treatment for OSA is Continuous Positive Airway Pressure (CPAP). CPAP is a continuous positive pressure given to the patient evenly throughout inspiration and expiration. This stinting of the airways helps to relieve some or most of the obstruction depending on the patients’ severity of the OSA and other factors. By doing this the patient is able to ventilate and therefore oxygenate better due to this constant flow of pressure. This helps to reduce the work of breathing, vital signs, hypoxemia, hypercapnia, and the list goes on. If the patient is a smoker to get them in a smoking cessation class as soon as possible, with nicotine patches if necessary. The diet will be a significant part of the treatment. This will allow, if obese, for them to lose weight and if they are not overweight, the diet and nutrition will help their overall wellbeing and help the body. Positional treatment is always an option. You can have the patient try to sleep on their side by using pillows and other techniques. Also, oral appliances can be made to help bring the bottom jaw forward hence bringing the base of the tongue forward to helping with the obstruction when the muscles relax. There are quite a few surgeries but most have less than a 50% chance of even working and most do not. Follow up labs and vital signs are essential for trending the results of those treatment.
The prognosis will always vary with each individual and it will also be dependent on what type or how many comorbidities they are dealing with. The increase work of the heart caused by the chronic hypoxemia stresses and affects the heart but it also causes defects in neural control of the respiratory centers of the brain. The prognosis will also vary due to severity and how compliant the patient is to the treatments that have been established for them. It’s up to the patient and physician to find what works for them. Education is key to a better prognosis and outcome of the individual.
OSA is a very frightening disease and can have life-threatening effects on the body. Even without another disease or co-morbidity, you still have a 7-10 times more of a chance to have a stroke or a heart attack just based on the effects of this condition. We are still researching and learning more about the disease, and the results of these studies have brought new therapies and ideas to light. This will in the future help save people’s lives and give them a better quality of life.
Vanessa Mower is a student at the Pima Medical Institute and the winner of our 2014 Student Writing Contest. Read more about her here.
Golbin J, et al. Obstructive Sleep Apnea, Cardiovascular disease, and Pulmonary Hypertentsion. American Thoracic Society, 2008;5(2):200-206. http://atsjournals.org/doi/full/10.1513/pats.200708-143MG.
Quan S. Cardiovascular consequences of Sleep-Disordered Breathing: Past, Present, and Future. AHA Journals. 2004;951-957. http://circ.ahajournals.org/content/109/8/951.full
Eckert D. Pathophysiology of Adult Obstructive Sleep Apnea. American Thoracic Society. 2008;144-153. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2628457/