First: What is bradycardia? It may not be a term you hear every day, but in medical diagnosis and research, bradycardia is often associated with sleep apnea. This makes it of natural interest to anyone exploring the causes and solutions of sleep apnea.
Often (but not always) associated with sleep apnea in babies, bradycardia is a medical term meaning a slow heart rate and applies to people of all ages. The American Heart Association (AHA) defines bradycardia as a heart rate of less than 60 beats per minute, but adds that what is "too slow" for each individual depends on the age and physical condition you have.
Physically active adults typically have a resting heart rate below 60 BPM, but this does not cause problems. During deep sleep, your heart rate may drop below 60 BPM.
Sleep apnea and bradycardia: cardiovascular links
So what’s the connection between sleep apnea and bradycardia? Obstructive sleep apnea is listed as a potential cause of bradycardia because it tends to interrupt your body's sleep patterns. A slow heart rate may mean you're not getting enough oxygen, and not getting enough oxygen is a symptom of sleep apnea, a condition that causes you to wake up throughout the night because your breathing is blocked.
In a broader sense, bradycardia is a condition that affects the heart, and sleep apnea has a well-known association with heart (i.e., cardiovascular) disease. A large number of published studies support this link; a 2007 study published in the European Respiratory Journal noted that there is substantial evidence supporting an independent association between OSA and cardiovascular disease as a good example.
Sleep apnea and bradycardia: The pediatric connection
However, the link between sleep apnea and bradycardia often also refers to apnea of infancy, or a specific type of sleep apnea common in infants.
Pediatrics, the official journal of the American Academy of Pediatrics, defines infantile apnea as “an unexplained pause in breathing for 20 seconds or more or a shorter period of breathing associated with bradycardia , cyanosis, pallor, and/or marked hypotonia. pause.
The reason most babies develop bradycardia is the same reason they have apnea, says Emory University School of Medicine. And bradycardia is often caused by apnea in infants. But other medical problems can sometimes be the cause; therefore, babies who have these seizures need to be evaluated.
The article goes on to list the following possible causes of sleep apnea and bradycardia in infants:
- Infect. This is a fairly common cause and is often looked for if a baby is apneic.
- hypoxemia. Because this means a low heart rate, bradycardia can lead to hypoxia.
- Airway problems. This includes obstruction of the nose or respiratory airways, including those caused by mucus.
- envirnmental factor. Hyperthermia or hypothermia, or "overhandling of a premature baby."
- premature birth. This is often classified as apnea of prematurity.
If a baby does have sleep apnea and bradycardia, what is the treatment? This usually depends on what the specific cause is; for example, if the cause is an infection, it will require a different treatment than a respiratory obstruction. See last week's infant apnea article for more details.
The efficacy of continuous positive airway pressure in the treatment of patients with cardiac arrhythmia and obstructive sleep apnea
Over the past few decades, obstructive sleep apnea (OSA) has been extensively studied as an independent risk factor for the development and progression of cardiac arrhythmias. Continuous positive airway pressure (CPAP) therapy lowers blood pressure, improves ejection fraction in patients with heart failure, and reduces the need for revascularization surgery in patients with coronary artery disease. However, there is little published discussion on the effects of CPAP therapy on arrhythmias in OSA patients. We aimed to summarize the scientific evidence on the utility of CPAP therapy in managing the recurrence and severity of different types of arrhythmias. English articles published before December 2016 were searched through the databases of PubMed, CENTRAL and Embase. All peer-reviewed experimental, comparative, and other observational studies in adults were considered eligible. Several studies have documented positive changes in arrhythmia frequency and severity following CPAP use, regardless of arrhythmia type, study method, or setting. However, existing evidence on the effects of CPAP therapy on arrhythmia frequency and severity is limited by data heterogeneity. Duration of CPAP application, treatment compliance, and baseline severity of OSA and heart disease are important confounders of CPAP treatment efficacy. We highlight the need to agree on a core set of relevant predictors of effect size.
Efficacy of continuous positive airway pressure in patients with cardiac arrhythmias and obstructive sleep apnea: What is the evidence?
Obstructive sleep apnea (OSA) is characterized by recurrent obstruction of the upper airway during sleep, resulting in respiratory arrest despite continued respiratory drive. Obstructive sleep apnea has been implicated as an independent risk factor for hypertension, heart failure, cardiac arrhythmias, coronary artery disease, stroke, sudden cardiac death, and mortality in general and specifically from cardiac causes. OSA has been highlighted as a risk factor for increased complications after cardiac surgery.
Additionally, some studies have found that OSA increases an individual's susceptibility to potentially life-threatening atrial and ventricular arrhythmias. Obstructive sleep apnea has been found to be 18 times more likely to cause cardiac arrhythmias than normal breathing. The mechanism of this adverse effect is not fully understood; however, it has been suggested that OSA creates an imbalance between sympathetic and vagal activity during sleep, which plays a major role in generating or exacerbating cardiac rhythm disturbances. Obstructive events can also lead to hypoxia, which in the case of obstruction can cause reflex bradycardia and increase blood pressure. In addition, hypoxia is associated with increased oxidative stress and the production of reactive oxygen species, which can lead to cell damage, ischemia, and abnormal myocardial excitability. These changes may induce atrial and ventricular arrhythmias. Furthermore, increased intrathoracic negative pressure causes acute stretching of the myocardial wall and intrathoracic vessels, as evidenced by proximal aortic dilation and increased left ventricular volume. These structural changes, along with increased transmural gradients, may create an arrhythmic environment that triggers atrial and ventricular arrhythmias. Finally, nocturnal obstructive events are often terminated by arousal accompanied by a surge in sympathetic nervous system activity, which results in significant increases in blood pressure and heart rate as well as coronary vasoconstriction and microischaemia. Therefore, sympathetic overstimulation can induce various tachyarrhythmias and myocardial repolarization disorders.
Based on the current understanding of the underlying mechanisms of OSA, several treatments for OSA have been promoted. While milder cases of OSA can be managed by losing weight, avoiding muscle relaxants, improving nasal patency, oral appliances, and avoiding sleeping on your back, in more severe cases, continuous positive airway pressure (CPAP) is a good option. This treatment recommends providing positive pressure through a mask to keep the upper airway open during sleep. Early research suggests that although CPAP therapy is effective for OSA, clinicians and researchers face significant problems with patient compliance and compliance. The main reasons for poor compliance with CPAP therapy are thought to be skin irritation due to mask application and difficulty in device handling. However, understanding all aspects of CPAP therapy use, including those of physicians, health care systems, and CPAP distributors, suggests that advocating for its continued use is desirable. Likewise, classifying the benefits of CPAP therapy in the context of several types of arrhythmias may help develop clinical guidelines for patients with arrhythmias to be screened for OSA and receive CPAP therapy to optimize outcomes. Therefore, a comprehensive review of information regarding the use of CPAP therapy in patients with OSA and arrhythmias is necessary to inform more rigorous and ethical clinical decision-making.
Three studies investigated the effects of CPAP therapy on sinus bradycardia in 119 patients. Four studies – 40 in total – evaluated second- and third-degree AV block in 74 patients. Six studies included 194 patients with sinus pause/arrest. Outcome measures included total number of episodes, average number of episodes per 24 hours, and number of episodes per patient. Several studies reported that CPAP therapy significantly reduced or completely prevented the recurrence of nocturnal sinus bradycardia, atrioventricular block, and sinus arrest. In one study, researchers found a positive trend in favor of therapeutic CPAP in reducing nocturnal sinus bradycardia and pauses. However, this result did not reach the level of statistical significance.
Hypoxia caused by obstructive sleep apnea increases carotid chemoreceptor activity, which in the case of obstruction increases vagal stimulation of the heart, triggering bradyarrhythmias. It has been observed that approximately 87% of OSA-related nocturnal bradyarrhythmias occur during the rapid eye movement (REM) phase of sleep due to instability of the autonomic nervous system. Continuous positive airway pressure therapy prevents the development of OSA-induced bradyarrhythmias by restoring normal breathing and eliminating the detrimental effects of hypoxia and autonomic changes during obstructive events. Several studies have reported a reduction in the frequency of nocturnal sinus bradycardia, atrioventricular block, and sinus arrest even after short-term use of CPAP (i.e., 2 nights). Interestingly, 2 studies excluded patients with abnormal electrophysiological studies that would eradicate the presence of sinus node or atrioventricular node dysfunction. In addition to the 48-hour Holter ECG, an insertable loop recorder was applied for long-term heart rhythm monitoring. Importantly, weekly analysis with insertable loop recorders detected arrhythmia in 22% of patients, whereas 48-hour Holter electrocardiography showed arrhythmia in only 13% of patients. Most detected episodes of bradycardia and pauses occur at night and show significant nocturnal variability in individual patients. In patients treated with CPAP, a trend towards a reduction in nocturnal bradycardia and pause frequency was reported, but did not reach a level of statistical significance. Conventional short-term ECG monitoring and lack of assessment of SA/AV node function may have contributed to these nonsignificant results. Likewise, given that previous studies have shown that bradycardia and pauses are more prevalent in patients with severe OSA, concomitant heart failure, longer obstructive events, and greater degrees of oxygen desaturation, demographic characteristics may underlie the nonsignificant results. Confounding factors should be considered in future research on this topic.
Sleep apnea treatment linked to improved heart function
Study finds CPAP helps breathing, reverses heart damage
Using a ventilator to treat sleep apnea can improve heart function and potentially prevent heart failure, according to British researchers. People with obstructive sleep apnea temporarily stop breathing while sleeping.
To treat this condition, doctors sometimes prescribe a mechanical therapy called continuous positive airway pressure, or CPAP. It uses a mask to gently force air into the breathing passages, keeping them open.
In a new study published online by the American Heart Association, researchers at the University of Birmingham in the United Kingdom used echocardiography to study heart structure and function in sleep apnea patients before and after CPAP treatment and compared the results with hypertension and hypertension. patient data for comparison. Healthy control group.
Gregory Lipp, who led the study, said they observed heart damage in sleep apnea patients even though they had no obvious symptoms. "Moderate to severe sleep apnea does result in significant structural and functional changes comparable to those seen in patients with hypertension."
Apnea patients were treated with CPAP for an average of six months before having an echocardiogram. Scans showed most of the heart damage had been reversed.
"CPAP therapy does reduce the thickness of the heart muscle wall," Lip said. "Our heart function also improved and the stiffness of the heart chambers improved."
Lip says that given the therapy's apparent role in improving heart structure and function, patients with moderate to severe obstructive sleep apnea should be considered for CPAP treatment, even if they don't have any symptoms of heart problems.
"We hope that these improvements will translate into significant reductions in the risk of stroke and coronary artery disease," he said, "but clearly this needs to be confirmed in large prospective randomized trials."