Module 5 - Consequences of Sleep Disordered Breathing Flashcards
What are the primary effects of OSA on cerebral function in children and adolescents?
OSA impacts cerebral function primarily in children and adolescents due to their developing brains. Sleep loss contributes more to neurocognitive deficits than hypoxemia.
Why is it unclear whether OSA has functional or anatomical consequences?
The effects of decreased alertness on higher cognitive functioning mimic cerebral damage from hypoxia. Daytime sleepiness measures are also not associated with objective measures of apnea burden, like AHI, hypoxemia, or sleep parameters.
What cerebrovascular diseases can a high apnea burden cause?
High apnea burden can cause cerebrovascular diseases such as stroke.
What are the effects of CPAP therapy on cerebral function?
CPAP reduces both objective and subjective daytime sleepiness and improves executive functioning. However, it does not alleviate depression symptoms, which occur in 40% of OSA patients. In younger patients with good compliance, CPAP can normalize all aspects of brain function.
What cardiovascular diseases are associated with OSA?
OSA is associated with coronary artery disease (CAD), heart failure (HF), and cerebrovascular diseases such as stroke, with an incidence rate between 30-50% in patients with these conditions.
How do OSA and cardiovascular diseases interact pathophysiologically?
The interaction is complex, but oxidative stress and endothelial dysfunction are key mechanisms leading to cardiovascular diseases in OSA. OSA also increases sympathetic activity.
What is the relationship between OSA and arterial hypertension?
OSA is an independent risk factor for arterial hypertension, which in turn is a risk factor for CAD, HF, and stroke. This makes it challenging to prove a causal relationship between OSA and CVD independent of hypertension.
How does CPAP therapy affect cardiovascular function in OSA patients?
CPAP reduces nocturnal sympathetic activation, oxidative stress, endothelial dysfunction, leptin levels, interleukins, CRP, platelet aggregability, and fibrinogen levels. It also lowers nocturnal and diurnal blood pressure in OSA.
What is the relationship between metabolic syndrome and obesity?
Metabolic syndrome, defined by a large waist, high BP, high fasting BG, and reduced HDL cholesterol, is strongly associated with obesity and its sequelae, contributing to cardiovascular risk.
How does white adipose tissue affect cardiovascular health?
White adipose tissue releases leptins and acids that contribute to inflammation and negative cardiovascular effects. In obesity, adipose tissue secretion is increased and altered due to relative hypoxia of adipocytes, particularly in intra-abdominal or visceral adipose tissue.
How does sleep affect metabolic syndrome?
Sleep restriction in healthy individuals causes insulin resistance, reduced leptin, increased ghrelin concentrations, and increased appetite. Chronic stress also alters energy uptake, leading to obesity.
How does OSA impact metabolic syndrome?
OSA is associated with a fivefold increase in metabolic syndrome. Leptin levels correlate with OSA severity, but causality is unclear due to the confounding effects of obesity.
How does CPAP therapy affect metabolic status?
CPAP improves glucose control and insulin sensitivity in non-diabetic patients. In overweight and Type 2 diabetes patients, CPAP has no significant effect on metabolic status.
How can weight loss improve OSA and metabolic outcomes?
A clinically meaningful reduction in body weight by about 20kg, coupled with counseling and a low-energy diet, improves OSA by over 60% and subsequently enhances metabolic outcomes.
What are the known consequences of CSA in heart failure patients?
Unlike OSA, the consequences of CSA in HF patients are unclear. Patients with HF have less daytime sleepiness than controls despite reduced total sleep time, and no correlation between ESS and AHI in HF, though there is a correlation between ESS and severity of HF.
What changes occur in sleep stages with CSA treatment?
Treatment leads to less Stage N1 sleep and more Stage N2 sleep, with no significant effect on SWS, REM, or arousals. It’s uncertain whether CSA profoundly disturbs sleep or only affects conventional sleep scoring.
Why is it difficult to study the neurobehavioral impacts of CSA in heart failure patients?
HF patients tend to be elderly, which disturbs sleep, and both HF and age affect general health and sleep quality. The relationship is partly due to oxidative stress and sympathetic activation.
How do the cardiovascular effects of CSA differ from those of OSA?
CSA is primarily associated with severe HF, and the oscillation of ventilation, HR, and SaO2 in CSA is distinct from OSA’s negative pressure swings and consecutive hypoxia. A failing heart is more vulnerable to stressors like increased BP and sympathetic activation, making OSA particularly detrimental in patients with established HF.
Are the cardiovascular consequences of CSA in HF patients clear?
The cardiovascular consequences of CSA are unclear, and it’s uncertain if CSA contributes to morbidity and mortality in CHF patients or is merely a phenomenon.
What effect does CPAP have on CSA?
CPAP reduces CSA by around 50%.
What is the relationship between CSA and neurobiological sequelae and CV sequelae?
There is no clear relationship between CSA and neurobiological sequelae, and the CV sequelae of CSA are not well established compared to OSA.
How does OSA impact the normal physiological changes during NREM sleep?
OSA disrupts the normal decrease in metabolic rate, sympathetic nerve activity, blood pressure, and heart rate, along with the increase in vagal tone. Cycles of hypoxia and CO2 retention alter sympathetic and parasympathetic activity, increasing ventilatory drive and creating negative intrathoracic pressure.
What are the cardiac effects of negative intrathoracic pressure during OSA?
Negative intrathoracic pressure increases right ventricular (RV) preload and pulmonary vasoconstriction, which can cause the right ventricle to dilate and bulge into the left ventricle (LV), impairing LV filling and reducing stroke volume. It also increases the transmural pressure across the LV walls, increasing effective afterload
How does OSA impact sympathetic and parasympathetic tone?
OSA increases sympathetic tone, raising systemic vascular resistance. Apnea termination arousals are associated with increased sympathetic tone and decreased vagal tone, leading to higher blood pressure and heart rate. High sympathetic tone persists during wakefulness and impairs vagally mediated heart rate variability.
How does intermittent hypoxia contribute to cardiovascular risks in OSA?
Intermittent hypoxia triggers oxygen free radical production and activates inflammatory pathways, predisposing patients to atherosclerosis and thrombosis.
How do coexisting conditions affect the mortality data for OSA?
Conditions like hypertension and obesity complicate the analysis of OSA’s impact on survival. Most mortality data come from retrospective or observational studies, which may have referral bias or lack sufficient data on severe OSA.
What did an early retrospective study by He reveal about survival and OSA in regard to treatment?
The study showed decreased survival in untreated patients with an AHI > 20/hr and unchanged survival when treated.
How do cardiovascular diseases impact OSA patients’ mortality?
An OSA study from 1976 to 1988 found that 53% of deaths were due to respiratory or cardiovascular causes. Additionally, the risk of mortality is higher for patients with moderate or severe OSA compared to the general population, with the presence of comorbidities further increasing this risk.
How does the severity of OSA affect mortality in patients of different ages?
In patients younger than 62 years, increased mortality is associated with heart failure or diabetes mellitus. In those older than 62 years, predictors include COPD, congestive heart failure, and diabetes mellitus. However, older patients with mild to moderate OSA seem resistant to the adverse effects of OSA on mortality.
What relationship exists between OSA and all-cause mortality?
Multiple studies indicate an increase in all-cause mortality associated with moderate to severe OSA, with an increased risk of cardiovascular events and mortality for severe OSA compared to those with normal sleep, snorers, or mild OSA.
What is the gender difference in mortality risk for OSA patients?
Studies show strong evidence of increased mortality in untreated middle-aged male patients with severe OSA. Women with severe OSA may also face increased mortality, though the evidence is not as strong.
How do sleepiness symptoms correlate with OSA’s adverse outcomes?
Studies indicate that adverse outcomes correlate more with measures of oxygenation than sleepiness, suggesting that intermittent hypoxemia, rather than sleep fragmentation, is associated with increased mortality. The Wisconsin-based cohort found increased cardiovascular mortality with severe OSA, regardless of sleepiness symptoms.
How does the timing of death differ for OSA patients?
OSA patients have a higher relative risk of sudden death from cardiac causes between midnight and 6 am compared to other times, contrasting with the general population, which has a nadir of sudden death risk during this period.
How variable is the severity of excessive daytime sleepiness (EDS) in OSA?
EDS severity is highly variable. Chronic sleep deprivation and fragmentation from respiratory events are believed to cause sleepiness, though hypoxemia may also play a role. No clear PSG variable explains EDS, and correlations between sleep fragmentation and cognitive functioning or EDS are modest.
