The National High Blood Pressure Education Program presents the complete Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Like its predecessors, the purpose is to provide an evidence-based approach to the prevention and management of hypertension. The key messages of this report are these: in those older than age 50, systolic blood pressure (BP) of greater than 140 mm Hg is a more important cardiovascular disease (CVD) risk factor than diastolic BP; beginning at 115/75 mm Hg, CVD risk doubles for each increment of 20/10 mm Hg; those who are normotensive at 55 years of age will have a 90% lifetime risk of developing hypertension; prehypertensive individuals (systolic BP 120-139 mm Hg or diastolic BP 80-89 mm Hg) require health-promoting lifestyle modifications to prevent the progressive rise in blood pressure and CVD; for uncomplicated hypertension, thiazide diuretic should be used in drug treatment for most, either alone or combined with drugs from other classes; this report delineates specific high-risk conditions that are compelling indications for the use of other antihypertensive drug classes (angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, beta-blockers, calcium channel blockers); two or more antihypertensive medications will be required to achieve goal BP (<140/90 mm Hg, or <130/80 mm Hg) for patients with diabetes and chronic kidney disease; for patients whose BP is more than 20 mm Hg above the systolic BP goal or more than 10 mm Hg above the diastolic BP goal, initiation of therapy using two agents, one of which usually will be a thiazide diuretic, should be considered; regardless of therapy or care, hypertension will be controlled only if patients are motivated to stay on their treatment plan. Positive experiences, trust in the clinician, and empathy improve patient motivation and satisfaction. This report serves as a guide, and the committee continues to recognize that the responsible physician's judgment remains paramount.

Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

Background Sleep-disordered breathing is prevalent in the general population and has been linked to chronically elevated blood pressure in cross-sectional epidemiologic studies. We performed a prospective, population-based study of the association between objectively measured sleep-disordered breathing and hypertension (defined as a laboratory-measured blood pressure of at least 140/90 mm Hg or the use of antihypertensive medications). Methods We analyzed data on sleep-disordered breathing, blood pressure, habitus, and health history at base line and after four years of follow-up in 709 participants of the Wisconsin Sleep Cohort Study (and after eight years of follow-up in the case of 184 of these participants). Participants were assessed overnight by 18-channel polysomnography for sleep-disordered breathing, as defined by the apnea–hypopnea index (the number of episodes of apnea and hypopnea per hour of sleep). The odds ratios for the presence of hypertension at the four-year follow-up study according to...

https://www.nejm.org/doi/pdf/10.1056/NEJM200005113421901

Prospective study of the association between sleep-disordered breathing and hypertension.

Population-based epidemiologic studies have uncovered the high prevalence and wide severity spectrum of undiagnosed obstructive sleep apnea, and have consistently found that even mild obstructive sleep apnea is associated with significant morbidity. Evidence from methodologically strong cohort studies indicates that undiagnosed obstructive sleep apnea, with or without symptoms, is independently associated with increased likelihood of hypertension, cardiovascular disease, stroke, daytime sleepiness, motor vehicle accidents, and diminished quality of life. Strategies to decrease the high prevalence and associated morbidity of obstructive sleep apnea are critically needed. The reduction or elimination of risk factors through public health initiatives with clinical support holds promise. Potentially modifiable risk factors considered in this review include overweight and obesity, alcohol, smoking, nasal congestion, and estrogen depletion in menopause. Data suggest that obstructive sleep apnea is associated with all these factors, but at present the only intervention strategy supported with adequate evidence is weight loss. A focus on weight control is especially important given the expanding epidemic of overweight and obesity in the United States. Primary care providers will be central to clinical approaches for addressing the burden and the development of cost-effective case-finding strategies and feasible treatment for mild obstructive sleep apnea warrants high priority.

Epidemiology of obstructive sleep apnea: a population health perspective.

ContextSleep-disordered breathing (SDB) and sleep apnea have been linked to
hypertension in previous studies, but most of these studies used surrogate
information to define SDB (eg, snoring) and were based on small clinic populations,
or both.ObjectiveTo assess the association between SDB and hypertension in a large cohort
of middle-aged and older persons.Design and SettingCross-sectional analyses of participants in the Sleep Heart Health Study,
a community-based multicenter study conducted between November 1995 and January
1998.ParticipantsA total of 6132 subjects recruited from ongoing population-based studies
(aged ≥40 years; 52.8% female).Main Outcome MeasuresApnea-hypopnea index (AHI, the average number of apneas plus hypopneas
per hour of sleep, with apnea defined as a cessation of airflow and 
hypopnea defined as a ≥30% reduction in airflow
or thoracoabdominal excursion both of which are accompanied by a ≥4% drop in oxyhemoglobin
saturation), obtained by unattended home polysomnography. Other measures include
arousal index; percentage of sleep time below 90% oxygen saturation; history
of snoring; and presence of hypertension, defined as resting blood pressure
of at least 140/90 mm Hg or use of antihypertensive medication.ResultsMean systolic and diastolic blood pressure and prevalence of hypertension
increased significantly with increasing SDB measures, although some of this
association was explained by body mass index (BMI). After adjusting for demographics
and anthropometric variables (including BMI, neck circumference, and waist-to-hip
ratio), as well as for alcohol intake and smoking, the odds ratio for hypertension,
comparing the highest category of AHI (≥30 per hour) with the lowest category
(<1.5 per hour), was 1.37 (95% confidence interval [CI], 1.03-1.83; P for trend=.005). The corresponding estimate comparing
the highest and lowest categories of percentage of sleep time below 90% oxygen
saturation (≥12% vs <0.05%) was 1.46 (95% CI, 1.12-1.88; P for trend <.001). In stratified analyses, associations of hypertension
with either measure of SDB were seen in both sexes, older and younger ages,
all ethnic groups, and among normal-weight and overweight individuals. Weaker
and nonsignificant associations were observed for the arousal index or self-reported
history of habitual snoring.ConclusionOur findings from the largest cross-sectional study to date indicate
that SDB is associated with systemic hypertension in middle-aged and older
individuals of different sexes and ethnic backgrounds.

/pdf/association-of-sleep-disordered-breathing-sleep-apnea-and-4rltgqnm1r.pdf

Association of Sleep-Disordered Breathing, Sleep Apnea, and Hypertension in a Large Community-Based Study

These practice parameters are an update of the previously-published recommendations regarding the indications for polysomnography and related procedures in the diagnosis of sleep disorders. Diagnostic categories include the following: sleep related breathing disorders, other respiratory disorders, narcolepsy, parasomnias, sleep related seizure disorders, restless legs syndrome, periodic limb movement sleep disorder, depression with insomnia, and circadian rhythm sleep disorders. Polysomnography is routinely indicated for the diagnosis of sleep related breathing disorders; for continuous positive airway pressure (CPAP) titration in patients with sleep related breathing disorders; for the assessment of treatment results in some cases; with a multiple sleep latency test in the evaluation of suspected narcolepsy; in evaluating sleep related behaviors that are violent or otherwise potentially injurious to the patient or others; and in certain atypical or unusual parasomnias. Polysomnography may be indicated in patients with neuromuscular disorders and sleep related symptoms; to assist in the diagnosis of paroxysmal arousals or other sleep disruptions thought to be seizure related; in a presumed parasomnia or sleep related seizure disorder that does not respond to conventional therapy; or when there is a strong clinical suspicion of periodic limb movement sleep disorder. Polysomnography is not routinely indicated to diagnose chronic lung disease; in cases of typical, uncomplicated, and noninjurious parasomnias when the diagnosis is clearly delineated; for patients with seizures who have no specific complaints consistent with a sleep disorder; to diagnose or treat restless legs syndrome; for the diagnosis of circadian rhythm sleep disorders; or to establish a diagnosis of depression.

/pdf/practice-parameters-for-the-indications-for-polysomnography-79szzyhm7q.pdf

Practice parameters for the indications for polysomnography and related procedures: an update for 2005.

Sleep-induced apnea and disordered breathing refers to intermittent, cyclical cessations or reductions of airflow, with or without obstructions of the upper airway (OSA). In the presence of an anat...

Pathophysiology of Sleep Apnea

Background: Clinical observations have linked sleepdisordered breathing, a condition of repeated apneas and hypopneas during sleep, with hypertension but evidence for an independent association has been lacking. Understanding this relationship is important because the prevalence of sleep-disordered breathing is high in adults. Objective: To test the hypothesis that sleep-disordered breathing is related to elevated blood pressure independent of confounding factors. Methods: The sample included 1060 employed women and men aged 30 through 60 years who had completed an overnight protocol as part of the Wisconsin Sleep Cohort Study. In-laboratory polysomnography was used to determine sleep-disordered breathing status, quantified as the number of apneas and hypopneas per hour of sleep (apnea-hypopnea index). Blood pressure was measured on the night polysomnography was performed. Results: Blood pressure increased linearly with increasing apnea-hypopnea index (P=.003 for systolic,P=.01 for diastolic, adjusted for confounding factors). The magnitude of the linear association increased with decreasing obesity. At a body mass index (weight in kilograms divided by the square of the height in meters) of 30 kg/m2, an apnea-hypopnea index of 15 (vs 0) was associated with blood pressure increases of 3.6 mm Hg for systolic (95% confidence interval, 1.3-6.0) and 1.8 mm Hg for diastolic (95% confidence interval, 0.3-3.3). The odds ratio for hypertension associated with an apneahypopnea index of 15 (vs 0) was 1.8 (95% confidence interval, 1.3-2.4). Conclusions: There is a dose-response relationship between sleep-disordered breathing and blood pressure, independent of known confounding factors. If causal, the high prevalence of sleep-disordered breathing could account for hypertension in a substantial number of adults in the United States. Arch Intern Med. 1997;157:1746-1752

https://jamanetwork.com/HttpHandlers/ArticlePdfHandler.ashx?journal=INTEMED&articleId=623690&pdfFileName=archinte_157_15_019.pdf

Population-Based Study of Sleep-Disordered Breathing as a Risk Factor for Hypertension

1. We recently showed that fatigue of the inspiratory muscles via voluntary efforts caused a time-dependent increase in limb muscle sympathetic nerve activity (MSNA) (St Croix et al. 2000). We now asked whether limb muscle vasoconstriction and reduction in limb blood flow also accompany inspiratory muscle fatigue. 2. In six healthy human subjects at rest, we measured leg blood flow («Q L) in the femoral artery with Doppler ultrasound techniques and calculated limb vascular resistance (LVR) while subjects performed two types of fatiguing inspiratory work to the point of task failure (3–10 min). Subjects inspired primarily with their diaphragm through a resistor, generating (i) 60 % maximal inspiratory mouth pressure (P M) and a prolonged duty cycle (TI/TTOT = 0.7); and (ii) 60 % maximal PM and a TI/TTOT of 0.4. The first type of exercise caused prolonged ischaemia of the diaphragm during each inspiration. The second type fatigued the diaphragm with briefer periods of ischaemia using a shorter duty cycle and a higher frequency of contraction. End-tidal P CO2 was maintained by increasing the inspired CO2 fraction (FI,CO2 ) as needed. Both trials caused a 25–40 % reduction in diaphragm force production in response to bilateral phrenic nerve stimulation. 3. «Q L and LVR were unchanged during the first minute of the fatigue trials in most subjects; however, «QL subsequently decreased (_30 %) and LVR increased (50–60 %) relative to control in a time-dependent manner. This effect was present by 2 min in all subjects. During recovery, the observed changes dissipated quickly (< 30 s). Mean arterial pressure (MAP; +4–13 mmHg) and heart rate (+16–20 beats min _1 ) increased during fatiguing diaphragm contractions. 4. When central inspiratory motor output was increased for 2 min without diaphragm fatigue by increasing either inspiratory force output (95 % of maximal inspiratory pressure (MIP)) or inspiratory flow rate (5 w eupnoea), «Q L, MAP and LVR were unchanged; although continuing the high force output trials for 3 min did cause a relatively small but significant increase in LVR and a reduction in «Q L. 5. When the breathing pattern of the fatiguing trials was mimicked with no added resistance, LVR was reduced and «Q L increased significantly; these changes were attributed to the negative feedback effects on MSNA from augmented tidal volume. 6. Voluntary increases in inspiratory effort, in the absence of diaphragm fatigue, had no effect on «Q L and LVR, whereas the two types of diaphragm-fatiguing trials elicited decreases in «QL and increases in LVR. We attribute these changes to a metaboreflex originating in the diaphragm. Diaphragm and forearm muscle fatigue showed very similar time-dependent effects on LVR and «Q L.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1469-7793.2001.0277k.x

Fatiguing inspiratory muscle work causes reflex reduction in resting leg blood flow in humans.

The relative contributions of hypoxia and hypercapnia in causing persistent sympathoexcitation after exposure to the combined stimuli were assessed in nine healthy human subjects during wakefulness...

Exposure to hypoxia produces long-lasting sympathetic activation in humans.

We tested the hypothesis that reflexes arising from working respiratory muscle can elicit increases in sympathetic vasoconstrictor outflow to limb skeletal muscle, in seven healthy human subjects at rest. We measured muscle sympathetic nerve activity (MSNA) with intraneural electrodes in the peroneal nerve while the subject inspired (primarily with the diaphragm) against resistance, with mouth pressure (PM) equal to 60 % of maximal, a prolonged duty cycle (TI/TTot) of 0.70, breathing frequency (fb) of 15 breaths min-1 and tidal volume (VT) equivalent to twice eupnoea. This protocol was known to reduce diaphragm blood flow and cause fatigue. MSNA was unchanged during the first 1-2 min but then increased over time, to 77 +/- 51 % (s.d.) greater than control at exhaustion (mean time, 7 +/- 3 min). Mean arterial blood pressure (+12 mmHg) and heart rate (+27 beats min-1) also increased. When the VT, fb and TI/TTot of these trials were mimicked with no added resistance, neither MSNA nor arterial blood pressure increased. MSNA and arterial blood pressure also did not change in response to two types of increased central respiratory motor output that did not produce fatigue: (a) high inspiratory flow rate and fb without added resistance; or (b) high inspiratory effort against resistance with PM of 95 % maximal, TI/TTot of 0.35 and fb of 12 breaths min-1. The heart rate increased by 5-16 beats min-1 during these trials. Thus, in the absence of any effect of increased central respiratory motor output per se on limb MSNA, we attributed the time-dependent increase in MSNA during high resistance, prolonged duty cycle breathing to a reflex arising from a diaphragm that was accumulating metabolic end products in the face of high force output plus compromised blood flow.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1469-7793.2000.00493.x

Barbara J. Morgan

Papers

Pathophysiology of Sleep Apnea

Population-Based Study of Sleep-Disordered Breathing as a Risk Factor for Hypertension

Fatiguing inspiratory muscle work causes reflex reduction in resting leg blood flow in humans.

Exposure to hypoxia produces long-lasting sympathetic activation in humans.

Fatiguing inspiratory muscle work causes reflex sympathetic activation in humans.