6. Risk Factors for Hypertension
More common and more severe in blacks
It is likely that increased salt intake is a
necessary but not sufficient cause for
hypertension
Excess alcohol intake increases risk
High cholesterol may also associated with the
development of hypertension
Hypertension may be more common among
those with certain personality traits, such as
hostile attitudes and time urgency/impatience
7. Stevens, VJ, Corrigan, SA, Obarzanek, E, et al, Arch Intern Med 1993; 153:849
Obesity and Hypertension
Obesity is associated with an increased risk of
hypertension, and weight gain appears to be a
main determinant of the rise in blood pressure
that is commonly seen with aging
Weight loss improves blood pressure
8. Why is Hypertension Important?
Hypertension is associated with a number of
serious adverse effects
The likelihood of developing these complications
varies with the blood pressure
The increase in risk begins as the blood
pressure rises above 110/75 mmHg and, at any
blood pressure, is importantly affected by the
presence or absence of other risk factors
10. What Causes Hypertension?
Increased sympathetic neural activity
Increased angiotensin II activity and mineralocorticoid
excess
Reduced adult nephron mass
may be related to genetic factors, intrauterine disturbance (eg,
hypoxia, drugs, nutritional deficiency), and post-natal
environment (eg, malnutrition, infections)
Hypertension is twice as common in those who have
hypertensive parents; genetic factors account for
approximately 30% of the variation in blood pressure
11. Benefit of Treating Hypertension
Antihypertensive therapy has been associated
with 40 percent reduction in stroke; 25 percent in
myocardial infarction; and more than 50 percent
in heart failure
It is estimated that control of hypertension to
below 140/90 mmHg could, in men and women,
prevent 19 and 31 percent of coronary heart
disease events
12. Modification Recommendation Approximate SBP
reduction
Weight
reduction
Maintain normal body weight (BMI 18.5 to
24.9 kg/m2)
5-20 mmHg per
10-kg weight loss
Adopt DASH
eating plan
Consume a diet rich in fruits, vegetables, and
low-fat dairy products with a reduced content
of saturated and total fat
8 to 14 mmHg
Dietary sodium
reduction
Reduce dietary sodium intake to no more than
100 meq/day (2.4 g sodium or 6 g sodium
chloride)
2 to 8 mmHg
Physical activity Engage in regular aerobic physical activity
such as brisk walking (at least 30 minutes per
day, most days of the week)
4 to 9 mmHg
Moderation of
alcohol
consumption
Limit consumption to no more than 2 drinks
per day in most men and no more than 1 drink
per day in women and lighter-weight persons
2 to 4 mmHg
The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood
Pressure, JAMA 2003; 289:2560
Lifestyle modifications in the management of hypertension
13. Obstructive Sleep Apnea and
Hypertension
Wisconsin Sleep Cohort Study
Dose-dependent relationship between severity of sleep apnea and risk
of developing hypertension
Odds for developing hypertension during a 4-8 year follow-up period
compared to subjects with no apneas or hypopneas was 2.0 if AHI was
5-15, and 3.0 if AHI>15
The Sleep Heart Health Study
A cross-sectional analysis of a large community-based multi-center
population showed an increase in odds of 1.4 for hypertension when
AHI > 30 compared to those with AHI < 1.5
The Nurses’ Health Study
Increase in risk of 1.6 for the development of hypertension over an 8-
year follow-up period in regular snorers compared to non-snorers
14. The Relationship between Obstructive
Sleep Apnea and Hypertension
The odds of having
hypertension is 37%
greater in persons with
obstructive sleep apnea
The odds of having
hypertension is 46%
greater in those who
spend greater percentage
of sleep time below 90%
oxygen saturation
Nieto, F. J. et al. JAMA 2000;283:1829-1836
15. Peppard et al. NEJM. 2000; 342:1378-1384
The Relationship between Obstructive
Sleep Apnea and Hypertension
Compared to those
with AHI=0, the odds of
having hypertension
was 42% greater if AHI
was 0.1-5, 2x greater if
AHI was 5-15, and
almost 3x greater if
AHI was more than 15
per hour
19. Tilkian AG, Guilleminault C. Ann Intern Med. 1976 Dec;85(6):714-9
Overnight Polysomnogram in a Patient with Obstructive Sleep Apnea
EEG
EOG
EKG
SBP
PAP
SAO2
RESP
20. The Sympathetic System
Many early studies demonstrated abnormal
autonomic activity in both animal models and in
humans with obstructive sleep apnea:
Increased norepinephrine levels
Increased muscle sympathetic nerve activity
21. Narkiewicz et al. Circulation 1999;100:2332-2335
Sympathetic System: Muscle Nerve
Activity
Compared muscle
sympathetic nervous activity
(MSNA) of blood vessels in
untreated and treated OSA
at baseline and after 1, 6, 12
months of CPAP
MSNA was similar during
repeated measurements in
the untreated group
In contrast, MSNA
decreased significantly over
time in patients treated with
CPAP
22. Sympathetic System: Norepinephrine
Dimsdale et al, Sleep 1995;18:377-81
24-hr urinary NE
increased 45% in apneic
(RDI>20) compared to
non-apneic patients.
CPAP treatment lowered
daytime plasma NE
levels by 23%; Placebo
had no effect on NE
levels
23. Treating Obstructive Sleep Apnea
Several trials have demonstrated improved
systolic and diastolic blood pressures with both
short-term and long-term CPAP use
Regular CPAP use has also shown to improve
blood pressure in patients with refractory
hypertension who were requiring three or more
antihypertensive medications
24. The seventh Joint National Committee on
Prevention, Detection, Evaluation, and
Treatment of High Blood Pressure
recommends evaluating for and treating
obstructive sleep apnea in adults with
hypertension
25. Obstructive Sleep Apnea and other
Cardiovascular Diseases
www.rjmatthewsmd.com/Definitions/img/osa-fig3.gif
26. Summary
Hypertension is a serious disease that affects many
people
Scientific evidence for a link between obstructive sleep
apnea and hypertension is compelling
Sleep apnea is thought to contribute to hypertension by
increasing sympathetic nervous system activity and
causing vascular dysfunction
Animal studies have demonstrated that sleep apnea can
cause hypertension
Human epidemiological studies confirm that untreated
sleep apnea increases the risk of having hypertension
27. Summary
CPAP stabilizes the upper airway, preventing collapse
and the acute cardiovascular and hemodynamic
consequences of obstructive sleep apnea
CPAP applied over several weeks reduces both systolic
and diastolic blood pressure by ~10 mm Hg. These
reductions are predicted to reduce stroke risk by 56%
and coronary heart disease event risk by 37%
The United States National Heart, Lung, and Blood
Institute now recognizes sleep apnea as a significant and
reversible cause of hypertension
These definitions apply to adults on no antihypertensive medications and who are not acutely ill. If there is a disparity in category between the systolic and diastolic pressures, the higher value determines the severity of the hypertension. The systolic pressure is the greater predictor of risk in patients over the age of 50 to 60.
Hypertension is the major risk factor for premature cardiovascular disease
Hypertension increases the risk of heart failure with the hazard increasing with the degree of blood pressure elevation
Hypertension is the most common and most important risk factor for stroke, the incidence of which can be markedly reduced by effective antihypertensive therapy
Hypertension is the most important risk factor for the development of intracerebral hemorrhage
Hypertension is a risk factor for chronic renal insufficiency and end-stage renal disease
Marked elevations in blood pressure can cause an acute, life-threatening emergency
1) During apnea:
Mueller maneuver = neg intrathoracic pressure as low as -80 cmH2O; Large negative ITP generated during obstructive apneas may increase LV transmural pressure causing greater myocardial oxygen demand and reduced cardiac output; neg ITP also stretches aorta and activate aortic baroreceptors causing intermittent inhibition of sympath to heart;
Hypoxia = chemoreceptors in carotid bodies, increase MV, symp of periph blood vessels, parasymp to heart; Chronic hypoxemia from apneic episodes may induce pulmonary vasoconstriction, and subsequent smooth muscle hypertrophy and vascular remodeling
Hypercapnia = central R, increase MV, symph vasoconstriction, augments chemoreflex response to hypoxia
2) EEG arousals - increase in sympath, activates upper airway dilator muscles and promotes systemic and pulmonary vascular constriction
3) Resumption of breathing - increase venous return, increase CO, already constricted periphs, result in acute increases in BP, increased venous return may distends RV, interventr septal shift toward left, reducing LV compliance and filling, labile BP