Aging dan Tidur pada

Gangguan KardioVaskular

Agung Dwi W W

Pokok Bahasan
Proses Aging dan gangguan
Kardiovaskular
Gangguan Tidur pada Kelainan
Kardiovaskular

Proses Aging dan gangguan

Kardiovaskular

Demografi Penuaan
US proporsi manula berusia 65 th dan lebih tua
meningkat dari 12.4 % (35 million) pada tahun
2000 menjadi 19.6 % pada 2030 (71 million) dan
82 million pada 2050.
Manula 80 th menjadi double dari 9.3 million
pada 2000 menjadi 19.5 million pada 2030 dan
lebih dari triple pada 2050.
Wanita 59 % dari manula 65 th pada 2000 dan
estimasi menjadi 56 % pada 2030
Populasi Dunia manula > 65 th meningkat dari
973 million atau 12 % pada 2030 dan 20 %
populasi pada 2050.

Penyakit Cardiovascular dan Penuaan

Penyakit kardiovaskular sering terdeteteksi pada manula
dan sering menjadi penyebab kematian
Hipertensi, atau 2/3 pada manula lebih dari 65 tahun
Heart failure (HF) sering terjadi pada manula dan Dx
KRS RS manula di AS
Profil penyakit berbeda dari dewasa muda.
Systolic, but not diastolic, tekanan darah meningkat
pada manula menjadi Systolic hypertension , terutama
pada wanita
Heart failure terjadi karena fungsi sistolik
Coronary artery disease (CAD) juga terjadi pada manula

Hub Usia, SBP dan risk CHD

Penyakit Kardiovaskular

Perubahan Vaskular
Age-Associated Changes

Cardiovascular Disease

Increased intimal thickness

Arterial stiffening
Increased pulse pressure
Increased pulse wave
velocity
Early central wave
reflections
Decreased endothelialmediated vasodilation

Systolic hypertension
Coronary artery obstruction
Peripheral artery obstruction
Carotid artery obstruction

Perubahan Jantung
Komponen Age-Associated
Changes

Cardiovascular
Disease

Atria

Increased left atrial size Atrial fibrillation

Atrial premature
complexes

Sinus node

Decreased maximal
heart rate Decreased
heart rate variability

Atrioventricul Increased conduction

ar node
time

Sinus node
dysfunction, sick
sinus
Type II block,
third-degree block

Perubahan Jantung
Komponen

Age-Associated
Changes

Cardiovascular
Disease

Valves

Sclerosis, calcification

Stenosis,
regurgitation

Ventricle

Increased left ventricular

wall tension Prolonged
myocardial contraction
Prolonged early diastolic
filling rate Decreased
maximal cardiac output
Right bundle branch
block
Ventricular premature
complexes

Left ventricular
hypertrophy
Heart failure (with or
without preserved
systolic function)
Ventricular
tachycardia,
fibrillation

Gagal jantung

Penyakit Katup Pada Manula

Perubahan Usia terjadi perubahan fibromuscular
skeleton pada jantung mengalami degenerasi dan
infiltrasi yang menyebabkan sklerosis
Sclerosis katub yaitu the aortic valve 30 % pada manula
usia 65 th
Bertambahnya usia lanjut menyebabkan calcification of
the aortic valve leaflets, aortic annulus, base of the
semilunar cusps, and the mitral annulus.
Aortic sclerosis berhubungan dg kejadian atherosclerotic
progression di pembuluh darah. Ini menjelaskan adanya
risk of MI dan kematian pada penderita aortic sclerosis
tanpa stenosis.
Risk factors : hypertension; hyperlipidemia; smoking;
end-stage renal disease; congenital bicuspid valves;
diabetes, shorter stature, and male sex.

Aritmia pada manula

Kehilangan sel pada penuaan di sinus node, sampai
atria, the central fibrous body, dan cytoskeleton jantung.
Perubahan ini merusak area sinus node hingg 90
percent of cells pada usia 75 th.
Kerusakan sinus menyebabkan sinoatrial conduction
menurun
Perubahan juga terjadi pada atrioventricular (AV) node
juga pada His bundle. Terjadi penurunan konduksi ke
ventrikel
Terjadi perubahan pola listrik jantung pada gambaran
EKG P-R interval meningkat dan gelombang R, S, dan T
amplitudonya menurun. QRS axis mergeser ke kiri

HEART FAILURE
HF penyebab utama kelainan pada Manula
HF menyumbang 20 % pada penderita manula
pada 65 th
Kematian meningkat hingga 85 % pada usia
lebih dari 85 tahun
Asymptomatic LV systolic dysfunction estimasi 3
hingga 5 % pada komunitas manula.
Insiden dan prevalens lebih tinggi pada Laki-laki
dari pada wanita. (CAD risk).

Approach to the Older Patient

with Heart Failure (HF)
Symptoms may be nonspecific in the older patient
suspect HF.
Consider HF diagnosis in patients with fatigue, dyspnea,
exercise intolerance, or low activity.
Diagnosis may be assisted by use of echocardiography
or serum markers of HF.
HF may be present in the older patient with preserved
systolic function (ejection fraction), especially older
women.
Aggressive treatment of hypertension or diabetes when
present may improve HF outcomes.

Approach to the Older Patient

with Heart Failure (HF)
Treat symptoms with a goal of improving quality of life
and morbidity:
Control blood pressure-systolic and diastolic.
Treat ischemia.
Control atrial fibrillation rate.
Promote physical activity.
Adjust medications for age and disease-related changes
in kinetics and dynamics.
Educate and involve patients, family members, or
caregivers in management of HF:
Monitor weight.
Consider use of multidisciplinary team approaches.

Hypertension
Diastolic (>90 mm Hg) dan atau systolic (>140 mm Hg)
hypertension hingga 2/3 pada manula 65 th dan 75 %
pada 80 th.
Prevalensi beragam karena Ras (atau genetics)
meningkat pad aorang kulit berwarna
The profile of hypertension is altered by aging. Systolic
hypertension becomes more prevalent with aging
Systolic blood pressure rises with aging in both men and
women but rises more steeply in women.
A large percentage of people are unaware that they have
hypertension, and hypertension is not controlled in many
older patients, especially older women and those older
than 80 years of age.

Approach to Hypertension in
Older Patients
Systolic and diastolic hypertension should be
treated; current recommendations are based on
brachial artery measurements:
Diastolic target is <90 mm Hg
Systolic target is <140 mm Hg
(individualization is necessary for patients older
than 80 years of age)
The focus should be on achieving blood
pressure control, not initial therapy

Approach to Hypertension in
Older Patients
Multiple medications are usually required in older
patients, and combinations should be based on
concomitant diseases
Drug dosing regimens should be adjusted for age- and
disease-related changes in drug metabolism and
potential drug-drug interactions
Patients should be monitored for adverse effects and
drug interactions, especially:
Postural hypotension and postprandial hypotension
Hypovolemia with diuretics
Hyperkalemia with angiotensin-converting enzyme,
angiotensin receptor blocker, or aldosterone
antagonists

Approach to the Older Patient with

Stroke
Prevention is key
Treat hypertension, diabetes, smoking, physical
inactivity, elevated lipids, obesity, and sleep
apnea and limit alcohol intake
Anticoagulate patients with atrial fibrillation (in
the absence of contraindications)
Acute stroke treatment
Evaluate rapidlyuse neuroimaging for
diagnosis and to guide therapy
Aspirin within 48 hr

Approach to the Older Patient with

Stroke

Anticoagulation is not recommended

Initiate rehabilitation early
Routinely evaluate and treat for depression
Secondary prevention:
Aspirin (at lower doses), clopidogrel, or aspirin
plus extended release dipyridamole
Aspirin + clopidogrel is not recommended
Consider warfarin for patients with strokes while
receiving aspirin

Gangguan Tidur pada Kelainan

Kardiovaskular

Normal sleep

The possible function of sleep

Protective behaviour
Energy conservation
Brain restoration
Homoeostasis
Improving immune function
Temperature regulation

Kleitmans dictum, Tell me first what is the function of wakefulness

and then I will tell you what is the function of
sleep.

The characteristics of sleep architecture

hypnogram
over a 7.5-hour sleep period

Characteristics of REM sleep

Arousal threshold

Relatively deep sleep. Increased arousal

threshold to various stimuli

EEG

Desynchronized (low amplitude with high-mixed

frequency, similar to that of stage 1)

EOG

Rapid eye movements (visualization of vivid

dreams, which are characteristic of this stage)

EMG

Absent; effective paralysisatonia of skeletal

muscles

Energy consumption Augmented metabolism and oxygen

consumption by the brain, leading to increased
brain temperature in humans
Cardiovascular

Variable blood pressure, more variable pulse

rate, change in blood flow
distribution ( to the brain)

Characteristics of REM sleep

Breathing

Less rhythmic; increased respiratory variability;

decreased chemosensitivity

Autonomic nervous
system

Increased sympathetic tone, relatively diminished

parasympathetic tone

Other physiological
phenomena

Penile erection in men (increased vaginal blood

flow in women)

Consciousness

In humans, awakening from REM sleep is

associated with dreaming

The possible functions of REM sleep and dreaming

Consolidation of memory and processing newly learned
material
Stimulation to the brain
Solving daytime problems and conflicts

Consequences of sleep deprivation

Behavioural

Sleepiness
Mood changes
Irritability, nervousness

(Both subjective and objective)

Depression/mania
Can turn to violence

Cognitive

Impairment of function

Newly learned skills Short-term

memory Complex tasks Slow
reaction time

Neurological

Mild and quickly reversible

Nystagmus, tremor, ptosis,

slurred speech, increased
reflexes (gag, tendon),
increased sensitivity to pain

Biochemical

Increased metabolic rate

Increased thyroid
activity Insulin resistance

In animals, decreased weight

despite increased caloric
intake (secondary to increased
energy requirement?)

Others

Hypothermia, perhaps
immune function impairment

The effect of behavioural state on the

cardiovascular system
Transition

Wakefulness NREM to
to NREM
tonic REM
sleep
sleep

Phasic REM
sleep

Heart rate

Cardiac
output

Blood
pressure

Total
peripheral
resistance

Minimal
changes

The predominant neurotransmitters in

the various behavioural states
Behavioural Acetylcholine Norepinephrine
state
(noradrenaline)

Serotonin
(5HT)

Wake

++

++

Non-REM sleep

REM
sleep

++

++

Changes in sleep content and length

with age

Infants
Children
Adults
Elderly
people

Sleep
time
(h)

Stages
12 (%)

Stages
34 (%)

REM
(%)

1316
812
69
58

1030
4060
4560
5080

3040
2030
1525
515

4050
2030
1525
1525

Gangguan Tidur

Hypersomnia
Sleep apnoea syndrome
Insomnia
Parasomnias: sleep walking,night mare,
Sleep enuresis

Obstructive sleep apnea and

cardiovascular disease
Obstructive sleep apnea (OSA), along with
smoking, diabetes, dyslipidemia, and
hypertension, is an important risk factor for
coronary artery disease.
In large epidemiological studies, the
association between heart disease and
OSA is independent of such confounders
as obesity and age.

The acute pathophysiological effects of the

apneaarousal cycle include:
The acute pathophysiological effects of
the apneaarousal cycle include:
hypoxemia
increased negative intrathoracic pressure
decreases in cardiac output
activation of the sympathetic nervous
system
acute hypertension.

Pathophysiological effects
Chronic pathophysiological changes associated
with this process include the
following persistent elevations:
sympathetic tone
platelet activation
inflammatory mediators
C-reactive protein
vascular endothelial dysfunction.
All of these effects have been suggested to
promote artherogenesis in OSA.

Other important cardiovascular

effects of OSA include
Essential hypertension. 40% of hypertensive adults have
some degree of sleepdi sordered breathing, which
increases to 80% in treatment-refractory hypertension.
Cardiac arrhythmias. Bradyarrhythmias, prolonged sinus
pauses, and increased ventricular ectopy are common;
atrial fibrillation is also markedly increased in people with
OSA.
Pulmonary hypertension. In most cases the elevations
are modest with the exception of the overlap of OSA and
chronic obstructive pulmonary disease, where pulmonary
hypertension and cor pulmonale are common (see
Respiratory disease and sleep, below).
Insulin resistance (see Other medical illness and sleep,
below).

Congestive heart failure

Several cardinal symptoms of congestive heart
failure (CHF), i.e., orthopnea and paroxysmal
nocturnal dyspnea, involve disruption of sleep.
Sleep-disordered breathing is common in CHF,
with 1530% of individuals with CHF diagnosed
with OSA, and 3040% diagnosed with central
sleep apnea (CSA).
OSA is believed to exacerbate CHF through its
effect on blood pressure, cardiac output, and
ventricular function.

Nocturnal angina
Nocturnal angina may herald an acute coronary
event. Several sleep-related factors predispose
to coronary artery ischemia at night:
nocturnal hypoxemia secondary to OSA
nocturnal autonomic surges associated with
REM sleep
nocturnal hypotension and bradycardia
associated with NREM sleep vasospasm
associated with Prinzmetals variant angina
(most commonly occurs between midnight and
07:00 during REM sleep).

Nocturnal arrhythmia and sudden death

Common and normal rhythm changes seen in sleep include:

sinus pauses
sinus bradycardia
first-degree AV block.
The Brugada syndrome is characterized by distinct ST segment
elevations in the right precordial ECG leads and is associated with a
mutation in a gene encoding a cardiac sodium channel.
A family history of sudden death is common. Kiroshi, a Japanese
term, is used to describe sudden death in otherwise healthy young
people following prolonged episodes of overwork and sleep
deprivation.
Both are causes of sudden cardiac death due to ventricular
fibrillation, predominantly between 20:00 and 08:00, affecting young,
healthy men without structural heart disease, with a higher
incidence in Asian countries.