Hypertension, Coronary Artery Disease, &

Congestive Heart Failure

Oleh:
dr. I Putu Agus Wismantara, SpJP

Bagian/SMF Kardiologi dan Kedokteran Vaskular

FK Unud-RSUP Sanglah Denpasar
HYPERTENSION
 EPIDEMIOLOGI
• Penderita di Amerika  60 juta orang
• Penderita di dunia  1 milyar orang
• Diprediksi pada tahun 2025  akan meningkat
menjadi 1,5 milyar orang ≈ 1/3 jumlah total
penduduk dunia

• Merupakan faktor risiko terjadinya infark

miokard, stroke, gagal jantung, gangguan irama
jantung

Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine, 8 th edition. 2007. Saunders Elsevier.
 Cardiovascular Mortality Risk Doubles with Each 20/10 mmHg
Increment in Systolic/Diastolic BP*

Cardiovascular mortality risk

8
8X
risk
6

4
4X
risk
2
2X
1X risk risk
0
115/75 135/85 155/95 175/105
Systolic BP/Diastolic BP (mmHg)

*Individuals aged 40–69 years Lewington et al. Lancet 2002;360:1903–13

7/21/20 PLEASE INSERT Presentation title 7
 Hypertension
More Than Just High BP

A complex syndrome in which neurohumoral and

metabolic abnormalities influence development
and progression of vascular disease and clinical
events

A complex inherited syndrome of cardiovascular risk factors

Hypertension Syndrome
Giles,TD, JCI Suppl,2005
Assessment of the Overall Cardiovascular Risk

Search for target organ damage

Cerebrovascular disease
- transient ischemic attacks
- ischemic or hemorrhagic stroke
- vascular dementia
Hypertensive retinopathy
Left ventricular dysfunction
Left ventricular hypertrophy
Coronary artery disease
- myocardial infarction
- angina pectoris
- congestive heart failure
Chronic kidney disease
- hypertensive nephropathy (GFR < 60
ml/min/1.73 m2)
- albuminuria
Peripheral artery disease
- intermittent claudication
- ankle brachial index < 0.9

2009 Canadian Hypertension Education Program Recommendations

The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. JAMA 2003.
 PENGUKURAN TEKANAN DARAH
• Pasien duduk tenang selama beberapa menit
(± 5 menit)
• Lakukan 2x pengukuran, dengan rentang
waktu 1-2 menit
• Pakai manset dengan ukuran yang sesuai
(pakai manset yang kecil untuk anak-anak)
• Posisi manset setinggi jantung

Pickering TG, et al. 2005. Recommendations for Blood Pressure Measurement in Humans. Hypertension. Journal of American Heart Association.
 PENGUKURAN TEKANAN DARAH
• Palpasi arteri brakial pada fossa antecubital,
tempatkan pertengahan manset tepat diatas
pulsasi arterial, dengan bagian bawah manset
2 - 3 cm diatas fossa antecubital.

Pickering TG, et al. 2005. Recommendations for Blood Pressure Measurement in Humans. Hypertension. Journal of American Heart Association.
 PENGUKURAN TEKANAN DARAH
• Baik pasien maupun pengukur tidak
diperbolehkan bicara saat pengukuran
dilakukan.

• Manset diinflasi minimal 30 mm Hg diatas titik

dimana pulsasi radialis menghilang.

• Kecepatan deflasi sekitar 2-3 mm Hg per detik.

Pickering TG, et al. 2005. Recommendations for Blood Pressure Measurement in Humans. Hypertension. Journal of American Heart Association.
 PENGUKURAN TEKANAN DARAH
• Korotkoff I  tekanan sistolik
• Korotkoff V  tekanan diastolik

Pickering TG, et al. 2005. Recommendations for Blood Pressure Measurement in Humans. Hypertension. Journal of American Heart Association.
 Faktor-faktor Risiko
• Umur, Laki-laki > 55 tahun, Perempuan > 65 tahun
• Merokok
• Dyslipidemia
• Kadar gula darah puasa 102-125 mg/dL
• Test toleransi glukosa abnormal
• Obesitas sentral (lingkar pinggang > 102 cm untuk laki-
laki, >88 cm untuk perempuan)
• Riwayat keluarga menderita penyakit kardiovaskular
pada usia <55 tahun untuk laki-laki dan <65 tahun untuk
perempuan

2007 Guidelines for the Management of Arterial Hypertension. ESH and ESC Guidelines. European Heart Journal.
 PATOFISIOLOGI HIPERTENSI
• Mekanisme terjadinya hipertensi primer dapat
terjadi melalui beberapa mekanisme, antara
lain:
– mekanisme neural,
– mekanisme renal,
– mekanisme vaskular,
– mekanisme hormonal

Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine, 8 th edition. 2007. Saunders Elsevier.
 Mekanisme Neural
• Aktivitas yang berlebih pada sistem simpatetis
dapat ditemukan pada fase awal hipertensi

Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine, 8 th edition. 2007. Saunders Elsevier.
 Mekanisme Renal
• Kerusakan pada kemampuan ginjal
mengeluarkan natrium berlebih.

• Natrium berlebih meningkatkan volume

plasma, meningkatkan curah jantung, dan
memicu respon autoregulasi yang
meningkatkan resistensi vaskular sistemik

Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine, 8 th edition. 2007. Saunders Elsevier.
 Mekanisme Vaskular
• Disfungsi sel endotel, aktivasi neurohormonal,
dan peningkatan tekanan darah menyebabkan
remodeling dari pembuluh darah, yang
memperparah kondisi hipertensi

Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine, 8 th edition. 2007. Saunders Elsevier.
 Mekanisme Hormonal

Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine, 8 th edition. 2007. Saunders Elsevier.
Klasifikasi etiologi

1. Hipertensi primer (esensial) -- 90 - 95 %

Etiologi tidak diketahui

2. Hipertensi sekunder -- 5 - 10 %
Etiologi diketahui -- dari sistem / organ lain
a. penyakit ginjal (hipertensi renal)
b. penyakit metabolik (DM, hipertiroid,
feokromositoma, hiperaldosteronisme primer)
c. penyakit jantung & pembuluh darah
d. obat-obatan (steroid, kontrasepsi, antidepresan)
e. kehamilan
Simtom : tidak spesifik
- tidak ada keluhan
- sakit kepala - vertigo
- sulit tidur
- berdebar-debar

Sign : tidak spesifik

- sehubungan dengan komplikasi
Komplikasi
A. Akut (krisis hipertensi)
berhubungan dengan tingginya tekanan darah
1. Hipertensi gawat (emergency)
2. Hipertensi darurat (urgency)

B. Kronik
berhubungan dengan aterosklerosis
1. Otak
2. Mata
3. Jantung
4. Ginjal
 HIGH BLOOD PRESSURE OR
HYPERTENSIVE DISEASE
DISEASE CLINICAL EVENTS

TIA

CEREBROVASCULAR STROKE

HIGH BP : DEMENTIA
- Genetic predisposition
ANGINA
- Life stye CARDIOVASCULAR
- Environment IMA

CHF

RENAL
ESRD
Treatment of Adults with Systolic/Diastolic Hypertension
without Other Compelling Indications
TARGET <140/90 mmHg
INITIAL TREATMENT AND MONOTHERAPY

Lifestyle modification A combination of 2 first line drugs may

be considered as initial therapy if the
therapy blood pressure is >20 mmHg systolic or
>10 mmHg diastolic above target

Long- Beta-
Thiazide ACEI ARB acting
blocker*
CCB

• BBs are not indicated as first line therapy for age 60 and above

ACEI, ARB and direct renin inhibitors are contraindicated in pregnancy and caution is
required in prescribing to women of child bearing potential

2009 Canadian Hypertension Education Program Recommendations

Terapi

1. Modifikasi gaya hidup (non farmakologik)

• diet rendah garam
• kendalikan berat badan
• tidak merokok
• tidak minum alkohol
• olah raga teratur
• hindari stress / relaksasi
2. Obat antihipertensi
a. obat lini pertama (first line drug)
• diuretik
• beta bloker
• antagonis kalsium/calcium channel blocker (CCB)
• penghambat “angiotensin converting enzyme”: (ACE inhibitor)
• angiotensin receptor blocker (ARB)

b. obat lain
• reserpin
• obat yang bekerja sentral (mis. Klonidin)
• alfa metil dopa (antihipertensi pada kehamilan)
• alfa bloker (mis. Prazosin, doxazosin)
1. Diuretik
Mekanisme kerja : mengurangi vol. Plasma
Efek samping : dehidrasi, hiperlipidemi, gangguan toleransi glukosa
Preparat : HCT (12,5 - 25 mg/hari)
Furosemid (20-40 mg/hari)

2. Beta bloker
Mekanisme kerja : mengurangi cardiac out put
Efek samping : bradikardi, bronkokonstriksi
Kontraindikasi : payah jantung, asma bronkial
Preparat : propranolol, atenolol, bisoprolol, metoprolol, carvedilol
3. Antagonis kalsium/calcium channel blocker (CCB)
Mekanisme kerja : relaksasi otot polos arteriol
Efek samping : sakit kepala
Kontra indikasi : payah jantung (relatip)
Preparat : - nifedipin, amlodipine, lercanidipine, felodipine
- diltiazem
- verapamil

4. Penghambat ACE
Mekanisme kerja : menghambat pembentukan angiotensin II
Efek samping : batuk
Kontraindikasi : hamil
Preparat : captopril, lisinopril, ramipril
 Control of Blood Pressure and
Antihypertensive Sites of Action
BP is controlled
via changes in
• Cardiac output
• Vasomotor tone
• Plasma volume 1 3

Heart
4 Diuretics

1 -Blockers
Postcapillary Venules
12 (Capacitance Vessels)

2 Ca Antagonist
Precapillary Arteriole
(Resistance Vessels)
3
ACE Inhibitors
1
Renin 12 AT1-RA
4 Activates
Angiotensin
3
Activates
Kidney Aldosterone 3
 ESH/ESC: Antihypertensive Treatment Preferred Drug
- ACE Aldo-
Diuretic ARB CCB
blocker inhibitor antagonist

Heart failure
• • • • •
Post-MI
• • •
Angina pectoris
• • • •
Diabetes
• •
Renal
dysfunction • •
Previous stroke
Any blood pressure lowering agent

Mancia G, et al. 2007 ESH/ESC Guidelines for the Management of Arterial Hypertension. J Hypertens 2007;25:1105-1187
CORONARY ARTERY DISEASE
 Pendahuluan
• Penyakit Jantung Koroner (PJK) adalah
sekelompok penyakit yang terdiri dari angina
pektoris stabil, angina pektoris tidak stabil,
dan infark miokard
• Ditandai dengan adanya sumbatan di
pembuluh darah arteri oleh plak aterosklerosis
 Sindrome Koroner Akut
• Suatu sindrom yang disebabkan oleh
trombosis akut akibat ruptur plak
aterosklerosis yang menyebabkan penurunan
aliran darah yang tiba-tiba
• Umunya terdapat nyeri dada yang khas
dengan/tanpa disertai perubahan EKG berupa
ST elevasi.
 Sequence of Events in Ischemic
Heart Disease

•Arrythmias
•Lost of muscle
•Angina MI
•Silent
Ischemia Remodeling

CAD
Progresif dilatation

Endothelial dysfunction
Heart Failure
Death
Risk Factor
Risk Factors of Coronary Heart Disease

Non
Modifiable Novel
Modifiable
• Dyslipidemia (LDL • Advanced age • Homocysteine
,HDL) • Male gender (post • Lipoprotein (a)
• Tobacco smoking menopausal • CRP & other
• Hypertension women) inflammatory
• Diabetes Mellitus, • Family history (1st markers
Metabolic degree relatives
Syndrome <55 male or <65
• Lack of Physical female)
Activity
Pathophysiology of Atherosclerosis
Endothelial Dysfunction
•Foam • Fatty •Intermediate •Fibrous • Complicated
• Cells •Streak • Lesion •Atheroma • Plaque •Lesion/Rupture

•oxidized LDL
•homocysteine
•smoking
•aging
•hyperglycemia
•hypertension

35-45 yrs 45-55 yrs 55-65 yrs >65 yrs

•Endothelial •Lipid accumulation•
•adhesion molecules Inflammation •MMP's
injury (ICAM, VCAM) •continued macrophage/lipid
•nitric oxide accumulation •CRP (hepatic)
•monocyte adhesion
•endothelin-1 •
•vasodilation •macrophage LDL uptakeleukocyte accumulation
•cytokines (IL-6,TNFa, IFNg)
 ACS
UAP NSTEMI STEMI

NYERI + + +
DADA YG
KHAS
CARDIAC - + +
MARKER
ST - - +
ELEVASI
 Assessing Chest Pain (Classic Angina)

 Location : usually retrosternal

 Radiation : neck, throat, lower jaw, teeth, ulnar
arm, left shoulder, interscapular, infrascapular,
epigastric
 Character : “Tightness,pressure,burning,
heaviness, aching, strangling, compression” –
Dull & deep
 Time of onset, duration, frequency
 Exacerbating & alleviating factors
“4 E’s : Exercise, Emotional Stress, Exposure to
Cold/Hot humid, Eating”
Relieved by : rest, relax, SL/NTG
 Associated symptoms : breath shortness,
sweating, dizziness, syncope, fatique
TERAPI

Tatalaksana awal sindrome koroner akut di

unit emergensi :
 Oksigen 4 l/mnt (saturasi dipertahankan >
90 %)
 Aspirin 160 mg (dikunyah)
 Nitrat diberikan 5 mg SL (dapat diulang 3
x) lalu drip bila masih nyeri
 Morfin iv bila nyeri tidak teratasi dengan
nitrat
Tatalaksana Sindroma Koroner Akut :
1. Anti iskemik : beta blocker, nitrat, CCB
 Beta blocker pd pasien tanpa kontraindikasi,
khususnya pasien takikardi
 Nitrat IV atau oral untuk nyeri dada akut
 CCB bermanfaat pd pasien dgn kontraindikasi beta
blocker dan pasien dgn angina vasospastik
2. Antiplatelet : aspirin, clopidogrel
 Aspirin dosis awal 160-325 mg dan selanjutnya 75-100
mg/hr
 Clopidogrel loading dose 300 mg, selanjutnya 75
mg/hr
 Yg direncanakan PCI, maka diberikan loading dose
clopidogrel 600 mg
3. Anti koagulan/anti trombin : Heparin
(UFH/LMWH)
 Pemilihan didasarkan pada resiko ischemia
dan perdarahan serta strategi awal yg akan
dilakukan.
4. Anti platelet intravena : penghambat
reseptor GIIb/IIIa
 Pasien dgn resiko sedang sampai tinggi,
khususnya pasien dgn troponin yg
meningkat, atau DM, tirofiban dpt diberikan
sbg terapi awal dan merupakan tambahan
anti platelet.
5. Terapi reperfusi atau revaskularisasi koroner
 Trombolitik/fibrinolitik (streptokinase,
alteplase) atau Percutaneous Coronary
Intervention (PCI) primer pada STEMI
 Early PCI pada NSTE-ACS

6. Terapi tambahan : ACE inhibitor /ARB dan

statin
Tatalaksana jangka panjang
 Perbaiki gaya hidup : berhenti merokok, olah
raga teratur dan diet
 Penurunan berat badan pd pasien obese
 Kontrol tekanan darah
 Intervensi terhadap profil lipid
 Meneruskan pemakaian anti platelet dan anti
koagulan
 Meneruskan ACE inhibitor (pd pasien dgn
LVEF ≤ 40 %, HT, DM dan CKD)
 Meneruskan beta blocker (pd pasien dgn
fungsi ventrikel kiri menurun dgn atau tanpa
gejala gagal jantung)
 ARB (bila intoleransi terhadap ACE inhibitor)
 Antagonis reseptor aldosteron
dipertimbangkan pada pasien pasca infark yg
mendapat ACE inhibitor dan beta blocker dan
dgn LVEF ≤ 40 % dan dgn DM atau gagal
jantung, tanpa disfungsi renal atau
hyperkalemia
 Rehabilitasi dan kembali ke aktivitas fisik
(dalam 4-7 minggu setelah perawatan)
CONGESTIVE HEART FAILURE
 AHA/ACC Guidelines for the Evaluation
and Management of Chronic Heart Failure

A. Definition of HF
• “Heart failure is a complex clinical syndrome that
can result from any structural or functional
cardiac disorder that impairs the ability of the
ventricle to fill with or eject blood.
• The cardinal manifestations of HF are dyspnea
and fatigue, which may limit exercise tolerance,
and fluid retention, which may lead to pulmonary
congestion and peripheral edema.”
ACC/AHA Guidelines 2001
 Forms of Heart Failure
Old paradigm
Forward vs Backward HF
Right-sided vs Left-sided HF
Low Output vs High Output HF

New Paradigm
Systolic vs Diastolic HF
Chronic vs Acute HF
 Acute Vs Chronic HF
Chronic HF
•  develops gradually
•  adaptive mechanisms
•  allow the patient to adjust the abnormality
and reduction in CO.

Acute HF
• Sudden cardiac dysfunction
• Rapid onset of sign an symptom secondary to
inadequate organ perfusion and/or congestion
of the venous bed.
 Classical Pathophysiology of HF
Primary Decreased SNS Release of
disease aortic stimulation Renin /
state pressure angiotensin
catecholamins

Decreased
cardiac Vasoconstriction Increased
vascular
output
volume
Ventricular Increased
dilatation afterload

Heart
Failure Increased
symptoms Preload
The Donkey Analogy
Ventricular dysfunction limits a patient's ability to perform the
routine activities of daily living…
 Classic Symptoms of
Heart Failure
• Dyspnea on exersion Fluid overload
• Lower extremity edema Fluid overload
• Orthopnea Fluid overload
• Paroxysmal nocturnal dyspnea Fluid overload
• Fatigue
Low cardiac output
 Signs of Heart Failure

• Elevated neck veins (jugular venous pressure)

• Positive abdominojugular reflux
• Rales or evidence of pleural effusion
• An S3
• Ascites
• Lower extremity edema
Signs and Symptom of ADHF
Hypotension
Cool extremities
Narrow pulse pressure
Low
Sleepiness, obtundation Perfusion
Elevated BUN, creatinine
Hyponatremia

Orthopnea
Paroxysmal Nocturnal Dyspnea
Neck vein distention
Ascites, edema
Congestion
Hepatojugular Reflux
Rales
Treatment options for patients with chronic
symptomatic systolic Heart Failure

M’c Murray JJV, et. al. Eur Heart J 2012; doi: 10. 1093/eurhj/ehs.104
Diuretics, ACE Inhibitors

Reduce the number of sacks on the wagon

ß-Blockers
Limit the donkey’s speed, thus saving energy
Digitalis Compounds

Like the carrot placed in front of the donkey

Thank You