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HIPERTENSI
Congestive
Heart FailurePenyusunSteven Octavianus ( 406117064 )
Reyjen ( 406117069 )
Pembimbing
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Epidemiologi
Dalam studi pustaka yang dilakukan oleh
Master, dkk (dikutip oleh Caird, 1985)
menemukan bahwa prevalensi hipertensi
pada orang-orang lanjut usia adalah sebesar
30-65%.
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Pendahuluan
Dengan makin meningkatnya harapan hidup
penduduk Indonesia, maka dapat diperkirakan
bahwa insidensi penyakit degeneratif akan
meningkat pula
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etiologi
Berdasarkan etiologinya, hipertensi dibagi
menjadi:
Hipertensi primer atau esensial
Hipertensi sekunder
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PENYEBAB
genetiklingkunganalkoholmerokokstressobesitas
estrogenpenyakit ginjaleklamsipre eklamsi
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KLASIFIKASISISTOLIK
(mmHg)
Diastolik
(mmHg)
Normal < 120 < 80
Pre-hipertensi 120139 80 - 89
Hipertensi stad. 1 140159 9099
Hipertensi stad. 2 160 > 100
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PENGUKURAN TEKANAN
DARAH Tidak minum kopi / merokok 30 menit sebelumnya
Cukup istirahat ( 5 menit berbaring )
Lengan tidak tertutup pakaian
Dipompa 20 30 mmHg di atas sistolik
Diturunkan 2 3 mmHg per-detik
Diulang lagi interval 15 detik
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attention
sistolik > 210 mmHg
diastolik > 120 mmHg
Diagnosis hipertensi pada satu kali
pengukuran
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EVALUASI
A. Anamnesis, meliputi :
1. Lamanya menderita hipertensi
2. Indikasi adanya hipertensi sekunder
3. Faktor-faktor resiko
4. Gejala kerusakan organ
5. Pengobatan hipertensi sebelumnya6. Faktor-faktor pribadi, keluarga dan lingkungan
B. Pemeriksaan fisik
Memeriksa tekanan darah
Mengevaluasi adanya penyakit penyerta & kerusakan organ target
Kemungkinan adanya hipertensi sekunder
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EVALUASI
C. Pemeriksaan penunjang
Tes darah rutin
Glukosa darah
Profil lemakAsam urat serum
Kreatinin serum
Kalium serumUrinalisis
Elektrokardiogram
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Pengobatan
NonFarmakologis
Farmakologis
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Blood Pressure Classification
BP Classification SBP mmHg* DBP mmHgLifestyle
Modification
Drug
Therapy**
Normal
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Lifestyle Modification
ModificationApproximate SBP Reduction
(range)
Weight reduction 5-20 mmHg/ 10 kg weight loss
Adopt DASH eating plan 8-14 mmHg
Dietary sodium reduction 2-8 mmHg
Physical activity 4-9 mmHg
Moderation of alcohol
consumption2-4 mmHg
JNC 7 Express. JAMA. 2003 Sep 10; 290(10):1314
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Impact of a 5 mmHg Reduction
Overall Reduction
Stroke 14%
Coronary Heart Disease 9%
All Cause Mortality 7%
Hypertension 2003;289:2560-2572.
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Kolesterol Red Meat Gula Garam
Dietary Approaches to Stop Hypertension
Protein Buah Sayur K, Ca, Mg
Lowers systolic BPin normotensive patients by an average of 3.5 mm HgIn hypertensive patients by 11.4 mm Hg
Latihan Fisik Teratur
Stop Alkohol dan merokok
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farmakologis
DIURETIK
PENGHAMBAT ADRENERGIK
VASODILATORPENGHAMBAT ENZIM KONVERSI
ANGIOTENSIN
ANTAGONIS KALSIUM
ANTAGONIS RESEPTOR ANGIOTENSIN II
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BP
HR
Stroke
Volume
SVR
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Thiazide Diuretics
Thiazides
Veins
Mechanism: inhibit Na/K pumps in the distal
tubule
Hydrocholorthiazide 12.5-25 mg daily
Chlorthalidone 12.5-50 mg daily
Effective first line agent and provides synergisticbenefit
As single agent more effective if CrCl >30 ml/min
Compelling indications: HF, High CAD risk,Diabetes, Stroke,
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Loop Diuretics
Thiazides
Loops
Veins Mechanism: Inhibit Na/K/Cl ATPase in ascendingloop of henle
Furosemide 20 mg BID
Typically only beneficial in patients with resistant HTNand evidence of fluid; effective if CrCl
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Aldosterone Receptor Antagonists
Thiazides
LoopsAldosterone Ant.
Am J Hypertension. 2003; 16:925-930.
Veins Mechanism: inhibit aldosteroneseffect at thereceptor, reducing Na and water retention
Examples:
Spironolactone 25 mg daily
Can provide as much as 25 mmHg BP reduction ontop of 4 drug regimen in resistant hypertension
Monitor SCr and K
Compelling indications: HF
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Nitrates
Thiazides
LoopsAldosterone Ant.
Nitrates
VeinsMechanism: Direct venodilation by release of nitric
oxide
Examples:
Isosorbide dinitrate 10 mg TID
IMDUR 30 mg daily
In renal patients with resistant hypertension additionto 3-4 drug regimen may help get patient to goal
Provide 8h nitrate free interval daily
Compelling indications: Angina
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ACEI & ARBs
Thiazides
LoopsAldosterone Ant.
Nitrates
ACEI
ARB
Veins
Mechanism: Inhibit vasoconstriction by inhibiting synthesis or
blocking action of angiotensin II; provides balanced vasdilation
Examples:
Enalapril 2.5-40 mg daily BID Lisinopril 5 40 mg daily
Irbesartan 150-300 mg daily
Losartan 25-100 mg Daily - BID
Monitor: SCr, K
Compelling indications: HF, post-MI,High CAD risk, Diabetes, CKD, Stroke
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Beta Blockers
Beta
Blockers
Heart
Mechanism: Competitively inhibit the binding ofcatecholamines to beta-adrenergic receptors
Examples:
Atenolol 25-100 mg PO daily
Metoprolol 25 -100 mg PO daily or BID
Carvedilol 6.25-25 mg PO BID
Monitor: HR, Blood Glucose in DM
Not contraindicated in asthma or COPD but usecaution
Compelling indications: HF, post-MI, High CADrisk, Diabetes
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Dihydropyridine Calcium Channel Blockers
DihydropyridineCCBs
Arteries
Mechanism: Decrease calcium influx
into cells of vascular smooth muscle
Examples:
Amlodipine 2.5-10 mg PO daily
Felodipine2.5-10 mg PO daily
Do not use immediate release nifedipine
Monitor: Peripheral edema, HR (can
cause reflex tachycardia)
Good add on agent if cost is not anissue
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Vasodilators
Dihydropyridine
CCBsHydralazine
Minoxidil
Arteries
Mechanism: Direct vasodilation of arterioles
via increased intracellular cAMP
Examples:
Hydralazine 20-400 mg BID-QID
Minoxidil 2.5-40 mg PO daily-BID
Monitor: HR (can cause reflex tachycardia),Na/Water retention
Hydralazine is an alternative in HF if ACEIcontraindicated
Consider minoxidil in refractory patients onmulti-drug regimens
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Chinese Menu Approach
Thiazides
Loops
Aldosterone Ant.
Nitrates
ACEI
ARB
Beta Blockers
Diltiazem
Verapamil
Via CentralMechanism:
Clonidine
DihydropyridinesHydralazine
Minoxidil
Alpha1Blockers
ACEIARB
Heart Arteries
Veins
Choose one agent from each category
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PROGNOSIS
Hipertensi yang tidak terkontrolmortalitas
me
silent killer
50% penderita dengan hipertensi ringan-
sedang yang tidak diberikan pengobatan 8-
10 tahun setelah onset kerusakan organ
prognosis memburuk
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KRISIS HIPERTENSI
Krisis hipertensi keadaan klinis yang
ditandai oleh tekanan darah yang
sangat tinggi dengan kemungkinan
akan timbulnya atau telah terjadikelainan organ target.
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KRISIS HIPERTENSI
Krisis Hipertensi meliputi 2 kelompok :
Hipertensi Darurat (emergency hypertension) :
Tekanan darah yang sangat tinggi & kelainan/kerusakantarget organ yang bersifat progresif tekanan darah harus
diturunkan segera (dalam beberapa menit atau jam) mencegah / membatasi kerusakan target organ yang terjadi.
Hipertensi mendesak (Urgency Hypertension) :
Tekanan darah yang sangat tinggi
Kelainan/kerusakan target organ yang progresif (-)Penurunan tekanan darah dapat dilakukan lebihlambat (dalam hitungan jam /hari).
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GEJALA
KRISIS HIPERTENSI
gejala dari organ target yang terganggu, yaitu:
nyeri dada
sesak napas gangguan jantung
diseksi aortamata kabur papilledema
sakit kepala hebat
gangguan kesadaran dan lateralisasi gangguan otak
gagal ginjal akut gangguan ginjal
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DIAGNOSIS
KRISIS HIPERTENSI
Berdasarkan :
tingginya tekanan darah, gejala, dan tandaketerlibatan organ target.
pemeriksaan fisikpemeriksaan laboratorium
ureum kreatinin
pemeriksaan penunjang
USG
EKG
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PENGOBATAN
Obat-obatan yang dipakai di Indonesia
Oral :Nifedipin
Kaptopril
KlonidinPropanolol
Parenteral :
Klonidin 150g
NitrogliserinNikardipin
Nitroprusid
Diltiazem
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Pengobatan hipertensi sekunder lebih mendahulukan pengobatan kausal.
Pengobatan hipertensi esensial ditujukan untuk menurunkan tekanan darah dengan harapanmemperpanjang umur dan mengurangi timbulnya komplikasi.
Upaya menurunkan tekanan darah dicapai dengan menggunakan obat antihipertensi.
Pengobatan hipertensi adalah pengobatan jangka panjang, bahkan mungkin seumur hidup.
Pengobatan dengan menggunakan Standart Triple Therapy(STT) menjadi dasar pengobatanhipertensi.
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Heart failure is generally divided into
Left Heart Failure Right Heart Failure
Cardiac problem with great implications to the respiratory system
This means less oxygen is reaching the organs make you feel tired and short
of breath.
A clinical syndrome where the hearts mechanical performance is
compromised and the cardiac output cannot meet the demands of the body
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How did I get it?
HeartFailure
Highblood
pressure
Valvulardisease
Viralinfection
Alcoholcoronarydisease
heartdisease
DIET
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Why water retention?
Fluid goes into legs and /or lungs
Heart cant pump against all this extra fluid
Kidneys hold onto fluid and salt because they think the person is dry.
Decreased blood flow to kidneys
Poor heart pump
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Myocardial Dysfunction
Systolic
Left ventricle has
reduced musclecontractility
Diastolic
Decreased left
ventricular filling Caused byventricularstiffness,
decreased rate ofrelaxation, orrapid heart rate
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Functional Assessment
No limitations of physical activityNo shortness of breath, fatigue, or heart palpitations
ordinary physical activity.Class I
Slight limitation of physical activity.
SOB, fatigue, heart palpitations Patient comfortable at rest.Class IISymptoms with minimal exertion
SOB, fatigue, heart palpitations
Patients comfortable at restClass III
Severe to complete limitation of activity
SOB, fatigue, heart palpitations, even at rest.Class IV
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High risk of HF, no structural heartabnormalityStage A
Structural heart disorder, no symptoms
Stage B Structural disorder, past or current HF
symptomsStage C
End-stage disease, requiring specializedtreatmentStage D
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High pressure system
Blood needs to be pumped to the entire body
Left ventricular muscle needs to be significant in size toact as a strong pump
Left sided failure results in backup of blood into the lungs
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Low pressure system
Blood needs to be pumped to the lungs right next to the
heart
Right ventricle is smaller than the left and does not need tobe as developed
Right sided failure results in back pressure of blood in thesystemic venous system (the periphery)
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Left Ventricular Heart Failure
heart disease
MIvalvulardisease
chronichypertension
dysrhythmias
Failure of effective forward pump
back pressure of blood into pulmonary circulation
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Left Ventricular Failure
increasing fluid in the alveoli decreases the lungs oxygenation capacity andincreases patient hypoxia
increasing pressure in the capillaries forces blood plasma into alveoli causingpulmonary edema
increasing pressure is transmitted to the pulmonary veins and capillaries
Pressure in left atrium rises
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Right Ventricular Heart Failure
Causes
Failure of the right ventricle to work as an effective forward pump
back pressure of blood into the systemic venous circulation causes venouscongestion
Most common cause is left ventricular failure
Systemic hypertension
Pulmonary embolism
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Congestive Heart Failure
Can present as edema
Pulmonary Peripheral Sacral Ascites
A condition where the hearts reduced stroke volumecauses an overload of fluid in the bodys other tissues
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Compensatory Measures - Starlings
Law
The more the myocardium is stretched, thegreater the force of contraction and the greaterthe cardiac output
The greater the preload (amount of bloodreturning to the heart), the farther themyocardial muscle stretches, the more forcefulthe cardiac contraction
After time or with too much resistance the hearthas to pump against, the compensation methodsfail to work
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Often presents as: Pulmonary edema
Pulmonary hypertension
Myocardial infarction
Often presents as:
Cardiomegaly - enlargement of the heart
Left ventricular failure
Right ventricular failure
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Progressive or acute shortness of breath
Labored breathing especially during exertion (ie: standing up, walking a few steps)
Awakened from sleep with shortness of breath (paroxysmal nocturnal dyspnea)
increasing episodes usually indicate the disease is worsening
Positioning
inability to recline in bed without multiple pillows
using more pillows to be comfortable in bed
Changes in skin parameters
pale, diaphoretic, cyanotic
mottling present in severe CHF
Increasing edema or weight gain over a short time
early edema in most dependent parts of the body first (ie: feet, presacral area)
Generalized weakness
Mild chest pain or pressure
Elevated blood pressure sometimes
to compensate for decreased cardiac output
Progression of Acute CHF
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Progression of Acute CHF
Hypercarbia (carbon dioxide retained in the blood) can cause CNS depression
slowing of the respiratory drive slowing of the respiratory rate
Pulmonary gas exchange is decreased leading to hypoxemia (oxygen in blood)& hypercarbia (carbon dioxide in blood)
Fluid will eventually enter & fill the alveoli
Fluid is forced from the pulmonary capillaries into the interstitial spaces between the
capillaries and the alveoli
Pulmonary venous pressure rises
Left ventricle fails as a forward pump
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Typical medication profile
diuretic - to remove
excess fluids
hypertension
medications
Digoxin - to increase
the contractilestrength of the heart Oxygen
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Wheezes heard in
any geriatric patientshould be consideredpulmonary edema untilproven otherwise(especially in the
absence of any historyof COPD or asthma)
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TERIMA KASIH
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