Hipertensi dan Dekompensasio.pptx

8/14/2019 Hipertensi dan Dekompensasio.pptx

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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


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


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

Hipertensi dan Dekompensasio.pptx

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