Oleh : Eli Halimah

HipertensiHipertensi atau tekanan darah (TD) tinggi adalah keadaan dimana TD lebih tinggi dari normalHipertensi bukan penyakit melainkan suatu kelainan, gejala dari gangguan pada mekanisme regulasi tekanan darahGejala-gejala hipertensi : - Nyeri kepala pagi hari sebelum bangun dari pembaringan dan akan lenyap setelah bangun - Gejala yg khas tidak ada - silent disease - Hipertensi hanya dapat diketahui dari pengukuran tekanan darah

Evolution in Understanding Cardiovascular Disease: Total Risk Perspective *Cardiovascular Disease Is an Interplay of Risk FactorsAgeGender SmokingDyslipidemiaHypertensionDiabetesMellitusKannel WB. Am J Hypertens. 2000;13:3S-10S; Poulter N. Am J Hypertens. 1999;12:92S-95S.

Partners in Healthcare Education, LLC 2009*EndothelialDysfunction CVDHypertension Dyslipidemia AtherosclerosisSmooth MuscleCell ContractionImpaired Bioavailability of Nitric OxideImpaired Vasodilation

Partners in Healthcare Education, LLC 2009

Hypertension Remains One of the Most Important Multipliers of CV RiskBP >140/90 mm Hg is associated with:277,000 deaths in 2003BP, blood pressure; CHF, congestive heart failure; MI, myocardial infarction.

Rosamond W et al. Circulation. 2007;115:1-103.

Chart1

0.690.740.770.91

First MIs

Current CHF

First Strokes

Eventual CHF

Sheet1

First MIs69%

Current CHF74%

First Strokes77%

Eventual CHF91%

Klasifikasi Hipertensi berdasarkan Tingginya Tekanan Darah Kisaran TD (mmHg) Kategori Diastolik : < 90 TD Normal 90 104 HT ringan 105 - 114 HT sedang > 115 HT berat

Sistolik, bila TD diastolik < 90 < 140 TD Normal 140 159 HT sistolik perbatasan > 160 HT sistolik

Classification of Blood Pressure for Adults(JNC 7, May 2003)

SystolicDiastolicNormal 100

PrehypertensionIndividuals with a systolic BP of 120-139 mm HG or a diastolic BP or 80-89 mm HG should be considered as pre-hypertensive and lifestyle modification initiated.

*JAMA. 2003:289:2560-2577.

Table 3. Lifestyle Modifications to Manage Hypertension*

Aetiology of HypertensionPrimary 90-95% of cases also termed essential of idiopathicSecondary about 5% of casesRenal or renovascular diseaseEndocrine diseasePhaeochomocytomaCusings syndromeConns syndromeAcromegaly and hypothyroidismCoarctation of the aortaIatrogenicHormonal / oral contraceptiveNSAIDs

Klasifikasi HT berdasarkan Etiologi1. Hipertensi esensial, primer atau idiopatik - HT ini tidak jelas etiologinya ( 90%) - Ciri-ciri : ada riwayat HT pada keluarga terjadi peningkatan reaktivitas vaskuler - Penyebab multifaktorial : genetik Lingkungan : masukan garam, obesitas, pekerjaan / jabatan, kepadatan penduduk - HT esensial merupakan kelainan kronik & biasanya progresif

2. Hipertensi Sekunder (6-8%)Disebabkan oleh penyakit lain atau obat tertentu

HT Renal ( HT Renovaskuler) Terjadi karena penyakit pada ginjal : - penyempitan pembuluh darah ginjal - kerusakan arteri ginjal

HT Endokrin - Kelainan korteks adrenal (Cushing syndrom) - tumor di medula adrenal (Feokromositoma)

Obat-obatan : - Kontraseptif hormonal - Kortikosteroid - Antidepresan trisiklik

Target Organ DamageHeartLVH, Angina, CHF, MIBrainStroke or TIADementiaChronic Kidney DiseasePeripheral Vascular DiseaseRetinopathyJAMA. 2003:289:2560-2577.

Kieran McGlade Nov 2001

Department of General Practice QUBThis left ventricle is very thickened (slightly over 2 cm in thickness), but the rest of the heart is not greatly enlarged. This is typical for hypertensive heart disease. The hypertension creates a greater pressure load on the heart to induce the hypertrophy.

Department of General Practice QUB

The left ventricle is markedly thickened in this patient with severe hypertension that was untreated for many years. The myocardial fibers have undergone hypertrophy.

Kerusakan Organ Akibat HipertensiKerusakan jantung- Jantung bekerja lebih keras dan pembuluh-pembuluh mengeras (menahan TD yang tinggi)- Infark Jantung- Infark otak, dengan kelumpuhan separuh badan (pecah pembuluh darah otak)- Kerusakan ginjal- Kerusakan selaput jala mata

If HTN diagnosed Evaluate for Cardiovascular Risk FactorsAge,Fm Hx, Lipids, Obesity, microalbuminuria, Inactivity,Smoking

Evaluate for Target Organ DamageLVH or reduced EF, Angina,stroke,dementia,Kidney disease, PAD,retinopathy

Think about Secondary Hypertension with any new onset Hypertension or uncontrolled hypertension

Physiology of the Renin Angiotensin SystemAng, angiotensin.Reid IA. Adv Physiol Edu. 1998;20:S236-S245.

Hypertension produces several types of structural change in the blood vessel wall

Blood vessel walls in hypertension may be narrowed in two ways: structural hypertrophy increase smooth muscle contraction producing vasoconstriction

Development of fibrinoid necrosis in malignant hypertension

CHARACTERISTICS of the HYPERTENSION SYNDROME Blood PressureDislipidemiaInsulin Resistance (IGT)Central Obesity Coagulation Factors( Fibrinolysis)Renal Changes (Microalbuinuria)Arterial and VentricularCompliance (LVH) All contribure Cardiovascular Risk

Panel Pemeriksaan Hipertensi(Evaluasi Awal)Tipe penyakit, etiologi, stratifikasi prognostik, Faktor risiko, Target Organ Damage (Sebagai dasar u/ menentukan pengobatannya)

Parameter :Hematologi rutin, HematokritUrinalisis rutin, ureum , kreatinin, asam urat, Mikroalbumin (urin)Glukosa puasa + 2 jam ppKolesterol, HDL/LDL, TrigliseridaApoA1/Apo BK, Na (serum/ urin 24 jam)Renin (PRA)

Tambahan : Foto toraks EKG

Panel Pengelolaan Hipertensi(Pemantauan)Panel ini berguna u/ melihat adanya efek samping obat maupun u/ deteksi dini adanya kerusakan organ akibat hipertensi

Parameter :Urinalisis Rutin UreumKreatininAsam uratGlukosa puasaMikroalbumin (urin)Kolesterol, HDL/LDLTrigliseridaApo A1/Apo BK, Na (serum)

Partners in Healthcare Education, LLC 2009*The traditional view of CVD is based on the Framingham Heart Study model of a stepwise increase in CVD risk with multiple independent risk factors.Recently, this model has evolved into a more dynamic one as new epidemiologic and clinical evidence has been published.The current model shows clustering of risk factors, such as hypertension, dyslipidemia, and diabetes along with smoking, gender, and increasing age, emphasizing the synergistic interaction of these risk factors. This dynamic, interactive effect of risk factors places individualseven those with mild levels of 2 risk factorsat profound risk for CVD.

Fuster V, Gotto AM Jr. Risk reduction. Circulation. 2000;102:IV94IV102. Kannel WB. Framingham study insights into hypertensive risk of cardiovascular disease. Hypertens Res. 1995;18:181-196.Kannel WB. Risk stratification in hypertension: new insights from the Framingham study. Am J Hypertens. 2000;13:3S-10S. Poulter N. Coronary heart disease is a multifactorial disease. Am J Hypertens. 1999;12:92S-95S.

Partners in Healthcare Education, LLC 2009*Hypertension and hypercholesterolemia impair vascular endothelial function by reducing the bioavailability of nitric oxide, an important contributor to vascular smooth muscle relaxation and consequential vasodilation.Nitric oxide depletion also accelerates other atherogenic mechanisms.The endothelium is damaged by the release of reactive molecular groups (eg, oxidants) and elevation of angiotensin II via upregulation of the AT1 receptor, which increases the deleterious effects of this vasoactive peptide.By downregulating AT1 receptor expression and activation, statins reduce BP as well as LDL-C.Although hypertension and hypercholesterolemia exert their major effect at the level of the resistance vessels (small arteries), these disorders also reduce the ability of large vessels to distend, a deleterious effect that is reversible with lowering of BP and LDL-C.Some studies have shown a BP-reducing effect of statins in patients with untreated hypertension as well as in those treated with angiotensin-converting enzyme inhibitors (ACEIs) or calcium channel blockers (CCBs) and suggest that statins may act synergistically with antihypertensive agents.

John S, Schmieder RE. Potential mechanisms of impaired endothelial function in arterial hypertension and hypercholesterolemia. Curr Hypertens Rep. 2003;5:199-207.Sander GE, Giles TD. Hypertension and lipids: lipid factors in the hypertension syndrome. Curr Hypertens Rep. 2002;4:458-463.Spieker LE, Noll G, Ruschitzka FT, Maier W, Lscher TF. Working under pressure: the vascular endothelium in arterial hypertension. J Hum Hypertens. 2000;14:617-630.Giannattasio C, Mancia G. Arterial distensibility in humans: modulating mechanisms, alterations in diseases and effects of treatment. J Hypertens. 2002;20:1889-1899.Borghi C, Dormi A, Veronesi M, Immordino V, Ambrosioni E. Use of lipid-lowering drugs and blood pressure control in patients with arterial hypertension. J Clin Hypertens. 2002;4:277-285.*Summary: Hypertension is associated with increased cardiovascular morbidity and mortality, leading to an estimated direct and indirect cost of $63.5 billion in 2006.Cardiovascular morbidity and mortality are high among patients with hypertension, which is evident in as many as 69% of patients suffering a first heart attack and 74% of those with congestive heart failure (CHF). In fact, according to a 2006 report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee, approximately 91% of patients with CHF had hypertension before the development of heart failure.1 This same report indicates that among the 2.4 million deaths that occurred in the United States in 2003,2 approximately 277,000 were attributable to high blood pressure. The estimated direct and indirect costs of hypertension in 2007 total $66.4 billion.1 ReferencesRosamond W, Flegal K, Friday G, et al. Heart disease and stroke statistics2007 update. Circulation. 2007;115:1-103.Centers for Disease Control and Prevention. Number of deaths, death rates, and age-adjusted death rates, by race and sex: United States, 1940, 1950, 1960, 1970, and 1980-2003. Available at: http://www.cdc.gov/nchs/fastats/pdf/mortality/nvsr54_13_t01.pdf. Accessed January 29, 2007.**SLIDE SUMMARY: PHYSIOLOGICALLY, THE RENIN ANGIOTENSIN SYSTEM HELPS TO REGULATE BLOOD PRESSURE AND BLOOD VOLUME BY RESPONDING TO EXTRACELLULAR FLUID VOLUME AND BLOOD PRESSURE REDUCTIONSThe diagram shows the cascade of events characteristic of the physiologic operation of the renin angiotensin systemReductions in blood volume and arterial pressure, perhaps caused by dehydration or blood loss, result in decreased firing of low- and high-pressure baroreceptors. This causes an increase in renal sympathetic nerve activity, which, together with decreases in renal artery pressure, glomerular filtration rate, and macula densa salt load, stimulates renin secretion1Renin secretion initiates processes resulting in increased plasma concentrations of angiotensin II, which causes vasoconstriction, renal sodium reabsorption, and thirst (stimulating fluid intake). These processes lead to restoration of blood volume and blood pressure1

Reid IA. The renin-angiotensin system: physiology, pathophysiology, and pharmacology. Adv Physiol Edu. 1998;20:S236-S245.***********