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Hipertensi
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Hypertension
and
Hypertensive Crisis
Hypertension
Blood pressure Pressure is generated when the heart contracts against the
resistance of the blood vessels.
Ohm's Law can be applied as follows: V = I x R
MAP = CO x SVR MAP = Estimated by DBP + (SBP - DBP)/3 CO = cardiac output SVR = systemic vascular resistance
Cardiac output can be broken down as: CO = SV x HR SV = Dependent on pre-load, contractility, after-load
Control of blood pressure
Blood pressure = Cardiac output x Peripheral resistance
Hypertension = Increased CO and/or Increased PR
Preload
Fluid volume
Renal sodium retention
Excess sodium intake
Genetic factors
Contractility Heart rate
Vasoconstriction
Sympathetic nervous system
Renin-angiotensin-aldosterone
system
Kaplan (1994)
Hypertension
Hypervolemia - Renal artery stenosis- Renal disease- Hyperaldosteronism- Aortic coarctation
Stress - Sympathetic activation
Pheochromocytoma - Increased cathecholamines
Stress - Sympathetic activation
Atherosclerosis Renal artery disease
- Increased Ang II Pheochromocytoma
- Increased cathecholamine Thyroid dysfunction Diabetes Cerebral ischemia
Cardiac Output
Systemic VascularResistance
Hypertension Guidelines
BP Classification WHO-ISH 2003 ESH-ESC 2003 BP-JNC 7
Optimal <120 / <80 <120/<80 Normal
Normal <130 / <85 120-129 /80-84 Prehypertension
High normal 130-139 / 85-89 130-139 / 85-89
Grade 1 Hypertension (mild)
140-159 / 90-99
(140-149 / 90-94)
140-159 / 90-99 Stage 1 Hypertension
Grade 2 Hypertension (moderate)
160-179 /100-109 160-179/100-109 Stage 2 Hypertension
Grade 3 Hypertension (severe)
> 180 / >110 > 180 / >110
Isolated Systolic Hypertension
> 140 / < 90 >140 / < 90 Isolated Systolic Hypertension
Essential (Primary) Hypertension
Primary or “Essential” Hypertension
1. Etiology - unknown
2. Accounts for approximately 90% of hypertension
3. Onset typically in the fifth or sixth decade of life
4. Strong family history - 70-80% positive family history
BP correlations are stronger among parent and child than between spouses, suggesting that environmental factors are less important than genetic ones
Certain races (e.g. African Americans) are at much higher risk of HT
Risk factors Race (More common and more severe in blacks) Age > 60 years Sex (men and postmenopausal women) Family history of CVD Smoking High cholesterol diet Co-existing disorders such as diabetes, obesity
and hyperlipidemia Sodium intake High intake of alcohol Sedentary life style
Secondary Hypertension
Secondary Hypertension 1. Identifiable underlying cause:
kidney disease renal artery stenosis hyperaldosteronism pheochromocytoma
2. Represents approximately 10% of all hypertension
3. Has specific therapy, and is potentially curable
4. Often distinguishable from essential hypertension on clinical grounds
Endocrine hypertension
Secondary hypertension 6-8%Renal 4-5%Miscellaneous ~2%Endocrine 1-2%
Primary hyperaldosteronism 0.3%Cushing’s syndrome <0.1%Pheochromocytoma <0.1%
COMPLICATIONS
The risks of hypertension The risks of hypertension are well recognised Cerebrovascular disease: Thromboembolic,
Intra cranial bleed, TIA Cardiovascular disease: MI, HF, CAD LVH -- enhanced incidence of HF, ventricular
arrhythmias, death following MI, and sudden cardiac death.
Peripheral vascular disease Renal failure
Impact of high-normal BP on CV risk
Optimal BP: <120/80 mmHg; normal BP: 120-129/80-84 mmHg; high-normal BP: 130-139/85-89 mmHg
Cumulative incidence of CV events
(%)
16
1210
86420
14
Optimal BP
Normal BP
1210
86420
0 2 4 6 8 10 12Years
Optimal BP
Normal BP
High-normal BPWomen
Men
Cumulative incidence of CV events
(%)
High-normal BP
Vasan RS, et al. N Engl J Med 2001;345:1291-1297
DIAGNOSIS
Diagnosis
Based upon the average of > 2 properly measured readings at each of > 2 visits (at least 3 to 6 visits, spaced over a period of weeks to months)
Apply to adults on no antihypertensive medications and who are not acutely ill.
If there is a disparity in category between the systolic and diastolic pressures, the higher value determines the severity of the hypertension.
White coat hypertension
"white-coat" or isolated office HT Approximately 20 to 25 % of ptspersistent office HT but repeatedly normal
when measured at home, at work, or by ABPM
more common in the elderly, but is infrequent (< 5%) in pts with office DP 105 mmHg.
Taken by a nurse or technician, rather than the physician
Masked hypertension
Elevated out-of-office readings despite normal office readings
Cardiovascular risk: similar as patients with sustained HT
This is consistent with the risk of hypertensive cardiovascular complications
Indications for ABPM
Suspected white coat HT Suspected episodic HT (eg, pheochromocytoma) HT resistant to increasing medication Hypotensive symptoms while taking
antihypertensive medications Autonomic dysfunction
EVALUATION
Aim
To determine the extent of target organ damage.
To assess the patient's overall cardiovascular risk status.
To rule out identifiable and often curable causes of hypertension
If HT diagnosed
Evaluate for Cardiovascular Risk Factors Age,Fm Hx, Lipids, Obesity, microalbuminuria,
Inactivity, Smoking
Evaluate for Target Organ Damage (TOD)LVH or reduced EF, Angina, stroke, Kidney disease, PAD, retinopathy
Think about Secondary Hypertension with any new onset Hypertension or uncontrolled hypertension
Physical examination Goal is to assess for target organ damage
(such as retinopathy) and clues to secondary causes
BP, P, R Vascular (including check all pulses) Thyroid Heart and Lungs Abdomen Neurologic
Testing
Hematocrit, urinalysis, and routine blood chemistries (glucose, creatinine, electrolytes)
Fasting lipid profile (total and HDL-C, TG) Electrocardiogram Testing for microalbuminuria Echocardiography - detect left ventricular
hypertrophy.
Testing for renovascular hypertension
Severe or refractory HT An acute rise in BP over a previously stable baseline Proven age of onset before puberty or above age 50. An acute ↑ Cr that is either unexplained or occurs after the
institution of therapy with an ACE-i or AIIRB Moderate to severe HT in a patient with diffuse atherosclerosis
or an incidentally discovered asymmetry in renal disease. A systolic-diastolic abdominal bruit that lateralizes to one side. Negative family history for HT. Moderate to severe HT in patients with recurrent episodes of
acute pulmonary edema or otherwise unexplained CHF.
Testing for other causes of identifiable hypertension
Elevated creatinine, a calculated GFR < 60 mL/min per 1.73 m2, or proteinuria.
Pheochromocytoma: paroxysmal elevations in BP - triad of headache, palpitations, and sweating.
Low-renin forms of hypertension (primary hyperaldosteronism): unexplained hypokalemia Measurement of plasma renin activity (PRA) and aldosterone concentration.
Cushing's syndrome: cushingoid facies, central obesity, ecchymoses, and muscle weakness.
Coarctation of the aorta: decreased peripheral pulses and a vascular bruit over the back.
TREATMENT
JNC VI and WHO–ISH blood pressure targets
JNC VII targets <140/90 mmHg in uncomplicated hypertension <130/85 mmHg in patients with diabetes or renal
disease <125/75 mmHg in patients with renal insufficiency
and proteinuria >1 g/24 hours
WHO–ISH targets <130/85 mmHg in young, middle-aged and diabetic
patients <140/90 mmHg in elderly patients
JAMA. 2003; 289:2560-2572J Hypertens 1999;17:151–183
Lifestyle Modification
Modification Approximate 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 consumption
2–4 mmHg
Drug treatment
Factors affecting choice of antihypertensive drug
The cardiovascular risk profile of the patient
Coexisting disordersTarget organ damage Interactions with other drugs used for
concomitant conditionsTolerability of the drugCost of the drug
Antihypertensive drug strategies
Reduce cardiac output -adrenergic blockers Ca2+ Channel blockers
Dilate resistance vessels Ca2+ Channel blockers Renin-angiotensin system blockers 1 adrenoceptor blockers Nitrates
Reduce vascular volume Diuretics Direct vasodilators
Anti-Hypertensive Drugs: Sites of Action
β BLOCKERS
Calsium Antagonist+
α BLOCKERS
HYDRALAZINE
Symphatetic
Activity
Cardiac Output
Renin
PERIPHERAL VASCULAR
RESISTENCE
ThiazidsACE-i
ARBs
Renin inhibitors
Choosing the right antihypertensive
Condition Preferred drugs Other drugs that can be used
Drugs to be avoided
Asthma CCBs -blockers/ARB/Diuretics/ACE-i
-blockers
Diabetes mellitus
-blockers/ACE-i/ ARB
CCBs Diuretics/-blockers
High cholesterol levels
-blockers ACE-i/ARB/ CCB -blockers/Diuretics
Elderly patients
CCBs -blockers/ACE-i/
ARB/- blockers
BPH - blockers -blockers/ ACE-i/ ARB/ Diuretics/ CCBs
Initial Drug Choices
Drug(s) for the compelling indications
Other antihypertensive drugs (diuretics, ACEI,
ARB, BB, CCB) as needed
With Compelling Indications
Stage 2 Hypertension (SBP >160 or DBP >100
mmHg) 2-drug combination for most (usually thiazide-type diuretic and ACEI or ARB or BB or CCB)
Stage 1 Hypertension(SBP 140–159 or DBP
90–99 mmHg) Thiazide-type diuretics for most. May consider ACEI, ARB, BB, CCB,
or combination
Without Compelling Indications
Not at Goal BP
Optimize dosages or add additional drugs until goal BP is achieved.
Consider consultation with hypertension specialist.
JNC 7 Medication Algorithm
Antihypertensive: Side-effects and Contraindications
Class of drugs
Main side-effects Contraindications/ Special Precautions
Diuretics (e.g. HCT)
Electrolyte imbalance, level of total and C-LDL,, glucose levels, UC, ↓C-HDL
Hypersensitivity, Anuria
-blockers (e.g. atenolol)
Impotence, Bradycardia, fatique
Hypersensitivity, Bradycardia, Conduction disturbances, Diabetes, Asthma, Severe cardiac failure
Class of drugs Main side-effects Contraindications/ Special Precautions
CCB (e.g. Amlodipine, Diltiazem)
Pedal edema, Headache
Non-DHP CCBs (e.g diltiazem)– Hypersensitivity, Bradycardia, Conduction disturbances, CHF, LV dysfunction. DHP CCBs–Hypersensitivity
-blockers (e.g. Doxazosin)
Postural hypotension Hypersensitivity
ACE-inhibitors (e.g. Lisinopril)
Cough, Hypertension, Angioneurotic edema
Hypersensitivity, Pregnancy, Bilateral renal artery stenosis
A-II RB Headache, Dizziness Hypersensitivity, Pregnancy,Bilateral renal artery stenosis
Antihypertensive: Side-effects and Contraindications
Hypertensive Crises
Definitions:
Acute life-threatening increase in BP
Hypertensive urgency: severe hypertension (usually SBP > 180 and DBP > 120 mmHg) without acute target organ damage (TOD)
Hypertensive emergency : severe HTN + TOD
Pathogenesis
Untreated essential hypertensionSudden withdrawal / non-adherence to
antihypertensive drug therapy Increase in sympathetic tone (stress, drugs) Renovascular hypertension, renal parenchymal
diseases, pheochromocytoma, or primary hyperaldosteronism.
Pressure damages vascular endothelium Platelets and fibrin activate
Clinical Manifestations
EncephalopathyAMI/USANephropathyAortic dissectionLV failure/cardiac decompensationEclampsia
Patient evaluation
Medical history Physical examination Laboratory evaluation
serumurine
Medication profile Drug use Fundoscopy EKG, CXR, head CT, echo
Laboratory evaluation
Urinalysis: protein, RBC, casts Cardiac enzymes- CKMB, troponinsElectrolytes, BUN, creatinineToxicology screenEKG, echo, angiography, X-rayThyroid, cortisol, BGLFTs
Therapeutic approach
Time frame - consider risk levelBP goal
Urgency: gradual; DBP to 110 in 24-48 hoursEmergency: MAP < 20 to 25% in 1 to 2 hours
Drug selection Route
Complications of rapid BP reduction in severe hypertension
Widening neurologic deficitsRetinal ischemia: blindnessAcute myocardial infarctionDeteriorating renal function
Drug treatment of hypertensive emergencies
Nitroprusside
Potent arterial and venous dilator Onset seconds, duration 1-2 minutes Immediate rebound ADR:
coronary “steal” cyanide toxicity
Hepatic conversion to thiocyanate Less toxic Cleared renally
Na thiosulfate antidote ototoxicity, encephalopathy, seizures Increase mortality post MI
May drop cerebral blood flow May increase intracranial pressure Recommended vs. toxic dose!
Approved dose max 10mcg/kg/minToxic at 4mcg/kg/min for 2-3 hrs
Protect from light
Nicardipine
Water soluble DHP CCB IV infusion, titratable effectsAs effective as nitroprussideOnset 5-15min, dur 4-6hDose independent of pt wt (5-15mg/h)
Parenteral drugs for treatment of hypertensive emergencies
Parenteral drugs for treatment of hypertensive emergencies
Nifedipine
Given SL, absorbed POonset 5min, peak 30-60, duration 6hdirect arterial dilation, decrease PVRunpredictable BP loweringcerebral, renal, cardiac ischemia- fatal!Elderly most prone to ADR
Do not use!
Oral agents
Limitation: slower onset of action and an inability to control the degree of BP reduction.
May be useful when there is no rapid access to the parenteral medications.
Nifedipine SL (10 mg) and captopril SL (25 mg) lower the BP within 10 to 30 minutes in many patients.
Major risk with these drugs is ischemic symptoms (eg, AP, MI, or stroke) due to an excessive and uncontrolled hypotensive response.
Should be avoided if more controllable drugs are available.
Treatment of specific hypertensive emergencies
Ischemic stroke or subarachnoid or intracerebral hemorrhage
The benefit of reducing the BP in these disorders must be weighed against possible worsening of cerebral ischemia induced by the thrombotic lesion or by cerebral vasospasm.
These cerebrovascular events are characterized by the abrupt onset of usually focal neurologic findings.
Acute pulmonary edema
Hypertension in patients with acute LF failure due to systolic dysfunction should be principally treated with vasodilators.
Nitroprusside or nitroglycerin with a loop diuretic is the regimen of choice for this problem.
Drugs that increase cardiac work (hydralazine) or decrease cardiac contractility ( labetalol or other beta blocker) should be avoided.
Angina pectoris or AMI
Acute coronary insufficiency frequently increases the systemic BP.
Intravenous parenteral vasodilators, principally nitroprusside and nitroglycerin, are effective and reduce mortality in patients with AMI, with or without hypertension.
Labetalol is also effective in this setting. Drugs that increase cardiac work (hydralazine) are
contraindicated
Withdrawal of antihypertensive therapy
Abrupt discontinuation of a short-acting sympathetic blocker (such as clonidine or propranolol) can lead to severe hypertension and coronary ischemia due to upregulation of sympathetic receptors.
Control of the BP can be achieved in this setting by readministration of the discontinued drug and, if necessary nitroprusside, or labetalol
Pregnancy
Usually due to preeclampsia or preexistent hypertension
Hydralazine is the treatment of choice Nicardipine or labetalol are alternatives in patients
who do not achieve adequate BP control with hydralazine.
Nitroprusside, ACE inhibitors, and A II RB are contraindicated
ACE inhibitors and AII RB can impair renal function in the fetus
Nah gambar di atas ada dua,Tata Surya dan Pulau Jawa. Takaran Alam ini Nah gambar di atas ada dua,Tata Surya dan Pulau Jawa. Takaran Alam ini kira2 kalau dihitung pakai matematika hasilnya:kira2 kalau dihitung pakai matematika hasilnya:
Tata Surya dibanding Galaksi Bima Sakti = 1 cm dibanding 1000 kmTata Surya dibanding Galaksi Bima Sakti = 1 cm dibanding 1000 kmJadi = sebuah neker dibanding sebuah pulau Jawa sebagai radiusnya.Jadi = sebuah neker dibanding sebuah pulau Jawa sebagai radiusnya.
Kalau Tatasurya sebesar kelereng, maka Galaksi Bima Sakti adalah sebesar Kalau Tatasurya sebesar kelereng, maka Galaksi Bima Sakti adalah sebesar Bola dengan Radius sepanjang pulau Jawa… pokoknya bayangin sendiri Bola dengan Radius sepanjang pulau Jawa… pokoknya bayangin sendiri
aja…karena saat itu kita ndak jelas seberapa ukuran kita..???aja…karena saat itu kita ndak jelas seberapa ukuran kita..???Padahal Galaksi tidak sekedar satu namun Milyaran…Padahal Galaksi tidak sekedar satu namun Milyaran…