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…