HIPERTENSI SMT VI KBK.ppt

7/30/2019 HIPERTENSI SMT VI KBK.ppt

1/64

Hypertension

and

Hypertensive Crisis


2/64

Hypertension


3/64

Blood pressure

Pressure is generated when the heart contracts against theresistance 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


4/64

Control of blood pressure

Blood pressure = Cardiac output x Peripheral resistance

Hypertension = Increased CO and/or Increased PR

Preload Fluid volumeRenal sodium

retention

Excess

sodium

intake

Genetic

factors

Contractility Heart rateVasoconstriction

Sympathetic

nervoussystem

Renin-

angiotensin-aldosterone

system

Kaplan (1994)


5/64

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 Vascular

Resistance


6/64

Hypertension Guidelines

BP Classification WHO-ISH 2003 ESH-ESC 2003 BP-JNC 7

Optimal 140 / < 90 Isolated Systolic

Hypertension


7/64

Essential (Primary)Hypertension


8/64

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


9/64

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, obesityand hyperlipidemia

Sodium intake

High intake of alcohol

Sedentary life style


10/64


11/64


12/64


13/64

Secondary Hypertension


14/64

Secondary Hypertension1. 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 onclinical grounds


15/64

Endocrine hypertension

Secondary hypertension 6-8%

Renal 4-5%

Miscellaneous ~2%

Endocrine 1-2%

Primary hyperaldosteronism 0.3%

Cushings syndrome


16/64

COMPLICATIONS


17/64

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


18/64

Impact of high-normal BP on CV risk

Optimal BP:


19/64

DIAGNOSIS


20/64

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 thesystolic and diastolic pressures, the higher value

determines the severity of the hypertension.


21/64

White coat hypertension

"white-coat" or isolated office HT

Approximately 20 to 25 % of pts

persistent office HT but repeatedly normalwhen 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 thanthe physician


22/64

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 ofhypertensive cardiovascular complications


23/64

Indications for ABPM

Suspected white coat HT

Suspected episodic HT (eg, pheochromocytoma) HT resistant to increasing medication

Hypotensive symptoms while taking

antihypertensive medicationsAutonomic dysfunction


24/64

EVALUATION


25/64

Aim

To determine the extent of target organ

damage.

To assess the patient's overallcardiovascular risk status.

To rule out identifiable and often curable

causes of hypertension


26/64

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 newonset Hypertension or uncontrolled hypertension


27/64

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


28/64

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.


29/64

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 Crthat is either unexplained or occurs after the

institution of therapy with an ACE-i or AIIRB

Moderate to severe HT in a patient with diffuseatherosclerosis 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 ofacute pulmonary edema or otherwise unexplained CHF.


30/64

Testing for other causes of identifiable

hypertension

Elevated creatinine, a calculated GFR < 60 mL/min per 1.73m2, 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) andaldosterone concentration.

Cushing's syndrome: cushingoid facies, central obesity,ecchymoses, and muscle weakness.

Coarctation of the aorta: decreased peripheral pulses and avascular bruit over the back.


31/64

TREATMENT


32/64

JNC VII and WHOISHblood pressure targets

JNC VII targets


33/64

Lifestyle Modification

Modification Approximate SBP reduction

(range)

Weight reduction 520mmHg/10 kg weight loss

Adopt DASH eatingplan

814 mmHg

Dietary sodium

reduction

28 mmHg

Physical activity 49 mmHg

Moderation of

alcohol consumption

24 mmHg


34/64

Drug treatment


35/64

Factors affecting choice of

antihypertensive drug

The cardiovascular risk profile of thepatient

Coexisting disorders

Target organ damage

Interactions with other drugs used for

concomitant conditions Tolerability of the drug

Cost of the drug


36/64

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


37/64

Anti-Hypertensive Drugs: Sites of Action

BLOCKERS

Calsium Antagonist+

BLOCKERS

HYDRALAZINE

Symphatetic

Activity

Cardiac

Output

Renin

PERIPHERAL

VASCULARRESISTENCE

Thiazids

ACE-iARBs

Renin inhibitors


38/64

Choosing the right antihypertensive

Condition Preferred drugs Other drugs that canbe used

Drugs to beavoided

Asthma CCBs -blockers/ARB/Diuretics/

ACE-i

-blockers

Diabetesmellitus

-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

C di ti l ith


39/64

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 140159 or DBP

9099 mmHg)

Thiazide-type diuretics

for most. May consider

ACEI, ARB, BB, CCB,

or combination

Without Compelling Indications

Not at Goal BP

Optimize dosages oradd additional drugs

until goal BP is achieved.

Consider consultation with hypertension

specialist.

JNC 7 Medication Algorithm


40/64

Antihypertensive: Side-effects and Contraindications

Class ofdrugs

Main side-effects Contraindications/Special Precautions

Diuretics

(e.g. HCT)

Electrolyte

imbalance, level of total andC-LDL,, glucoselevels, UC, C-HDL

Hypersensitivity, Anuria

-blockers(e.g. atenolol)

Impotence,Bradycardia,fatique

Hypersensitivity, Bradycardia,Conduction disturbances,Diabetes, Asthma, Severecardiac failure


41/64

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, LVdysfunction.DHP CCBsHypersensitivity-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


42/64

Hypertensive Crises


43/64

Definitions:

Acute life-threatening increase in BP

Hypertensive urgency: severehypertension (usually SBP > 180 and DBP> 120 mmHg) without acute target organdamage (TOD)

Hypertensive emergency : severe HTN +TOD


44/64

Pathogenesis

Untreated essential hypertension

Sudden withdrawal / non-adherence to

antihypertensive drug therapy Increase in sympathetic tone (stress, drugs)

Renovascular hypertension, renal parenchymal

diseases, pheochromocytoma, or primaryhyperaldosteronism.

Pressure damages vascular endothelium

Platelets and fibrin activate


45/64

Clinical Manifestations

Encephalopathy

AMI/USA Nephropathy

Aortic dissection

LV failure/cardiac decompensation Eclampsia


46/64

Patient evaluation

Medical history

Physical examination

Laboratory evaluation

serum

urine

Medication profile

Drug use

Fundoscopy

EKG, CXR, head CT, echo


47/64

Laboratory evaluation

Urinalysis: protein, RBC, casts

Cardiac enzymes- CKMB, troponins

Electrolytes, BUN, creatinine

Toxicology screen

EKG, echo, angiography, X-ray

Thyroid, cortisol, BG

LFTs


48/64

Therapeutic approach

Time frame - consider risk level

BP goal Urgency: gradual; DBP to 110 in 24-48 hours

Emergency: MAP < 20 to 25% in 1 to 2 hours

Drug selection Route


49/64

Complications of rapid BP reduction insevere hypertension

Widening neurologic deficits Retinal ischemia: blindness

Acute myocardial infarction

Deteriorating renal function


50/64

Drug treatment of

hypertensive emergencies


51/64

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


52/64

May drop cerebral blood flow

May increase intracranial pressure

Recommended vs. toxic dose!

Approved dose max 10mcg/kg/min

Toxic at 4mcg/kg/min for 2-3 hrs

Protect from light


53/64

Nicardipine

Water soluble DHP CCB

IV infusion, titratable effectsAs effective as nitroprusside

Onset 5-15min, dur 4-6h

Dose independent of pt wt (5-15mg/h)


54/64

Parenteral drugs for treatment of hypertensive emergencies


55/64

Parenteral drugs for treatment of hypertensive emergencies


56/64

Nifedipine

Given SL, absorbed PO

onset 5min, peak 30-60, duration 6h

direct arterial dilation, decrease PVR unpredictable BP lowering

cerebral, renal, cardiac ischemia- fatal!

Elderly most prone to ADR

Do not use!


57/64

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 theparenteral medications.

Nifedipine SL (10 mg) andcaptoprilSL (25 mg) lower theBP 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 uncontrolledhypotensive response.

Should be avoided if more controllable drugs are available.
http://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/181147&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_a_k/41777&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_a_k/41777&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/181147&drug=true


58/64

Treatment of specific

hypertensive emergencies


59/64

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 bythe thrombotic lesion or by cerebral

vasospasm.

These cerebrovascular events arecharacterized by the abrupt onset of usually

focal neurologic findings.


60/64

Acute pulmonary edema

Hypertension in patients with acute LF failure due

to systolic dysfunction should be principally treated

with vasodilators. Nitroprusside ornitroglycerin with a loop diuretic is

the regimen of choice for this problem.

Drugs that increase cardiac work (hydralazine) or

decrease cardiac contractility (labetalolor other

beta blocker) should be avoided.
http://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/183014&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/182768&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_a_k/124123&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/139235&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/139235&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_a_k/124123&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/182768&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/183014&drug=true


61/64

Angina pectoris or AMI

Acute coronary insufficiency frequently increasesthe systemic BP.

Intravenous parenteral vasodilators, principallynitroprusside and nitroglycerin, are effective andreduce mortality in patients with AMI, with orwithout hypertension.

Labetalol is also effective in this setting. Drugs that increase cardiac work (hydralazine) are

contraindicated
http://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/183014&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/182768&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/139235&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_a_k/124123&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_a_k/124123&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/139235&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/182768&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/183014&drug=true


62/64

Withdrawal of antihypertensive therapy

Abrupt discontinuation of a short-acting

sympathetic blocker (such as clonidine or

propranolol) can lead to severe hypertension andcoronary 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, orlabetalol
http://embedded/utod/utd?type=4&displaytype=1&file=drug_a_k/62879&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/214749&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/183014&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/139235&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/139235&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/183014&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/214749&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_a_k/62879&drug=true


63/64

Pregnancy

Usually due to preeclampsia or preexistenthypertension

Hydralazine is the treatment of choice

Nicardipine orlabetalol are alternatives in patientswho do not achieve adequate BP control withhydralazine.

Nitroprusside, ACE inhibitors, and A II RB are

contraindicated ACE inhibitors and AII RB can impair renal function

in the fetus
http://embedded/utod/utd?type=4&displaytype=1&file=drug_a_k/124123&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/180656&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/139235&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/183014&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/183014&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/139235&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_l_z/180656&drug=truehttp://embedded/utod/utd?type=4&displaytype=1&file=drug_a_k/124123&drug=true


64/64

Nah gambar di atas ada dua,Tata Surya dan Pulau Jawa. Takaran Alam inikira2 kalau dihitung pakai matematika hasilnya:

Tata Surya dibanding Galaksi Bima Sakti = 1 cm dibanding 1000 km

Jadi = sebuah neker dibanding sebuah pulau Jawa sebagai radiusnya.

Kalau Tatasurya sebesar kelereng, maka Galaksi Bima Sakti adalah sebesarBola dengan Radius sepanjang pulau Jawa pokoknya bayangin sendiri

ajakarena saat itu kita ndak jelas seberapa ukuran kita..???

Padahal Galaksi tidak sekedar satu namun Milyaran

HIPERTENSI SMT VI KBK.ppt

Documents

Transcript of HIPERTENSI SMT VI KBK.ppt