dr. rukma_cardio (cardiovascular emergency)
Post on 08-Apr-2015
406 Views
Preview:
TRANSCRIPT
CRISES HYPERTENSION
R RUKMA JUSLIMSUBDEP JANTUNG RSAL
DR RAMELAN
DEFINITION
H. Emergency≈ Acute end organ damaged
(CV;Renal;CNS;Eyes)H.Urgency
≈ Without acute end organ damagedMalignant Hypertension
≈ Elevated BP + Encephalopathy or Acute nephropathy
Target Organ Damage (TOD)
• CNS : encephalopathy, stroke
• Occular : papiledema, blurring of vision
• Cardiac : ADHF, AP, aortic dissection
• Renal : azotemia, hematuria, proteinuria, oliguria
• Hematologic : microangiopathic hemolytic anemia
CLASSIFICATION
Normal : < 120/80
Prehypertension : 120-139 – 80-89
Stage I : 140-159 – 90-99
Stage II : >160/100
Crises : ≥ 180/110
EPIDEMIOLOGY
30% Undiagnosed
Framingham Heart Study:
3,3% 30-39 yrs ; 6,2% 70-79 yrs
♂ > ♀
(1939) Untreated malignant hypertension » 1 year mortality 79%
ETIOLOGY
Essential/primary hypertension
Secondary hypertension
CONTRIBUTING TO CRITICAL INCREASE IN BP
Factors in the pathomechanism of Factors in the pathomechanism of hypertensive crisishypertensive crisis
FURTHER INCREASE IN BLOOD PRESSURE AGGRAVATED ENDOTHELIAL DAMAGE LEAD TO
TISSUE ISCHEMIA
LOCAL FACTORS
• FG, Free radicals
• Endothelial damage
• Platelet-aggregation
• Mitogenic and migration factors
proliferation
• Myointimal proliferation
SYSTEMIC FACTORS
• Renin, A II, catecholamine,
ET
• Vasopressin, pressure
natriuresis
• Hypovolemia
Kaplan, N : Critical Hypertension
Critical degree of hypertension
Local effect Systemic effect (RAA,cathecol,Vasopres)
Endothelian damage ↓
Platelet deposition Pressure natriuresis
Mitogenic & migration factors Hypovolemia
Myointimal proliferation Increase of vasopressors
Vascular damage & Tissue ischemia
SYMTOMP & SIGNS
Headache Focal Neurological sign
Consciousness Retinopathy
Seizures AMI (angina)
Left Ventricle Failure
Acute Renal Failure
Subjective and Laboratory Subjective and Laboratory Symptoms of Hypertensive Crisis Symptoms of Hypertensive Crisis
Cardiac symptoms
palpitation
rhythm disturbances
Chest pain
dyspnea
General symptoms
sweating
flush
pallor
dizziness
fear of death
tinnitus
epistaxis
Ocular symptoms
flashes
spotted vision
dimmed vision
diplopia
blindness
Renal symptoms
oliguria
hematuria
proteinuria
Electrolyte disturbances
azotemia
uremia
Cerebral symptoms
headache
dizziness
nausea
daze
focal symptoms
cramp
coma
Zamplagione B et al : Hypertension 1996
Management of Hypertension
Life style modification
Management of Hypertensive urgency • Goal : prevent to the target organ damage
• Therapeutic consideration :
• Use oral drugs
• Sub lingual drug ?!
• Reach the BP 160/100 mmHg in 24 hours, normal after 24-48 hours
Management of Hypertensive Emergency
JNC 7
• Reduce mean arterial BP by no more than 25% (within minutes to 1 hours)
• If stable , to 160/100 to 110 mmHg (within next 2 to 6 hours)
• If well tolerated and stable, gradual reduction toward a normal BP can be implemented in the next 24 to 48 hours
Management of crises hypertension
Examination :
(Physical; Neurological; Funduscopic)
Laboratory
ECG ; Radiological
↓↓↓↓
URGENCY OR EMERGENCY
↓ ↓
Oral Intravenous
Initial evaluation of patients with a hypertensive emergency
• Laboratory Evaluation– Hematocrit and blood smear– Urine analysis– Automated chemistry : creatinine, glucose,
electrolytes– Electrocardiogram– Chest radiograph
Pathways for management of patients with severe hypertension, defined as blood pressure (BP) in excess of 180/120 mmHg.
Severe HypertensionBP > 180 / 110
EncephalopathyProgressing target organ damage
Yes(HT Emergency)
No
New onset(HT Urgency)
Prior similar experience;Negative workup(Uncontrolled HT)
Admit to ICUBaseline lab
Baseline lab
Oral Rx
Reinstitute oral Rx
Follow closely
Parenteral Rx
Workup foridentifiable causes:
Renovascular HT
The Kidney and Hypertension, Bakris, 2004
Ideal Pharmacological Agent
Fast acting
Rapidly reversible
Titratable
Without significant Side Efect
Diuretics
Usually needed to maintain efficacy of other drug
Onset : 5 – 15 minutes
Duration: 2 – 3 hours
SE : Hypovolemic, Hypokalemia
Dose : 20 – 40 mg in 1-2 repeated
Sodium Nitropruside
Most hypertensive emergencies; caution with high intracranial pressure / azotemia
Onset : Immediate
Duration: 1-2 minutes
SE : Nausea, vomiting, muscle
twitching, cyanide intoxication
Dose : 0,25 – 10 µg/kg/min
Nitroglycerin
Coronary ischemia
Onset : 2-5 minutes
Duration: 5-10 minutes
SE : headache, vomiting, tolerance
with prolonged use.
Dose : 5-100µg/min
Nicardipine
Most hypertensive emergencies; caution with acute HF. Strong cerebral & coronary vasodilator. 100 times more water soluble than nifedipin (titratable)
Onset : 5-10 minutes
Duration: 4-6 hours
SE : Headache, tachycardia, local
phlebitis
Dose : 5-15 mg/h
Labetolol
Most hypertensive emergencies, except acute HF.
Onset : 5-10 minutes
Duration: 3-6 hours
SE : Vomiting, burning in throat,
dizziness, nausea, heart block,
orthostatic hypotension
Dose : 20-80 mg bolus every 10 min 2
mg/min
Berbagai Macam Sediaan Parenteral Calcium Channel Bloker
Drug Coronary Vasodilation
Suppressionof Cardiac
Contractility
Suppressionof SA Node
Suppressionof AV Node
Verapamil
(phenylalkylamine)
++++ ++++ +++++ +++++
Diltiazem
(benzothiazepin)
+++ ++ +++++ ++++
Nicardipine
(dihydropyridine)
+++++ 0 + 0
Classification Calcium Antagonists
Generation: First Second Third Latest
VerapamilNifedipineDiltiazem
FelodipineIsradipineNicardipineNimodipineNisoldipineNitrendipine
FelodipineIsradipineNicardipineNimodipineNisoldipineNitrendipine
Amlodipine Lercanidipine(hydrophilic) (lipophilic)
Prototype Tissue selectivity Tissue selectivity Tissue selectivity gradual onset gradual onset Plasma controlled membrane controlled
J Clin Basic Cardiol 1999;2:155
Basic Properties Of The Ccb Nicardipine (Nc), Nifedipine (Nf), Diltiazem (D) and
Verapamil (V)
Nc Nf D V
Systemic vasodilatation
Myocardial depression
Block AV conduction
Vasoselectivity
++
0
0
++++
++
+
0
+++
+
+
+
+
+
+++
++
0
NICARDIPINE VS DILTIAZEM
NICARDIPINE DILTIAZEM
Target organ Arteriole (ca Channel)
Arteriole (ca Channel)
Clinical effect Vasodilatation : BP decreased
Vasodilatation : BP decreased
Heart Rate ↑
Cardiac inotropic
(-) (-)
PERDIPINE Nicardipine injection 2 / 10 mg
MEKANISME KERJA
Menghambat influx ion Ca ke dalam intra sel, dengan memblokade channel calcium ( Ca Channel Blocker / CCB ), sehingga terjadi
penghambatan kontraksi otot .
Sifat vasoselektif tinggi hanya dimiliki oleh PERDIPINE, maka penghambatan ini terutama terjadi pada otot polos pembuluh darah, khususnya pembuluh darah arteri.
DOSIS & PEMAKAIAN• Hipertensi akut selama operasi : 2 – 10 µg/kg/menit secara IV infus drip• Untuk penurunan yang cepat : 10 – 30 µg/kg bolus • Hipertensi emergensi : 0,5 – 6 µg/kg/menit secara IV infus drip
Perdipine mempunyai 2 kemasan :
- 2 mg (isi 2 cc) untuk bolus injeksi
- 10 mg (isi 10 cc) untuk infus drip
Untuk pemakaian dengan infus drip, direkomendasikan menggunakan cairan infus 100cc dan mikro drip (1cc=60 tetes).
Lamanya pemakaian setelah tekanan darah turun dan terkontrol tergantung dari keputusan klinisi untuk pindah ke oral
DOSIS & PEMAKAIAN (Cont’d)
• Penambahan tetesan tergantung dari dosis.Mis. Dimulai dengan dosis 0.5 dengan 15 tetesan monitor, bila dalam 5-15 menit tidak ada perubahan TD naikkan tetesan menjadi 20 tetes (Tidak harus langsung menjadi 30 tetes) tapi dapat bertahap
• Pada pemakaian Perdipine harus disertai dengan monitor tekanan darah & detak jantung
• Apabila ada keputusan untuk pindah ke oral, maka 1 jam sebelum Pd di aff obat oral diberikan dahulu Dosis Pd mulai di turunkan (Tappering Off).
top related