Kul v - Angina
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Transcript of Kul v - Angina
Edited by :
ESTI DYAH UTAMI, M.Sc., Apt.
ANGINA PECTORIS
DEFINISI
Definisi…?
Rasa tidak enak di dada sebagai akibat dari suatu iskemik miokard tanpa adanya infark
Adl penyakit jantung iskemik berkurangnya pasokan oksigen (adanya aterosklerosis koroner atau spasme arteria koroner) dan menurunnya aliran darah ke dalam miokardium.
Dapat berkembang menjadi infark miokard.
Angina pectoris
Angina pectoris is a primary symptom of myocardial ischemia, which is the severe chest pain that occurs when coronary blood flow is inadequate to supply the oxygen required by the heart. Chest pain caused by transient myocardial ischemia due to an imbalance between myocardial oxygen supply and demand.
Transient Myocardial ischemia
Severe Chest pain
Myocardial Blood Flow
Myocardial O2 Demands
Angina Pectoris
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Angina pectorisTypical Symptom a heavy strangling or pressure-like pain, sometimes may feel like indigestion, usually located in substernal area or precardium, but sometimes radiating to the left shoulder, left arm, jaw , neck, epigastrium or back.
ANGINA PEKTORISMerupakan gejala utama iskemia miokard yg terjadi bila tdp ketidakseimbangan antara suplai O2 ke jtg dgn kebutuhan
O2 jtg
Terjadi penumpukan asam laktat
timbul nyeri yang khas dgn gejala berupa:Serangan nyeri hebat di bawah tulang dada yang menjalar
ke pundak, leher, rahang atau lengan kiri atas
Serangan berkisar antara 5 – 10’
TIPE ANGINA
Types of Angina1. Stable Angina.
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2. Unstable Angina.
3. Variant Angina.
1. ANGINA STABIL
ANGINA KLASIK = ANGINA STABIL KRONIK = ANGINA OF EFFORT
serangan timbul pada waktu penderita sedang melakukan kerja fisik.
PENYEBAB : aterosklerosis dan spasme stress / emosi exposure udara dingin iskemia jtg dg anemia
Stable angina Angina klasik (angina stabil kronik),
terjadi karena adanya aterosklerosis koroner dan timbul gejalanya setelah kerja fisik, emosi atau makan;
Is caused by narrowed arteries due to atherosclerosis
Occurs when the heart works harder Usually lasts a short time Is relieved by a rest or angina medicine
2. UNSTABLE ANGINA Angina tidak stabil, ditandai meningkatnya frekuensi
dan lama serangan angina, terjadi baik waktu istirahat maupun kerja fisik. Biasanya angina tidak stabil akan cepat berkembang menjadi infark miokard apabila tidak ditangani secara serius dan tepat.
Often occurs at rest Is more severe and lasts longer than stable
angina Episodes of pain tend to be changing in the
character, frequency, duration as well as precipitating factors
Is caused by episodes of increased coronary artery tone or small platelet clots occurring in the vicinity of an atherosclerotic plaque.
Merupakan tipe angina pectoris yg dapat berubah menjadi infark miokard ataupun kematian. Telah lama dikenal sebagai gejala awal dari
infark miokard akut (IMA) risiko terjadinya IMA dan kematian.
60-70% penderita IMA dan 60% penderita mati mendadak pada riwayat penyakitnya yang mengalami gejala angina pectoris tidak stabil.
IMA terjadi pada 5-20% penderita angina pectoris tidak stabil dengan tingkat kematian 14-80%.
3. VARIANT ANGINAAngina varian (Prinzmetal), terjadi karena adanya
vasospasem koroner yang dipacu oleh rangsangan pada reseptor α1 dan biasanya gejala timbul pada waktu istirahat
Timbul pada waktu istirahat antara tengah malam dan pagi buta.
Penyebab : spasme koroner Usually occurs at rest Tend to be severe Is relieved by angina medicine (vasodilators) Is caused by a transient spasm in a coronary artery
Angina variant Angina variant adalah angina yang
diakibatkan kejang sementara arteri jantung di mana serangan nyeri timbul spontan dalam keadaan istirahat dan kebanyakan di malam hari.
Angina timbul apabila terjadi ketidakseimbangan antara suplai oksigen dengan kebutuhan oksigen miokardium.Gangguan timbul disebabkan oleh :
Suplai menurun→ adanya arteriosklerosis koroner atau spasme arteria koroner
Kebutuhan meningkat→ kerja fisik
Variant Angina .(Prinzmetal)
Chest pain at rest due to coronary artery spasm
ECG changes:
Acute elevation of ST segment
The baseline ECGWith chest pain ,
marked ST segment elevation
Return of the ST segment to the baseline after
nitroglycerin administration
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PATHOPHYSIOLOGY OF ANGINA
An imbalance between the myocardial oxygen supply and demand.
>O2
demandO2
supply
Pathophysiology
The difference of Arteriovenous oxygen pressure
O2
demandO2
supplyWall tension
Heart rate
Contractility
Coronary blood flow
Angina
Aortic Diastolicpressure
Coronary Vascularresistance
VentricularPressure
VentricularVolume
>
the duration of diastole
The underlying cause is
• Atheroscelerotic changes
Fissuring of atheroscelerotic plaques
Platelet aggregation
Thrombosis
Coronary artery spasm
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MANAGEMENT OF ANGINA
Management of Angina
Management of Stable Angina
Management of Unstable Angina
Management of Variant Angina
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Management of Stable Angina
1- General measures.2- Drug Treatment.3- Coronary artery revascularization.
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Stop smoking Reduce weight
Treat Hypertension , Hypercholestrolimia
and Diabetes
AVOID Severe exertion Heavy meal Emotions Cold Weather
General measures
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• Graduated exercise may open new collaterals
a. For an acute attackb. For immediate pre-exertional prophylaxisc. For long-term prophylaxisd. Antiplatelet therapy.
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Treatment of an acute attack of anginaSublingual nitroglycerin (0.5 mg ) or
isosorbide dinitrate (5 mg ) or Oral spray nitroglycerin (0.4 mg/metered
dose), isosorbide dinitrate(1.25 mg/metered dose)
Relief within 1-3 min. Persistence of pain
Repeat nitroglycerin at 5 min. interval (3 tab. max.)
Relief not relieved
InfarctionHOSPITALIZATION25
Immediate pre-exertional prophylaxis of AnginaSublingual nitroglycerin (0.5 mg) or isorbide dinitrate (5 mg) should be taken 5 min. before effort.
For Long term prophylaxis:Long acting nitrates, Ca++ channel blockers,b-blockers or combinations of these drugs.
Antiplatelet therapy:Aspirin in small dose (75-150 mg daily orally)or Dipyridamole (75 mg t.d.s orally)
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Coronary artery bypass grafting (CABG)
Percutaneous Transluminal coronary Angioplasty (PTCA)For patients not responding to
adequate medical therapy
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Management of Unstable AnginaNitrate
+b-blocker+
Aspirin (low dose) and/or Heparin orThrombolytic (stryptokinase)to minimize risk of infarction
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Management of Variant Angina
Nitrates and/or Ca++ Channel blockers
For the acute attack & prophylaxis
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Treatment of angina Lifestyle changes NitratesMedication β-blockers Calcium channel
blockersSurgery : CABG ( coronary artery bypass
graft) PTCA (percutaneous
transluminal coronary angioplasty)
OBAT ANTIANGINA (ANTIANGINAL DRUGS)
What are the antianginal drugs?
Organic nitrates.
Calcium channel blockers.
b- adrenoceptor blockers.
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NITRATES
Veins
Arteries
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Relaxation of smooth muscles Dilatation
Cellular Mechanism of Vasodilatation
Nitrates Formation of Nitric oxide (NO)
Activation of Guanylate cyclase
Synthesis of cyclic GMP
Relaxation of Vascular smooth muscles
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N.B. (-SH) groups are required for formation of NO.
Effect of Nitrates :On Stable Angina :
Venodilatation Arteriolar dilatation
Preload Afterload
Myocardial Oxygen demand
2- Redistribution of coronary flow towards subendocardium3- Dilatation of coronary collateral vessels.
1-
On Variant Angina :
Relax smooth muscles of the epicardial coronaries relieve coronary artery spasm
On Unstable Angina :
Dilatation of epicardial coronary arteries + reducing O2 demands
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Preparations :Short acting
For acute attacksLong acting
For antianginal prophylaxis
Nitroglycerin (sublingual, buccal spray)Isosorbide dinitrate(sublingual, buccal spray)
Nitroglycerinoral SR (6.25-12mg) 2-4 times/day - 2% ointment (1-1.5 inch/4hrs)- patches (1 patch=25mg)/day
Isosorbide dinitrate (oral) 10-40mg t.d.s.Isosorbide mononitrate (oral) 20mg/12 hrs.
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Duration of Action of Various Preparations of Organic Nitrates
Preparation Duration of action
" Short-acting"1-Nitroglycerin
2- Isosorbide dinitrate
a) Sublingual b) Spray
a) Sublingual b) Spray
10-30 min 10-30 min
Up to 60 min. 1.5 hours
" Long-acting" 1-Nitroglycerin
2- Isosorbide dinitrate 3-Isosorbide mononitrate
a) Oral; sustained releaseb) Ointmentc) Transdermal patches Oral Oral
4-8 hours3-6 hours 8-12 hours
4-6 hours 6-10 hours
Adverse Reactions :1- Postural Hypotension &
Syncope2- Tachycardia
5- Throbbing Headache
4- Facial Flushing
3- Drug Rash
6- Prolonged high dose Methaemoglobinaemia
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b-blockers are effective in STABLE & UNSTABLE angina
In contrast they are not useful for vasospastic angina (Variant) {Prinzmetal}& may worsen the condition. This deleterious effect is likely due to an increase in coronary resistance caused by the unopposed effects of catecholamines acting at a-adrenoceptors.
The effectiveness of b-adrenoceptor blockers in the treatment of exertional angina is attributable to a fall in myocardial O2 requirement at rest & during exertion due to :
1- A -ve chronotropic effect (particularly during exercise).2- A -ve inotropic effect. 3- A reduction in arterial blood pressure (particularly systolic pressure) during exercise.
Mechanism of antianginal action:
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However the net effect of b-blockers is to myocardial O2 requirement particularly during exercise; their potentially deleterious effects can be balanced by concomitant use of nitrates
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Rate & contractility
Undesirable effects of b-blockers in treatment of angina:
Systolic ejection period & left ventricular end diastolic vol. Myocardial O2 requirements
Dosage and Route of Administration
Drug Route Dosage
Propranolol Oral 30-360 mg/day in 2-4 divided doses
Nadolol Oral 40-80 mg ONCE daily
Atenolol Oral 50-100 mg ONCE daily
Metoprolol Oral 50-100 mg TWICE daily
Adverse Reactions :
CHF A-V block Bronchospasm
Cold extremities Worsening
symptoms of PVDHypotension
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Fatigue & weakness
Mask signs of Hypoglycemi
a
Nightmares , Hallucinations , Depression.
Plasma Triglycerides & HDL Cholesterol Discontinuation after
long ttt exacerbates Angina
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Adverse Reactions :
CHF A-V block
Peripheral Vascular disease
Hypotension
Contraindications :
Bronchial asthma
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Verapamil (80-160 mg) /8 hrDiltiazem (60-120 mg) /8 hrDihydropyridine group
Nifedipine (10-40mg) /8 hrAmlodipine 5mg/day
Used in treatment of all types of angina.
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BlockVoltage -dependent calcium channels (L-type) in cardiac and smooth muscles.
CALCIUM
Mechanism of anti-anginal action :
1 - Coronary artery dilatation and relief of coronary spasm (variant angina)
• (Verapamil & Diltiazem)• Decrease HR.• Decrease contractility• Decrease AV conductivity
• Arteriolar dilatation
Vascular resistance
Afterload
2 -Decrease myocardial O2 demand due to:
Dosage and Route of Administration
Drug Route Dosage
Verapamil Oral 80-160 mg every 8 hours
Nifedipine Oral 10-40 mg every 8 hours
Diltiazem Oral 60-120 mg every 8 hours
Adverse reactions :
DizzinessAnkle
edema HypotensionHeadache
FlushingConstipation
A-V block & HF only with Verapamil &
Diltiazem
Reflex Tachycardia with
Nifedipine
3 - Bradycardia.
Contraindications of Verapamil & Diltiazem:
1 - HF
2 - Sinus or A-V node disease.
b-blocker + Long
acting Nitrate
b-blocker + Nifedipine
Verapamil or Diltiazem +
Nitrate
b-blocker + Nitrate + Nifedipine
??
?
?
b-blockers block reflex tachycardia produced by nitrates•Nitrates attenuate the increased left ventricular end-diastolic volume associated with b-blockers
b-blockers decrease reflex tachycardia produced by nifedepine.
•Verapamil or Diltiazem decrease tachycardia produced by nitrates.
•In patients with stable angina not controlled by two types of antianginal drugs the use of three agents may provide improvement.
OBAT-OBAT ANGINAPEKTORIS
I. NITRAT ORGANIKMK :
otot polosNirat organik NO reaktif
( radikal bebas )
guanilat siklase
GMP c GMP
Defosforilasi miosin
Relaksasi otot polos
“ Nitrat organik tidak memberikan efek langsung pada jantung “
Sediaan :1. NO3 kerja singkat
ex : - gliseril trinitrat sublingual or spray yg mpy durasi 30 menit.- gliserol trinitrat transdermal yg brp plester dgn durasi 24 jam.
2. NO3 kerja lama lebih stabil dan efektif ex : isosorbid dinitrat oral Warning NO3 :Nitrat organik +Vasodilator lain hipotensi
-hidralazin -prazosin -nifedipin
II. Beta blokerdigunakan untuk profilaksis angina pektoris akibat kerja fisik.
MK : menghambat reseptor beta, shg
menurunkan frek.denyut jtg & kontraktilitas miokard, shg kebutuhan oksigen miokard juga akan berkurang.
Sediaan :1. Kardioprotektif beta bloker :
- Propranolol- Timolol- Metoprolol*
2. Kardioselektif beta bloker :- Atenolol- Asebutalol- Metoprolol
III. Ca AntagonisMK :
Menghambat masuknya ion Ca ekstraselluler pada membran sel
jantung dan otot polos
Menimbulkan efek lgs inotropik dan kronotropik negatif dan
memperlambat konduksi AV
Vasodilatasi
Sediaan : - Nifedipin- Verapamil- Diltiazem
Pada Angina tidak stabil, kemungkinan resiko Infark miokard akan meningkat, maka terapinya :1.NO3 + Beta bloker.2.Antiplatelet : aspirin 3.Antikoagulan : heparin
TERIMAKASIH