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

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.

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

BACK MAIN EXIT INDEX NEXT

PATHOPHYSIOLOGY OF ANGINA

An imbalance between the myocardial oxygen supply and demand.

demandO2

supply

Pathophysiology

The difference of Arteriovenous oxygen pressure

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

MANAGEMENT OF ANGINA

Management of Angina

Management of Stable Angina

Management of Unstable Angina

Management of Variant Angina

Management of Stable Angina

1- General measures.2- Drug Treatment.3- Coronary artery revascularization.

Stop smoking Reduce weight

Treat Hypertension , Hypercholestrolimia

and Diabetes

AVOID Severe exertion Heavy meal Emotions Cold Weather

General measures

• Graduated exercise may open new collaterals

a. For an acute attackb. For immediate pre-exertional prophylaxisc. For long-term prophylaxisd. Antiplatelet therapy.

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)

Coronary artery bypass grafting (CABG)

Percutaneous Transluminal coronary Angioplasty (PTCA)For patients not responding to

adequate medical therapy

Management of Unstable AnginaNitrate

+b-blocker+

Aspirin (low dose) and/or Heparin orThrombolytic (stryptokinase)to minimize risk of infarction

Management of Variant Angina

Nitrates and/or Ca++ Channel blockers

For the acute attack & prophylaxis

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.

NITRATES

Arteries

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

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.

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

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.

Duration of Action of Various Preparations of Organic Nitrates

Preparation Duration of action

" Short-acting"1-Nitroglycerin

2- Isosorbide dinitrate

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

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:

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

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

Fatigue & weakness

Mask signs of Hypoglycemi

Nightmares , Hallucinations , Depression.

Plasma Triglycerides & HDL Cholesterol Discontinuation after

long ttt exacerbates Angina

45BACK MAIN EXIT INDEX NEXT

Adverse Reactions :

CHF A-V block

Peripheral Vascular disease

Hypotension

Contraindications :

Bronchial asthma

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.

47BACK MAIN EXIT INDEX NEXT

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

Kul v - Angina

Documents

Transcript of Kul v - Angina

ANGINA PEKTORIS

Presentasi Angina

Referat Angina

Angina Pectoris.docx

Patofisiologi Angina

Angina Ludwig Atau Angina Ludovici Atau Abses Leher Dalam

Stable Angina

Ludwig Angina

Angina Ppt

angina unstable

Askep Angina

Angina Pectoris

Makalah Angina

Jurnal Angina

Sa-14. Paduan Fe-c (Materi Kul v)

Angina Pectoris1

Angina Pektoris

Unstable Angina

Angina Ludwig

Angina Ludovici