Angina Pectoris USW
-
Upload
nadia-indri -
Category
Documents
-
view
233 -
download
4
description
Transcript of Angina Pectoris USW
ANGINA PECTORIS
ANGINA PECTORIS
Angina pectoris is the result of myocardial ischemia caused by an imbalance between myocardial blood supply and oxygen demand
occurs when the Oxygen Supply to the Myocardium is insufficient for its needs.
ANGINA-CORONARY OCCLUSION
CORONARY OCCLUSION
Classification
Stable angina= effort angina, = angina related to myocardial
ischemia. Typical presentations :
chest discomfort and associated symptoms precipitated by some activity (running, walking, etc.) with minimal or non-existent symptoms at rest.
STABLE ANGINAOccurs on exercise, emotion or eating.Caused by increase demand of the heart and
by a fixed narrowing of coronary vessels, almost always by atheroma.
Coronary obstruction is ‘fixed’Blood flow fails to increase during increased
demand
a form of acutely developing and rapidly reversible left ventricular failure results which is relieved by taking rest and reducing the myocardial workload.
ClassificationUnstable anginaUnstable angina (UA) (also "crescendo angina;"
this is a form of acute coronary syndrome) is defined as angina pectoris that changes or worsens.
It has at least 1 of these 3 features:it occurs at rest (or with minimal exertion),
usually lasting >10 min;it is severe and of new onset (i.e., within the prior
4–6 weeks); and/orit occurs with a crescendo pattern (i.e., distinctly
more severe, prolonged, or frequent than before).
UNSTABLE ANGINAThis is characterized by pain that occurs with
less excertion , cumulating pain at rest.The pathology is similar to that involved in
Myocardial Infraction, namely platelet-fibrin thrombus associated with a ruptured atheromatous plaque, but without complete occulation of the vessels.
ClassificationMicrovascular angina= Syndrome X characterized by angina-like chest painThe cause of Microvascular Angina is
unknown, but it appears to be the result of poor function in the tiny blood vessels of the heart, arms and legs.
prognosis is excellent.
ANGINA: SYNDROME XTypical , exertional angina with positive
exercise stress testAnatomically normal coronary arteriesReduced capacity of vasodilation in
microvasculatureCalcium channel blockers and Beta blockers
are effective.
VARIANT ANGINA (PRINZMETAL’S ANGINA)
UncommonOccurs at rest generally during sleepCaused by Large Coronary Artery SpasmUsually associated with atheromatous diseaseAbnormally reactive and hypertrophied
segments in the Coronary ArteryDrugs aimed at preventing & relieving
Coronary spasm.
ANGINAL EQUIVALENT SYNDROME
Patient’s with exertional dyspnea rather than exertional chest pain
Caused by exercise induced left ventricular dysfunction
ANGINA: SILENT ISCHEMIAVery Common
More episodes of Silent than Painful angina in the same patient.
Difficult to diagnose
Generally Exercise testing.
DIAGNOSIS1. STRESS (EXERCISE) TEST.2. ECG3. CHEST X-RAY4. CARDIAC ANGIOGRAPHY/ CARDIAC
CATHETERIZATION5. ERGONOVINE TEST6. BLOOD TEST (BIO-MARKERS)
1. EXERCISE TEST/STRESS TESTUsed to measure heart’s response to exerciseAlternatively the patient recieves an injection
of a radioisotope (generally Thallium) which makes the heart visible to a special-linked camera
90% accuratedoesn’t identify the exactly where and how
the coronary arteries are blocked.
2. ECGProvides info about the changes or damages
to the heart muscleDoesn’t detect the narrowing of the coronary
arteriesDuring an Anginal attack the ECG may show 1. S-T phase depression.2. T- phase inversion and/or3. Ventricular arrythmia ECG- more abnormal with Unstable Angina
where the elevation in S-T segment is found.
STABLE ANGINA
At Rest
After Excercise
3. CHEST X-RAY
Performed to rule out any lung disease or heart damage that may be causing the pain.
Also may reveal enlargement of heart
4. CARDIAC ANGIOGRAPHY/ CARDIAC CATHETERIZATIONShows the precise size and location of
blockages within the Coronary arteriesA cathereter is inserted through the blood
vessels from the forearm or groinIt is snaked through arteries till it reaches
the heartA fluid is pumpedSo the arteries and the heart are clearly
visible
5. ERGONOVINE TEST
Generally done if the person is assumed to suffer from Coronary Spasm
Done along with angiographyThe artery-narrowing drug—Ergonovine or
Ach is given to cause Coronary SpasmThe persons response to ergonovanine is
measured
6. BLOOD TEST/BIOMARKERS
Lipid profileC-reactive protein and B-type natriuretic
proteinThese tests are predictive of the moratality of
heart disease
TREATMENT3 Classes of drugs used according their mode
of action
1. NITRATES2. - ADRENOCEPTOR ANTAGONISTS3. CALCIUM CHANNEL ANTAGONISTS4. ANTIPLATELET DRUGS
NITRATESProdrugsSources of Nitric OxideEg:- Nitroglycerin, Isosorbide Dinitrate Isosorbide-5-Mononitrate
TOXICITY OF NITRATESHeadacheIncreased mortalityRecurrence of Myocardial InfractionDizzinessFlushingRapid heart beatRestlessnessDry mouthSkin rashNausea
CALCIUM CHANNEL ANTAGONISTSDisrupt Ca++ through Ca++ channels-ve ionotrpic effect2 types:-1. Dihydropyridine (amlodipine, nifedipine,
nicardipine)2. Non-Dihydropyridine
1. Phenylalkylamine (verapamil, gallopamil)2. Benzodiazapenes (diltiazem)3. Non-selective (bepridil, mibefradil)
MECHANISM OF ACTION
-ADRENOCEPTOR ANTAGONOSTS
Important in prophylaxis of angina and treating unstable angina
Decrease O2 consumption by the heartEffects on coronary vessels-not importantAvoided in variant angina as they increase
the chances of spasm
PHARMACOLOGICAL ACTIONS
MECHANISM OF ACTION
COMPARITIVE TOXIC EFFECTS
COMBINATION THERAPY1. Nitrates + -blockers :- in stable angina2. Ca++ channel blockers + -blockers :-in
stable angina when the treatment with nitrates and -blockers has failed.
3. Ca++ channel blockers + Nitrates :- in unstable angina
4. All 3 together:- when the combinations of 2 drugs has failed, where:-
1. Nitrates:- decrease Preload2. Ca++ channel Blockers:- decrease Afterload3. -blockers:- decrease heart rate and
myocardial contractions