The word ‘angina’ means I cry.’ Angina pectoris is used to denote cardiac pain of short duration due to inadequate blood supply to the cardiac musculature. As a result of this, pain producing factors (some metabolites) accumulate and stimulate the nerve endings resulting in pain.
The most important symptom of Angina Pectoris is pain. This has got the following characteristics:
If the pain lasts for more than 30 minutes it may indicate unstable angina, myocardial infarction or other alternate possibility.
Patient may look pale and anxious. He is motionless and still, with a tightly closed fist kept over the precordium. Pulse rate may be increased and systolic and diastolic blood pressures may be little elevated. At the site of pain in the arms a few tender spots may be present.
Cardiac finding is usually nil except tachycardia; sometimes there may be evidence of cardiac enlargement or aortic second sound (A2) may be accentuated. Atrial sound (S,) may be palpable and audible, this may give rise to a gallop rhythm. Apical systolic murmur due to papillary muscle dysfunction, paradoxical splitting of the second heart sound, even precordial bulge may be present. Evidences of diabetes, xanthomatosis xanthelasma, Tendinous xanthoma, hypertension, thyrotoxicosis, myxoedema, orthostatic hypotension, aortic stenosis, aortic regurgitation, mitral stenosis, occlusive peripheral arteries, hypertrophic cardiomyopathy, mitral valve prolapse, peripheral arterial disease, etc. may be present. Supraventricular or ventricular arrhythmia may be present as a cause or effect relationship. Angina pectoris may be of different types.
This is classical angina pectoris which is prOvoked by effort or exercise, relieved by rest or by taking nitroglycerin, is short lasting and often recurrent. ECG shows ST segment depression.
It is of recent onset (less than 3 months), clinical picture is more severe but not so characteristic, pain may occur at rest at night, more frequent, usually 3 episodes per day and very often leads to myocardial infarction. It is of longer duration (15 minutes or more) and may not improve with nitrates. Patients with accelerated stable angina, i.e. when induced with minimal provocation, lasts longer, occurring at rest is also included under unstable angina. ECG shows transient ST and T changes simulating sub-endocardial injury pattern but serum enzymes remain at normal level. Coronary angiography shows significant obstruction (>80%) in one or more larger coronary arteries. There is controversy regarding the relative merits of medical and surgical treatment.
Variant Angina Pectoris (Prinzmetal’s angina)
It is more common in women under 50. The pain is typical but may occur at rest without any provocating factor. It characteristically occurs in the early morning often awakening the patient from sleep. No history of previous myocardial infarction is usually seen. It often recurs in cyclic fashion with waxing and waning and sometimes may have a fixed time each day. The ECG shows ST elevation as is seen in acute myocardial infarction transiently. Focal coronary spasm of proximal epicardial coronary arteries is the usual factor associated with various types of arrhythmias and conduction defects. Both surgical and medical treatment are advocated. Rapid relief of pain is observed with sublingual nitrates and nifedepine. B-blocker may increase coronary vasospasm though they are used in the management where spasm is associated with fixed stenosis.
This type of angina occurs when patient lies down. This is usually seen in presence of heart failure. In recumbent position the central blood volume is increased and myocardial tension is also increased. In such patients severe coronary artery disease is usually present.
This type of angina occurs at night awakening the patient from sleep as with variant angina. It is usually precipitated by vivid dreams. Severe coronary artery disease is usually associated with this condition.
Here pain of angina pectoris is same as in chronic stable angina but with normal coronary arteriogram. After exercise ECG shows ST segment depression. Possibly these patients have an abnormal coronary vascular reserve. In response to vasoconstrictive influences there may be an abnormal increase In coronary vascular reserve. In response to vasodilatation for increased myocardial oxygen demand. Probably some local factors which autoregulate coronary vascular resistance such as endothelium derived relaxing factor (EDRD), paracrine hormones and endothelin are responsible. Abnormalities in the release of these hormones or their effect on the smooth muscles is responsible for precipitating a clinical atack Long term prognosis is better in comparison to usual angina pectoris.
https://butanoblog.com/ The most important member of a family is the housewife. He lives as a pillar of a family. Women…
Staphylococcal Pneumonia It may be a primary respiratory infection or secondary to staphylococcal focus anywhere in the body. It is…
It is the commonest of all specific pneumonias. AETIOLOGY Predisposing causes Age: All ages but 50% of cases are below…
DEFINITION OF CHRONIC BRONCHIAL ASTHMA BRONCHIAL ASTHMA is a chronic reversible inflammatory destructive disease of the airways characterised by recurrent…
DEFINITION BRONCHIECTASIS SINGS is a condition of permanent abnormal dilatation of the larger bronchi. AETIOLOGY AND PATHOGENESIS Acquire Obstruction Obstruction…
DEFINITION OF CHRONIC BRONCHITIS PATIENT Chronic bronchitis may be defined as a disease characterised by cough and sputum for at…