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SURGICAL DISORDERS OF THE PERICARDIUM


Acute and chronic pericarditis are entities, which need separate management and approach. The acute process (acute pericarditis) may be caused by viral and/or bacterial infection, uraemia, myocardial infarction, Tuberculosis and neoplastic infiltration of the pericardial layers. There are two types: specific and non-specific.

Non-specific itself consists of purulent pericarditis and pericardial effusion, and also pericarditis after uraemia, but tuberculosis pericarditis should be considered as a specific type. The main physical findings in case of acute pericarditis are common weakness, fatigue, high temperature and specific so called Marker’s sign.

Friction rub, which is audible during the heart motions, is consisting of three elements:
  • Atrial systole
  • Ventricular systole
  • Atrial diastole
There are also characteristic changes in ECG (elevation of ST segment and pointed T waved). These changes occur in all leads exception aVR and V1. Intermittent atrial fibrillation, supra-ventricular tachycardia and heart flattering occur in about 29% of patients with acute pericarditis. Acute pericarditis is itself limited lesion. It limits itself spontaneously after two to six weeks, when the main signs disappear. The signs are exacerbated in supine position.

The treatment of the acute pericarditis includes the use of NSAID’s as the first step in the process of treatment. If there is no evidence of improvement within the 48 hours, if the chest pain and high temperature doesn’t subside, we should use steroid e.g. prednisone (10mg per day) and the broad spectrum antibiotics.

Pericardial Effusion:
Pericardial effusion may be with little and/or in great quantity and if left untreated, can cause cardiac temponade and the base for the development of the pericardial adhesions. In case when the cardiac temponade does occur, pericardiocentesis should be used. It should be performed at the left sternal angle in the fourth intercostal space under ECG monitoring. When the point of the needle approaches pericardial layers, there is a little click and ST wave depression. Even the small amount of the fluid, which we receive from pericardium, is sufficient to cease the cardiac temponade and moreover, investigation of the evacuated effusion also plays an important role in the treatment. The main signs of cardiac temponade are tachynoea, tachycardia, low arterial pressure and high venous pressure, which clinically are revealed in the distended veins.

Pathogenesis:
There are three factors:
  • Volume of effusion
  • Intensivity of effusional process
  • Distensibility of the pericardium
When the pressure due to effusion equiblirizes the pressure in the right chambers of the heart, then pericardial temponade occurs. The main sign of the cardiac temponade is paradoxical pulse (a 10mmHg fall in the arterial pressure during inspiration). Heart sounds are feeble and not audible. Alteration of R wave in ECG is also characteristic sign of cardiac temponade.

Differentiation of Cardiac Temponade:
  • For haemorrhagic shock, low arterial pressure, tachypnoea and tachycardia are also characteristic. During pericarditis, in 50% of patients occurs chronic renal insufficiency and uraemia
  • Tuberculosis pericarditis is characterized by cough, weakness, sweat, subfebrile temperature (37 – 37.2C) etc.
  • Purulent pericarditis often results as a result of pneumonia or penetrating cardiac injury. If the adhesive type of pericarditis occurs then surgical treatment is a method of choice. Two incisions are applied now-a-days. Most commonly we use so called left anterior intercostal incision; but at some clinics, they use sternostomy, which makes much larger approach to the pericardium but it more complicated as well. Early types of adhesions must be dissected, first on the left ventricular surface and then on the right. If there is any evidence of cardiac insufficiency, then some kinds of shunt may be applied
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This article has been written by Dr. M. Javed Abbas.
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19:53 09/02/2003