Changing haemodynamics in patient with papillary muscle dysfunction.

Abstract

A patient with papillary muscle disease caused by myocardial infarction was studied before and after injection ofphenylephrine. The pulmonary wedge pressure was normal at rest. However, pressures and murmur changes, occurring spontaneously and after injection ofphenylephrine, suggested that intermittent severe mitral regurgitation contributed significantly to the recurrent episodes of acute left heartfailure presented by this patient. Case report A 53-year-old woman was admitted with a 6-month history of recurrent pulmonary oedema associated with chest pain. Except for mild diabetes, she had been previously healthy. Between the episodes of acute left heart failure, she was feeling relatively well, complaining only of atypical chest pain and of mild dyspnoea on effort. Clinical examination on admission showed a woman in no distress. Her blood pressure was IIO/70 mmHg (14.6/9.3 kPa) and the pulse was regular, 70/minute.The jugular pulse and pressure were normal, the edge of the liver was palpated 3 cm under the costal margin, and no peripheral oedema was present. The lungs were clear. The left ventricle was enlarged on palpation and a prominent lower left sternal impulse was felt. The first heart sound was reduced in intensity and the pulmonary closure sound was accentuated. A grade 3/6 pansystolic murmur was heard at the apical area, conducted to the axilla, and along the left sternal border, followed by a third heart sound and a short mid-diastolic rumble. The murmur varied only slightly from day to day. The chest x-ray showed moderate enlargement of the left ventricle and left atrium. There were signs of pulmonary venous congestion and of pulmonary arterial hypertension.Acute subvalvar mitral regurgitation was considered to be the most likely diagnosis at this stage. Right heart catheterization was performed under local anaesthesia. Pethidine 50 mg and promethazine hydrochloride 50 mg were given intramuscularly i hour before catheterization. No shunts were detected. The pulmonary artery pressure was 56/24 mmHg (7.4/ 3.2 kPa) at the beginning ofthe procedure. While attempting to record a reliable pulmonary wedge pressure, the main pulmonary artery pressure was observed to vary spontaneously, finally dropping to i8/8 mmHg (2.4/ 1.1 kPa) about 30 minutes after the first measurement was obtained. At that time, the mean pulmonary wedge pressure was 9 mmHg (r.2 kPa), with a v wave of 14 mmHg (I.9 kPa). The systemic blood pressure as measured by sphygmomanometer was unchanged at 110/70 mmHg (14.6/9.3 kPa); the heart rate was 120/ minute. The murmur was barely audible.Phenylephrine, i mg diluted in IO ml of normal saline, was injected intravenously. Within i minute, the blood pressure rose to I50/90 mmHg (I9.9/II.9 kPa) and the heart rate dropped to ioo/minute. A giant v wave appeared on the pulmonary wedge tracing (Fig. i) while the pulmonary artery pressure rose to 84/30 mmHg (II.2/3.9 kPa) (Table). The patient complained of chest pain and of increasing dyspnoea. The murmur became much louder. These changes persisted...

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