The intensive care of the coronary crisis

This article was first published by JRSM in Volume 58 issue 2, February 1965. Our full back archive is available online at jrs.sagepub.com.

The mortality among patients admitted to hospital following acute myocardial infarction is distressingly high and is in the order of 25% to 40%. In the series of 543 hospital admissions for acute myocardial infarction described by Honey and Truelove, ¹ 36% died during the first eight weeks. Sixty-three deaths occurred during the first 24 h and the subsequent death rate declined steadily towards the end of the first week. These figures are similar to those reported by Wahlberg, ² Brown et al., ³ Robinson et al. ⁴ and Julian et al. ⁵ Some of the factors responsible for death can be listed under the following headings: (1) Disturbances of rhythm (ventricular fibrillation, asystole, heart block, tachycardia). (2) Myocardial failure. (3) Peripheral vascular failure. (4) Biochemical changes. (5) Embolism. (6) Respiratory disturbances. (7) Drugs.

Knowledge of the changes taking place in acute myocardial infarction is often fragmentary. A special care and investigation unit has been set up at Hammersmith Hospital in association with the Postgraduate Medical School of London and the Medical Research Council. The Unit has been designed for a pilot study, not only to observe physiological changes but also to determine the value of such an organisation in the routine care of patients in this serious condition.

A side-ward attached to the main male medical ward has been set aside entirely as a care and study room for patients with acute myocardial infarction. The room is divided by curtains to separate the patient from the electronic recording apparatus when necessary. Figure 1 shows a general view of the room and recording apparatus which includes a multichannel direct writing recorder with two pressure channels, two electrocardiographic, one phonocardiographic and one respiration channel. The input plugs of the channels are arranged on the wall at the head of the patient’s bed. The outputs are recorded on a direct writer and displayed on a four-channel oscilloscope. Rectal and skin temperatures are recorded by an electric thermometer. A dye dilution recorder is used for measuring the cardiac output.

Figure 1.

The special ward for the intensive care and investigation of the patient with an acute myocardial infarction (reproduced from Shillingford and Thomas ⁶ with kind permission).

A Lown ‘cardioverter’ ⁷ is available for pacing or defibrillation as required and includes an auditory alarm system operating according to a pre-set heart rate. A closed-circuit television camera is mounted above the patient’s bed and relayed to screens in the registrars’ laboratories and nurses’ room. Instruments and drugs necessary for investigation and treatment are stored in the room. Electrical signals from the room can be transmitted via a cable and stored on an eight-channel magnetic tape recorder in a nearby laboratory. This instrument has five DC channels, two AC and one channel for speech and will run continuously for 24 h.

The patient at all times is under the full care of the consultant physician and his staff and all research procedures are integrated with the care of the patient. Any procedures undertaken in the study of the patient have been designed to give the minimum discomfort while yielding the maximum information on his condition and response to treatment.

Patients suspected of having an acute myocardial infarct on clinical and electrocardiographic grounds are admitted to the unit. After routine clinical examination, standard electrocardiogram and chest X-ray, two leads of the electrocardiogram are recorded continuously, the first chosen to show P waves most clearly for analysing rhythm, the second to show the greatest ST-T changes. Arterial and venous pressures are measured by introducing fine polythene catheters percutaneously under local anaesthesia into the brachial artery and antecubital vein by the Seldinger technique. The tip of the venous catheter lies in the region of the great veins and the arterial catheter about 10 cm above its point of insertion. These catheters are attached to P23Gb Statham strain-gauge manometers. When measurements are not being made the lumen of each catheter is filled with heparin (5000 U/mL). The catheters are bandaged to the patient’s forearm allowing complete freedom of movement. The catheters are also used for withdrawing arterial and venous blood samples without disturbing the patient and without the necessity for further needle puncture.

The cardiac output is measured by the dye dilution method using the photoelectric earpiece and Coomassie blue dye. Blood investigations include arterial pO₂, pCO₂, pH, lactic acid, pyruvate and serum electrolyte estimations.

When a patient is not under personal supervision an alarm system, in which a buzzer rings when the heart rate goes below or above pre-set levels, is in operation. In the event of cardiac arrest, the established hospital drill is put into operation. The medical or nursing staff nearest to the patient begin closed cardiac massage and ventilate the lungs while the duty anaesthetist, thoracic surgical registrar and other assistants are called to the ward by the loud-speaker system. All the necessary equipment and drugs for resuscitation are at hand.

The hemodynamic changes observed in a series of patients during the acute changes of myocardial infarction are being reported in full elsewhere. ⁸ There appears to be a wide range of changes from low cardiac output and high peripheral resistance to high cardiac output and low peripheral resistance in patients who are seriously ill. The effect of drugs such as oxygen and morphine has been studied. ⁹ Figure 2 shows the usual effect of oxygen on the blood pressure. It will be seen that when the patient is breathing oxygen (approximately 40%) there is a rise in the blood pressure of about 5 to 10 mmHg as compared with when he is breathing air, together with a slight fall of cardiac output. Associated with this is a rise of blood pO₂ from 64 to over 250 mmHg.

Figure 2.

The effect of breathing oxygen and air alternately on the arterial blood pressure of a patient with an acute mnyocardial infarction.

Figure 3 illustrates a reaction that may occur with the administration of morphine: 3 mg of morphine sulphate was given slowly intravenously to a man aged 72 who had had a myocardial infarction 7 h previously. The administration was followed by a very considerable fall in the blood pressure and slowing of the heart beat; the patient’s reaction was that of going to sleep. Raising the legs restored the blood pressure to its previous level.

Figure 3.

The effect on the blood pressure of 3 mg of morphine sulphate injected intravenously, in one patient with an acute myocardial infarction.

The number of patients treated so far is small and we must await a larger series before drawing any conclusions about the long-term value of such a unit. Two things are certain, however: a few patients who would otherwise die will be saved and a clearer understanding of the haemodynamic and other changes taking place in this condition, and a more rational use of drugs, will ensue.