Leisa J. Freeman

Dynamic causes of angina pectoris

Angina pectoris was linked with coronary arterial disease well over a century ago, but the linkage presented the Victorian physician with problems because he saw it as neither simple nor direct: some patients had severe disability and died with relatively little coronary disease whereas others lived to a ripe old age with an astonishing amount of arterial narrowings. The dilemma was resolved by Colbeck’ who postulated that dynamic factors such as coronary arterial spasm must cause acute and subacute obstructions. Coronary arteriograms made it possible for the contemporary physician to see the narrowings that were the counterparts of the rigid stenoses he had seen in the postmortem examination, albeit less severe in appearance when the vessel was distended by pulsatile blood flow. Cause and effect were believed to have been demonstrated. It seemed so simple then to explain the symptom of angina on the basis of an organic vascular handicap; the worse the blockage, the more severe the symptoms. Bypass the stenosis and all would be well. The patient was amazed by such a simple explanation because he knew that his symptoms varied widely from day to day and month to month. Dynamic factors fell into disrepute and became the diagnosis of the “diagnostically destitute”.2 The increased use of arteriograms allowed repeated examinations of the patient’s arteries. A problem began to emerge, because there was no difference in the coronary appearance when the patient had minimal symptoms and when he had numerous attacks of angina each day and his condition was called “unstable” or “preinfarction”. When the patient’s symptoms improved there were no new collaterals to explain why this happened.3 Recordings of thousands of arteriograms showed that two patients might have the same degree of coronary stenoses, yet one might have severe and life threat-

Hyperventilation in Cardiac Rehabilitation

Seventy-six out of the first 100 consecutive patients enrolled in a cardiac rehabilitation programme were considered to hyperventilate. The diagnosis was made on the basis of four or more clinical findings documented from the history, examination and electrocardiogram. Thirteen percent had an organic cause, the remaining 66 were found to hyperventilate with activity (39%), emotion (44%) or as a habit (17%). The cardiovascular effects of hyperventilation are outlined and a method of rebreathing training is explained. The opinion is expressed that hyperventilation is one of the maladaptive coping strategies commonly adopted by patients with coronary illness. Activity programmes are unlikely to be successful if it is not recognized clinically and treated.

Two cases of pregnancy with coarctation of the aorta

An increasing number of women with previously repaired coarctation of the aorta are now becoming pregnant; uncorrected coarctation may also present for the first time in pregnancy with hypertension. There are vital issues pertaining to maternal risk and management.

Role of the Nurse Counsellor in Managing Patients with the Hyperventilation Syndrome

A hyperventilation clinic was established specifically to deal with patients referred from the accident and emergency department with the hyperventilation syndrome. This was run by a staff nurse, who counselled the patients and taught abdominal breathing techniques and relaxation. In 30 patients so managed, 63% said their symptoms were much better or had completely gone and in only 6% was there no improvement; 43% had previously had more than one attendance at the A&E department, but following treatment only 2 patients represented during 5 months of follow up. The use of a nurse counsellor seems to be a simple and effective approach to managing these patients and considerably reduces both casualty and outpatient physician time.

Heart rate response, emotional disturbance and hyperventilation

The heart rate and electrocardiographic responses were documented in 40 subjects undergoing hyperventilation provocation tests. Forced overbreathing produced a similar mean heart rate increase in all subjects, regardless of whether the result of the provocation tests suggested the hyperventilation syndrome. In contrast subjects diagnosed as hyperventilators by virtue of prolonged hypocapnia in response to psychological provocation showed significant increased heart rate responses compared to the remaining subjects (p less than 0.001). Significant electrocardiographic abnormalities were also produced. The view is presented that the hypocapnia may allow persistence of the cardiovascular responses in the presence of emotional challenge.

The effect of the Type A behaviour pattern on myocardial ischaemia during daily life

Twenty-eight subjects completed 2 Type A questionnaires. Just under half the patients were considered Type A. Painful episodes of myocardial ischaemia occurred more frequently in Type A patients during a stressful period of ambulatory Holter monitoring compared to a later date. This difference could not be explained in terms of severity of disease or length of myocardial ischaemia. Rather it seemed to reflect increased reporting of somatic symptoms on the background of a greater sensitivity to environmental stress. Type A patients may thus present themselves earlier than their Type B peers.

Breathing and Thinking: Unacknowledged Coronary Risk Factors

Health is a quality of life we enjoy when we can take a vigorous part in the world around us and yet keep the internal milieu in a balanced, orderly and stable condition. In varying degrees we are all vulnerable to loss of integrity of the internal self-regulating systems through such influences as the external environments changing too fast for our adaptive mechanisms, loss of control, lack of sleep, inadequate supplies of energy and information for the tasks on hand, and a want of social assets.

Hyperventilation and Ischaemic Heart Disease

It is increasingly obvious that the paradigms that hold sway over cardiology at present are not providing adequate solutions. Risk factor management has been disappointing [1] and coronary artery bypass grafting is not the simple answer to angina pectoris, usually considered to be due solely to the rigid coronary atheromatous narrowings demonstrated at angiography [2].