Shock or severe cardiac failure developing in the course of acute myocardial infarction is an ominous event with a grave prognosis. Despite its frequent occurrence, the precise haemodynamic alterations which occur in cardiogenic shock have not been clearly defined. To date there is no uniform agreement about the therapeutic management of these severely ill patients and the widely different therapeutic measures being advocated only emphasise the uncertainty about the precise pathogenesis of shock complicating acute myocardial infarction. This thesis reviews developments in the concept of myocardial infarction and describes haemodynamic and respiratory studies in patients with acute myocardial infarction. The investigations show that nearly all patients with recent myocardial infarction have abnormal cardio-respiratory function. Even in patients with so called 'uncomplicated' myocardial infarction cardiac output is in the low normal range and the mixed venous oxygen saturation is reduced. A number of these patients have a raised pulmonary arterial pressure. Mismatching of ventilation and perfusion results in arterial hypoxia. The clinical diagnosis of left ventricular failure is not always easy and the abnormal cardio- respiratory function suggests that sub -clinical left ventricular failure is a relatively common finding in acute myocardial infarction. In patients with cardiogenic shock or clinical left ventricular failure, the disorders of cardiac and pulmonary function are more marked but the similarity of the abnormalities suggests that left ventricular failure is present in both groups. The finding of raised pulmonary arterial pressures in the patients with cardiogenic shock is in accord with this view. In general the more severely ill the patient the greater is the degree of cardiac failure and respiratory abnormality. The thesis also documents attempts to treat the impaired left ventricular function in cardiogenic shock by digitalis and acid-base correction and comments on the failure of this approach. The failure to alter the course of cardiogenic shock by pharmacological agents is similar to the reports of many other investigators. Pain and anxiety are present in many of these patient and this can be relieved by opiates, but recent reports have suggested that morphine can produce marked hypotension in patients with acute myocardial infarction and that morphine should be used with great caution, if at all. A detailed examination of the circulatory effects of morphine and heroin in myocardial infarction is presented. The results suggest that morphine is a suitable analgesic for the relief of pain in acute myocardial infarction.