Abstract
The circulatory, arterial blood gas tension and
metabolic changes following acute myocardial infarction
have been studied serially in patients with and without
cardiogenic shock. The effects of oxygen administration
on these changes has been investigated. Follow-up
studies have been undertaken following recovery from
shock and at various stages of convalescence in most
patients.
Cardiogenic shock has been shown to be associated
with a severe impairment of left ventricular function
with a reduced cardiac output and markedly reduced
stroke volume* an elevated central venous pressure and
an inadequate compensatory increase in systemic
vascular resistance. These circulatory changes were
accompanied by a very considerable degree of arterial
blood hypoxaemia, as well as a metabolic acidosis,
lactic acidaemia and hyperglycaemia.
In uncomplicated acute myocardial infarction the
circulatory changes were found to be highly variable.
The cardiac output and stroke volume varied from
normal to very low values. The systemic vascular
resistance varied between high and low values, resulting
in the maintenance of the blood pressure at moderate to
normal levels. Uncomplicated acute myocardial
infarction was accompanied by only a mild degree of
arterial blood hypoxaemia and a complete lack of
metabolic disturbance.
The patients without shock showed a normal
rise in arterial blood oxygen tension when breathing
oxygen. In contrast, those with shock showed a
relatively small increase of arterial blood oxygen
tension following oxygen therapy. This impaired
response has been shown to be due to the shunting of
about 25% of the cardiac output through vessels
inaccessible to pulmonary gas exchange. These
patients are therefore in urgent need of oxygen and
this must be given in as high a concentration as possible.
The circulatory effects of oxygen therapy in
patients with uncomplicated myocardial infarction are
similar to those found in normal subjects - that is,
a fall in heart rate and cardiac output with a slight
increase in systemic vascular resistance and arterial
blood pressure. It is possible that the poor and variable
response of arterial blood oxygenation in cases of
cardiogenic shock accounts for the less marked and
equally variable circulatory response to such therapy.
Recovery from cardiogenic shock was found to be
associated with a reduction in tachycardia and central
venous pressure with an increase in blood pressure*
stroke volume and cardiac output and only small variable
changes in systemic vascular resistance. The
arterial hypoxacmia, metaoolic acidosis and lactic
acicaemia progressively declined with recovery.
Progressive recovery from uncomplicated acute
myocardial infarction was associated with a reduction
in central venous pressure and an increase in strrke
volume. There was a progressive increase in the
arterial blood oxygen tension levels towards normal
with increasing recovery.
The pathophysiological and therapeutic implications
of these findings are discussed.
