ALTERNATION OF THE MAMMALIAN HEART‐BEAT AND OF THE ARTERIAL PULSE
Authors: MacWilliam J. A. 
Published: December 2014

Typical systolic alternation in the cat's ventricle, not in the auricle, is very common in simple chloroform anæsthesia in the normal type I., not in type II.; it is much less frequent under anæsthesia with chloroform and urethane. In susceptible hearts systolic alternation is favoured by vagus stimulation, acceleration of rhythm, increased arterial resistance, inadequate respiration, and the occurrence of premature contractions. It is not a necessary consequence of any of these. It is opposed by slowing of rhythm and lowering of blood‐pressure; it is occasionally abolished by a premature contraction.

A brief phase of weakening, with or without systolic alternation, may occur after a period of excessively rapid excitation; this apparently depends on a fatiguing effect of forced excitations at an early phase of recovery from preceding contractions.

Systolic alternation depends on a defect of effective participation at the smaller beats of varying portions of the musculature from deficient recuperation in some portions. This is due, in cases with excessive arterial resistance or after premature contraction, to prolongation of the absolute refractory period, in others (vagus, chloroform) to slowing of recovery after that period—in the relative refractory period.

Vagus alternation affords evidence of direct action of the nerve on the ventricle additional to that stated in a former paper.

An essential feature is the functional inequality, depending on toxic influences, local differences of coronary blood‐supply, etc., of different portions of the ventricular musculature, not simply a general depression and weakening of the whole ventricle.

Typical diastolic alternation of the ventricles (not of the auricles), with equal timing of the rhythm, may occur in both types I. and II., under the influence of experimental conditions or as a very temporary phase, e.g. during recovery from certain effects of vagus inhibition, and from auricular acceleration, increased inflow into the heart, or premature contraction with compensatory pause and increased filling.

Incomplete relaxation at alternate beats may, under some of the same conditions, be attended by varying degrees of prematurity of alternate beats.

Alternately incomplete relaxation is removed, temporarily at least, by slowing of rhythm, or by compression of vena cava inferior, or by inhalation of amyl nitrite.

Increased arterial resistance may set up diastolic alternation, or alternate premature beats, or systolic alternation.

Diastolic alternation has a different mechanism of production from systolic alternation, the former depending on undue duration of the ventricular curves in relation to the rate of excitation (from auricle, etc.) and a failure in the adequate shortening of the ventricular curves when the rhythm is accelerated.

Alternation in the duration of A‐V intervals, a longer interval following a somewhat premature auricle beat, sometimes accompanies incomplete relaxation at alternate beats. Typical pulses alternans, with equal timing of the beginnings of the alternating pulse‐waves or with slight delay of the smaller wave, may occur apart from the existence of systolic alternation of the ventricle, and be due to alternate variation in the degree of relaxation and filling between the beats; typical diastolic alternation with equal timing of the V. rhythm, or with some prematurity of alternate V. beats depending on A‐V nodal rhythm; beats led by S‐A and A‐V nodes alternately, producing alternation of the arterial pulse in two ways, which are described.

Some of these modes of causation can be distinguished by other modes of examination (e.g. electrogram), while others cannot.

Pulsus alternans may or not co‐exist with systolic alternation of the ventricle, varying with associated conditions of relaxation and filling; ventricular alternation may be masked in this way, so far as the arterial pulse shows.

Under apparently similar experimental conditions there is much individual variation, in both cats and rabbits, as regards the tendency to the development of systolic and diastolic alternation.

Part of the expenses of this investigation was defrayed by a grant from the Medical Research Council. I have to thank Professor G.
Spencer Melvin for his co‐operation in a number of the early experiments.