Saturday 2 July 1966
REFLECTIONS ON CARDIOPULMONARY
RESUSCITATION
H. R. S. HARLEY
M.S. Lond., F.R.C.S.
CONSULTANT THORACIC SURGEON, UNITED CARDIFF HOSPITALS
THE purposes of this communication are to review the
pulmonary and circulatory disturbances during cardio-
pulmonary resuscitation (C.P.R.), to compare and deter-
mine the place of the closed and open methods of
performing it, and to assess when efforts to save the
patient should be abandoned. By C.P.R. is meant the
combination of intermittent positive-pressure ventilation
with rhythmic compression of the heart (cardiac massage)
either by sternal compression, when the chest is closed, or
by direct compression after the chest and pericardium
have been opened. Discussion will be confined to the
period during which both cardiac compression and
artificial ventilation are required; but it is not proposed
either to define the techniques of these procedures or to
describe important associated measures, such as the use
of cardiac stimulants, electrical defibrillation, or stimula-
tion of the heart, or the correction of acid-base upsets.
Although neither the closed nor the open chest method
is new (Safar et al. 1963), the former did not come into
widespread use until the work of Kouwenhoven et al.
(1960) popularised it and gave us a resuscitative method
of the greatest value. Other good accounts of this tech-
nique are given by Hiigin (1961), Brook et al. (1962),
Safar et al. (1962, 1963), and Stephenson (1964). Safar
et al. (1962) showed that in cardiac arrest rhythmical
compression of the sternum failed to ventilate the patient,
and that some form of intermittent-positive-pressure
respiration is essential.
Recent physiological studies made in the course of
resuscitation show that during cardiac arrest and the
whole period of resuscitation the functions of the lungs
and circulation are seriously deranged. Some of these
studies will now be considered.
Disturbance of Pulmonary Function
Ventilation-perfusion relationships are severely dis-
turbed during C.P.R. This results in a large intrapulmonary
venous-arterial shunt and a pronounced increase in the
physiological dead-space. The shunt produces a large
alveolo-arterial oxygen tension difference (Gilston 1965),
unrelieved by oxygen, and severe arterial hypoxsemia.
The arterial oxygen tension is usually less than 100 mm.
Hg even during adequate ventilation with pure oxygen,
when it should be over 650 mm. Hg (Comroe et al. 1962).
Del Guercio et al. (1965) found the venous admixture
during closed and open chest C.P.R. to be 38-3% and
46-7% respectively, whereas the normal figure is only 3%.
The large physiological dead-space is part of the
ventilatory problem, for it is associated with a reduction
in the proportion of total ventilation which supplies
7453
perfused alveoli. This is partly why, despite appa
good minute ventilation, the arterial PC02was rai
some 50% of 37 patients during closed-chest C.P.R
were investigated by Gilston (1965). The hyperca
may be aggravated by airway obstruction due to i
vomit or other causes.
Thus ideally, in order to maintain satisfactory te
of oxygen and carbon dioxide in-the arterial bloo
patient should be ventilated with large tidal and m
volumes of pure oxygen. The ventilation-perfusion
probably persists for some hours after a satis
heart-beat has been re-established.
Causes of Disturbed Pulmonary Function
The causes of disturbed pulmonary function m
divided into pre-existing and exciting. The pre-ex
causes include low-cardiac-output states, pulmonar
pulmonary vascular disease, and surgery, togethe
its complications—especially the cardiac and p
pulmonary ones.
Several exciting causes may arise during and af
period of resuscitation. Of these, pulmonary o
which is nearly always found at necropsy in fatal
is important. This may be induced by several f
such as left ventricular failure, which may have pr
and caused the cardiac arrest, or pulmonary
hypertension, which may result from C.P.R. in the pr
of mitral-valve incompetence (vide infra). Other
include inhaled vomit and the administration intrave
of strong solutions of sodium bicarbonate (8-4% s
bicarbonate contains about 7 times as much sod
does physiological saline solution). Finally the
hypoxia which follows cardiac arrest may dama
pulmonary capillaries and make them more perm
especially as their hydrostatic pressure is raised.
The low cardiac output provided by C.P.R. undou
contributes importantly to the abnormal venti
perfusion relationships, for these occur in othe
output states, such as cardiogenic or hypovo
hypotension. Incoordination of ventilation and
chest cardiac compression, and the complicati
closed-chest C.P.R. (fractures of costochondral junct
sternum, pneumothorax, hxmothorax, hsemopericar
may also play their part.
Disturbance of Circulatory Function
When cardiac arrest occurs, the circulation ceas
a sudden steep rise of venous pressure accompa
similar fall of arterial pressure so that the two a
mately equilibrate at about 20-25 mm. Hg. Thi
venous pressure then distends the arrested, is
heart and will, in my opinion, quickly destroy its f
in these circumstances, unless cardiac compres
started soon. This almost certainly explains the
of Kouwenhoven et al. (1957) that in dogs ope
electrical defibrillation was unlikely to restore the