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I use PACs when I am dealing with a patient
who is hypotensive / shocked, and I cannot rely on right atrial pressure
as a guide to LV preload. Examples of this are refractory cardiogenic
shock, myocardial contusion, myocardial ischemia complicating septic
shock, or sepsis in a patient with previous myocardial disease. On
occasion it is necessary to perform right heart catheterization in a
patient who is not responding to conventional therapy.
The oximetric (continuous cardiac output)
pulmonary artery catheter has been advocated as a useful guide to early
aggressive resuscitation, particulary in trauma. The stroke volume, CVP
and PCWP and mixed venous oxygen saturation are used to guide fluid
resuscitation. Although none of these are hard endpoints of resuscitation,
the logic of this approach is that it prevents under and
over-resuscitation, particularly when large amounts of volume are being
given. The counter argument is that patients are rarely over-resuscitated,
and non invasive monitors such as the esophageal doppler may provide more
rapid (and less hazardous) measurement of stroke volume.
You will undoubtedly work with physicians who
believe that PACs are the bedrock of critical care, and others that they
are a faddish cult (Robin 1985). Much of the information derived from PACs
cannot be predicted by clinical examination (Connors 1983). I believe that
they have greatly helped our understanding of cardiovascular physiology
in critical illness, so much so that, in many cases, particularly in
sepsis, we can now predict PAC findings without catheterizing the right
heart.
What follows is thirteen tips
for using invasive pressure monitors:
-
There is no “normal”
CVP or wedge pressures: you must follow a trend and look at responses to
therapy, principally fluid boluses.
-
Abnormal hearts –
those with acutely ischemic ventricles, fibrotic or contused myocardiums,
are less compliant, and require higher filling pressures to project a
“normal” stroke volume. They progressively dilate until there is
sufficient muscle stretch to eject this volume. This is why the ejection
fraction progressively falls.
-
It is preferable to
use stroke volume rather than cardiac output as the measured response to
therapy, as the latter is influence by heart rate, which may be fast for
a variety of reasons, and mask a poorly performing ventricle (in sepsis
the cardiac output is characteristically high and the stroke volume
low).
-
A low mixed venous
oxygen saturation (SvO2) is usually an indication of
under-resuscitation, and volume loading is required. It is worthwhile to
match this process withlactic acid concentration. An increased SvO2 is
difficult to interpret: it may indicate inability to extract oxygen, it
may indicate a hyperdynamic circulation.
-
Normal hearts have
huge physiologic reserve, and can cope very well with high filling
volumes, consequently, you should never go wrong with aggressively
volume loading shocked patients: you will adequately fill abnormal
hearts without injuring normal hearts. Always aim your CVP and PCWP
targets high!
-
The first treatment
for all kinds of shock, including cardiogenic, is volume, volume and
more volume.
-
A little extravascular
lung water is probably less harmful than vasoactive drugs: do not skimp
on the fluids for fear of flooding the lungs.
-
There is no magic
mathematical formula which allows you to figure out the influence of
PEEP on PCWP and CVP: if transalveolar pressure is kept constant, the
trend should be consistent.
-
The pulmonary artery
catheter is a monitor not a therapy: it is not a surrogate for
resuscitative therapy or source control.
-
During the
resuscitative process, it should rapidly become apparent to you the CVP
and PCWP that the patient’s heart “likes” (in terms of stroke volume and
CVP). This is important with regard to fluid mobilization (“deresuscitation”)
and redistribution.
-
If the patient’s blood
pressure or stroke volume begins to fall and the filling pressures are
higher than those at which optimal stroke volume/cardiac output was
obtained, then the patient has likely mobilized fluid, and is now
“overloaded”: preload reducing agents such as nitrates and diuretics are
required.
-
An evolving increase
in the stroke volume likewise represents hypervolemia: the patient will
autodiurese if the kidneys are functioning normally.
-
Be cautious with the
use of derived variables from pulmonary artery catheters. I speak in
particular of the “systemic vascular resistance” (SVR). There is,
unquestionably, and abnormality in peripheral resistance (PR) in all
forms of distributive shock, and appropriate vasoconstriction (and thus
high PR) in hypovolemic and cardiogenic shock. Unfortunately, there is
no easy method for measuring PR. The SVR is calculated from the equation
for change in pressure/flow, which is MAP-CVP/CO. The problem with this
equation is the pulsatility of cardiac output flow – it is determined by
the heart rate. A fast heart rate for the same stroke volume will lead
to the measurement of a lower SVR than before. The PR may not have changed.
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