Specific use effects, Cardiac function, Bradycardia – ZOLL Thermogard XP IVTM Physician Manual User Manual

Page 26: Arrhythmia, Specific use effects 25, Cardiac function 25, Bradycardia 25, Arrhythmia 25

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ZOLL IVTM™ System

Physicians' Manual

600248-001 Rev 3

25

Specific Use Effects

Cardiac Function

The use of any central catheter brings with it potential for alterations in cardiac
function. Hypothermia applications bring attendant risks of bradycardia and
ventricular arrhythmia. IVTM catheters do not carry additional risk in this respect
when used in a normothermia application since the intention is to maintain the patient
at a normal body temperature. The discussion below explains this in more detail.

Bradycardia

The induction of bradycardia is not a particular risk of normothermia applications of
the IVTM System .

Bradycardia is an inevitable result of hypothermia. Cardiac tissue is an excitable
tissue. Bjornstad et al [11] studied the cardiac effects of hypothermia in dogs. There
is a linear increase in the duration of the epicardial monophasic action potentials
(MAP) and ventricular effective refractory period (VERP) with decreasing temperature
from normal to 25°C. Bradycardia that does not revert with a return to normothermia
requires further investigation.

Arrhythmia

The induction of ventricular arrhythmia is not a particular risk of normothermia
applications of the IVTM System except insofar as this is theoretically possible with
any central line insertion due to direct physical cardiac irriation.

Ventricular arrhythmia are of concern in hypothermia. Cooling reduces the
monophasic action potential. As a result, Bjornstad et al [11] showed a
corresponding decrease in the fibrillation threshold during electrophysiological
testing. Similar work has been done by Mortensen et al (1993) and Bjornstad et al
(1995) with little evidence that agents that alter ion channel behavior can modify the
effect.

The effects of hypothermia upon an individual heart will worsen with the extent of pre-
existing cardiac disease. Conventional wisdom is that ventricular fibrillation cannot
be reversed at temperatures below 25-28°C and that coma is induced somewhere
below 30°C[28][29]. However Thomas & Cahill [30] reported electromechanical
cardiac recovery at 25.6°C and DaVee & Reineberg [31] at 20°C.

There exists a specific risk with any system that relies upon cardiac output, such as
the IVTM catheters, for heat exchange. In the event that the catheter system is used
in patients that are moderately to severely hypothermic (i.e. below 32°C) it is possible
that fibrillation will occur and be irreversible until the heart is warmed. With no
cardiac output , there is no mechanism to raise that patient’s core temperature.
Death would ensue unless the patient was on coronary bypass or could be rapidly
rewarmed by other means.

In the usual cardiovascular situation, the patient is warmed to the mid-30’s prior to
disconnection from the bypass pump so that this situation does not arise.

In Neurological hypothermia, it is important not to depress the cardiac temperature
below 30ºC. The CoolGard 3000 is limited by design to prevent the selectio of set-
point temperatures to below 32ºC as a result.

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