Objectives of this presentation
Review the common pathophysiology – Cause – Affect of the reasons cardiopulmonary arrest occurs in clinical practice and then
review the current views on basic and advanced cardiac life support and provide my personal views on the subject based on
over 35 years of clinical and some years of experimental research experience. Some of my experience comes from my emergency
medical technician experience. In this regard I am able to carefully compare, in my opinion, the drastic differences as well
as similarities between CPR in animals and CPR in humans. The title reminds us of which patients should be resuscitated.
Pathophysiology
Cardiac Arrest leads to dysoxia in the brain mitochondria... energy failure. Calcium influx into mitochondria AND THE cytosol
occurs leading to a literally melt down of cellular enzyme pathways making even getting and using oxygen into the metabolic
energy manufacturing pathways. Also it should be remembered that ROS production, following the restarting of perfusion occurs
and these oxygen radicals combine with inducible NO and produces peroxylnitrite. This compound literally blows the cell up!
It is like intracellular TNT. The cells most vulnerable are in the brain & heart (the heart by a factor of half that of the
most sensitive areas of the brain (cortical-subcortical occulocephalic reagions involved with visual recognition). Within
a few minutes of severe dysoxia as seen with cardiac arrest, this area is rendered into various stages of cell injury and
death – from Stage I where no morphological changes are seen on scanning EM to Stage V where cells are literally autolyzing.
It is estimated by some that the percentage of the number of cells reaching the stage IV level of cell injury, where the 'point
of no return' is for recovery must reach approximately 35-45% before irreversible neuro-injury occurs, so long as this primary
'hit' does not propagate into a secondary injury caused by reperfusion injury mechanisms. These can be suppressed by such
things as hypothermia, the most important, and use of neuro-excitation blockers such as lidocaine, calcium channel blockers,
superoxide radical blockers and scavengers, etc., but the most important is the IMMEDIATE USE OF LOCAL AND REGIONAL – GLOBAL
HYPOTHERMIA starting at the time of the arrest and lasting at least several hours post resuscitation.
Principle goal of CPR or the new term cardiopulmonary and cerebral (CPCR) circulation
To resume normal or near normal blood flow and oxygenation to the brain and heart within a maximum of only several minutes.
From my experience that means at the maximum 5 minutes and at the minimum 3 minutes. Any time period beyond this critical
5 minutes leads to impairments that could be life-long. EVERY SECOND IS IMPORTANT.
In review of 10 cases that were successfully resuscitated it appears that the use of Doppler flow detection using the cornea
of the eye in dogs and cats as the landing zone for the pediatric flat probe of the Doppler Blood Flow Detector to assess
cranial blood flow during CPCR Provide adequate blood flow was the most accurate means, outside of visual and palpable assessment
of cardiac performance, was the best means of determining the meeting of the principle objective – the normalization of enough
blood flow to prevent cardio-cerebral injury past the point of no return where pet function after the arrest would be poor,
with such things as permanent blindness or cerebral palsy. It appeared in the analysis of the ten survivors with good neuro
function that other organ systems were also resuscitated adequately to prevent irreversible injury, including spinal cord,
lung, liver, GI tract, kidney and endocrine organs if the brain and heart were resuscitated adequately.
