The amount of blood flow that CPR can generate – as currently performed – is very limited, hardly reaching one fourth of the normal blood flow.
Such low blood flow is not able to generate in the aorta – the large vessel that comes right off the heart to supply blood carrying oxygen to the rest of the body – the pressure needed to ensure that enough blood carrying oxygen flows through the coronary arteries and the cerebral arteries. To increase the aortic pressure, pharmacological agents able to induce constriction of vessels (i.e., vasoconstrictive agents) in peripheral tissues and other organs that are not at immediate risk of suffering permanent injury from ischemia, is necessary.
Epinephrine is currently the vasoconstrictive agent of choice. However, epinephrine while producing the necessary vasoconstriction it also accentuates the energy deficit of the heart muscle (by stimulating cardiac cells when there is limited oxygen availability). This effect, limits its efficacy, and recent studies have shown that among individuals who are successfully resuscitated, those who receive epinephrine during CPR do worse than those who do not.
Vasopressin is another vasoconstrictive agent that can be used during CPR. However, vasopressin has a longer duration of action than epinephrine and its effect persists after cardiac activity has been restored in vasoconstriction is no longer desired.
At Resuscitation Therapeutics, we believe there is a need of new vasoconstrictive agents – specifically designed for CPR – that are able to elicit the needed peripheral vasoconstriction only for the duration of CPR and without accentuating the energy deficit of the heart muscle.
Future development - Stay tuned