Welcome to PERFUSION POLICIES 101. This will be a continuing series provided to assist your programs with that one puzzle piece we all run into now and then- that one time that an unexpected patient condition may give you pause…
The intention here is to disseminate some basic recipes that have probably been implemented at countless institutions, for God knows how long. The usual disclaimers obviously apply:
Due Diligence is the Responsibility of the Reader!
Use the information as you feel fit, recognizing that this is information gleaned from multiple sources, it is recruited from the public domain of the internet, with no implied assurance of accuracy- but is cogent, and based on logical and reasonable clinical rationale.
Frank Aprile 🙂
Protamine Administration and Reaction
Protamine is a basic protein originating from salmon sperm that effectively neutralizes heparin. A number of hemodynamic effects are suggested after protamine neutralization of heparin. Guffin et al. showed a 50% reduction in postoperative bleeding with protamine doses adjusted to unneutralized heparin, suggesting an advantage to aboiding protamine overdosing and its anticoagulant and proinflammatory effects. This is accomplished with use of heparin-protamine titration assay utilizing a Hepcon analyzer.
After the patient is off cardiopulmonary bypass (CPB) and is hemodynamically stable, heparin is reversed with protamine sulfate. This is accomplished by utilizing a Hepcon analyzer. If protamine titration assay is not available, a dosage of 1.3mg protamine/mg of heparin is used. Before starting protamine, the perfusionist should be notified by anesthesia and all pump suctions should be truned off. If not notified, ask if protamine has been started. Protamine is associated with a wide variety of cardiovascular responses that do not appear to be related to speed or total dose of administration. However, it seems prudent to administer protamine slowly in patients with impaired cardiovascular function or previous exposure to protamine. Some commonly seen hemodynamic profiles are:
- No change.
- Systemic vasodilatation with decreased arterial blood pressure and decreased ventricular filling pressures (volume, CaCl2 or a peripheral alpha agonist are useful treatments).
- With pulmonary artery vasoconstriction, there is an elevation in PA pressure, the heart dilates and CVP increases. If right ventricle failure occurs, systemic BP and left-sided ventricular filling pressures decrease. (the treatment consists of inotropic support until right heart function returns to normal. Rarely, reinstitution of CPB may be necessary).
- Myocardial depression and left ventricular failure manifested by increases in left ventricle (LV) filling. This may be more common in patients with preexisting LV dysfunction. (Additional inotropic and/or vasodilator support may be required).