WHY IDENTIFY THE RIGHT VENTRICULAR INFARCT?
It is important to recognize the signs of a right ventricular infarct because treatment differs significantly between patients with an RVI and those with other infarct sites.
The traditional field treatment for an MI is aspirin and oxygen, with nitroglycerin and morphine for pain (often referred to as MONA). Some services now administer angiotensin converting enzyme (ACE) inhibitors, clopidogrel, and beta-blocking drugs as well.6
Patients were given high-flow oxygen for years, although some authors have recently cast doubt on the routine use of high-flow oxygen in myocardial infarctions and called for controlled studies to evaluate its effectiveness as opposed to low-flow oxygen.7 American Heart Association guidelines no longer recommend high-flow oxygen, except when hypoxia is present; however, there is no evidence that hypertherapeutic oxygen harms when used in the field.
Nitroglycerin has been the mainstay of treatment for ischemic chest pain, followed by IV opioids when adequate nitroglycerin therapy does not reduce the pain.
The rationale for giving nitroglycerin has been that it will vasodilate both sides of the systemic circulation, reducing both preload (venous return) and afterload (forward systemic resistance), which reduces the workload on the heart and therefore oxygen and glucose consumption. It is also thought to vasodilate the coronary circulation, which improves coronary artery circulation, both direct and collateral, increasing oxygen and glucose delivery to ischemic tissues. However, nitroglycerin cannot do anything to correct complete obstruction from ruptured plaques or platelet aggregations (clots).
The American Heart Association's Handbook of Emergency Cardiovascular Care, Guidelines CPR-ECC 2005 states that nitroglycerin is contraindicated in RVI.8
The rationale for giving morphine is that by making the patient pain-free, endogenous catecholamine release and vasoconstriction (Alpha-1 effect) will be lessened, and the workload on the heart will be decreased; however, morphine causes histamine release, and histamine is a vasodilator. Vasodilation can lower venous return and preload to the damaged right ventricle, thus affecting cardiac output.
Morphine has been shown to increase infarct size9 and lessen blood flow through coronary arteries by as much as 13%.10 Some have questioned the efficacy of morphine in MI, but the American Heart Association still grants it a Class IC classification with the stated precaution: "Use with caution in right ventricular infarction."11
FOCUS ON THE PROBLEM
The right ventricle is not designed to provide systemic circulation. Its purpose is to pump blood through the lungs and pulmonary circuit. Thus, the pressures it is required to produce are less, and it has a thinner wall than the left ventricle, which must pump blood throughout the body.
Its functional abilities are dependent upon preload, or the volume of venous return to the heart, principally during diastole, since veins do not have muscular walls to keep blood moving as do the arteries. The right atria and ventricle have relatively little "suction" from contractions to pull blood into them.
So a reduction in venous return will result in diminished pumping pressure by the right ventricle, diminished pulmonary circulation, diminished left ventricular filling, diminished cardiac output, diminished systemic blood pressure and, if not corrected, possible dysrhythmias, shock and death.12,13
If one understands that heart muscle, or myocardium, is perfused by the coronary artery system, and that the coronary arteries primarily fill with blood during diastole and are dependent upon pressures in the aorta immediately after the left ventricle contracts, one can easily understand that a drop in stroke volume as a result of lessened preload will eventually result in a drop in coronary artery filling pressures. If there is an obstruction in one or more of the coronary arteries, the blood supply to myocardial tissue will be further compromised, since collateral circulation (blood flow through arterial branches not affected by the obstruction) is dependent upon adequate filling pressures.