The autonomic nervous system evolved to preserve human life as it tried to survive in a hostile environment (saber tooth tigers, mammoths, etc.) with frequently scarce resources (feast or famine). The two automatic divisions that define the autonomic nervous system require no conscious effort to function; the ‘fast tract’ (sympathetic nervous system) speeds up system functions so we can fight off or run away from life threats, and the ‘slow tract’ (parasympathetic nervous system) preserves scarce energy resources.
Think about it this way - imagine you are in the back of your ambulance with a very large patient who decides to become uncooperative. In fact, he becomes downright unfriendly. Without any conscious effort on your part, the sympathetic nerves in your body begin to fire, stimulating the sympathetic alpha and beta receptors that will help prepare you for this situation. Like pushing any on/off button, the results depend on the connection.
Starting from the top, your pupils dilate to maximize light gathering and improve vision. The diameter of your bronchioles increases, as does your respiratory rate (Beta 2 stimulation), thus increasing oxygen delivery and carbon dioxide removal. At the same time, heart rate and contraction strength increases (Beta 1 stimulation), as does blood return to the heart when non-essential blood vessels are constricted (Alpha stimulation). Together, this increases cardiac output that fills dilated blood vessels in skeletal muscle (Beta 2 stimulation) that need the additional oxygen and energy to fuel your ability to ‘fight or flee’ your threatening patient. Talk about pumped up!
Obviously, you wouldn’t want to have to maintain this level of activity on a continuous basis. Once the patient is out of your ambulance, stimulation of the sympathetic nervous system begins to subside, allowing a return to baseline activity. Once back at the station, you can move into a “rest and refuel” mode with help from the parasympathetic nervous system, which slows the heart rate, decreases heart contractility and lowers overall energy requirements, thus conserving residual fuel supplies while increasing blood flow to your digestive system to maximize absorption and processing of replacement nutrients.
Now imagine it is many, many years later and your coronary arteries have become plaque-laced time bombs that decide today is detonation day. You experience the classics: substernal chest pain radiating to your left arm and neck, sweating and shortness of breath. In short, you think you’re going to die.
A segment of your heart muscle is missing its normal blood supply, causing ischemia - and that hurts. You become tachycardic from anxiety, pain and fear, increasing the demand for oxygen and nutrients that are already in short supply from the occlusion. This escalates the ischemia and potential for heart muscle damage. Because of your medical background, you ask your spouse to drive you to the hospital. But she’s on to you and has already called the ambulance.
You know the drill: O2, IV, monitor, aspirin, nitro, 12 lead, transport … but wait - a new medication? Metoprolol? Atenolol? A beta 1 blocker? Why?
Fortunately, the EMTs quickly get a handle on your chest pain, so the drive to the nearest appropriate medical facility is unrushed and there’s time to explain.
Your personal paramedic says to you, “Your Beta 1 receptors are in overdrive, causing your heart rate and contractility to increase, which causes an increase in oxygen usage because of the elevated energy consumption. If the beta 1 receptor is blocked, the heart rate and contractility decreases, as does oxygen consumption. Right now, in your heart, if we decrease the oxygen demand, we decrease ischemia. This decreases the potential for heart muscle damage and limits the appearance of abnormal rhythms like ventricular fibrillation. The overall effect: improved survival from your heart attack!” (Don’t you just hate well-informed EMTs?).
But what she says is true. Many studies have shown consistent survival benefit from beta blockers in patients suffering a myocardial infarct. However, there are still conflicting views concerning early administration of beta blockers. One recent study suggested that early beta blocker administration saves heart muscle, while a recent editorial pointed out that early intravenous administration poses potential complications and later administration of oral beta blockers is equally effective and safer.
Bottom line: while route, administration or timing may vary, and while systems differ, there is consensus that at some point during your heart attack you will want the beta block benefit.
References
- 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care: Part 8: Stabilization of the Patient with Acute Coronary Syndromes. Circulation. 2005;112;89-110.
- ACC/AHA/AHRQ/CMS/JCAHO Practice Advisory: Commitment to Respond to COMMIT/CSS-2 Trial Results Beta Blocker Use for Myocardial Infarction (MI) Within 24 Hours of Hospital Arrival. Retrieved June 15, 2007 from http://www.americanheart.org/downloadable/heart/1115211365285COMMIT%20Beta%20Blocker%20FACT%20Sheet.pdf
- Ibanez B, Prat-Gonzalez S, Speidl WS, et al. Early Metoprolol Administration Before Coronary Reperfusion Results in Increased Myocardial Salvage: Analysis of Ischemic Myocardium at Risk Using Cardiac Magnetic Resonance. Circulation. 2007;115;2909-2916.
- Bates, ER. Role of Intravenous B-Blockers in the Treatment of ST-Elevation Myocardial Infarction: Of Mice (Dogs, Pigs) and Men. Circulation; 2007;2904-2906.