Muscarinic receptors are coupled to the Gi-protein ; therefore, vagal activation decreases cAMP. Gi-protein activation also leads to the activation of K ACh channels that increase potassium efflux and hyperpolarizes the cells. Increases in vagal activity to the SA node decreases the firing rate of the pacemaker cells by decreasing the slope of the pacemaker potential phase 4 of the action potential ; this decreases heart rate negative chronotropy.
The change in phase 4 slope results from alterations in potassium and calcium currents, as well as the slow-inward sodium current that is thought to be responsible for the pacemaker current I f. By hyperpolarizing the cells, vagal activation increases the cell's threshold for firing, which contributes to the reduction the firing rate.
Similar electrophysiological effects also occur at the AV node; however, in this tissue, these changes are manifested as a reduction in impulse conduction velocity through the AV node negative dromotropy. In the resting state, there is a large degree of vagal tone on the heart, which is responsible for low resting heart rates.
There is also some vagal innervation of the atrial muscle, and to a much lesser extent, the ventricular muscle. These agents can be used to maintain the patient's perfusion status in a symptomatic bradycardia en route to specialized care; however, keep a heightened suspicion of MI. If an infarction is present, chromotropic and inotropic medication would be minimized to prevent excessively increased oxygen demand from the myocardium before arrival at the ED and cath lab.
Electrical intervention for symptomatic bradycardias in the prehospital setting involves transcutaneous pacing. For cases of third-degree heart block in which there is complete atrioventricular dissociation, or in a rapidly deteriorating patient, this is the primary treatment. There are a couple of considerations with regard to pacing, one of which is that transcutaneous pacing is painful.
The increased sympathetic response to pain can in itself act as a stimulant, but there are more humane ways to accomplish this, such as using atropine. Sedatives are therefore given to facilitate pacing, which presents its own set of dilemmas. The sedative may dampen any remaining sympathetic stimulus to maintain heart rate and respirations. Also, it becomes more difficult to assess the effectiveness of treatment when the patient's mental status has been altered. Finally, pacing itself lessens the diagnostic effectiveness of ECGs, so on arrival at the ED, not only is the patient's mental status unreliable from sedation, but the paced rhythm may have masked ECG changes.
These are factors to be considered when ordering pacing. Nevertheless, it is the indicated treatment for third-degree block or a deteriorating patient with bradycardia Figure 2. In this case, the report was given to the ED physician, who asked that in addition to aspirin and two large IVs, the patient be given 0. Atropine is one of the oldest drugs in the medical pharmacopeia. It was used in ancient times, not as a chronotropic agent, but as a cosmetic drug.
The belladonna plant, which is a source of atropine, means "beautiful lady" in Italian. It was known for its ability to redden cheeks and dilate the pupils, thereby enhancing beauty. Atropine has also been a first-line treatment for bradycardia for hundreds of years.
In modern times it is used to antagonize the effects of acetylcholine, which plays a large role in regulating the sinoatrial node and transmission of impulses to the atrioventricular node in the heart. It is accepted practice to treat bradycardias with SA nodal input by giving atropine.
There have been conflicting views regarding treatment with atropine for bradycardias resulting from heart blocks. The American Heart Association, as well as most EMS protocols, recommends pacing without delay in treatment of high-degree heart blocks, which include both Mobitz II and third-degree blocks.
Keeping the creed "First do no harm" in mind, it is difficult to go straight to the painful administration of transcutaneous pacing. It is an equally difficult decision to sedate a patient who is minimally responsive.
Therefore, questions arise concerning the use of atropine as an initial treatment and what factors might be considered beforehand. The focus is on atropine, because there is much confusion and debate among paramedics on its role and implementation, especially in regard to heart block. Opinions about the use of atropine in heart block generally follow one of three statements: a It is relatively contraindicated in high-degree blocks; b atropine is ineffective for high-degree blocks and should therefore not be considered; c the ACLS guideline says atropine should be considered, but should not delay prompt pacing.
So what are the considerations at play? There is not much guidance on the issue in ACLS or in most protocols, so the statement "consider atropine but do not delay pacing" has not been entirely clear to many medics. A major source of confusion on the issue stems from the fact that a common cause of high-degree heart block is myocardial infarction. Since the actions of atropine are to block the binding of acetylcholine to muscarinic receptors, thereby a reducing vagal input at the SA node, and b increasing conduction velocity through the AV node, the thought is that atropine would be a poor choice for reducing oxygen demand in heart-block therapy when an MI is present.
This case study was intended to take some of the mystery out of the decision of whether to use atropine in treating high-degree heart block along with pacing. The discussion hopefully provides some clarity in the standard that is already in place. Working up these cases in a logical manner will provide guidance on treatment, minimize adverse effects and improve patient outcomes.
In the scenario, there are indeed factors pointing in the direction of right ventricular or septal MI, especially the V1 ST segment elevations and pathological Q-waves. Confounding the interpretation, however, the possibility exists that the Q-waves were residual indicators of previous MI. The ST segment elevations in lead V1 may be entirely due to a prior existing left bundle branch block, which often has ECG features of an elevated ST segment.
The point here is that what looks like MI on the ECG can be misleading, possibly leading a medic to not use atropine in heart block. Furthermore, making a diagnosis based on ECG interpretation can be difficult in any practice, especially in a prehospital setting. Therefore, the initial decision of whether to treat the bradycardia with atropine or pacing should be primarily based on the patient's hemodynamic presentation.
This is the basis for the perception that atropine is ineffective in wide-complex Mobitz II block. A wide QRS complex is an indication that the electrical origin of ventricular depolarization is not from the SA or AV nodes, but from the ventricles themselves. The point that must be made here is that bundle branch blocks a don't always show the RSR morphology that is, they don't always have two distinct points at the apex and b bundle branch blocks prolong the QRS width, appearing falsely to be a ventricular rhythm, especially when it's hard to discern the P-wave.
The point here is that a Mobitz II block is commonly a block in the bundle branches and therefore shows widened QRS patterns similar to a ventricular rhythm. Again, careful consideration of the patient's hematological status and presenting appearance must be made before deciding to withdraw atropine therapy. This was true in Mrs. Jones' case, in which two out of three atrial depolarizations caused ventricular contraction, but not rapidly enough to keep the tissues adequately perfused.
Stated another way, if there is ventricular response to nodal impulses in a BBB and the patient is symptomatic, it cannot be argued that atropine will have no effect.
Given that an acute MI would ordinarily exclude the use of atropine's accelerating effects, the question now is, would the risk of harm by giving atropine in MI outweigh its usefulness? The decision is especially crucial in a poorly perfused patient like Mrs. Jones, for whom the adverse effects of pain from pacing and the risks of sedation may be large.
To continue the theme described above, it must be recognized that along with false positive readings for MI, there are also commonly true MIs in which there are absolutely no ECG signs.
An example of how timing can make an ECG falsely normal is to obtain an ECG during a phase when the T-wave is moving upward from an inverted position ischemia to an upright position and pulling the depressed ST segment upwards with it.
For a small period of time, the ECG will appear to be completely normal, when in fact death is imminent. The point is that an ECG is a flash in time.
Although decisions in the emergency setting must be made with speed, having the benefit of establishing a trend will lead to better-quality decisions. This luxury is generally not available to paramedics in the field; therefore, emphasis must be on the patient's lack of perfusion from bradycardia in order to make a decision regarding atropine.
As stated, it is difficult to make a treatment decision based solely on ECG signs; therefore, we base the decision of whether to use atropine primarily on patient presentation. However, one case in which the use of atropine can more confidently be excluded is left coronary artery infarct.
The signs of LCA infarct are usually the more classic signs of "heart attack" because the LCA branches supply such a large area of myocardium. The highly sensitive presentation is a history of severe, crushing, substernal, radiating chest pain, diaphoresis and characteristic ECG indications of hypoxic left myocardium.
The problem from a diagnostic standpoint is that the interventricular septum containing the bundle branches is supplied by the septal branch of the LAD. So a LAD infarct may give high-degree heart block signs, yet it would be incorrect in this case to irritate the myocardium further by giving atropine as the primary treatment.
Left-sided infarction has a classic presentation. In addition, the intact SA node will usually respond to hypoperfusion with tachycardia. Thus, in the case of high-degree block in the face of left-sided MI, patient presentation can again, along with tachycardia, guide the treatment, in this case away from atropine. Jones did not show most of the classic signs of LAD infarct, but what if she was in the midst of a right coronary artery infarction?
Should this possibility exclude the use of atropine in a symptomatic patient? RCA infarct is more difficult to identify because the signs are more subtle, but in addition to inferior lead II, III, aVF and V4R ST segment changes, there are common right-sided features of a hypotension, b jugular venous distension, with c clear breath sounds. Jones did have slight crackles, but these may have been a chronic condition resulting from her recent MI.
Otherwise, she fits the picture. Our next question then is, does atropine help or hinder our treatment in the case of RCA infarct? First, it must be understood that just as the septal branch of the LAD supplies the interventricular septum and bundle, the nodal branches of the RCA supply the SA and AV nodes via different branches. So both infarct locations will affect signal conduction. But there is a major difference between right and left coronary infarct.
Read below for the explanation. Atropine increases the firing of the sinoatrial node atria and conduction through the atrioventricular node AV of the heart by blocking the action of the vagus nerve. With 3rd-degree block, there is a complete block and disassociation of the electrical activity that is occurring in the atria and ventricles. There is a partial block in the electrical impulses from the atria SA to the ventricles, and thus the effects of atropine would not significantly change the status of the ventricles.
This block can also rapidly progress to 3rd-degree block. To summarize, atropine may speed the firing rate of the SA node atria , but the ventricles are not responding to anything the atria SA node puts out. Thus, the heart rates will not increase. There may be some action at the AV-node with atropine, but the effect will be negligible and typically not therapeutic.
In most cases, atropine will not hurt the patient with 3rd-degree block unless they are unstable and cardiac pacing is delayed in order to administer atropine. It is important to note that Mobitz II and complete heart block may be associated with acute myocardial ischemia. If atropine is used when there is ongoing myocardial ischemia this may worsen myocardial ischemia because of an increase in oxygen consumption.
The increased heart rate will also reduce the diastolic filling time which may worsen coronary perfusion. Since new-onset Mobitz II and complete heart block are commonly associated with myocardial infarction, it is recommended to maintain a slow HR in order to increase the diastolic filling time.
Any time you increase HR, the diastolic filling time is reduced and this reduces the coronary perfusion. Transcutaneous pacing should be the first line action for symptomatic Mobitz II and symptomatic complete heart block. Now back to the bradycardia drugs Epinephrine and Dopamine Epinephrine and dopamine are second-line drugs for symptomatic bradycardia.
They are both used as infusions in the bradycardia algorithm if atropine is ineffective. ACLS guidelines state that if bradycardia is unresponsive to atropine, an equally effective alternative to transcutaneous pacing is the use of an IV infusion of the beta-adrenergic agonists dopamine or epinephrine. Prior to the use of ACLS drugs in the treatment of symptomatic bradycardia, contributing factors of the bradycardia should be explored then ruled out or corrected.
As this is what our unit uses. Kind regards, Jeff. I wish I knew the answer to it, but the American heart Association has not made any information about this change readily available in their literature. I am continuing to work on updates on the site and as soon as I get these complete, I will be doing a deep dive into this to see if I can determine what the scientific.
The total dose should be restricted to avoid Atropine-induced tachycardia, increased myocardial oxygen demand and the potential for worsening cardiac ischemia or increasing infarction size. Please, what is broad complex bradycardia?
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