Wild Iris Medical Education
COURSE PRICE: $20.00
CONTACT HOURS: 2
This course is available until February 1, 2013.
ACCREDITATION / APPROVAL
Wild Iris Medical Education (CBRN Provider #12300) is approved as a provider of continuing education for RNs, LVNs, and respiratory therapists by the California Board of Registered Nursing.
Wild Iris Medical Education, Inc., is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's Commission on Accreditation.
The planners and authors of this CE activity have disclosed no relevant financial relationships with any commercial companies pertaining to this activity.
This course is in the process of being revised in order to reflect the American Heart Association's 2010 Guidelines for CPR and Emergency Cardiovascular Care.
Copyright © 2010 Wild Iris Medical Education, Inc. All Rights Reserved.
COURSE OBJECTIVE: The purpose of this course is inform pre-hospital healthcare providers and nurses about current guidelines for emergency cardiac care and ongoing research in the field.
Upon completion of this course, you will be able to:
The 2006 revision of the American Heart Association (AHA) Emergency Cardiac Care (ECC) guidelines represented some of the most radical changes seen in many years. The shift in emphasis was based on many peer-reviewed studies, and it was expected that survival rates would improve (AHA, 2005a). The first studies of the new techniques are very encouraging, with increased survival rates of 15% to 45% being reported (Ewy, 2009). This change in emphasis, termed by some “cardiocerebral resuscitation,” deemphasizes ventilation, oxygenation, and defibrillation in favor of well-performed chest compressions in order to maintain perfusion to vital organs and provide adequate coronary artery pressure (Ewy, 2005).
Good Advanced Cardiac Life Support (ACLS) starts with good BCLS skills. The focus of the cardiac care guidelines for healthcare providers is to provide high-quality CPR for cardiac arrest patients. This emphasis will carry over to your ACLS and Pediatric Advanced Life Support (PALS) skills as well.
Start by establishing unresponsiveness using the shake and shout method. If you are a lone healthcare provider with an unresponsive patient, your next step will be determined by what type of cardiac arrest you expect. If the patient has most likely gone into sudden cardiac collapse, the lone rescuer should first call the emergency response number and get an Automated External Defibrillator (AED), if available. If the unresponsive patient has likely gone into an asphyxial arrest (e.g., drowning), the lone healthcare provider should provide about two minutes of CPR before calling for help (AHA, 2005b). If there is more than one person available, at least one person should start the process of CPR while another activates the emergency response system.
The head-tilt-chin-lift is the preferred method of opening the airway of an adult patient. If trauma is involved or suspected, use the jaw-thrust method. However if ventilations are ineffective using the jaw-thrust and readjustment still does not provide an effective airway, then the head-tilt-chin-lift may be used (AHA, 2005b). The head-tilt-chin-lift is performed by placing one hand on the victim’s forehead with the other hand on the chin and tilting the head back. Resist the temptation to lift up on the neck instead of the chin. This can cause hyperextension of the neck and partially close the airway.
After opening the airway, look, listen, and feel for breathing. Place your ear over the victim’s mouth to listen and feel for adequate breathing. While doing this, you should be looking at their chest to see if it rises. Do this for at least five seconds but no longer than ten seconds (AHA, 2005b). If apnea or agonal, ineffective breathing is detected, give two rescue breaths. Each breath should be delivered over one second. Use any delivery method available, such as mouth-to-mouth, mouth-to-mask, or bag-mask device (with or without oxygen). A good rescue breath will cause the chest to rise. If chest rise is not seen, readjust the airway and attempt ventilation again.
After giving the two rescue breaths, check for a carotid pulse. Use two fingers to find the trachea, and slide your fingers into the groove on either side. Feel for a pulse for at least five seconds but not longer than ten seconds (AHA, 2005b). If a pulse is found but breathing is absent, rescue breathing should be continued. The rescue breaths should be delivered at a rate of one breath every 5–6 seconds or 10–12 per minute. If no definite pulse is found, move the patient to a hard surface, such as a backboard or the floor, and start chest compressions. If the pulse is so weak that you’re not sure it’s really there, start compressions anyway. A slow weak pulse will not maintain adequate perfusion, and the patient can benefit from the compressions.
The importance of delivering high-quality compressions cannot be over emphasized. These compressions will be hard, fast, and deep but will allow full recoil of the chest between compressions. Interruptions will be kept to an absolute minimum.
Good hand position is necessary for effective compressions. For an adult patient, the middle of the patient’s chest or between the nipples is used. Place the heel of one hand on the sternum and the other hand on top with the fingers linked. Position your body directly over the patient’s chest and keep your elbows locked and arms straight.
Compressions should be delivered at a rate of at least 100 per minute. A feedback device such as a metronome should be used to maintain the proper rate. For an adult patient, the chest should be compressed 1-1/2 to 2 inches.
Allowing the chest to recoil completely between compressions is essential. Compression of the chest during CPR raises the intrathoracic pressure. This forces the blood out of the heart chambers. When the chest recoils, a negative intrathoracic pressure is produced. This allows blood to return to the heart, feeding the coronary arteries and filling the heart chambers so that the next compression will be even more effective. This effect is cumulative. Successive compressions will continue to increase coronary artery pressure and organ perfusion. Failure to allow full recoil will result in a continuous positive pressure in the chest and will result in a reduced cardiac output (AHA, 2005b).
Every time there is a pause in compressions, the perfusion pressure falls. Once compressions begin again, it will increase, but slowly. In order to optimize perfusion of the heart and brain, interruptions in compressions should be kept to an absolute minimum and limited to no more than 10 seconds. Compressions should be interrupted for ventilations only in the absence of an advanced airway. Each breath should be delivered over one second, and CPR should be resumed quickly (AHA, 2006a).
After an advanced airway is placed (such as an ET tube, or laryngeal airway), the compressions should not be paused and ventilations should be done at one breathe every 8 seconds. Higher ventilation rates are not indicated, and local protocols may call for even lower rates. With the reduced perfusion that even high-quality compressions provide, these low ventilation rates provide adequate perfusion/ventilation ratios. Hyperventilation can actually reduce survival by not allowing negative intrathoracic pressure during recoil and decreasing venous return (AHA, 2005b).
The recommended compression-to-ventilation ratio for adult patients is 30:2, with a brief pause to deliver the breaths (AHA, 2006a). Five cycles of the 30:2 compressions/ventilations should be delivered, which should take approximately 2 minutes (AHA, 2005b). Only then is the pulse check repeated. All BCLS and ACLS interventions are completed around the 2 minutes of CPR, which helps keep pauses in compressions to an absolute minimum.
The 30:2 compression/ventilation ratio is based on a consensus of experts rather than clear evidence (AHA, 2005b). Some emergency medical services (EMS) and hospitals may elect to give even more compressions. Ratios of 50:2, 100:2 or greater may be seen depending on the location in which you practice. More recent studies have shown benefits with compression-only CPR (Kern, 2009). Early in resuscitation, circulation is more important than ventilation, and the more chest compressions a patient receives, the better myocardial perfusion will be maintained. The oxygen present in the lungs and blood at time of collapse can support perfusion for as long as 10 minutes (Kern, 2009). As more studies are reported, guidelines are likely to change, so local protocol should be followed.
Delivery of chest compressions is tiring, and the emphasis on fast, hard compressions makes it even more so. Research has shown that compressions can become ineffective after 1 to 3 minutes (AHA, 2005b). After their technique has deteriorated, rescuers may mistakenly believe they’re still doing effective compressions for several minutes. In order to get the best and most effective compressions, the AHA recommends that personnel be rotated every 2 minutes, or at the end of every fifth cycle (AHA, 2005b).
Healthcare providers have had “ABC” (airway, breathing, circulation) drilled into them from the very beginning of their career. It is thus common to prioritize the same way. Some suggest that rescuers should think the other way around, or “CBA.” The highest priority is to maintain circulation with high-quality chest compressions, then breathing, and then attention to airway as needed to facilitate breathing (Ewy, 2009). The order in which we approach an unconsciousness should not change, just our priority of our thought process.
Studies into the physiology of cardiac arrest have divided the event into three phases. The first 5 minutes are termed the electrical phase. The most important action during this time is defibrillation, and it is during this time that success rates are the highest. This phase can be prolonged by high-quality CPR. If cardiac arrest is left untreated in the first phase, it moves into the circulatory phase. The heart has been without perfusion, and high-quality chest compressions are the most important action. Defibrillation will be ineffective or even detrimental. The third phase is metabolic, and research in this area is ongoing, with hypothermia being the most promising approach (Ewy, 2009).
If a victim collapses due to a sudden cardiac event, high-quality compressions should be started while an AED is brought to their side, whether the patient is pediatric or adult. Consider the circumstances of the collapse. If the victim is unresponsive from a respiratory event (most common in pediatrics) or from an asphyxial event, such as drowning, CPR should be performed for a period of 2 minutes prior to the application of an AED. The AED should be applied without interrupting compressions until it is ready to analyze. EMS providers will seldom arrive on scene of a cardiac arrest while the patient is still in the electrical phase. Unless bystanders have provided immediate and continuous high-quality chest compressions, deliver 200 compressions before attempting defibrillation (Ewy, 2009).
The recommendation for defibrillation is one shock at a time for patients in a shockable rhythm (AHA, 2005c). Research shows that the average hands-off time to deliver three shocks is about 40 seconds, which allows the coronary artery pressure to fall greatly (AHA, 2005c). This makes it important to continue compressions until you are ready to deliver a shock. There should be no more than 5 seconds from the time of the last compression to shock delivery for the most effective outcome. The increased coronary artery pressure will make successful conversion more likely.
After delivering a shock, there is no pulse check. Chest compressions should be started immediately and 2 minutes of CPR performed before a pulse check is done. Even if the patient has an organized rhythm, the compressions will not harm the patient. Most of the time if a rhythm is present, cardiac output is still too low to provide adequate perfusion, and the patient benefits from the assistance (AHA, 2006).
The energy doses given to adult victims depend on the type of defibrillator:
The first step in the foreign body airway obstruction (FBAO) sequence for the adult is to distinguish between mild and severe airway obstructions. Intervention is indicated only if the obstruction is severe. The signs of severe obstruction include respiratory difficulty, poor air exchange, cyanosis, or an inability to cough or talk. The AHA recommends that only one question be asked, and that question is “Are you choking?” If the victim nods yes, position yourself behind them and wrap your arms around them. Make a fist with one hand and place the thumb (flat side) against the abdomen between the naval and the xiphoid process. Place the other hand on top of your fist. Using both hands with an upward and inward motion, give abdominal thrusts until the foreign body has been dislodged or the patient goes unresponsive (AHA, 2006a).
If the patient becomes unresponsive, activate an emergency response before proceeding any further if you are by yourself. If you are with others, have them do so as soon as you recognize that the victim is in distress.
Management of an unresponsive patient with an airway obstruction is not unlike that of a pulseless and apneic patient. Studies show that chest compressions can produce intrathoracic pressures as high or higher than abdominal thrusts. Therefore, CPR is performed as it would be for a pulseless victim, with one exception. As the airway is opened, look inside the mouth for any foreign body. If a foreign body is seen, remove it, taking care not to push it further down the trachea. Blind finger sweeps are not recommended because of the potential damage to the mouth or throat—or even the healthcare provider’s finger (AHA, 2005b).
Assessment of a patient with cardiovascular compromise must be systematic and organized. The information gathered will vital to making good treatment decisions. An organized step-by-step approach is offered, with mnemonics and other memory aids. These steps can be taken while good CPR is being performed. They are divided into 5 quadrads (AHA, 2006b).
The first quadrad encompasses the primary survey, and it has already been completed if CPR is being performed. This is the ABCDs that we have been doing for many years.
The second quadrad expands on the ABCs and is used to perform a secondary survey.
If the patient has converted to a perfusing rhythm or if you are caring for a cardiac patient who has not yet arrested, continue on with the last 3 quadrads.
Quadrad 3 is the baseline treatment given for every patient with cardiovascular compromise. These are:
Quadrad 4 is assessment of vital signs:
Quadrad 5 is a consideration of the elements of adequate systemic perfusion.
The pulseless arrest algorithms reflect the BCLS guidelines and their emphasis on continuous CPR. Interventions are carefully timed to minimize interruptions.
Ventricular fibrillation (V-fib) is the most common rhythm seen in the out-of-hospital cardiac arrest victim. It is a chaotic rhythm with no organization. The foci in the ventricles are firing randomly and none are conducting, ultimately causing the heart to quiver uselessly. No pumping action occurs, and there is no cardiac output. V-fib may be categorized as course or fine. Course V-fib occurs early in the arrest and is characterized by more electrical activity than fine V-fib. If the patient remains in V-fib, the electrical activity will gradually decrease because of hypoxia and acidosis. Without intervention, it will progress to flat line or asystole (AHA, 2005d).
Ventricular fibrillation (V-fib).
Ventricular tachycardia (V-tach) is a tachycardia, or fast heart rhythm, that originates in one of the ventricles of the heart. It may present itself in one of two ways—monomorphic or polymorphic. Monomorphic is the more common of the two types. All of the QRS complexes will have the same morphology, indicating that they originate from the same location in the ventricles. Polymorphic V-tach originates from multiple locations, causing the complexes to take on different shapes and sizes. Torsades de pointes, or “twisting of the points,” is one of the more commonly recognized polymorphic V-tachs. V-tach may or may not have pulses, so the pulse check should be done with care. If pulses are clearly palpable, the tachycardia algorithm should be used. If pulses are not clearly felt, it is treated as V-fib.
Ventricular tachycardia (V-tach).
The treatment of choice for V-fib/pulseless V-tach is defibrillation, assuming the patient is still in the electrical phase of the arrest. If not, or if there is a doubt, the patient may benefit from doing two minutes of CPR prior to defibrillation (AHA, 2005d). Defibrillate at 360J with a monophasic defibrillator, 150J for a truncated biphasic, or 120J for a rectilinear biphasic. Start CPR after immediately after defibrillation—no pulse check or rhythm check.
Several activities may take place during the 2-minute cycle of CPR. If not already in place, IV or IO access should be established. A vasopressor may be given as soon as venous access is available. Charge the defibrillator before the cycle of CPR is completed. Do a pulse and rhythm check at the end of the cycle. If the rhythm is no longer shockable, go to the appropriate algorithm. If the rhythm is still V-fib or pulseless V-tach, defibrillate at 360J with a monophasic defibrillator, 200J for a truncated biphasic, or 150J for a rectilinear biphasic. After the shock, resume CPR immediately without an additional pulse or rhythm check. Continue CPR for 2 minutes and give an antiarrhythmic during compressions. Again, have the defibrillator charged and ready at the end of the cycle and do a pulse and rhythm check. If the rhythm is still V-fib or pulseless V-tach, then defibrillate at 360J with a monophasic defibrillator, 200J for a truncated biphasic, or 200J for a rectilinear biphasic (AHA, 2005c).
The cycle is repeated with vasopressors and antiarrhythmics as long as the patient remains in V-fib or pulseless V-tach. All subsequent shocks should be delivered at the highest energy level. Intubation or the insertion of an advanced airway should be considered at this point, however the need for intubation should be weighed against the need for continuous chest compressions. If adequate airway and ventilations are achieved by bag valve mask (BVM), advanced airways may be deferred until the patient is more stable (AHA, 2005d).
Asystole (flatline or complete cardiac standstill) is often a confirmation that death has occurred. There is no electrical activity occurring from either the atria or the ventricles. Confirmation of this rhythm should be made by viewing it in at least two different leads. At times, very fine V-fib can be mistaken for asystole.
Asystole (flatline).
Pulseless electrical activity (PEA) is not, in itself, a rhythm. There is organized electrical activity seen on the monitor that could be expected to produce a pulse, but there is little to no actual mechanical activity occurring, and so no pulses are being generated. The rhythm generated may look like a number of normal or aberrant rhythms (see graphs below). The only method of detecting whether the rhythm matches the heartbeat is to check a pulse.
Pulseless electrical activity (PEA).
An early consideration with either of these rhythms is whether this is a sudden unexplained event or if it is truly an end-of-life event. This is often easier to determine in a hospital setting, where medical history and advanced directives are more readily available. Information from family members, advanced directives, hospice workers and local protocols should be considered in determining whether any resuscitation should be attempted.
If either of these arrhythmias is present and the determination has been made to resuscitate, start CPR. Establish an IV or IO line as soon as possible. Vasopressors may be given as soon as venous access is in place.. In the event of asystole or PEA, the healthcare provider must address the “Hs” and “Ts” in the differential diagnosis. By identifying the cause, a cure may be found. Often, the cause is irreversible.
After two minutes of CPR, perform a pulse and rhythm check. If asystole or a bradycardic PEA is still present, continue CPR immediately and give 1 mg of atropine.
Repeat the cycle of vasopressors and atropine as long as the patient remains in asystole or PEA. Intubation or placement of an advanced airway should take place as soon as it becomes necessary. Again, weigh the benefit of continuous compressions and consider postponing placement if good ventilation is obtained with a BVM.
There is no benefit to defibrillating asystole. Pacing is also not used in either of these dysrhythmias, as there is no perfusing cardiac rhythm (AHA, 2005d).
Peripheral IV access should be established as soon as possible for the administration of medications and fluids. If access is difficult and results in delayed therapy, the adult intraosseous (IO) route may be used. IO has the advantage of being quick and easy to place. Any medications or IV fluids that go through an IV can be delivered through an IO, and uptake is almost as rapid. The location and technique of placement depends on which device is used, but possible sites include the distal femur, humeral head, tibial plateau, and the manubrium.
Should attempts at establishing an IV or IO fail, endotracheal (ET) administration can be considered as a last resort, although this route is no longer advocated by the American Heart Association. The IV or IO route is greatly preferred because it will provide a more predictable drug delivery and pharmacological effect (AHA, 2005d). Doses should be doubled for ET delivery and followed with a bolus of saline, to a volume of at least 5–10 ml.
Medications given in pulseless arrests fall into two general categories. Vasopressors are given for their alpha adrenergic properties in hopes that they will increase perfusion to the brain and heart. This makes return of spontaneous circulation more likely. Antiarrhythmics are used to convert nonperfusing and hypoperfusing rhythms. Neither class of drugs has been shown to increase survival rates (AHA, 2005d).
A vasopressor should be the first medication considered, after oxygen, in any pulseless arrest. There is evidence that vasopressors can facilitate the return of spontaneous circulation (ROSC) during a code, even though they have not been shown to increase the rate of neurologically intact survival to hospital discharge. The two recommended vasopressors are epinephrine and vasopressin (AHA, 2005, Part VII).
Epinephrine is the most familiar and commonly given medication during an emergency cardiac event. During cardiac arrest, the primary beneficial effects are secondary to the alpha-adrenergic receptor-stimulating properties. This causes an increase in myocardial and cerebral blood flow during CPR and increases peripheral vascular resistance. The dosing for epinephrine is 1 mg IV/IO of the 1:10,000 solution given every 3–5 minutes. High-dose epinephrine is not recommended as a routine therapy. Vasopressin can be given as an alternative to epinephrine as either the first or second dose. Dosing for vasopressin is 40 units given IV/IO, one time only. If resuscitation continues for more than 20 minutes after vasopressin is administered, continue with epinephrine 1 mg every 3–5 minutes (AHA, 2005d).
Amiodarone is the preferred antiarrhythmic for V-fib/pulseless V-tach. Studies have shown that it increases short-term survival to hospital admission when compared to other antiarrhythmics and placebos (AHA, 2005d). It does not increase survival to hospital discharge, nor does any other antiarrhythmic studied. Amiodarone has multiple effects on the myocardium, affecting the sodium, calcium, and potassium channels. It is also an alpha and beta adrenergic blocker. It has many side effects and interactions with other drugs and should only be given by those very familiar with its administration. The V-fib/pulseless V-tach dose for amiodarone is 300 mg rapid IV/IO push. If the rhythm has not converted after 10 minutes, it may be followed by an additional dose of 150 mg IV/IO. If amiodarone coverts the rhythm, consider an amiodarone drip (AHA, 2005d).
Lidocaine is considered an alternative for V-fib/pulseless V-tach if amiodarone is not available (AHA, 2005d). Lidocaine decreases the automaticity of the myocardium, which helps to reduce fibrillation, especially in ischemic tissue. In a pulseless patient, give 1–1.5 mg/kg IV initially. If the arrhythmia persists, doses of 0.5–0.75 mg/kg IV push can be administered at 5–10 minute intervals to a maximum dose of 3 mg/kg. If the rhythm converts, a lidocaine drip at 1–4 mg/min should be considered (Nursing2006 Drug Handbook, 2006).
Another antiarrhythmic that can be considered with the V-fib/pulseless V-tach is magnesium sulfate. Hypomagnesemia can appear transiently in acute myocardial infarction (AMI) and is associated with ventricular arrhythmias. Magnesium is only given, however, with torsades de pointes and documented hypomagnesemia. A dose of 1–2 g diluted in 10 mL D5W IV/IO is administered over at least 5 minutes.
Procainamide is not recommended in the V-fib/pulseless V-tach cardiac arrest patient because of the long period of infusion and uncertain efficacy in emergency situations (AHA, 2005d).
Neither a vasopressor nor an antiarrhythmic, atropine interrupts the parasympathetic nerve impulses in the central and autonomic nervous systems, allowing an increase in the heart rate, systemic vascular resistance, and blood pressure. It has been shown to be beneficial in asystole, certain bradycardias, and PEA, although the studies of the medication are limited. The dose for pulseless rhythms is 1mg given every 3–5 minutes to maximum dose of 3mg (Nursing2006 Drug Handbook, 2006).
The placement of an advanced airway can take significant time, which may cause a prolonged interruption of CPR. Healthcare providers should weigh the need for compressions against the need for the advanced airway. If adequate ventilations can be accomplished by a bag-mask device and no immediate risk for occlusion or aspiration is seen, it may be prudent to delay placement of an advanced airway until several cycles of CPR have been performed and several shocks have been delivered (AHA, 2005d). This requires maintenance of excellent bag-mask skills. If this procedure is not frequently performed, it should be practiced in a lab setting often enough to maintain the skills properly.
Advanced airways can include endotracheal tube (ETT), laryngeal mask airway (LMA), or a Combitube. Whichever device is chosen, it should be placed by the most experienced person available who has mastered the skill through practice, frequency of placement, and education. If an attempt to place an advanced airway fails, a cycle of CPR and bag-mask ventilation should be performed before any subsequent attempts are made. All equipment should be checked and close at hand before compressions are stopped for the placement attempt (AHA, 2005d).
Bradycardia (slow heart rate) is generally considered to be a resting heart rate of fewer than 60 beats per minute. It is typically symptomatic only when the heart rate drops below 50 beats per minute, and it may lead to cardiac arrest. The bradycardia algorithm covers symptomatic bradycardia as well as atrioventricular (AV) blocks. Remember the first rule of cardiac care: treat the patient, not the monitor. Many people, especially well-conditioned athletes, have resting heart rates in the 50s, 40s, and even lower. Just because the monitor shows a slow heart rate does not mean that the patient will need immediate treatment.
The primary and secondary exam that has already been performed is essential to making treatment decisions. If bradycardia is accompanied by signs and symptoms of poor perfusion, such as chest pain, shortness of breath, altered mental status, hypotension, or shock, the rhythm should be treated immediately. If the patient has adequate perfusion, observation may be all that is needed until a physician can do full work-up.
Pacing should be considered right away for symptomatic bradycardia (AHA, 2005d). If an IV or IO line is in place, atropine may be used first. If not, pacing should be initiated without delay. Clean the skin and clip excess hair to enhance adhesion and conduction. Place the pacemaker pads in the recommended position by following the manufacturer’s guidelines. Be aware, however, that many hospitals and cardiologists may prefer anterior-posterior pad placement to the apex-sternum placement. Be sure that the monitoring leads are also in place. Pacing can be very painful, so consider sedation and analgesia if it can be accomplished quickly.
The pacemaker rate should be set at a heart rate for an adult patient, usually 60–80 bpm. When setting the current, start low and increase until capture is seen on the monitor. This is characterized by pacemaker spikes consistently followed by a wide QRS complex. Check for a pulse that correlates with the monitor rhythm using a site other than the carotid. Once capture is achieved, increase the current another 2 mA and maintain that setting. Sedation should be considered if it was not done before starting. An unresponsive patient may become responsive and very uncomfortable with successful pacing.
Atropine (see also above) is one of the first medications to consider for sinus bradycardia as well as 1st-degree or 2nd-degree type I AV blocks. Atropine is rarely effective on high-degree blocks such as 2nd-degree type II or third-degree and may cause further deterioration in condition. Be aware that patients with transplanted hearts don’t respond to atropine because their hearts have been denervated. The suggested dose is 0.5 mg IV every 3–5 minutes to maximum dose of 3 mg for symptomatic bradycardia. Remember that bradycardic rhythms require an initial dose of 0.5 mg, whereas asystole and PEA require 1 mg doses. The maximum total of tropine (3 mg) is the same for both bradycardia and asystolic rhythms (Nursing2006 Drug Handbook, 2006). If atropine and pacing fail and the patient remains hypotensive, an epinephrine infusion can be considered. The dosing for an epinephrine infusion is 2–10 mcg/min titrated to the patient’s response.
Another medication to consider for symptomatic hypotension and bradycardia is dopamine. It is a catecholamine agent with dose-related dopaminergic and beta and alpha adrenergic agonist activity. The usual dose is 2–20 mcg/kg/min. The effect is rate dependent, and the rate should be titrated as needed:
The dopamine infusion can be administered alone or along with epinephrine (Nursing2006 Drug Handbook, 2006).
Isuprel is a medication that is no longer advocated in the treatment of bradycardia and is currently not advocated for arrest scenarios (AHA, 2005d).
Tachycardia (fast heart rate) is generally considered to be a resting heart rate over 100 beats per minute in an adult. Fast rates may be benign or they can be very dangerous. This will depend on the patient’s age, underlying heart condition, and duration of the arrhythmia. The faster the rate, the less likely it is that it will be tolerated for any length of time.
As with all of the algorithms, start with the basics of airway, breathing, and circulation and correct any problems. Obtain an initial ECG reading as soon as possible. Remember that if the rate is less than 150, the patient’s symptoms are probably not related to the rate, so look for other causes. Treatment decisions are made on the basis of three factors: whether the rhythm is stable or unstable, whether the QRS is narrow or wide, and whether the rhythm is regular or irregular.
Tachycardias are evaluated on the basis of the stability of the patient, the width of the QRS complex, and the regularity of the rhythm. The stability of the patient is determined during the primary and secondary survey. If the patient has signs of poor perfusion, such as chest pain, hypotension, shortness of breath, or altered mental status, consider immediate synchronized cardioversion. If IV access is in place, sedation may be considered if it can be done without significant delay. The first energy dose is 100J to 200 J for monophasic machines or 100J to 120J for biphasic machines. Subsequent shocks, if needed, should be 200 J, 300 J, then 360 J for monophasic machines. There is no clear consensus about energy levels for biphasic machines. If the rhythm is PSVT or atrial flutter, it may respond to a lower dosage, so 50 J may be attempted first (AHA, 2005d).
If the patient is stable and tolerating the tachycardia well, there is more time for decision making. Establish an IV if one is not already in place. Obtain a 12-lead ECG for a better look at the arrhythmia. Determine the width of the QRS complexes. This will determine the next steps of treatment. If the QRS complex is less than 0.12 seconds, it is considered narrow; if it is greater than or equal to 0.12 seconds, it is considered wide (AHA, 2005d).
If the QRS complex is narrow in any lead, determine next whether the rhythm is regular or irregular. With a narrow, regular rhythm, vagal maneuvers can be considered, either as a treatment or as a diagnostic tool. They are generally simple to perform and are successful in about 20% of cases. However, they should not be performed if the patient has severe coronary artery disease, has had a recent heart attack, or has a reduction in blood volume. A patient with any of these conditions could experience detachment of blood clots resulting in CVA, vertigo, cardiac arrhythmias, or even arrest.
Valsalva’s maneuver has fewer complications than other methods, but it depends on the patient’s cooperation and ability to perform the maneuver. Some methods to try may include having the patient bear down (as if having a bowel movement), forcibly exhale while keeping their mouth and nose closed, blow into a large syringe against the plunger, or blow into an occluded straw. Carotid sinus massage must be done with great care as carotid plaques can be dislodged causing a CVA. If vagal maneuvers fail to convert the rhythm, the medication of choice is adenosine (AHA, 2005d).
Adenosine (Adenocard) depresses the pacemaker activity of the SA node, reducing the heart rate and the ability of the AV node to conduct impulses from the atria to the ventricles (Nursing2006 Drug Handbook, 2006). It is also especially effective on reentry tachycardias that involve the AV node. It has been shown to be effective in over 90% of paroxysmal supraventricular tachycardias (PSVT).
Supraventricular tachycardia (or re-entrant tachycardia).
When giving adenosine, location and speed are key considerations. The half-life of this medication is only about 5 seconds, so it needs to get from the IV injection site into central circulation very quickly. The IV site should be as proximal as possible, preferably in the ante cubital (AC) with the largest catheter possible. Give 6 mg IV by rapid bolus injection followed immediately by 20 ml of normal saline flush by rapid bolus injection. If the arrhythmia has not converted after about a minute, a second dose of 12 mg is delivered in the same manner as the first. This dose may be repeated once more, if necessary. Remember that you are chemically cardioverting the patient’s heart, so conversion may be followed by a short period of asystole, chest pain, hypotension, arrhythmias, and nausea. These side effects are usually self-correcting and short-lived.
There are a few other medications to be aware of when giving adenosine. Dipyridamole (Persantine) may potentiate the effects of adenosine. Because of this, a smaller dose may be needed. Patients on theophylline may not respond well to adenosine; therefore, a higher dose may be needed. Use adenosine with caution in patients taking carbamazepine (Tegretol). Higher degrees of heart block may occur with concurrent use of this medication or with methylxanthines because they antagonize the effects of adenosine. Caffeine also may antagonize the effects of adenosine, so a higher dose may be needed, and it is possible that the patient may not respond at all.
If the tachycardia does not convert with adenosine, or if the rhythm is irregular, consider diltiazem hydrochloride (Cardizem). This medication is a calcium channel blocker, which prevents the passage of calcium ions across the myocardial cell membrane and vascular smooth cells and thus slows the heart rate (Nursing2006 Drug Handbook, 2006). It causes dilation of the coronary and peripheral arteries, which decreases afterload and reduces the workload of the heart. It should be avoided in patients with a known history of Wolff-Parkinson-White syndrome, sick sinus syndrome, and high-degree AV blocks unless the patient has a pacemaker in place. It should also be avoided in patients receiving oral or IV beta blockers, as severe hypotension can occur.
The most common form of regular wide complex tachycardias is monomorphic ventricular tachycardia. Ventricular filling time is short, and cardiac output can drop quickly. Usually, adult patients will quickly become unstable in this arrhythmia. If the patient is stable, consider a trial of antiarrhythmics. Monitor the patient closely and, if at any time they become unstable, proceed with cardioversion (AHA, 2005d).
Monomorphic ventricular tachycardia.
For stable V-tach give 150 mg of amiodarone over 10 minutes (Nursing2006 Drug Handbook, 2006). This may be facilitated by diluting the drug with 20 to 30 ml of D5W. Repeat the dose as needed until the rhythm converts, the patient becomes unstable, or a maximum dose of 2.2 g in a 24-hour period is given.
If amiodarone is not available, consider lidocaine (AHA, 2005d). The initial dose is 1 to 1.5 mg/kg. Repeat 0.5 to 0.75 mg/kg every 5 to 10 minutes to a maximum total dose of 3 mg/kg. A maintenance infusion of 1 to 4 mg/min should be started if the arrhythmia converts.
Although procainamide is not recommended for V-fib/pulseless V-tach, it can be considered for stable V-tach (AHA, 2005d). It can also be used for stable, irregular wide complex tachycardias. Procainamide reduces automaticity in all pacemakers and slows intraventricular conduction. It also has vasodilatory effects, especially with rapid administration and high doses. Give procainamide at a rate of 20 mg/min IV until the arrhythmia is suppressed, hypotension occurs, the QRS widens by > 50% from baseline, or the maximum dose of 17 mg/kg is given. If the arrhythmia is suppressed by procainamide, start a maintenance infusion at 1 to 4 mg/minute.
The three most common irregular wide complex tachycardias are a polymorphic V-tach (such as torsades de pointes), aberrantly conducted A-fib, or pre-excited A-fib (such as A-fib with WPW syndrome) (AHA, 2005d). A polymorphic V-tach is one in which different foci of the heart are initiating the impulse. It tends to have a poorer prognosis than monomorphic V-tach and usually deteriorates quite quickly into a pulseless arrhythmia. It is often associated with a prolonged QT interval prior to collapse. If this has been documented, stop any medications that may prolong the QT interval, and then correct problems such as electrolyte imbalance or drug overdose.
Polymorphic V-tach.
If medications are needed, consider a ventricular antiarrhythmic. If the patient is in torsades de pointes, has documented hypomagnesemia, or has documented long QT interval, magnesium may be considered (AHA, 2005, Part VII). Give a dose of 1 to 2 g diluted in D5W over 5 to 60 minutes. Slower rates are preferred in the stable patient. If it is a polymorphic V-tach other than torsades, it is treated as a regular wide complex tachycardia with amiodarone. If amiodarone is not available, consider lidocaine as an alternative.Patients in polymorphic V-tach become unstable quickly, so be prepared for defibrillation. This rhythm is usually too irregular to cardiovert, as most monitors cannot synchronize to it. Treat as a pulseless rhythm and be prepared to start compressions after defibrillation.
If the rhythm is a new onset atrial fibrillation (A-fib), treat as an irregular narrow-complex tachycardia, with the initial focus on rate control. Conversion of the rhythm can be done later under more controlled circumstances, unless the patient is unstable. If the patient has a documented pre-excitation syndrome such as WPW, do not use medications which block the AV node, calcium channel blockers, or beta blockers. These drugs can actually increase the rate.
Atrial fibrillation (A-fib).
Most cases of sudden cardiac death are immediately preceded by acute myocardial infarction (AMI), or heart attack; therefore, early recognition and prompt aggressive care of this condition is very important.
The overall goal that directs all therapies and protocols is for the patient to get the treatment they need in the shortest time possible. The interval between onset of symptoms and delivery of definitive care has many stages where delay may occur. The first and longest delay is from the time of onset of symptoms to the decision by or for the patient to seek care. It’s very important to call 911 early, and public education in this matter should be aggressive and ongoing. Emergency dispatchers should be trained to ask a series of questions while dispatching an ambulance. If they determine that the patient is having signs or symptoms of an AMI, they should advise the patient to immediately chew an aspirin (160 to 325 mg), as long as the patient does not have an aspirin allergy or recent gastrointestinal bleeding.
Pre-hospital emergency medical service (EMS) personnel need to rapidly recognize an ACS and deliver the patient to an appropriate facility in a timely manner. EMS should also have protocols in place to initiate care and notify the receiving facility to prepare for a cardiac patient. Pre-hospital 12-lead ECG can significantly shorten the time to definitive care and are becoming the gold standard in most areas.
Finally, the hospital emergency department should be ready to rapidly evaluate the patient and facilitate definitive care.
The first healthcare provider to encounter any patient with signs and symptoms of ACS should begin with general assessment and treatment as previously outlined in the 5 quadrads. Further assessment covering cardiac history, signs and symptoms, risk factors for cardiac disease, and screening for the administration of fibrinolytics should be completed in less than 10 minutes. A 12-lead ECG should be obtained as quickly as possible.
Specific care for ACS includes the mnemonic MONA, which stands for morphine, oxygen, nitroglycerin, and aspirin. Oxygen delivery should begin first and should be titrated to the patient’s SaO2 levels. Even in the absence of hypoxemia, oxygen is still appropriate for the early treatment of ACS. Non-enteric coated aspirin, 160 mg to 325 mg, should be chewed as soon as possible. This may be deferred in the presence of recent GI bleed or true aspirin allergy. Nitroglycerin should be administered by sublingual tablet or spray as long as the patient has a systolic BP over 100 mmHg and a pulse between 50 and 100. A dose of 0.4 mg is given every 3–5 minutes while the symptoms persist and the vital signs remain stable. Once 3 doses of nitroglycerin have been given, morphine may be given for persistent symptoms (AHA, 2005e).
Once the patent has been assessed, they will be stratified into 1 of 3 categories—STEMI, NSTEMI, and indeterminate—and this will determine subsequent treatment.
If the patient has a left-bundle branch block that is new or presumed to be new, or if the patient has ST-segment elevation >1 mm (0.1 mV) in 2 or more contiguous precordial leads or 2 or more adjacent limb leads, they are classified as having an ST-segment elevation MI, or STEMI. Most patients in this category have blockage of a coronary artery.
ST-segment elevation myocardial infarction (STEMI).
The goal of treatment is early reperfusion to eliminate or minimize necrosis of the heart muscle. This can be done with fibrinolytics or by performing percutaneous coronary intervention (PCI ). In many instances, PCI is superior to fibrinolytic administration because the restoration of vessel patency occurs more often and there’s a lower rate of reocclusion. Fibrinolytics can have the advantage of being available in smaller hospitals, and they are very effective when administered within 3 hours of symptom onset. Hospitals should have protocols in place that take into account their capabilities and available resources (AHA, 2005e).
Patients demonstrating ischemic ST-segment depression of at least 0.5 mm (0.05 mV) or dynamic T-wave inversion with chest pain or discomfort are classified as non–ST-segment elevation MI (NSTEMI). High-risk patients with unstable angina are also included in this category, as are patients who have ST elevation more than 0.5 mm but lasting less than 20 minutes.
Generally, patients with ST-segment depression do not have a complete coronary artery blockage and may not even be having an ACS. However, patients with chest pain and positive or elevated serum cardiac markers, diffuse or widespread ECG abnormalities, or heart failure have an increased risk of major acute cardiac event, or MACE. Patients displaying ST-segment depression may be having a posterior MI; this should be confirmed with diagnostic tests. Treatment options for these patients can include beta-adrenergic blockers, clopidogrel, heparin therapy, and/or glycoprotein IIb/IIIa inhibitors as well as early PCI. These patients should not receive fibrinolytics (AHA, 2005e).
If the patient has normal or nonspecific ECG changes, they are considered indeterminate pending further evaluation. Patients with a normal or nondiagnostic ECG will seldom be having an ACS. Evaluation will include cardiac markers and possibly a stress test. Therapies should be considered on the basis of risk verses benefit (AHA, 2005e).
This information covers the early, basic care of most cardiac patients encountered. Many factors can complicate care, such as drug overdose, hypothermia, trauma, or pregnancy, and are beyond the scope of this course. Providers who can expect to encounter such conditions regularly will need additional education appropriate to their situation. Remember that the guidelines for cardiac care are just that, guidelines. Local protocol should be the ultimate authority for any care given.
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