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This course will expire or be updated on or before April 30, 2015.
ABOUT THIS COURSE
You must score 70% or better on the test and complete the course evaluation to earn a certificate of completion for this CE activity.
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Wild Iris Medical Education is an approved provider for paramedic and EMT continuing education in California by the Coastal Valleys EMS Agency: CE Provider #49-0057.
This course is appropriate for EMTs, paramedics, and first responders.
Wild Iris Medical Education, Inc. provides educational activities that are free from bias. The information provided in this course is to be used for educational purposes only. It is not intended as a substitute for professional health care. See our disclosures for more information.
Copyright © 2012 Wild Iris Medical Education, Inc. All Rights Reserved.
COURSE OBJECTIVE: The purpose of this course is to inform healthcare professionals about current guidelines for emergency cardiac care.
Upon completion of this course, you will be able to:
The 2010 revision of the American Heart Association (AHA) Emergency Cardiovascular Care (ECC) guidelines included many updates. Most significant was the change from A-B-C (airway, breathing, chest compressions) to C-A-B (AHA, 2010). The 2005 guidelines deemphasized ventilation, oxygenation, and defibrillation in favor of well-performed chest compressions, and this was further expanded in 2010. Additionally there are changes in the depth and number of compressions and in medication protocols, such as atropine no longer being recommended for pulseless electrical activity or asystole.
Good Advanced Cardiovascular Life Support (ACLS) starts with good Basic Life Support (BLS) 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 the patient is unresponsive and not breathing or does not have normal breathing (only gasping) and you are a lone healthcare provider, 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 2 minutes of CPR before calling for help (AHA, 2011). 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.
After assessing the patient and activating the emergency response system, check for a carotid pulse by using two fingers to find the trachea and sliding your fingers into the groove on either side. Feel for a pulse for 5 to 10 seconds (AHA, 2011).
If a pulse is found but breathing is absent, rescue breathing should commence. The rescue breaths should be delivered at a rate of one breath every 5 to 6 seconds or 10 to 12 per minute (AHA, 2011). 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. The compressions need to be hard, fast, and deep while also allowing for full recoil of the chest between compressions. Interruptions need to be kept to an absolute minimum.
Good hand position is necessary for effective compressions. For an adult patient, place the heel of one hand on the center of the patient’s chest on the lower sternum and the other hand on top with the fingers linked. Position your body directly over the patient’s chest and keep your arms straight and elbows locked using your body weight to compress (Pozner, 2011b).
Compressions should be delivered at a rate of at least 100 per minute. Higher numbers of chest compressions with fewer interruptions yield better chances for a return of spontaneous circulation (ROSC) and survival with good neurologic function (AHA, 2010).
The depth of compressions has been changed in the 2010 guidelines to at least 2 inches for the adult patient (from 1-1/2 to 2 in the 2005 guidelines) (AHA, 2010).
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.
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 as soon as 1 minute (Pozner, 2011b). 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, 2011).
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, 2010).
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 the initial 30 compressions are delivered, the airway is opened and the provider delivers 2 breaths. (If two providers are involved in the resuscitation, one maintains chest compressions while the second prepares the airway to give breaths immediately following the thirtieth compression.) Each breath should be delivered over 1 second with any delivery method available, such as mouth-to-mouth, mouth-to-mask, or bag-mask device (with or without oxygen). A good breath will cause the chest to rise. If chest rise is not seen, readjust the airway and attempt ventilation again.
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 1 second, and CPR should be resumed quickly (AHA, 2011).
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 1 breath every 6 to 8 seconds (about 8 to 10 breaths per minute) (AHA, 2010). 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 (Pozner, 2011b).
The recommended compression-to-ventilation ratio for adult patients is 30:2, with a brief pause to deliver the breaths. Five cycles of the 30:2 compressions/ventilations should be delivered, which should take approximately 2 minutes. Only then is the pulse check repeated. All BLS and ACLS interventions are completed around the 2 minutes of CPR, which helps keep pauses in compressions to an absolute minimum (AHA, 2011).
Benefits have been shown with compression-only CPR. 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).
Studies into the physiology of cardiac arrest due to ventricular fibrillation have divided the event into three phases.
The first 4 to 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. High-quality CPR administration while a defibrillator is being obtained improves survival, but if cardiac arrest is left untreated in the first phase, it moves into the hemodynamic, or circulatory, phase (Pozner, 2011b).
In the hemodynamic phase (from 4 to 10 minutes after sudden cardiac arrest), the heart has been without perfusion. Studies are inconclusive as to whether a full 2 to 3 minutes of CPR prior to defibrillation is beneficial in this phase. “Providers should consider both patient downtime and their own response time when deciding whether to postpone defibrillation to provide CPR” (Pozner, 2011b).
The third phase, defined as greater than 10 minutes of pulselessness, is called the metabolic phase. The treatment is based on post-resuscitative measures, including hypothermia. If the patient does not obtain a perfusing rhythm during this phase, the patient generally does not survive (Pozner, 2011b).
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. The AED should be applied without interrupting compressions until it is ready to analyze. Attach the electrode pads by peeling away the backing and placing one pad on the upper-right side of the patient’s bare chest (to the right of the sternum directly below the clavicle) and the other to the left of the left nipple a few inches below the left armpit. The AED will analyze the rhythm and determine if a shock is appropriate. If needed, a shock will be delivered and chest compressions should immediately follow.
The recommendation for defibrillation is one shock at a time for patients in a shockable rhythm (Pozner, 2011b). Continue compressions until you are ready to deliver a shock, with 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 (Pozner, 2011b).
Biphasic defibrillators are preferred due to the lower energy doses needed for defibrillation. Pozner (2011b) recommends all defibrillations be delivered at the highest available energy dose in adults (360 J for a monophasic defibrillator and 200 J for a biphasic defibrillator). This has the potential to decrease interruptions in CPR and is supported by a study of out-of-hospital cardiac arrest patients treated with either low or high doses.
As Susie, a med-surg nurse, was walking back into the hospital after her lunch break she saw her 60-year-old patient, Sam, smoking in the parking lot. As she got closer to him she saw him collapse on the sidewalk. Susie ran up to Sam and shook him and shouted, “Are you okay?” Sam did not reply. Susie looked for signs of breathing but did not see any. She quickly scanned the area and saw a bystander and yelled for her to go into the hospital and get help.
Susie checked Sam’s carotid pulse but did not find one within 10 seconds. She immediately started compressions hard and fast at the rate of at least 100 per minute. After 30 compressions she used the head-tilt-chin-lift maneuver and gave 2 breaths, watching for Sam’s chest to rise each time. She then resumed giving compressions and ventilations at a rate of 30:2 until help arrived.
The bystander returned from inside the hospital with a hospital AED that was located in the lobby. The bystander said that the code had been called. In the meantime, the bystander opened up the AED, turned it on, followed the instructions, and applied the patches. While she was doing this, Susie continued giving compressions and ventilations. The AED announced it was analyzing, and Susie and the bystander stood clear and a shock was delivered. Susie quickly resumed compressions and could see the ED staff running to them.
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 (Berg, 2010). For obese patients or patients in the last stages of pregnancy, use chest thrusts instead of abdominal thrusts (AHA, 2011).
If the patient becomes unresponsive and you are by yourself, activate an emergency response before proceeding any further. 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 (Berg, 2010).
Assessment of a patient with cardiovascular compromise must be systematic and organized. The information gathered will be vital to making good treatment decisions.
Patients may have implanted defibrillators or pacemakers. These can usually be identified by a hard lump beneath the skin of the upper chest or abdomen about the size of a silver dollar to half the size of a deck of cards, with an overlying scar. This is not a contraindication to using an AED, but avoid placing the electrode pads over the devices, since they may interfere with one another.
Additionally, be mindful of medication patches. The patch may interfere with the transfer of energy to the heart or may cause burns to the skin. If you identify a patch, remove it and wipe the area clean before attaching the electrode.
Be sure to look for medical cards, bracelets, or necklaces that may give important information vital for proper care. For example, an ICD (implantable cardioverter defibrillator) card may have important information about the device and a link to the physician’s phone number.
The BLS survey has already been completed if CPR is being performed. This is the C-A-B plus defibrillation described above in “Basic Life Support.”
The ACLS survey expands on the BLS.
The pulseless arrest algorithms reflect the BLS guidelines and their emphasis on continuous CPR. Interventions are carefully timed to minimize interruptions.
Ventricular fibrillation (VF) is a 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.
VF may be categorized as coarse or fine. Coarse VF occurs early in the arrest and is characterized by more electrical activity than fine VF. If the patient remains in VF, the electrical activity will gradually decrease because of hypoxia and acidosis. Without intervention, it will progress to flat line or asystole (see rhythm strip under “Unshockable Rhythms” below) (AHA, 2011).
Coarse ventricular fibrillation (VF).
Ventricular tachycardia (VT) 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 VT 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 VTs.
VT 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 VF.
The treatment of choice for VF/pulseless VT is defibrillation followed by excellent CPR, assuming the patient is still in the electrical phase of the arrest. Defibrillate at 360 J with a monophasic defibrillator, manufacturer’s recommended energy dose (or 200 J as recommended by Pozner), followed by equivalent or higher subsequent doses, for a biphasic defibrillator (2011a). Start CPR 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 intraosseous (IO) access should be established. 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 VF or pulseless VT, defibrillate at 360 J with a monophasic defibrillator, manufacturer’s recommendation equivalent or higher than previous dose for biphasic. After the shock, resume CPR immediately without an additional pulse or rhythm check. Continue CPR for 2 minutes and give a vasopressor. Epinephrine should be given during compressions (40 units vasopressin may be substituted for the first or second dose of epinephrine). Epinephrine may be given every 3–5 minutes.
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 (Neumar, 2010). Consider quantitative waveform capnography for intubated patients, and if PETCO2 is less than 10mm Hg, attempt to improve CPR quality. 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 VF or pulseless VT, then defibrillate at 360J with a monophasic defibrillator, manufacturer’s recommendation at or above previous dose for biphasic (AHA, 2011). Resume CPR for 2 minutes, then administer an antiarrhythmic. Give a 300 mg bolus of amiodarone during CPR and look for and treat reversible causes (the Hs and Ts, or hypovolemia, hypoxia, hydrogen ion [acidosis], hypo-/hyperkalemia, hypothermia, tension pneumothorax, cardiac tamponade, toxins, pulmonary or coronary thrombosis).
The cycle is repeated by alternating shocks followed by vasopressors and antiarrhythmics as long as the patient remains in VF or pulseless VT. All subsequent shocks should be delivered at the highest energy level. If adequate airway and ventilations are achieved by bag-mask, advanced airways may be deferred until the patient is more stable. CPR with a supraglottic advanced airway or endotracheal intubation should include 8–10 breaths per minute with continuous chest compressions (AHA, 2011).
As nurse Susie was delivering compressions to Sam in the hospital parking lot, the emergency department team arrived on the scene. One ED nurse took over compressions while another started giving breaths with the bag-mask in the same ratio Susie had been using (30:2). While that was being done, the patient was moved onto a gurney and transported into the emergency department.
As he arrived, another nurse cut open Sam’s gown and set up the cardiac monitor. It showed ventricular fibrillation. The whole code team was now assembled and prepared to defibrillate. The patient was shocked and CPR was immediately continued. While compressions were being delivered, IV access was obtained. After 2 minutes of CPR, a rhythm of VF was obtained. The patient was shocked and CPR was restarted.
One mg of epinephrine was given intravenously, and an advanced airway was considered. It was determined to be too risky to take a break to intubate. After another 2 minutes of CPR, a sinus rhythm was obtained, the carotid pulse was checked, and a pulse was found. There had been a return of spontaneous circulation, and the team began Sam’s post-resuscitation care.
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 VF can be mistaken for asystole. For treatment, see “pulseless electrical activity” below.
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 asystole or PEA is present and the determination has been made to resuscitate, start CPR. Establish an IV or IO line as soon as possible. One mg epinephrine (or 40 units vasopressin for the first or second dose of epinephrine) 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 2 minutes of CPR, perform a pulse and rhythm check. If asystole or a bradycardic PEA is still present, continue CPR immediately. Continue to give epinephrine every 3–5 minutes.
Repeat the cycle of vasopressors and CPR 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 bag-mask.
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, 2011).
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 or while attempting to establish IV or IO access. The IV or IO route is greatly preferred because it will provide a more predictable drug delivery and pharmacological effect. ET doses should be 2–2.5 times the standard IV dose for ET delivery and diluted in 5–10 mL of sterile water or normal saline (Neumar, 2010).
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 a 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, 2011).
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, 2011).
Epinephrine is the most familiar and commonly given medication during an emergency cardiac event. It is thought to have a stimulatory effect on adrenergic receptors causing vasoconstriction and increased myocardial and cerebral blood flow during CPR. 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 (AHA, 2011).
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 (Pozner, 2011a). Vasopressin increases arterial blood pressure through nonadrenergic peripheral vasoconstriction.
Amiodarone is the preferred antiarrhythmic for VF/pulseless VT. 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 VF/pulseless VT 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 in 3–5 minutes (AHA, 2011).
Lidocaine is considered an alternative for VF/pulseless VT if amiodarone is not available (Pozner, 2011a). Lidocaine decreases the automaticity of the myocardium, which helps to reduce fibrillation, especially in ischemic tissue. In a pulseless patient, give 1 to 1.5 mg/kg IV/IO initially. If the arrhythmia persists, doses of 0.5–0.75 mg/kg IV/IO push can be administered at 5–10 minute intervals to a maximum dose of 3 mg/kg.
Another antiarrhythmic that can be considered with the VF/pulseless VT 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 5–20 minutes (AHA, 2011).
Atropine use during PEA/asystole is unlikely to have a therapeutic effect and is no longer recommended for routine use in PEA/asystole (AHA, 2010).
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, 2011). This requires maintenance of excellent bag-mask skills. Advanced airway management “must never be made at the expense of performing excellent CPR and early defibrillation” (Pozner, 2011a).
Advanced airways include endotracheal tube (ETT), laryngeal mask airway (LMA), or a laryngeal tube. 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. Chest compressions can continue while some advanced airway devices such as a laryngeal mask airway, laryngeal tube or esophageal-tracheal tube is placed.
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. Once placed, an ET tube must be confirmed by waveform capnography, secured, and monitored continuously (AHA, 2011).
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 may lead to cardiac arrest. The bradycardia algorithm covers symptomatic bradycardia as well as atrioventricular (AV) blocks.
Remember the first rule of cardiac care (and all assessment): 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.
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.
For symptomatic bradycardia, give a 0.5 mg bolus of atropine, which may be repeated every 3–5 minutes to a maximum of 3 mg. If atropine is ineffective, prepare for transcutaneous pacing or a dopamine or epinephrine infusion (AHA, 2011).
Pacing should be considered along with dopamine or epinephrine infusions for symptomatic bradycardia if atropine is ineffective (AHA, 2010). To set up for pacing, 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.
If transcutaneous pacing fails, transvenous pacing may need to be initiated.
Paced rhythm, with the spikes indicated by arrows. (Source: Adapted from Glenlarson.)
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.
Atropine is one of the first medications to consider for sinus bradycardia as well as first-degree or second-degree type I AV blocks. Atropine is rarely effective on high-degree blocks such as second-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 (AHA, 2011).
If atropine fails and the patient remains hypotensive, transcutaneous pacing or a dopamine or epinephrine infusion can be considered. The dosing for an epinephrine infusion is 2–10 mcg/min titrated to the patient’s response, and dosing for dopamine is 2–10 mcg/kg/min.
Both dopamine and epinephrine have vasoconstricting as well as chronotropic effects. Dopamine is a catecholamine agent with dose-related dopaminergic and beta- and alpha-adrenergic agonist activity. The effect is rate dependent. At lower doses (2–10 mcg/kg/min) it has a greater effect on inotropy and heart rate; at higher doses (>10 mcg/kg per minute) it also has vasoconstrictive effects, and the rate should be titrated as needed.
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 circulation, airway, and breathing 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 BLS and ACLS 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. For synchronized cardioversion, the energy doses are as follows:
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, 2010).
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 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 and the rhythm is regular, the medication of choice is adenosine (AHA, 2010).
Supraventricular tachycardia (or re-entrant tachycardia).
In tachycardia, adenosine may be considered if the complex is regular and narrow. Adenosine increases AV block. 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 antecubital (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 (AHA, 2011).
The dose of adenosine might need to be adjusted for patients taking certain medications. Larger doses may be required for patients taking theophylline or theobromine or who consume large amounts of caffeine. Patients taking dipyridamole or carbamazepine or those with implanted hearts may require smaller doses. When injecting adenosine through a central vein, the dose may also need to be reduced.
If the patient is stable and the rhythm is narrow, and vagal maneuvers and adenosine haven’t worked, or the rhythm isn’t regular, consider a beta-blocker or calcium channel blocker (AHA, 2011).
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, treat with antiarrhythmics. Adenosine may be used for regular wide-complex tachycardia with a monomorphic QRS complex (see dosing above). Monitor the patient closely and, if at any time they become unstable, proceed with cardioversion (AHA, 2010).
Monomorphic ventricular tachycardia.
Antiarrhythmic infusions, such as procainamide, amiodarone, and sotalol, may be considered for stable wide QRS VT.
Procainamide, though not considered for VF/pulseless VT, can be considered for stable wide-complex VT (AHA, 2010). It 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 20–50 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 1–4 mg/minute. Avoid the use of procainamide if the QT is prolonged or the patient has CHF (AHA, 2011).
For stable wide QRS VT, give 150 mg of amiodarone over 10 minutes. Repeat the dose as needed until the rhythm converts or the patient becomes unstable. Follow by maintenance infusion of 1 mg/min for the first 6 hours (AHA, 2011). The maximum dose is 2.2 g in a 24-hour period.
Sotalol may be considered as an alternate antiarrhythmic for VT with a wide QRS. The first dose is 100 mg (1.5 mg/kg) IV over 10 minutes, and repeat as needed if VT recurs. Avoid if the QT interval is prolonged.
The three most common irregular wide complex tachycardias are a polymorphic VT (such as torsades de pointes), aberrantly conducted atrial fibrillation, or pre-excited atrial fibrillation (such as atrial fibrillation with Wolf Parkinson White syndrome) (Pozner, 2011a). A polymorphic VT is one in which different foci of the heart are initiating the impulse. It tends to have a poorer prognosis than monomorphic VT 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.
If the patient is in torsades de pointes, has documented hypomagnesemia, or has documented long QT interval, magnesium may be considered. Give a dose of 2 g IV followed by a maintenance infusion. Slower rates are preferred in the stable patient (Pozner, 2011a). If it is a polymorphic VT other than torsades, it is treated as a regular wide-complex tachycardia with amiodarone. Patients in polymorphic VT 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, 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 that block the AV node, calcium channel blockers, or beta blockers. These drugs can actually increase the rate.
Atrial fibrillation. (Source: J. Heuser.)
If a cardiac arrest patient has a return of spontaneous circulation (ROSC), there are important objectives for his/her post-resuscitation care:
The decision to stop resuscitation efforts may be difficult. Pozner (2011a) recommends considering the following based on physician survey data and clinical practice guidelines:
Joe is a patient of nurse Susie’s on the med-surg floor. While she was down the hall in the hospital pharmacy, the telemetry tech called Susie to let her know that Joe’s cardiac monitor was reading tachycardic at 167 bpm. Susie rushed to Joe’s room, where he was sitting up in bed talking with his family. Susie took Joe’s vital signs and found him to be otherwise stable.
While she was glad to see he was not symptomatic, Susie still called the rapid response team (the house nursing supervisor, a designated ICU nurse, and a respiratory therapist) for help and requested the code cart be brought to the bedside, knowing Joe could deteriorate. When the team arrived, Susie explained to Joe the rationale for what she had done as she placed him on the bedside cardiac monitor and attached a BP cuff and pulse oximeter. The team confirmed a continuing tachycardia, with a wide and regular QRS complex. Nurse Susie told Joe to prepare for a strange sensation, and the ICU nurse gave him 6 mg adenosine intravenously by rapid IV push, followed with a NS flush.
After the adenosine was administered, Joe was still tachycardic. His level of consciousness (LOC) became altered, and he began to grasp at his chest, becoming hypotensive and hypoxemic with a weak pulse. Since Joe’s condition was now unstable, the code team was called. The team physician sedated him quickly and then proceeded with cardioversion. With synchronized cardioversion, Joe returned to a sinus rhythm.
Everyone breathed a sigh of relief.
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 is 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 is 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 above in the BLS and ACLS surveys. 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 only be used for patients who are dyspneic, hypoxemic, or have obvious signs of heart failure, titrated to keep the patient’s SaO2 levels at or above 94%. 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 three doses of nitroglycerin have been given, morphine may be given for persistent symptoms (AHA, 2010).
Once the patent has been assessed, they will be stratified into one of three categories—ST elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (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 two or more contiguous precordial leads or two 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. The PCI door-to-balloon time is 90 minutes if the facility is equipped. If not equipped, the door-to-departure goal is 30 minutes. Fibrinolytics can have the advantage of being available in smaller hospitals. The door-to-needle goal time for fibrinolytics is 30 minutes. Hospitals should have protocols in place that take into account their capabilities and available resources (AHA, 2011).
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 (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, 2011).
If the patient has normal or nonspecific ECG changes, he or she is 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 versus benefit (AHA, 2011).
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.
American Heart Association (AHA). (2011). Advanced cardiovascular life support: provider manual. Dallas, TX: American Heart Association.
American Heart Association (AHA). (2010). Highlights of the 2010 American Heart Association guidelines for CPR and ECC. Dallas, TX: American Heart Association.
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