Implications for practice and what we need to knowAs cath lab professionals, our practice is constantly becoming more complex and diverse. We are also engulfed in technology in the pursuit of improving quality of life for our patients. Why? The answer is sudden cardiac arrests (SCA), also referred as sudden cardiac death. About 325,000 SCA occur annually in the United States, of which 163,221 SCA take place out-of-hospitals.1 There are numerous contributors to SCA:2,8,10 • An unusually rapid heart rate of unknown cause that comes and goes, even when at rest. The result is a malfunction in the heart’s electrical system that leads to ventricular tachycardia and ventricular fibrillation, the immediate cause of SCA. • Preexisting heart condition: 75% of SCA had a previous heart attack. • Coronary heart disease (CHD) or coronary artery disease (CAD): Risk factors include high blood pressure, diabetes, high cholesterol, inactivity, overweight, smoking and poor diet. Roughly 330,000 CHD deaths take place out-of-hospital annually. CHD is also the leading cause of death in women. • Bradyarrhythmias account for approximately 20-30% of all SCA. • Valvular heart disease: The most common cause of SCA is aortic stenosis. • Syncope: A temporary loss of consciousness, described by patients as “fainting” or “passing out.” • Cardiomyopathy: hypertrophic or dilated; in both cases, the heart’s muscle is abnormal. This is also a condition that affects the heart’s electrical system conductivity. • Low ejection fraction (EF): EF is the percentage of blood pumped out of a heart chamber during the contraction phase of each heartbeat (systole). Normally, the left ventricle pumps 55 to 75% of the blood within that chamber out to the body with each heartbeat. Patients at risk of SCA are hard to identify. That’s why cath lab professionals are at the forefront and uphold the most critical role: patient education. As we apply the nursing process, we obtain a thorough family-medical history from our patients. Remember to peek outside the box (heart). Look at the whole package. Encourage patients to seek regular follow ups with their physicians for EKG, management of blood pressure, blood sugar, lipids and weight control. Background The first external pacemaker was designed and built by the Canadian electrical engineer John Hopps in 1950. A substantial external device, it was somewhat crude and painful to the patient in use. The pacemakers built in the late 1950s were bulky, relied on external electrodes, and external electric shocks were frequently too traumatic for young heart block patients. The early devices were all asynchronous; the first atrioventricular (AV) synchronous pacemaker, which simulated a true physiologic state, was first implanted into a human in 1958 by a Swedish team using a pacemaker designed by Rune Elmqvist and Åke Senning.1,7 The device failed after three hours. A second device was then implanted which lasted for two days. The world’s first implantable pacemaker patient, Arne Larsson, survived the first tests and died in 2001 after having received 22 different pacemakers during his lifetime. These devices have steadily improved since the primitive models of the early 1950s, shrinking in size as they grew in reliability, complexity and popularity. As device technology and therapy applications have grown, cath lab professionals’ responsibilities have evolved as well, evolving outside of the operating room (OR) and critical care arena, since initially the implantable converter defibrillator (ICD), also known as an automated implantable cardioverter defibrillator (AICD), was implanted via thoracotomy with the device inserted in a subcutaneous abdominal pocket and defibrillator patches applied to the pericardium. Nowadays more than 80% of devices are implanted in cath lab suites versus OR and followed by cardiac telemetry unit care versus critical care unit. Since the first implant of an AICD in the U.S. in February 1980 at Johns Hopkins Hospital, the device has become increasingly popular as a life-saving device for the treatment of lethal arrhythmias such as ventricular tachycardia (VT), specifically, ventricular fibrillation (VF), the most common cause of cardiac arrest.4,7,10 It is estimated that more than 70% of VF victims die before reaching the hospital. In the U.S. alone, approximately 456,076 people died in 1998 from SCA. Today, each year about 310,000 deaths are from unexpected SCA, among adults prior to reaching an emergency room.1,8,10 EMS treats about 107,000 to 240,000 of cardiac arrests in the U.S. annually. Of these cardiac arrests treated by EMS, 21,000 to 91,000 cases (20-38%) are found in VF or VT.9 The number of cardiac device implants in the U.S. has steadily increased, with substantial reductions in patient length of stay, as shown in data collected from 1997 to 2004. This study showed steady increases in the number of AICDs and pacemakers (PMs) implanted between 1997 and 2004. Approximately 153,000 PMs and 29,000 AICDs were implanted in 1997, and 178,000 PMs and 67,000 AICDs were implanted in 2004 in the U.S., increasing 19% and 60%, respectively, since 1997.3 The good news is that electronic pacing devices like the AICD are being implanted into patients to remedy these faulty electrical impulses. As a consequence, understanding the everyday experience of patients undergoing an AICD implant is an important consideration in their nursing management and ongoing care. How the Automatic Implantable Cardioverter Defibrillator (AICD) Works in Regulating the Heartbeat It might sound peculiar, but the heart itself is powered by a generator, the sinoatrial (SA) node, often called the heart’s natural pacemaker, which produces electrical impulses that travel through the heart muscles and stimulate it to contract. Ventricular tachycardia occurs when the electrical impulses are generated from one of the ventricular chambers of the heart, rather than the sinoatrial (SA) node. The electrical impulse does not run through the heart normally, causing irregular contraction, rapid heartbeat, and ineffective, lesser pumping of blood to the brain and body. The result is that the body and the brain do not receive enough oxygenated blood; the patient may say “I felt my heart pounding,” with effects ranging from fainting spells, blackouts, temporary blind spots, dizziness and eventual unconsciousness to possible cardiac arrest. If VT isn’t treated immediately, it can be life threatening. Likewise, when a patient develops VF, the heartbeats become very fast and irregular. The heart just quivers and unless effective CPR and defibrillation is given in 5 to 10 minutes, VF causes death.1,5 How the Heart’s Electrical System Works The heartbeat begins with an electrical signal in a group of cells called the sinus node, or SA node. The SA node is located in the right atrium, the upper right chamber of the heart. In a healthy adult heart at rest, the SA node fires off an electrical signal to begin a new heartbeat 60 to 100 times a minute. From the SA node, the electrical signal travels through special pathways to the right and left atria. This causes the atria to contract and pump blood into the heart’s two lower chambers, the ventricles. The electrical signal then moves down to a group of cells called the atrioventricular (AV) node, located between the atria and the ventricles. Here, the signal slows down just a little, allowing the ventricles time to finish filling with blood. The electrical signal then leaves the AV node and travels along a pathway called the bundle of His. This pathway divides into a right bundle branch and a left bundle branch. The signal goes down these branches to the ventricles, causing them to contract and pump blood out to the lungs and the rest of the body. The ventricles then relax, and the heartbeat process starts all over again in the SA node.11 A problem with any part of this process can cause an arrhythmia. For example, in atrial fibrillation, a common type of arrhythmia, electrical signals travel through the atria in a fast and disorganized way. This causes the atria to quiver instead of contract. Now all four chambers have received these signals and beat at the proper time — as a team. That electrical signal phenomenon spreads from the SA node throughout the entire heart in less than one second. This electrical signal journey is what an EKG records and measures. For a patient predisposed to such life-threatening arrhythmias, it could take up to 20 minutes for EMS to reach them and deliver the initial defibrillator shock, by which time the patient could have succumbed if unattended. The practical advantage of the AICD is that it detects life-threatening ventricular arrhythmias and effectively terminates the arrhythmia by delivering a programmed shock within seconds; this shock of 15-30 joules converts the arrhythmia and restores to normal the electrical rhythm of the heart, giving our patient a new lease on life. Compare the magnitude of this internal shock to an initial external shock of 200 joules (J). The optimal energy level for successful defibrillation as determined by the American Heart Association (AHA) Committee on Emergency Cardiovascular Care (ECC) for Advanced Cardiac Life Support (ACLS) protocols stipulate successive shocks of 200 J, 300 J, and 360 J energy levels for monophasic defibrillation.5,6 The shock has to be strong enough for it to penetrate and reach the heart, a procedure that can be extremely painful. In the matter of lower-energy biphasic waveform shocks, the AHA guidelines note an initial shock of 100 to 150 J is often sufficient with a biphasic defibrillator for the first defibrillation shock and 150 J for subsequent shocks. In fact, 200 joules is the recommended maximum amount for biphasic defibrillation.6 By comparison, an AICD shock of just 8.3 joules is something no more painful than a healthy thump on the chest. However, the AICD can deliver other appropriate electrical signals as programmed by the cardiologist. The AICD can do the following things; • Pacing. If a run of VT isn’t too fast, the device delivers several pacing signals in a row. These signals may stop the run and help the heart return to a normal rhythm. • Cardioversion. If the pacing doesn’t work, cardioversion can be used. In cardioversion, a mild shock is sent to the heart to stop the fast heartbeat. • Defibrillation. If VF is detected, a stronger shock is sent. This shock can stop the fast rhythm and help the heartbeat back to normal rhythm. • Pacemaker. The device can also sense when the heart beats too slowly, sending small electrical impulses to the heart muscle to stimulate the lower chambers of the heart (ventricles) and maintain a suitable heart rate. Because ventricular arrhythmias continue to threaten CHF patients and many anti-arrhythmic agents have not been well suited for use in these patients, a sophisticated ICD has shown encouraging results. Biventricular (BiV) pacing, also called cardiac resynchronization therapy (CRT), is used to synchronize the pumping of the heart’s ventricles with the pumping of the heart’s atria, returning the heartbeat and blood flow to normal. Heart failure causes a delay in the contractions of the ventricles, causing the left and right ventricle to pump “out of sync.” This leads to a rapid or irregular heartbeat, as well as the left ventricle not being able to pump enough blood to the body. Biventricular pacing is a new form of therapy for patients with heart failure (NYHA) class III. This combination device will now monitor the heart’s rhythm, provide protection against SCA and synchronize the contraction of the left ventricle, which improves cardiac function of the heart. Implications for Practice: What We Need to Know The following is more than just a disclaimer; these guidelines do not substitute for physicians’ orders or maintaining an open line of communication with the physician. To prepare your patient, written orders are required; however, in the event of no written orders, nurses must be proactive and notify the physician to obtain such needed orders to prepare the patient in a timely manner. Perform a baseline evaluation, including past history, allergies, vital signs, and a functioning intravenous (IV) line with an 18-20 gauge heparin IV lock (heplock). IV line and IV fluids: The IV line is preferred in the left arm when permissible, arm precautions when warranted. This IV line will serve for fluids, antibiotics, moderate “conscious” sedation and possible contrast injection (venogram) if necessary. Maintain precaution for patients with heart failure, review documented EF. As a rule of thumb we run IV fluids at the same rate as the EF, when in doubt, KVO (keep-the-vein-open) the IV line. Informed consent: It is a process of communication between the patient or their legal surrogate and physician that results in the patient’s authorization or agreement to undergo a specific medical intervention. In Florida, the informed consent law (Florida Medical Consent Law 766.103) requires that the patient be advised of three things: 1) the nature of the procedure; 2) the substantial risks and hazards of the procedure; and 3) the reasonable alternatives to the procedure (including, when appropriate, the option of doing nothing). After learning of these things, if a patient consents to the procedure, then informed consent has taken place. Healthcare professionals who witness consents are ethically obliged to assess the patient’s understanding of the proposed treatment and to inform the physician if there is reason to believe the patient has any misunderstanding regarding the nature, purpose, inherent risks or alternatives of his or her treatment. Medications: Patients may take their regular meds with a small amount of water the morning of the procedure, except for blood thinners (warfarin). Patients will have been asked to stop any blood thinners 5–7 days before the procedure. For inpatients on blood thinners [heparin, enoxaparin (Lovenox)], these medications will need to be stopped. Heparin requires more than six (6) hours. Always call the implanting physician for instructions or clarification. Surgical preparation: Pre-surgical skin preps or scrubs are as per your hospital guidelines. Patients will take a shower with soap and hair clippers when warranted from neck to chest (above the nipple line) as part of the skin preparation. NPO: Patients won’t be allowed to eat or drink anything for 8 hours, usually after midnight the day before or after breakfast for evening cases. Take precaution with diabetic patients: hold insulin and assess blood sugars. Pre-op or on-call antibiotics: Verify patient allergies and time of procedure, and start antibiotics within one hour from actual surgical cut time of procedure. Take precaution with underlying renal failure by reviewing labs for creatinine, blood urea nitrogen (BUN) and glomerular filtration rate (GFR) that may further nephrotoxicity to our patient. Pertinent laboratory data: Obtain CBC with platelets, a basic metabolic panel (BMP), APTT (if indicated: heparin) and PT/INR (if indicated: warfarin) for coagulation analysis. All are important. Be alert for and report elevated WBC, low hemoglobin/hematocrit and platelet count, or electrolyte imbalance (low or high K+). Review renal function: creatinine, blood urea nitrogen (BUN) and glomerular filtration rate (GFR). The procedure itself is performed under local anesthesia and moderate sedation. The patient is connected to backup pacer-defibrillator electrode pads. The anterior electrode pads are normally placed to the right of the upper part of the sternum and below the clavicle. However, since the chest is exposed and surgically prepped, placement of the first pad should be located posterior on the patient’s back, between the scapulas to the left of the spine. The second pad (apex) is placed to the left of the nipple in the mid-axillary line. This technique is the preferred method by most electrophysiologists to assess VF/VT rhythm and will result in a greater percentage of current passing through cardiac tissue and will increase the chances of successful defibrillation.8 Every AICD is tested by inducing an arrhythmia with a computer program and observation as to whether the device delivers the required therapy under sedation. Recovery from the procedure requires a chest x-ray and ECG with a brief overnight observation under cardiac telemetry. The patient will need to have their arm (same side where the device was implanted) in a sling. For new device implants, they will need to keep that arm still for at least 24 hours and should not raise it above their head for several weeks, thus allowing the new lead coil implanted to heal securely in place. Some of the complications of post pacer or ACID implant are failure to capture, failure to pace and failure to sense that may lead to an arrhythmia, causing hemodynamic instability related to a multitude of factors. Other common complications are hematoma at the site and infection. The healthcare professional needs to assess, document, implement and reevaluate these patients. We play a key role in facilitating maximum recovery — physically, psychologically and emotionally. Prior to discharge, patients will be shown how to examine the incision site and look for signs of infection daily, such as increased redness, increased tenderness, swelling around the incision and drainage from the incision. Patients should also report a fever over 100°F that lasts longer than 24 hours. The patient’s device will be rechecked by the pacemaker representative to handle your patient’s specific needs as instructed by the physician. Full recovery takes 6–10 weeks. Always follow and instruct your patients according to the implanting physician protocols (orders). Different Types of Pacemakers • Single chamber pacemaker: Uses one lead in the upper (1- Right atrium) or lower (2- Right ventricle) chamber of the heart. • Dual chamber pacemaker: Uses one lead in the upper (1- Right atrium) chamber and one lead in the lower (2- Right ventricle) chamber of your heart. • Biventricular pacemaker: (Figure 3) Uses three leads placed in the heart: 1- Right atrium, 2- Right ventricle, and 3- Left ventricle (via the coronary sinus vein). • Pulse generator: houses the battery and a tiny computer. • Leads: Wires that send impulses from the pulse generator to the heart muscle, as well as sense the heart’s electrical activity. Each impulse causes the heart to contract. The pacemaker may have 1–3 leads to treat the heart problem. About the author: Reynaldo “Rey” Grullon, BSN, RN is Clinical Coordinator of The Alliance Heart Institute for Leesburg Regional Medical Center and The Villages Regional Hospital. A graduate from Niagara University, a U.S. Army Nurse Corps Veteran, a member of the Society of Invasive Cardiovascular Professionals (SICP) and Alliance of Cardiovascular Professionals (ACVP). As clinical coordinator for a multi-office cardiology practice, he was recipient of the 2001 Office Nurse of the Year Award for Clinical Excellence by the American Association of Office Nurses for innovative education and leadership in Office Nursing. Reynaldo can be contacted at email@example.com Acknowledgements: Special gratitude to Theresa Gentile, RN, CEN and Luis De La Vega, RCIS for their friendship, for sharing their expertise and for providing countless contributions to this article. We work together at Central Florida Health Alliance with the commitment to quality care and service excellence to improve the health of our community.
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