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Learn more on telemetry monitoring and cardiac arrhythmias
By the completion of this exercise, the learner will be able to:
- Define the terms and recall the basic anatomy and physiology of the heart.
- Briefly discuss the variations of telemetry monitoring and how to assess a telemetry strip.
- Identify the characteristics of normal sinus rhythm, as well as its variations (sinus arrhythmia, sinus bradycardia, sinus tachycardia, sinus arrest, and sick sinus syndrome).
- Identify supraventricular arrhythmias on telemetry such as premature atrial contractions, atrial tachycardia, atrial flutter, atrial fibrillation, and wandering pacemaker and illustrate their basic pathophysiology, risk factors, protective factors, signs and symptoms, telemetry features, other associated diagnostic tests, nursing care and basic treatment/management.
- Identify junctional arrhythmias on telemetry such as Wolff-Parkinson-White, premature junctional contractions, junctional escape rhythm, accelerated junctional rhythm, and junctional tachycardia and illustrate their basic pathophysiology, risk factors, protective factors, signs and symptoms, telemetry features, other associated diagnostic tests, nursing care and basic treatment/management.
- Identify ventricular arrhythmias on telemetry such as premature ventricular contractions, idioventricular rhythms, ventricular tachycardia, Torsades de Pointes, ventricular fibrillation, asystole and pulseless electrical activity and illustrate their basic pathophysiology, risk factors, protective factors, signs and symptoms, telemetry features, other associated diagnostic tests, nursing care and basic treatment/management.
- Identify heart blocks on telemetry such as a first degree, second degree type I, second degree type II, or third degree SA and AV blocks as well as bundle branch blocks and illustrate their basic pathophysiology, risk factors, protective factors, signs and symptoms, telemetry features, other associated diagnostic tests, nursing care and basic treatment/management.
The heart consists of four chambers: the right atrium which accepts deoxygenated blood from the body via the veins, the right ventricle which pumps that deoxygenated blood to the lungs via the pulmonary artery, the left atrium which accept newly oxygenated blood from the pulmonary veins, and the left ventricle which pumps oxygenated blood to the rest of the body via the aorta. These four chambers are separated with four one-way, pressure-activated valves. The tricuspid valve is a three-flap valve that separates the right atrium from the right ventricle. The pulmonary valve is a three-flap valve that separates the right ventricle from the pulmonary artery. The mitral valve is a double-leaflet valve that separates the left atrium from the left ventricle and may also be called the bicuspid valve because of its construction. Finally, the aortic valve is a three-flap valve that separates the left ventricle from the aorta (American Heart Association [AHA], 2016). Please see Figure 1 (below) for further details.
Figure 1: Cardiac Anatomy and Blood Flow
The contraction of the heart muscle is a highly coordinated and precisely timed series of events. During diastole, the atria fill from the venous systems, and passive filling of the ventricles occurs. The atria contract simultaneously, filling the ventricles with the remainder of the blood via the open mitral and tricuspid valves, also known as the atrioventricular or AV valves. In systole, the full ventricles contract, closing the mitral and tricuspid valves (this is what we hear as S1) and opening the aortic and pulmonary valves (or semilunar valves) to allow the blood into the pulmonary artery and aorta. Once empty, decreased pressure inside the ventricles causes the semilunar valves to close again while the atria fill. This valve closure causes the second heart sound, or S2, which marks the start of diastole. Ventricular filling may be heard as S3, or if the ventricles are resistant and filling is slow, S4. The contraction is initiated by an electrical impulse in the sinoatrial (SA) node, also known as nature’s pacemaker. The impulse is transmitted from the SA node through the atria via Bachman’s bundle and the internodal pathways to the atrioventricular (AV) node. It passes through the AV node down through the ventricles via the bundle of His, the right and left bundle branches, and the Purkinje fibers. A healthy, properly functioning SA will keep the heart pumping between 60 and 100 times per minute. If the SA node becomes damaged the AV node, the heart’s first back-up plan, will create its own electrical impulse 40-60 times per minute if it does not receive an impulse from the SA node. Finally, the Perkinje fibers can also act as a tertiary pacemaker, but only at a rate of 20-40 beats per minute (bpm). The ability of a cardiac cells to contract after receiving a signal is called contractility. This electrical signal has a depolarizing effect on the cardiac cells. The ability of a cardiac cell to initiate an impulse is called automaticity, its ability to react to the impulse is called excitability, and the ability for a cell to transmit an impulse is called conductivity. The signal from the SA node triggers rapid depolarization, which consists of sodium (Na+) quickly entering the cells and calcium (Ca+) moving slowly into the cells. Repolarization can be broken down further into three stages: early repolarization consists of Na+ channels closing, the plateau phase consists of Ca+ moving into the cell and potassium (K+) moving out of the cell, and rapid repolarization consists of the Ca+ channels closing and K+ moving out of the cell rapidly. The resting phase between impulses consists of actively pumping K+ in and Na+ out of the cell. During the resting phase the cell is impermeable to Na+ diffusion but K+ can diffuse out of the cell slowly (Buss, 2011).
The term arrhythmia refers to a heart that has either an abnormal rate or abnormal rhythm. General signs and symptoms of arrhythmia include anxiety, blurry vision, chest pain, difficulty breathing, syncope, confusion or foggy thinking, fatigue, excessive sweating, weakness, dizziness, and lightheadedness. The National Institutes of Health (NIH) list risk factors for arrhythmia as follows:
- Increased age
- Air pollutants such as particulates and gases
- Family history or genetics- there is an increased risk for arrhythmia if a patient’s parent or another immediate relative has been diagnosed, as well as increased risk with certain inherited cardiac conditions and genetic mutation (malfunctioning ion channels for example)
- Alcohol abuse
- Tobacco or illicit drug use (especially cocaine and amphetamines)
- Certain medical conditions- such as aneurysm, rheumatoid arthritis, lupus, diabetes mellitus, cardiomyopathy, eating disorders, myocardial infarctions (MIs), congestive heart failure (CHF), hypertension, hypoglycemia, chronic obstructive pulmonary disease (COPD), obesity or sleep apnea
- Race/ethnicity- atrial fibrillation (afib) is more common in Caucasians, while many of the risk factors for arrhythmia are more common in African Americans
- Sex- afib is more common in men, supraventricular tachycardias (SVT) are more common in women
- Following surgery- there is an increased risk of atrial flutter in the weeks following major heart, lung, or esophagus surgery.
There are specific risk factors for individual arrhythmias that will be covered later throughout this learning activity. The NIH also lists protective factors, which includes a heart-healthy lifestyle of regular exercise, a diet high in fruits, vegetables and fiber and low in saturated fats and salt, avoiding illicit drugs, tobacco, and excessive alcohol, and managing stress on a regular daily basis. (USDHHS, n.d.a). In counseling patients regarding diet and lifestyle choices to limit their risk for arrhyth
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During the nurse’s assessment of a known or potential arrhythmia patient, the nurse should pay special attention to auscultation of the patient’s heart sounds as well as palpating peripheral pulses and auscultating for the apical pulse if necessary. While auscultating, note any irregularity to the heart rhythm as well as any audible murmurs. Check for lower extremity swelling, which may indicate heart failure and/or fluid overload. Auscultate the lungs and note any crackles or other adventitious sounds. Be sure to ask the patient for a full history of present illness, including all medications and any signs or symptoms of arrhythmias or risk factors for arrhythmias (i.e. coughing may indicate exposure to pollutants or tobacco smoke). If labs are needed, thyroid stimulating hormone, a metabolic profile with electrolytes, a toxicity screen and any drug levels should be included as these are common reversible causes of many arrhythmias. A chest x-ray may be ordered to assess for various lung abnormalities but also for cardiomegaly. If abnormalities are seen on the patient’s tests, additional more invasive testing may be done after the ECG. This may include an echocardiogram to assess the heart’s size, shape, and function, a cardiac catheterization to assess for complications of heart disease, or an electrophysiology study (EPS) to assess the heart’s electrical activity. A cardiac catheterization carries an increased risk of bleeding, infection, vessel or heart damage, blood clot formation/embolization, or development of a new arrhythmia. In an EPS, a wire is inserted to stimulate the heart and trigger an arrhythmia in order to assess risk as well as test potential treatments (USDHHS, n.d.a.).
Telemetry Monitoring Basics
The American Heart Association (AHA) publishes guidelines regarding who inside a hospital is an appropriate candidate for ECG monitoring. These guidelines exclude patients admitted to the intensive care unit (ICU), as these patients are significantly more complicated and are more often than not in need of monitoring. On a medical surgical floor that decision is more nuanced and complicated. The AHA outlines four major rationale for monitoring a patient on a medical or surgical floor in a hospital:
- To detect cardiac arrest sooner and therefore reduce the time to defibrillation
- To recognize deteriorating conditions (early afterdepolarizations or non-sustained arrhythmias)
- To facilitate management of arrhythmias (even if not life-threatening)
- To facilitate diagnosis of an arrhythmia or a cause for certain signs/symptoms (Sandau et al., 2017).
In addition to these general goals of telemetry monitoring the AHA guidelines recommend monitoring in these specific circumstances (See Table 1 below):
Table 1: Recommended Electrocardiographic Monitoring of Adult Hospitalized Patients
(Sandau et al., 2017)
Despite all of these very specific and comprehensive indications for monitoring, a recent study in hospitalized patients by Dai et al. (2016) found that the initial ECG was prompted by the patient’s reports of signs or symptoms in over half of the cases. In less than 20% of cases it was prompted by a change in vital signs. Listening to patients carefully and acting quickly when they report signs and symptoms of an arrhythmia are an essential part of excellent nursing care. This same study found that patient outcomes improved significantly across the entire hospital when nurses and other staff were adequately and regularly educated about the various signs and symptoms of an MI or arrhythmia (Dai et al., 2016).
A hospital in Delaware published findings in 2015 regarding the effects of instituting the AHA guidelines in their hospital regarding the monitoring of adult patients. In a similar period prior to implementing the AHA guidelines, they saw a decrease in the total number of alarms in a month from 4,106 to 3,094. Of these alarms, just 78 were emergencies, just 29 were clinically relevant, just 14 lead to a change in treatment, and just a single alarm in the two-month period examined was truly life-threatening. They concluded that life-threatening events are rare, and that reducing unnecessary telemetry use is not likely to miss life-threatening events of any clinical importance (Kansara et al., 2015). Similarly, Dressler, Dryer, Coletti, Mahoney & Doorey (2014) found that when the telemetry orders in their Electronic Medical Record were embedded with the list of approved AHA indications for telemetry monitoring as well as the appropriate associated predetermined durations for those orders they saw a 43% reduction in their number of monitored patients per week. They saw a 47% reduction in the average length of telemetry monitoring on a single patient and a reduction in cost for their telemetry monitoring services from an average of over $18,000 per day to less than $6,000 per day. They also instituted an order for a complete nursing assessment at the conclusion of the telemetry order to determine if the patient was in fact safe to discontinue monitoring, and if not, to contact the ordering provider for a new order. During this time they saw no significant change in the hospital census, the number of rapid responses called, the number of code blues called, or the number of mortalities (Dressler et al., 2014). A 2016 study by Cantillon et al. looked at the effect of standardized telemetry inclusion criteria being established as well as an off-site centralized monitoring unit, or CMU. This allows the telemetry to be monitored remotely. In their study, the inclusion criteria being standardized reduced the telemetry census by over 15%. They saw no significant change in cardiopulmonary arrests after instituting the changes. During the study they had 979 patients with rhythm or rate changes within one hour of emergency response team activation, and 772 (79%) of these were CMU detected and 105 were provided discretionary direct emergency response team notification. The CMU also provided advanced warning of 27 cardiopulmonary arrests which lead to 25 cases of successful cardiopulmonary resuscitation (Cantillon et al., 2016).
In order to better identify an abnormal rate/rhythm, it is important first to fully understand what a normal rate and rhythm refers to. As previously mentioned, a normal rate being generated from the SA node is 60-100 bpm. Rhythm is more complicated to define, but not impossible. Because the electrical impulses in the heart are what trigger contraction, the rhythm of the heart can easily and non-invasively be determined and monitored electronically via electrodes placed on the surface of the skin in specific locations. These electrodes are able to sense and record the electrical currents from the heart and use that information to graph a heart rhythm. The classic example of this is the 12-lead echocardiogram (ECG or EKG), which uses 12 different views to create a complete picture of the heart electronically. This is done using six limb leads and six precordial (V) leads. The limb leads provide information about the heart’s frontal (vertical) plane using three bipolar leads (I-III) and three unipolar (aVR, aVL, and aVF). All six limb leads produce a positive deflection on ECG with the exception of aVRwhich produces a negative deflection (the waves are upside down). The precordial leads (V1-6) are all unipolar and provide information about the heart’s horizontal plane. A modified chest lead (MCL1-6) may be used in lieu of a precordial lead. They give the same information about the horizontal plane of the heart but are bipolar. A rhythm strip gives a detailed picture of the electrical information gathered from one or more lead(s) simultaneously. The transmission of the electrical activity to a computer which generates the pictograph can be hardwired, as is commonly seen in emergency departments (EDs) and intensive care units (ICUs) or transmitted from a small portable box to a main computer for monitoring as is seen in telemetry (Diehl, 2011). The 12 leads of an ECG are characterized as follows:
- Lead I: a bipolar limb lead with current that runs from right to left, with a negative electrode on the right arm (RA) and a positive electrode on the left arm (LA) or chest. It is helpful in detecting atrial arrhythmias and hemiblocks
- Lead II: a bipolar limb lead with current that runs from the negative electrode on the RA or below the right clavicle to a positive electrode down on the left lower extremity (LL) or below the lowest palpable rib on the left midclavicular line. It produces a high-voltage deflection on ECG with tall P, R, and T waves. It is helpful for routine monitoring, or to detect sinus or atrial arrhythmias.
- Lead III: the final bipolar limb lead with current that runs down from the negative electrode on the LA to the positive electrode on the LL. It is especially helpful in detecting inferior wall MIs.
- aVR: an augmented unipolar limb lead with a negative deflection (the onlylimb lead with negative deflection). The positive electrode should be placed on the RA.
- aVL: an augmented unipolar limb lead with a positive deflection, the positive electrode on the LA, and useful in detecting lateral wall infarctions.
- aVF: an augmented unipolar limb lead with a positive deflection, the positive electrode on the LLE (or “foot”), and useful in detecting inferior wall infarctions.
- V1: the first precordial (or chest) lead, unipolar, biphasic, with the electrode placed to the right of the sternum at the 4th intercostal space- useful for its good view of P wave, QRS complex, and ST segment, and helpful in detecting ventricular arrhythmias, ST segment changes, bundle branch block (BBB), and ectopic beats
- V2: the second precordial (or chest) lead, unipolar, biphasic, with the electrode placed to the left of the sternum at the 4th intercostal space- useful in detecting ST segment elevation.
- V3: the third precordial (or chest) lead, unipolar, biphasic, with the electrode placed on the left half of the chest, between the sternum and the midclavicular line at the 4th/5th intercostal space- useful in detecting ST segment elevation.
- V4: the fourth precordial (or chest) lead, unipolar, biphasic, with the electrode placed on the left half of the chest, at the midclavicular line and the 5th intercostal space- useful in detecting ST segment and/or T wave changes.
- V5: the fifth precordial (or chest) lead, unipolar, positive deflection, with the electrode placed on the left half of the chest, at the anterior axillary line and the 5th intercostal space- useful in detecting ST segment and/or T wave changes.
- V6: the sixth precordial (or chest) lead, unipolar, positive deflection, with the electrode placed on the left half of the chest, at the midaxillary line and the 5th intercostal space.
As previously mentioned, the MCLs may be used in conjunction with the limb leads in lieu of the precordial leads. The MCL1is similar to V, but the negative electrode is placed on the left upper chest, the positive electrode is placed just to the right of the sternum at the 4th intercostal space, and a ground electrode placed on the right upper chest just below the clavicle. This produces a negative deflection waveform and is helpful in detecting premature ventricular contractions (PVCs), ventricular tachycardia, SVT, bundle branch defects, P wave changes, or to confirm pacemaker wire placement. MCL6is another alternative to MCL1to monitor ventricular conduction, but the negative lead is placed below the left shoulder, the positive electrode is placed on the left half of the chest at the midaxillary line and the 5th intercostal space (same location as V6), and a ground electrode is placed just below the right shoulder (Diehl, 2011). As previously mentioned, in most cases only one lead will be monitored at a time, and proper selection of the most appropriate lead for a particular patient is key in successful cardiac monitoring. The AHA recommends the V1lead when attempting to distinguish between ventricular tachycardia and aberrancy in adult patients. In pediatric patients, the AHA recommends lead II be used as supraventricular arrhythmias are more common in children than ventricular arrhythmias and P waves are best visible in inferior leads (Sandau et al., 2017).
Prior to applying electrodes, skin should be prepped. It should be washed, dried, any hair trimmed, and if needed the skin may be rubbed briskly with a dry, clean washcloth to remove dead skin cells and improve electrode contact. If the electrode is a snap design, the lead wire should be attached to the electrode prior to applying the electrode to the patient. If a clip design, the electrode can be applied to the patient first and the lead wire attached second. In a traditional 12-lead ECG, ten electrodes are placed: on the RA, RL, LA, LL and V1-6positions. While this is the most complete picture of the heart, this system is not conducive to ambulatory patients that may need monitoring for hours or even days (see Figure 2 below). The Mason-Likar system is a variation in which the four limb leads are moved to the torso to reduce motion artifact. The RA/LA electrodes are placed medial to the deltoid muscle in the infraclavicular fossa about 2 cm below the clavicle, while the RL/LL electrodes are placed along the anterior axillary line halfway between the ribs and the iliac crest (Diehl, 2011). The AHA guidelines recommend against leads on the limbs and advocates for placing all leads on the patient’s torso to allow for increased mobility and reduced artifact (Sandau et al., 2017).
Figure 2: Traditional ten-electrode placement for ECG monitoring
There are three primary options for placement of lead wires on ambulatory patients, depending on the telemetry system being used in an individual facility. A three-lead wire system (see Figure 3 below), which is the simplest system, includes a positive, a negative, and either a LL or a ground electrode that can all be placed and adjusted depending on the desired lead to be monitored (Diehl, 2011).
Figure 3: Three electrode versus five electrode placement for ECG monitoring
A five-lead wire system (see Figure 4 below) utilizes a RA, RL (ground), LA, LL and a single chest (C) electrode. Electrode positions may be identical for multiple leads, which means a lead selector switch on the monitor needs to be adjusted instead of the electrodes themselves (Diehl, 2011).
Figure 4: Five electrode placement for ECG monitoring
A third alternative is the five-lead wire EASI system (see figure 5 below), which uses just five lead wires to project a complete three-dimensional view of the heart’s conduction just as a 12-lead ECG would do. This reduced lead continuous 12-lead ECG has:
- the E lead in the center of the sternum at the 5th intercostal space
- the A lead on the left midaxillary line at the 5th intercostal space
- the S lead in the center of the upper sternum at about the first intercostal space
- the I lead at the right midaxillary line at the 5th intercostal space
- a ground lead placed anywhere on the torso (Diehl, 2011)
Figure 5: EASI system for ECG monitoring
Once a readout has been produced, it should be printed and labeled with the patient’s name and ID number, date, and time if not already included. Your interpretation of the patient’s cardiac rhythm may also be noted on the printout, as well as any current medications, signs/symptoms, or activities that may be affecting the rhythm. When reading an ECG printout or telemetry strip, the measurements are standardized (see Figure 6 below). The horizontal axis represents time in seconds (s), while the vertical axis represents amplitude in millimeters (mm) or voltage in millivolts (mV). A small box or square represents 0.04s and 1 mm or 0.1 mV. Five small boxes make up one large box, which represents 0.2s and 5 mm or 0.5 mV. Based on these numbers, 15 large boxes make up a 3 second strip, and 1500 small squares make up one full minute (Diehl, 2011).
Figure 6: An ECG Grid
A normal heart rhythm (see figure 7 below) has a P wave, a QRS complex, a T wave, and occasionally a U wave. Other measurements that should be taken into account include the PR interval, the ST segment, and the QT interval. An understanding of normal in all these items helps a healthcare provider identify when something is abnormal much faster.
The P wave is the first component, and this represents atrial depolarization. Normal amplitude is 2-3 mm, and normal duration is 0.06-0.12s. It should be smooth, rounded and upright in leads I, II, aVF, and V2-6, negative in lead aVR, and variable in leads III, aVL, and V1. If the P wave meets all of these characteristics and proceeds each QRS, this tells us that the impulse originated in the SA node as it should. Some variables you might see include a P wave that is:
- Peaked, notched or enlarged may indicate atrial hypertrophy secondary to COPD, pulmonary embolism (PE), valvular disease, or CHF
- Inverted may indicate retrograde or reverse conduction up from the AV node
- Variable may indicate impulses that are coming from various sites within the heart, such as in wandering pacemaker, irritable atrial tissue or damage near the SA node
- Absent may indicate conduction by a route other than the SA node, such as a junctional rhythm, afib, or a ventricular arrhythmia (Diehl, 2011).
The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex. It represents the time it takes for the conduction impulse to travel from the atria to the AV node and through the bundle of His and right and left bundle branches. Normal duration for the PR interval is 0.12-0.2s (twice the QRS complex). A lengthened PR interval may indicate a conduction delay such as an AV block or digoxin (Lanoxin) toxicity. A PR interval that is too short may indicate the impulse was not originated in the SA node such as a junctional arrhythmia or pre-excitation syndrome (Diehl, 2011).
The QRS complex represents depolarization of the ventricles. Normal amplitude is 5-30 mm and normal duration is 0.06-0.1s (half of the PR interval) measured from the beginning of the Q wave to the end of the S wave. The Q and S waves will have a negative deflection while the R wave will have a positive deflection in leads I-III, aVL, aVF, and V4-6. The deflections will be reversed in leads aVRand V1-3. Some possible variations in the QRS include:
- A deep Q wave (> 25% amplitude of the R wave) or a wide Q wave (>0.04s) may indicate a possible MI
- A notched R wave may indicate a BBB
- A widened QRS (> 0.12s) may indicate a ventricular conduction delay
- An absent QRS may indicate an AV block or ventricular standstill (Diehl, 2011).
The ST segment represents the end of ventricular conduction and depolarization to the beginning of recovery and repolarization. It is measured from the end of the S wave (called the J point) to the beginning of the T wave. It should be isoelectric (at the established baseline, not above or below) with a positive amplitude of no more than 1mm and a negative amplitude no less than -0.5mm below the baseline. An ST segment that is elevated (amplitude > 1mm) may indicate myocardial injury, while an ST segment that is depressed (< -0.5mm below baseline) may indicate myocardial ischemia or digoxin (Lanoxin) toxicity (Diehl, 2011). The AHA guidelines suggest that hospitals develop clear interdisciplinary protocols regarding which patients would benefit from ST segment monitoring, as changes in the ST segment or the adjoining T wave are often the first indicators of myocardial ischemia. Ideally, the AHA recommends computer software that allows for the simultaneous monitoring of the ST segment on all 12 leads in these at-risk patients. They also comment that ST segment changes may also be caused by hyperkalemia, hypothermia, an expected reaction post-defibrillation, electrolyte abnormalities, pericarditis, or BBB. Specifically, they recommend ST segment monitoring to be continuous for patients:
- In early phase acute coronary syndrome (ACS)
- Following an MI with revascularization
- With a newly diagnosed left main coronary artery lesion
- With vasospastic angina
- After non-urgent percutaneous coronary intervention (PCI) with suboptimal results
- During open heart surgery (Sandau et al., 2017).
The T wave represents ventricular recovery and repolarization. It should appear round and smooth with an amplitude of 0.5 mm in leads I-III. Its deflection should be upright in leads I, II, and V3-6, negative in lead aVR, and variable in leads III, aVF,aVL, and V1-2. If the T wave is:
- taller, peaked, or tented it may indicate myocardial injury or hyperkalemia
- inverted in leads I, II, or V3-6may indicate myocardial ischemia
- notched or pointed it may indicate pericarditis, which is inflammation of the pericardium, the double layer of connective tissue that covers the heart (Diehl, 2011).
The QT interval is measured from the beginning of the Q wave to the end of the T wave and represents ventricular depolarization and repolarization. Normal duration is 0.36-0.44 but can vary with age, sex, heart rate (HR). It should be less than half the time between consecutive R waves in any patient. A prolonged QT interval puts the patient at increased risk for a very serious arrhythmia called Torsades de Pointes (TdP). This may be caused my medication (see Table 2 below) or congenital. If a patient’s QT interval is shortened, this may indicate digoxin (Lanoxin) toxicity or hypercalcemia (Diehl, 2011).
Table 2: Drugs that may increase the QT interval
In addition to the above list, the AHA also cautions about the risk of QT prolongation with azithromycin (Zithromax), ciprofloxacin (Cipro), moxifloxacin (Avelox), citalopram (Celexa), escitalopram (Lexapro), ondansetron (Zofran) and fluconazole (Diflucan). The AHA also recommends monitoring and recording the corrected QT (QTc) by correcting the QT interval for HR. Regular monitoring is recommended in patients who have recently started antiarrhythmics such as dofetilide (Tikosyn), ibutilide (Corvert), sotalol (Betapace), disopyramide (Norpace), procainamide (Procan), quinidine and maybe amiodarone (Cordarone), dronedarone (Multaq) and flecainide (Tambocor) as well; patients with a history of prolonged QTc or risk factors for TdP; patients undergoing targeted temperature management; patients with inherited prolonged QT with unstable ventricular arrhythmias; patients with medically or metabolically induced prolonged QTc; patients with drug overdose or toxicity; and patients with moderate to severe hypokalemia or hypomagnesemia (Sandau et al., 2017).
The U wave is not consistently seen, but when present it represents the recovery and repolarization of the Purkinje fibers. It should be upright and rounded. If it is prominent it may indicate hypercalcemia, hypokalemia, or digoxin (Lanoxin) toxicity (Diehl, 2011).
The process of interpreting a telemetry strip will become faster and easier with repetition, but initially following a set-wise approach can be helpful. This is one such approach:
- Determine the rhythm: measure the distance between consecutive P and then R waves using paper and pencil or a caliper? Are they regular (consistently spaced)? A variation of less than 0.04s is OK. If not regular, is there a pattern?
- Determine the rate: this can be done in a number of ways. You can simply count the number of P (atrial rate) and then R (ventricular rate) waves in a 6 second strip and multiply by ten. You can count the number of small boxes/squares between consecutive P waves and then R waves and divide by 1500 (the number of small squares in one minute). The sequence method estimates HR based on the thicker black lines outlining the big squares/boxes. Locate a P wave that lands on a thicker black line. Locate the next P wave and determine how many big boxes are between them:
- One big box: HR of 300
- Two big boxes: HR of 150
- Three big boxes: HR of 100
- Four big boxes: HR of 75
- Five big boxes: HR of 60
- Six big boxes: HR of 50
Repeat this process with the R waves to determine the ventricular rate.
- Evaluate the P waves- are they present with every QRS? Are they similar size and shape? Are they normal configuration?
- Measure the PR interval duration by counting the number of small squares and multiplying by 0.04s. Measure form the beginning of the P wave to the beginning of the QRS complex. It should be consistent, measuring 0.12-0.2s and about twice the QRS complex.
- Measure the QRS duration from the beginning of the Q wave to the end of the S wave by counting the number of small squares and multiplying by 0.04s. Normal duration is 0.06-0.1s or about half the PR interval. Do they occur with every P wave? Are they consistent size and shape?
- Evaluate the T waves to see if they are present with every QRS complex and deflect in the same direction on each lead? Its deflection should be upright in leads I, II, and V3-6, negative in lead aVR, and variable in leads III, aVF,aVL, and V1-2. Are they normal and consistent amplitude and shape?
- Measure the QT interval from the beginning of the Q wave to the end of the T wave by counting the number of small squares and multiplying by 0.04s. A normal QT interval will be 0.36-0.44s or less than half the time between consecutive R waves.
- Evaluate for any other characteristics, such as ectopic (extra) beats, ST segment abnormalities (elevation or depression), or the presence of U waves (Diehl, 2011).
Normal Sinus and Not-So-Normal Sinus Rhythms
Normal sinus rhythm (see Figure 8 below) has a consistent regular rhythm, a rate of 60-100 bpm, a P wave preceding every QRS complex, normal PR and QT intervals, and normal/upright T waves. In addition, all P waves and QRS complexes are similar in size and shape (Diehl, 2011).
Figure 8: Normal Sinus Rhythm
Sinus arrhythmia is a normal variant (see Figure 9 below). The HR is still 60-100, but the rhythm is irregular and cyclic, varying with the patient’s respirations. This is related to the reduction in vagal tone and an increase in HR during inspiration and an increase in vagal tone and decrease in HR during exhalation. It should produce no symptoms. The difference between P-P and R-R intervals is usually > 0.12s, a P wave precedes every QRS complex, there are normal PR and QT intervals, and normal/upright T waves. In addition, all P waves and QRS complexes are similar in size and shape. It is important to notify the healthcare provider if the patient has recently started taking digoxin (Lanoxin). (Diehl, 2011).
Figure 9: Sinus Arrhythmia
Sinus bradycardia (see Figure 10 below) is a regular rhythm but a rate that is less than 60 bpm. The QT interval may also be slightly prolonged, but a P wave precedes every QRS complex, there is a normal PR interval, and normal/upright T waves. In addition, all P waves and QRS complexes are similar in size and shape. It occurs typically as a result of automaticity in the heart’s SA nodes decreasing due to excess vagal stimulation (such as Valsalva maneuver, carotid sinus massage, or vomiting) or decreased sympathetic stimulation (such as sleep or deep relaxation). It may also be due to hyperkalemia, increased intracranial pressure, hypothyroidism, hypothermia, glaucoma, SA node disease, cardiomyopathy, myocarditis, myocardial ischemia (especially after an inferior wall MI that involves the right coronary artery, which feeds the SA node). It can also be caused by certain medications (beta blockers, digoxin (Lanoxin), calcium channel blockers, lithium (Lithobid), sotalol (Betapace), amiodarone (Cordarone), propafenone (Rhythmol) and quinidine. If the condition is asymptomatic, such as in elite athletes, no treatment is required. Monitor the patient’s vital signs, airway, breathing, and pulse carefully. Sinus bradycardia may produce dizziness, hypotension, decreased level of consciousness (LOC), confusion, cool/clammy skin, blurred vision, chest pain, or bradycardia-induced syncope (Stokes-Adams attack). Sinus bradycardia in a child is an ominous sign and should be taken and monitored very seriously. If treatment is required, an underlying cause should first be identified and corrected. In the interim, or if an underlying cause cannot be identified immediately, transcutaneous pacing can be used until a more definitive plan can be established or medications such as atropine, epinephrine, or dopamine can be given to increase the HR (Diehl, 2011). After administration of atropine, be watchful for difficulty swallowing (USDHHS, n.d.a.).
Figure 10: Sinus Bradycardia
Sinus tachycardia (see Figure 11 below) is a regular rhythm with a rate of 100-160 bpm. There will be a P wave preceding every QRS complex, normal PR interval, a shortened QT interval, and normal/upright T waves. In addition, all P waves and QRS complexes are similar in size and shape, but P waves may have a higher amplitude and become superimposed on the preceding T wave. Sinus tachycardia may be caused by exercise, increased stress, hypovolemia, pain, hemorrhage, CHF, cardiogenic shock, pericarditis, PE, sepsis, or hyperthyroidism. It can also be prompted by certain medications such as excessive alcohol, caffeine, or nicotine intake, cocaine, amphetamines, atropine, dopamine, dobutamine, epinephrine, isoproterenol (Isuprel), or aminophylline. Sudden onset of sinus tachycardia following an MI may indicate extension of the infarction. The increased heart rate causes increased myocardial demands and decreased cardiac output due to reduced ventricular filling time, which can lead to angina, palpitations, decreased peripheral perfusion, hypotension, syncope, nervousness/anxiety, and blurred vision. Monitor the patient’s vital signs, airway, breathing, and pulse carefully. Monitor LOC and attempt to keep the environment as calm as possible. If untreated, tachycardia can lead to heart failure (as evidenced by respiratory crackles, S3 heart sounds, and jugular venous distention) or cardiogenic shock. If treatment is required, an underlying cause should first be identified and corrected. In the interim, or if an underlying cause cannot be identified immediately, medications such as beta blockers (metoprolol [Lopressor] or atenolol [Tenormin]) and/or calcium channel blockers (verapamil [Calan]) may be given to reduce the heart rate. (Diehl, 2011). If beta blockers are used, be watchful for first-degree heart block development or reports of digestive complaints, trouble sleeping, or erectile dysfunction. If calcium channel blockers are selected, be watchful for signs of afib, lower extremity swelling, hypotension and reports of digestive complaints (USDHHS, n.d.a.).
Figure 11: Sinus Tachycardia
Sinus arrest (see Figure 12 below) or atrial standstill is secondary to a lack of electrical activity in the atrium from the SA node. The patient will have a previously regular rhythm, followed by one or more missing beats. If just one or two beats are missed, it is considered a sinus pause, while three or more beats is considered a sinus arrest. The length of the pause is not a multiple of the previous R-R intervals and commonly ends with a junctional escape beat. When present, there will be a P wave preceding every QRS complex, normal PR and QT intervals, and normal/upright T waves. In addition, all existing P waves and QRS complexes are similar in size and shape. It closely resembles third degree SA block and can be caused by SA node disease (fibrosis or idiopathic degeneration), increased vagal tone (such as Valsalva maneuver, carotid sinus massage, or vomiting), acute inferior wall MI, acute infection, chronic coronary artery disease, acute myocarditis, cardiomyopathy, hypertensive heart disease or sick sinus syndrome. Medications that may cause sinus arrest include digoxin (Lanoxin), quinidine, procainamide, salicylates, or excessive dosages of beta blockers such as metoprolol (Lopressor) or propranolol (Inderal). If asymptomatic, no treatment may be necessary. Normal adults may have 2-3 second pauses during sleep or due to increased vagal tone or hypersensitive carotid sinus disease. However, a prolonged pause or arrest (usually 7 seconds or more) can cause syncope, which may lead to falls, injuries, car accidents, or other secondary injuries, and any pause over 2-3 seconds should be noted and considered significant. The patient may also have hypotension, altered mental status (AMS), dizziness, blurred vision, and cool/clammy skin. Monitor the patient’s vital signs, airway, breathing, and pulse carefully. If treatment is required, an underlying cause should first be identified and corrected. In the interim, or if an underlying cause cannot be identified immediately, a transcutaneous pacemaker may be used as well as medications such as atropine or epinephrine to prevent circulatory collapse until more definitive and long-term treatment can be established (Diehl, 2011).
Figure 12: Sinus Arrest
Sick sinus syndrome (SSS) refers to a wide variety of SA node abnormalities (see Figure 13 below). The syndrome can refer to both disturbances in way impulses are either generated or conducted. It is more common over the age of 60. The rhythm is irregular and the rate may vary. P waves usually precede each QRS. The QRS complex, T wave, PR interval, and QT interval are usually within normal limits but vary with rhythm changes. It typically presents with an insidious and progressive onset of bradycardia and episodes of sinus arrest or SA block with varying periods of rapid afib. There can also be periods of atrial tachyarrhythmias such as atrial flutter or atrial tachycardia dispersed amongst periods of bradycardia, a condition known as bradycardia-tachycardia (or brady-tachy) syndrome). It may also present as a lack of appropriate response by the SA node to increase the HR during exercise. It can be caused by fibrosis of the SA node (increased age, atherosclerotic heart disease, hypertension, or cardiomyopathy), trauma to the SA node due to surgery, pericarditis, or rheumatic heart disease, or autonomic disturbances. It can also be provoked by medications such as digoxin (Lanoxin), beta blockers, or calcium channel blockers. It can develop after an inferior wall MI that involves the right coronary artery, which feeds the SA node. Symptoms may include symptoms of cardiomyopathy (such as crackles, an s# sound, and a dilated/displaced left ventricular apical pulse), AMS, hypotension, blurry vision, or syncope. If asymptomatic, no treatment may be necessary. If symptomatic, monitor the patient’s mental status, vital signs, airway, breathing, and pulse carefully. If treatment is required, an underlying cause should first be identified and corrected. In the interim, or if an underlying cause cannot be identified immediately, atropine or epinephrine may be administered for symptomatic bradycardia, or metoprolol (Lopressor) or digoxin (Lanoxin) may be given for tachyarrhythmias (although these may worsen underlying SA node disease) (Diehl, 2011). If digoxin (Lanoxin) is given, look for reports of nausea and the development of other arrhythmias such as heart block (USDHHS, n.d.a.). Transcutaneous pacing may also be recommended as a short-term solution. Anticoagulants should be given to reduce the risk of blood clots and stroke if the patient develops afib (Diehl, 2011). If anticoagulants are prescribed, be mindful to educate the patient and family regarding the risks of bleeding and be watchful for signs/symptoms of this in the future (USDHHS, n.d.a.).
Figure 13: Sick Sinus Syndrome
Atrial or supraventricular arrhythmias affect the atrium. The AHA lists common symptoms of atrial arrhythmias as angina, shortness of breath, dizziness, lightheadedness, syncope, or heart palpitations (AHA, 2016). Premature atrial contractions (PACs) are ectopic or premature beats that do not originate in the SA node but instead from an irritable or ectopic spot elsewhere in the atria (see Figure 14 below). Unfortunately, this erroneous signal may be conducted through the AV node and the rest of the heart just as any other impulse. They can be caused by excessive alcohol or nicotine use, anxiety, extreme fear or fatigue, infection, coronary or valvular heart disease, acute renal failure, hypoxia, pulmonary disease, digoxin (Lanoxin) toxicity, or electrolyte imbalances. They are rarely dangerous in patients without heart disease and typically asymptomatic. The ECG strip will show a premature P wave with an abnormal configuration compared to the others and an irregular rate. If conducted, a normal QRS will follow. If not, no QRS will appear. The SA node is typically able to reset itself, causing a normal sinus beat to follow but slightly earlier. If PACs occur every other beat, this is called bigeminy, and every third beat trigeminy. Two PACs in a row are called a couplet. If symptomatic, the patient may report palpitations, fluttering, or the feeling of skipped beats. If symptomatic, monitor the patient’s vital signs and pulse. If treatment is required, an underlying cause should first be identified and corrected (Diehl, 2011).
Figure 14: Premature Atrial Contraction
Atrial tachycardia is also known as supraventricular tachycardia or SVT. The AHA reports it is more common in children, and more often found in women than men (AHA, 2016). This rhythm has an atrial rate of 150-250 bpm. This rapid rate may lead to a shorter diastole, reduced atrial kick and cardiac output, reduced coronary perfusion, and myocardial ischemia. This can eventually lead to angina, heart failure, or an MI if untreated. Atrial tachycardia can be with block (not every impulse is conducted through the AV node, so atrial and ventricular rates will differ), multifocal (multiple atrial foci firing impulses leads to various different P wave configurations and an irregular rhythm), or paroxysmal (starts and stops suddenly, regular rhythm). It can be caused by excessive caffeine or other stimulants, marijuana use, electrolyte imbalances, hypoxia, stress, MI, cardiomyopathy, congenital anomalies, Wolff-Parkinson-White (WPW), valvular heart disease, SSS, cor pulmonale, hyperthyroidism, hypertension, or digoxin (Lanoxin) toxicity. In atrial tachycardias, the QRS complex and QT interval is usually normal but may be shorter with the faster rate. ST segment changes and T wave inversion may occur if ischemia develops. Symptoms may include palpitations, blurry vision, syncope and hypotension. If symptomatic, monitor the patient’s mental status, airway/breathing, vital signs and pulse carefully. If treatment is required, an underlying cause should first be identified and corrected if possible. Carotid sinus massage may be a treatment option for younger patients but should be avoided in elderly patients. Potential risks include hypotension, bradycardia, vasodilation, ventricular arrhythmias, stroke and cardiac standstill. Valsalva maneuver is another option for vagal stimulation but carries many of the same risks. Medications such as digoxin (Lanoxin), beta blockers, adenosine (Adenocard) or calcium channel blockers may be used to reduce the HR (Diehl, 2011). If adenosine (Adenocard) is used, watch for the development of chest pain, SOB, and flushing (USDHHS, n.d.a.). If medications are unsuccessful or inappropriate, synchronized cardioversion or atrial overdrive pacing may also be used (Diehl, 2011). Synchronized cardioversion works by precisely timing (at the peak of the R wave) a low-energy shock to the heart in order to restore a normal rhythm. The patient will be premedicated with a sedative, anxiolytic, and/or analgesic medication intravenously. Caution should be advised, as cardioversion can lead to new or worsening arrhythmias or a clot embolism (USDHHS, n.d.a.).
Figure 15: Atrial Tachycardia
Atrial flutter is an SVT with an atrial rate of 250-350 bpm. The impulse is typically generated form a single atrial focus and results from circus reentry and increased automaticity. The ECG for this rhythm (see Figure 16 below) has a classic and unmistakable sawtooth pattern as the P waves lose their distinction and the waves blend together. T waves are not usually discernible, and the QRS complexes may be widened if P waves are superimposed. It is often associated with a second degree block, which does not allow all impulses through the AV node, resulting in a slower ventricular rate. If the ventricular rate is below 40 or above 150, cardiac output may be compromised. This can lead to reduced ventricular filling and coronary perfusion, angina, heart failure, pulmonary edema, hypotension, or syncope. It is often caused by conditions that raise the atrial pressure or cause atrial hypertrophy such as severe mitral valve disease, hyperthyroidism, pericardial disease, or primary myocardial disease. It can also be seen in patients with recent cardiac surgery, acute MI, COPD, and systemic arterial hypoxia. If symptomatic, monitor the patient’s mental status, airway/breathing, vital signs and pulse carefully. If treatment is required, an underlying cause should first be identified and corrected if possible. Treatment will focus on rate control and converting to a normal rhythm. In a stable patient, direct current cardioversion (DCCV) may be considered if the atrial flutter has been present for less than 48 hours. If present for more than 48 hours, the risk of thromboembolism is greater and cardioversion should not be considered unless the patient is adequately anticoagulated or a transesophageal echocardiogram (TEE) has been done to rule out the presence of a clot. If the patient is unstable, synchronized cardioversion should be considered (Diehl, 2011).
Figure 16: Atrial Flutter
Atrial fibrillation, commonly referred to as afib, is the most common arrhythmia (about 2 million people affected in the U.S.). It is defined as chaotic, random electrical activity in atrial tissue with an impulse rate of 400-600 per minute, which results in loss of atrial kick and quivering instead of coordinated contractions in the atria. The ECG baseline will have no discernible P waves but instead erratic waves called fibrillatory waves that may be coarse or fine (see Figure 17 below). It may be preceded by or caused by PACs. There is an irregularly irregular transfer of impulses through the AV node to the ventricles, leading to an irregular ventricular rate and corresponding irregular pulse. It can be caused by cardiac surgery, hypotension, PE, COPD, electrolyte imbalances, mitral insufficiency or stenosis, hyperthyroidism, infection, coronary artery disease (CAD), acute MI, pericarditis, hypoxia, or atrial septal defects. It can also be triggered by excessive caffeine, alcohol, or nicotine in combination with fatigue and stress. Medications such as aminophylline or digoxin (Lanoxin) may also trigger afib. If left untreated, afib can cause heart failure, angina, syncope, cardiovascular collapse, thrombus and/or embolism formation. If the ventricular rate is greater than 100, it is termed uncontrolled afib. On physical exam, the peripheral pulses may be different from the apical rate due to weaker contractions that do not produce a palpable pulse. Acute symptoms may include lightheadedness or hypotension due to reduced cardiac output. In patients with chronic afib, assess for symptoms of embolism such as PE or stroke. If symptomatic, monitor the patient’s mental status, airway/breathing, vital signs and pulse carefully. Any underlying cause should first be identified and corrected if possible. Similar to atrial flutter, treatment is targeted at controlling the rate (below 100) with medications if needed, and cardioverting to a normal rhythm if possible. Just as above, synchronized cardioversion is most successful if done within the first 48 hours of afib development. Patients should be adequately anticoagulated. Vagal stimulation with carotid sinus massage or Valsalva maneuvers may also slow the ventricular rate temporarily. Medications such as digoxin (Lanoxin), propranolol (Inderal), quinidine, amiodarone (Cordarone), and verapamil (Calan) are often given to maintain normal sinus rhythm and control the ventricular rate after cardioversion. Radiofrequency ablation is sometimes required in patients with refractory ectopic sites in the atria (Diehl, 2011). Ablation procedures use either a radiofrequency (high-energy) catheter, cryoablation (cold) or a laser to create a focal area of scar tissue to prevent the extraneous electrical activity from a specific ectopic site. The patient is pre-medicated with an anxiolytic and the procedure carries many of the same risks as a cardiac catheterization (USDHHS, n.d.a).
Figure 17: Atrial Fibrillation
Wandering pacemaker is an irregular rhythm that occurs when the heart's pacemaker changes from the SA node to another area above the ventricles or the AV junction. It is commonly transient and rarely serious. This leads to a rhythm with a normal rate of 60-100 bpm but varying P waves and PR intervals (see Figure 18 below). The QRS complex, T wave, and QT interval are usually normal, but the ventricular rate may be slightly irregular. It may be caused by increased vagal tone, digoxin (Lanoxin) toxicity, or heart disease such as rheumatic carditis. Wandering pacemaker is often asymptomatic and requires no treatment other than monitoring, but not always. If symptomatic, monitor the patient’s mental status, airway/breathing, vital signs and pulse carefully. If treatment is required, an underlying cause should first be identified and corrected if possible (Diehl, 2011).
Figure 18: Wandering Pacemaker
There are five main junctional arrhythmias that originate in the AV junction, which is the area around the AV node and the bundle of His. They occur when the SA fails as the heart’s main pacemaker or the impulse fails to conduct properly. This abnormal signal from the AV junction may cause upward or retrograde depolarization of the atria, which appears as inverted P waves in leads II, III and aVFwhere you would normally see them upright. Another key to spotting a junctional arrhythmia is the PR interval. If a rhythm has an inverted P wave but a normal PR interval (0.12-0.2s), it is likely an atrial arrhythmia. If a rhythm has an inverted P wave and a shortened PR interval (<0.12s), it likely originated in the AV junction (Diehl, 2011).
Wolff-Parkinson-White (WPW) syndrome is typically a congenital rhythm disorder seen in young children and young adults age 20-35. In this condition, impulses bypass the AV node through the bundle of Kent, travelling directly from the atria to the ventricles abnormally fast. This can lead to circus reentry, retrograde conduction or reentrant tachycardia. On ECG, this appears as a shortened PR interval (<0.1s) and a widened QRS complex (>0.1s) with a slurred beginning called a delta wave due to abnormal ventricular depolarization (see Figure 19 below). In asymptomatic patients, monitoring may be the only treatment necessary. WPW can also lead to tachyarrhythmias such as afib or atrial flutter, thus necessitating additional treatment such as radiofrequency ablation and/or rate-controlling medications like amiodarone (Cordarone) (Diehl, 2011).
Figure 19: A Delta Wave
A premature junctional contraction (PJC) is an irregular ectopic beat that originates from the AV junction. It appears on ECG with an inverted P wave due to the retrograde depolarization of the atria that may fall before, during, or after the QRS. If the P wave occurs prior to the QRS complex, the PR interval is shortened (<0.12s). The QRS complex, T wave, and QT interval are usually normal (see Figure 20 below). It can be caused by digoxin (Lanoxin) toxicity, excessive caffeine intake, inferior wall MI, rheumatic heart disease, valvular disease, hypoxia, heart failure, or swelling of the AV junction following surgery. PJCs are often asymptomatic and do not require treatment other than monitoring, or the patient may report palpitations or a quickening in their chest. Their pulse may be irregular. If cardiac output is compromised, they may show signs of hypotension or report dizziness, lightheadedness, blurry vision, or develop syncope. If symptomatic, monitor the patient’s mental status, airway/breathing, vital signs and pulse carefully. If treatment is required, an underlying cause should first be identified and corrected if possible (Diehl, 2011).
Figure 20: Premature Junctional Contraction
Junctional escape rhythm is a rapid succession of beats that occurs after a conduction delay from the atria. It is a compensatory mechanism to prevent ventricular standstill. It appears on ECG with a rate of 40-60 bpm and an inverted P wave due to the retrograde depolarization of the atria that may fall before, during, or after the QRS. If the P wave occurs prior to the QRS complex, the PR interval is shortened (<0.12s). The QRS complex, T wave, and QT interval are usually normal (see Figure 21 below). It can be caused by SSS, vagal stimulation, digoxin (Lanoxin) toxicity, inferior wall MI or rheumatic heart disease. This rhythm may be asymptomatic depending on their age and cardiovascular fitness level, or they may show signs of reduced cardiac output such as hypotension, decreased urine output or syncope. If symptomatic, monitor the patient’s mental status, airway/breathing, vital signs and pulse carefully. If treatment is required, an underlying cause should first be identified and corrected if possible. Atropine may be indicated to speed up the patient’s HR or a transcutaneous temporary pacemaker may be used until a permanent one can be implanted (Diehl, 2011).
Figure 21: Junctional Escape Rhythm
An accelerated junctional rhythm is very similar to the junctional escape rhythm above, but at a faster rate. This is especially problematic if the atria depolarize after the ventricles (the P wave follows the QRS) as this prevents the atrial kick, which is blood being pumped into the ventricles from the atria. It appears on ECG with a rate of 60-100 bpm (or > 80 bpm in toddlers up to age 3) and an inverted P wave due to the retrograde depolarization of the atria that may fall before, during, or after the QRS. If the P wave occurs prior to the QRS complex, the PR interval is shortened (<0.12s). The QRS complex, T wave, and QT interval are usually normal (see Figure 22 below). It can lead to decreased cardiac output with symptoms of hypotension, dizziness, confusion, syncope, decreased urine output and weak peripheral pulses. If symptomatic, monitor the patient’s mental status, airway/breathing, vital signs and pulse carefully. If treatment is required, an underlying cause should first be identified and corrected if possible. Pacing may be indicated with a transcutaneous temporary pacemaker until a permanent one can be implanted (Diehl, 2011).
Figure 22: Accelerated Junctional Rhythm
Junctional tachycardia a three or more consecutive PJCs in a row. It originates from an irritable focus in the AV junction with increased automaticity, overriding the SA node. The rate on ECG is 100-200 bpm. The rhythm strip indicates an inverted P wave due to the retrograde depolarization of the atria that may fall before, during, or after the QRS. If the P wave occurs prior to the QRS complex, the PR interval is shortened (<0.12s). The QRS complex, T wave, and QT interval are usually normal, but if the rate is increased may not be visible (see Figure 23 below). The significance of this rhythm depends on the rate, the underlying cause, and any accompanying or preexisting heart disease. It is most often caused by digoxin (Lanoxin) toxicity, but can also be related to hypokalemia, inferior or posterior myocardial ischemia or MI, congenital heart disease, or swelling of the AV junction after surgery. A lack of atrial kick and a high ventricular rate can quickly combine forces to produce reduced cardiac output. Assess for symptoms of hypotension, dizziness, confusion, syncope, decreased urine output and weak peripheral pulses. If symptomatic, monitor the patient’s mental status, airway/breathing, vital signs and pulse carefully. If treatment is required, an underlying cause should first be identified and corrected if possible. Vagal maneuvers may temporarily reduce the HR, and medications such as verapamil (Calan) may be indicated to slow the heart down further. Pacemakers, either temporary or permanent, or ablation therapy are sometimes indicated in cases of resistant or recurrent junctional tachycardia (Diehl, 2011).
Figure 23: Junctional Tachycardia
Ventricular arrhythmias start in the ventricle below the bundle of His and can be very dangerous, requiring immediate medical attention. For that reason, they should be studied, understood, and quickly recognized. The AHA lists common signs and symptoms as dizziness, palpitations, shortness of breath, nausea, altered level of consciousness, or cardiac arrest. It is often caused by reduced coronary blood flow, cardiomyopathy, inflammation related to sarcoidosis, sepsis, problems with the aorta, or certain medications/drugs (AHA, 2016). The myocardium is depolarized along a different pathway, causing widened QRS complexes on ECG. In addition, characteristic signs of ventricular arrhythmias include an absent P wave due to lack of atrial depolarization and a QRS and T wave that deflect in opposite directions due to the difference in the action potential during ventricular depolarization and repolarization. Without the atrial contraction or kick, cardiac output can decrease by 30%, causing hypotension, angina, syncope and/or respiratory distress (Diehl, 2011).
A premature ventricular contraction (PVC) is an ectopic beat caused by electrical irritability in the ventricular conduction system or muscle tissue. This may be caused by electrolyte imbalances, metabolic acidosis, hypoxia, myocardial ischemia or infarction, illicit drugs (cocaine, amphetamines), tricyclic antidepressants, ventricular hypertrophy, increased sympathetic stimulation, myocarditis, excessive alcohol or caffeine intake, antiarrhythmics medication, or tobacco use. If frequent or sustained, PVCs can reduce cardiac output. They can also be a precursor to more serious arrhythmias. PVCs can occur in couplets, bigeminy, or trigeminy. On ECG, PVCs appear wide and abnormally shaped at irregular intervals. There is no P wave, or a retrograde P wave may interfere with the ST segment. The QRS complex is > 0.12s with a deflection opposite that of the T wave (see Figure 24 below). There may or may not be a compensatory pause following the PVC, which should equal two regular P-P intervals. Patients with PVCs that are in couplets, bigeminy, or are variable in shape may indicate a more serious condition and require immediate medical evaluation. Patients with frequent PVCs may describe palpitations or experience hypotension or syncope. If asymptomatic, treatment beyond monitoring may not be necessary. If symptomatic, monitor the patient’s mental status, airway/breathing, vital signs and pulse carefully and place on continuous ECG monitoring. If treatment is required, an underlying cause should first be identified and corrected if possible. Antiarrhythmic medications such as procainamide (Procan), amiodarone (Cordarone) or IV lidocaine may be indicated (Diehl, 2011).
Figure 24: Premature Ventricular Contractions
Idioventricular rhythms are the hearts safety mechanism to avoid ventricular standstill if no impulse is received by the SA node or the AV node above the bundle of His. The cells of the His-Purkinje system will generate electrical impulses at 20-40 bpm. Cardiac output is markedly reduced with such a slow rate and no atrial kick. If just a single beat is seen, it is called a ventricular escape beat. If multiple beats occur consecutively at a regular rate of 20-40 bpm, it is called idioventricular rhythm. If the rate is above 40, it is called accelerated idioventricular rhythm (see Figure 25 below). On ECG, the P wave will be absent, the QRS will be widened (>0.12s), the QT interval will be prolonged, and the T wave will deflect opposite from the QRS complex (see Figure 26 below). Signs and symptoms include palpitations, dizziness, lightheadedness, hypotension, weak peripheral pulses, syncope, decreased urine output, or confusion. It may be caused by myocardial ischemia or infarction, digoxin (Lanoxin) toxicity, beta blockers, pacemaker failure, or metabolic imbalances. It may accompany third degree heart block. In a symptomatic patient, the underlying cause should be identified and corrected if possible. Monitor the patient’s mental status, airway/breathing, vital signs and pulse carefully and place on continuous ECG monitoring. Treatment should focus on increasing cardiac output by increasing the heart rate and establishing a normal rhythm. Atropine may be given or a transcutaneous pacemaker may need to be used until a permanent treatment plan can be established. Never give lidocaine or other antiarrhythmic medications to someone with idioventricular rhythm as this may suppress their last safety mechanism (Diehl, 2011).
Figure 25: Accelerated Idioventricular Rhythm
Figure 26:Idioventricular Rhythm
Ventricular tachycardia, or V-tach, is a series of three or more PVCs consecutively. The ventricular rate exceeds 100 bpm. It may be a precursor to ventricular fibrillation and sudden cardiac death, and for that reason should be identified and treated without delay. It may occur in short bursts without symptoms or be sustained. On ECG, the atrial rate cannot be determined and the ventricular rhythm is usually regular with a rate of 100-250 bpm. The QRS complex is widened (>0.12s) and typically with an increased amplitude. The QRS may be uniform (monomorphic) or variable (polymorphic). If the T wave is present, it deflects opposite from the QRS complex and the QT interval is not measurable (see Figure 27 below). It may be a result of myocardial ischemia or infarction, CAD, valvular heart disease, heart failure, cardiomyopathy, electrolyte imbalances, digoxin (Lanoxin) toxicity, procainamide toxicity, quinidine toxicity, cocaine use, or the proarrhythmic effects of some antiarrhythmic medications. If patients are stable, they still need quick and close attention as they can decompensate quickly. Poor cardiac output may lead to decreased level of consciousness, dizziness, lightheadedness, hypotension, weak peripheral pulses, syncope, decreased urine output, or confusion. Assess the patient carefully for vital signs, level of consciousness, mental status, airway/breathing, and pulse carefully and place on continuous ECG monitoring. If no pulse is present, defibrillation and CPR should be started immediately. If a pulse is present yet the patient is unstable hemodynamically, synchronized cardioversion may be appropriate. If hemodynamically stable and the rhythm is monomorphic, amiodarone (Cordarone) could be administered first. If the medication is ineffective then cardioversion is recommended. In a patient who is stable with polymorphic ventricular tachycardia, treatments with beta blockers, lidocaine, amiodarone (Cordarone), or procainamide (Procan) could be attempted prior to cardioversion therapy. For those with chronic ventricular tachycardia, an implantable cardioverter-defibrillator may be recommended (Diehl, 2011).
Figure 27: Ventricular Tachycardia
Torsades de pointes (TdP), which means twisting around the points, is a polymorphic ventricular tachycardia. It shares many of the same characteristics of ventricular tachycardia above, plus a rotation of the QRS complexes deflecting above and below the baseline.The rate is 150-250 bpm, the rhythm is irregular, and the QRS complexes are wide with varying amplitude (see Figure 28 below). It may be paroxysmal and appear or cease suddenly. It may deteriorate into ventricular fibrillation. It is often caused by something reversible, such as medications (Diehl, 2011). The AHA also lists the following risk factors for QT prolongation and potential TdP (see Table 3 below):
Table 3: General Risk Factors and Indicators for Impending TdP:
Other causes of TdP includes electrolyte imbalances and myocardial ischemia. Therefore, treatment includes correcting the underlying cause. In addition, mechanical overdrive pacing may be utilized to override the ventricular rate. Magnesium sulfate or electrical cardioversion are also options that should be considered if other treatment options do not work (Diehl, 2011).
Figure 28: Torsades de Pointes
Ventricular fibrillation, or V-fib, is a chaotic rhythm of electrical activity. The impulses are arising from multiple different foci in the ventricles. It produces significant contraction and no cardiac output. If untreated, sudden cardiac death will occur. It may be caused by myocardial ischemia or infarction, untreated ventricular tachycardia, underlying heart disease, acid-base imbalance, electric shock, severe hypothermia, electrolyte imbalances, drug toxicity (including digoxin [Lanoxin]) or severe hypoxia. On ECG, V-fib appears as fibrillatory waves with no discernible P waves, QRS complexes, or T waves. The larger the waves, the higher the electrical activity in the heart and the easier it is to convert it back to a usable and acceptable rhythm (see Figure 29 below). Patients are in full cardiac arrest, with no detectable pulse or blood pressure, and unresponsive. Shivering or electric razors can interfere with ECG monitors and even mimic ventricular fibrillation, so assess the patient first. Treatment for ventricular fibrillation is defibrillation, but CPR can help improve survival until the defibrillator arrives and is set up. Defibrillation causes myocardium to depolarize and allow the SA node to resume normal pacemaker duties. Intubation to facilitate gas exchange and medications such as epinephrine or vasopressin are also key components to help the heart respond to defibrillation and recover afterwards. Other medications that may be given during resuscitation include amiodarone (Cordarone), lidocaine, procainamide (Procan), or magnesium sulfate (Diehl, 2011).
Figure 29: Ventricular Fibrillation
Asystole or ventricular standstill corresponds with no electrical activity and no cardiac output. It should be confirmed in more than one ECG lead to confirm. It is predominantly related to inadequate blood flow to the heart such as MI, severe electrolyte disturbances, massive PE, prolonged hypoxemia, severe acid-base disturbances, electric shock, drug overdose, cardiac tamponade, or hypothermia. On ECG, it looks like a mostly flat line except for fluctuations from chest compressions during CPR (see Figure 30 below). In a patient with an implanted pacemaker, pacer spikes may still be present. Assess the patient rapidly yet carefully- they will be unresponsive and have no pulse or blood pressure if truly in asystole. Treatment includes CPR initially with repeated doses of epinephrine. Transcutaneous pacing should be initiated if possible, as well as correcting the underlying cause if possible. (Diehl, 2011).
Figure 30: Asystole
Pulseless electrical activity (PEA) is similar to asystole in that the heart is not contracting and there is no cardiac output. The primary difference between the two is that in PEA, the heart’s electrical impulses are preserved. In PEA, the ECG will show organized electrical activity, yet the patient will be unresponsive without a pulse or measurable blood pressure. It can be caused by hypovolemia, hypoxia, acidosis, tension pneumothorax, cardiac tamponade, massive PE, hypothermia, electrolyte imbalances, massive acute MI, or drug overdose. CPR in conjunction with epinephrine is the recommended treatment of choice initially, following by correcting the underlying cause if possible. If untreated, PEA can lead to asystole (Diehl, 2011).
Sinoatrial blocks, or SA blocks, occur when the SA node discharges regularly but some or all of those discharges are delayed or blocked in transit through the atria. There are three degrees of SA block:
- First degree SA block is a delay between the SA node firing and depolarization of the atria. This type of SA block cannot be seen on the ECG as there is no specific indicator for SA node activity within the electrocardiograph. Typically, it is asymptomatic with only monitoring required. Underlying causes should be treated if possible
- Second degree SA block is further broken down into type I and II:
Type I (see Figure 31a below): conduction time becomes progressively longer with each beat (causing an irregular rhythm and a progressively longer P-P interval) until an entire PQRST cycle is missed or dropped. The resulting pause is less than 2x the shortest P-P interval.
Type II (see Figure 31b below): conduction time is normal and the rhythm is regular until a single impulse is blocked. The resulting pause is a multiple of the previous P-P interval.
- In third degree SA block (see Figure 31c below) some impulses from the SA node are blocked completely, causing sinus pauses. The pause is not a multiple of the previous R-R intervals. This appears similar on ECG to sinus arrest, but is due to lack of impulse conduction, not lack of impulse formation. The pause can be indefinite and typically ends with a sinus beat (in contrast to sinus arrest which typically ends with a junctional escape beat) (Diehl, 2011).
Figure 31: SA Blocks: Second Degree, Type I and II and Third Degree
Atrioventricular block (AV block) involves the blocking of the electrical impulses from the SA node at the AV node. In AV blocks, atrial rates are regular with a rate of 60-100. Ventricular rates vary depending on the type and severity of the block. If slowed significantly, the reduced ventricular rate can reduce cardiac output and produce signs and symptoms of lightheadedness, hypotension and confusion. AV blocks can be caused by inferior wall or anteroseptal MI, digoxin (Lanoxin) toxicity, acute myocarditis, calcium channel blockers, beta blockers, cardiac surgery or radiofrequency ablation procedure, congenital abnormalities, or cardiomyopathy (Diehl, 2011). There are three degrees of AV block:
- First degree AV block is simply a consistent delay of the impulses as they pass through the AV node, but every impulse does eventually pass through. It may be temporary or permanent. On ECG, it will present with a longer than normal PR interval (>0.2s) and a regular rate (see Figure 32a below). Typically, it is asymptomatic with only monitoring required. Underlying causes should be treated if possible (Diehl, 2011).
- Second degree AV block- this is further broken down into type I and type II
- Type I, or Wenckebach/Mobitz type I, block is characterized by progressively longer delay with each heartbeat until a beat is finally missed, and the cycle then restarts. It may be caused by an MI, CAD, rheumatic fever, or certain medications. It can also be caused by increased vagal stimulation. Treatment focuses on resolving the underlying condition, as this will resolve the consequent block as well. If it occurs during an MI, it may progress to a more serious form. On ECG, the atrial rhythm is regular (P-P interval), yet the ventricular rhythm is regularly irregular (R-R interval). The PR interval progressively lengthens on each beat until a P wave fails to conduct and a QRS complex is missing (See Figure 32b). Patients are usually asymptomatic but may present with signs of reduced cardiac output such as hypotension and dizziness/lightheadedness if the ventricular rate is slow. In a symptomatic patient, atropine and/or a temporary pacemaker is indicated to help AV conduction. Any underlying cause should be assessed and corrected if possible (Diehl, 2011).
- Type II, or Mobitz type II, block- less common yet more dangerous than type I. In type II AV block, impulses pass through the AV node regularly until a single beat fails to conduct occasionally. It can be caused by an anterior wall MI, severe CAD or degenerative changes. The ventricular rate tends to be slower, thus decreasing cardiac output and causing symptoms such as hypotension and dizziness. The ratio of conducted to dropped beats can be as low as 2:1. On ECG, the atrial rate will be regular but the ventricular rate may not be. There will simply be missing QRS complexes. The QRS complexes may be wide and the PR interval may be prolonged but consistent (see Figure 32c below). As the number of dropped beats increases, patients may report fatigue, dyspnea, chest pain, or lightheadedness. Pulse may be slow and blood pressure low. If symptomatic, atropine, dopamine or epinephrine may be given to increase HR and improve cardiac output and oxygen to treat hypoxia. Transcutaneous pacing may also be indicated until a permanent pacemaker can be safely placed (Diehl, 2011).
- Third degree AV block, or complete heart block, occurs when all impulses are permanently or temporarily blocked at the AV node. The atrial rate will continue at 60-100 bpm, with regular P waves on ECG. However, the ventricular rate will be 40-60 bpm (if originating from the AV node) or 20-40 bpm (if originating from the Purkinje system) with no connection or coordination between the two (see Figure 32d below). It is most commonly congenital, but may be caused by CAD, an anterior or inferior wall MI, degenerative changes, digoxin (Lanoxin) toxicity, calcium channel blockers, beta blockers, or a surgical injury. With a decreased ventricular rate and no atrial kick, cardiac output can drop dangerously low, causing severe fatigue, dyspnea, chest pain, lightheadedness, altered mental status, loss of consciousness, hypotension, pallor, diaphoresis, bradycardia, and variable pulses. Atropine, dopamine, epinephrine and/or a temporary pacemaker may be utilized to increase the ventricular rate and improve cardiac output. The underlying cause may be resolved, or a permanent pacemaker inserted (Diehl, 2011).
Figure 32: Atrioventricular Block
Bundle branch block (BBB) is a potential complication of an MI. Either the left or the right bundle branch does not conduct impulses. If the block happens further down the left bundle branch, it is called a hemiblock. If the block occurs as the HR increases, it is called rate-related. Ventricular depolarization is prolonged because the signal travels down one bundle branch and then across to the opposite ventricle via myocardial cell to cell conduction. This leads to a widened QRS complex on the strip (>0.12s). Leads V1and V6to help determine which side of the heart is affected. A right BBB (see Figure 33a below) can be caused by an anterior wall MI, CAD, cardiomyopathy, cor pulmonale, or PE. The QRS may be double notched in lead V1, which is an rsR due to late right ventricular depolarization, and a negative T wave. In lead V6you may see a widened S wave. A left BBB (see Figure 33b below) may be caused by hypertension, aortic stenosis, degenerative changes of the conduction system, or CAD. If left BBB occurs with an anterior wall MI, it may indicate complete heart block and require pacemaker placement. A wide S wave will be seen after the widened QRS complex in lead V1with a positive T wave. In lead V6you will see a tall, notched R wave with an inverted T wave. Most patients are asymptomatic, although if symptomatic they may cause syncope and require pacing or cardiac resynchronization therapy (CRT) to help the ventricles get back in sync (Diehl, 2011).
Figure 33: Bundle Branch Block
A. Right BBB
B. Left BBB
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