Patients can display a variety of EKG changes for reasons other than acute myocardial infarctions (AMI). Many of these have been mentioned in previous chapters. This chapter will look at some of these deviations from normal as they relate to EKG tracing and cardiac monitor irregularities. When examining these changes, always do so with the patient in mind. Patient past history, symptoms, vital sign assessment, and events surrounding the presentation should be considered when making definitive decisions about EKG changes. Also, comparing the patient’s EKG with a prior EKG is an important facet of interpretation. Correlate lab studies and put the entire picture into perspective before arriving at a final decision.
Today’s cardiac monitors have the capacity to recognize many changes to waveforms, including ST segment elevations, QTc intervals, etc. One of the problems that health care personnel must be aware of is called alarm fatigue. Technology affords the medical world in many ingenious ways to “watch” the patient and with this comes more noises, bells, and alarms to bring changes to the attention of those who are caring for the ill or injured individual. Guard against becoming lax regarding responding to alarms. Always check the patient. Make sure that there is clear understanding about what the alarms mean. Be familiar with the mechanics of the monitoring equipment including retrieving important information and creating a hard copy of events. Never assume that alarms are simply patient movement or the loss of a lead wire.
EKG Changes Associated with Processes Other Than Myocardial Infarction lists the EKG changes that occur with factors other than an AMI.
EKG Changes Associated with Processes Other Than Myocardial Infarction
Both hypo and hyperkalemia can create changes in EKG morphology. Hypokalemia will be noted as a depressed or flattened T wave, depressed ST segments, and/or the presence of a U wave. A U wave is an extra waveform after the T wave. It can be present in other processes as well. Dysrhythmias which can occur with low potassium are ventricular in nature and include the development of torsades de pointes (EKG changes associated with hypokalemia).
Hyperkalemia is noted to have diffuse, high, peaked T waves and broad QRS complexes. These T waves are not restricted to certain areas of the heart. The P wave is also important in high potassium situations as the PR interval will prolong and then flatten and sometimes disappear. The cardiotoxic effects of hyperkalemia which creates the wide QRS complexes can predispose the patient to PVCs and subsequent ventricular fibrillation (EKG changes associated with hyperkalemia).
EKG changes associated with hypokalemia
EKG changes associated with hyperkalemia
As has been noted in previous chapters, calcium is a necessary electrolyte for the normal functioning of the heart. Hypocalcemia can be a dangerous electrolyte imbalance. This causes the QT interval to lengthen which can be a precursor of torsades de pointes. The QT interval should be less than half the entire length of the cardiac cycle. Some causes of hypocalcemia are pancreatitis, hydrogen fluoride burns, and the administration of multiple units of blood. The ST segment can also be flattened. Hypercalcemia can cause the QT interval to shorten (EKG changes associated with hypocalcemia).
Hypomagnesemia can present with similar changes to the EKG as hypokalemia with the presence of U waves and nonspecific T wave changes as well as the prolongation of the QT interval. This places the patient at high risk for torsades de pointes and other ventricular dysrhythmias such as PVCs, ventricular tachycardia, and ventricular fibrillation. Some causes of low magnesium are diuresis, increased calcium, increased ingestion of vitamin D, administration of steroids, chemotherapy, and the development of sepsis.
Hypermagnesemia can cause a prolonged PR interval, a widened QRS, and elevated T waves. Complete heart block can occur with this electrolyte disturbance. Etiologies of high magnesium include renal failure, administration of magnesium, and use of antacids.
EKG changes associated with hypocalcemia
The biggest issue with environmental problems is that of hypothermia. Bradycardia is the most common dysrhythmia, including a slow atrial fibrillation. All intervals have a tendency to prolong. The J wave or Osborne wave is the most distinguishing characteristic for this environmentally related concern. This is an extra “hump” or positive deflection in the EKG tracing between the ST segment and the T wave at the “J point” (J wave).
Be aware that when individuals are presenting with hypothermia, they may be shivering or trembling. When this happens, artifact on the EKG can cause misinterpretations. Be sure to distinguish between artifact and what might appear to be atrial flutter, atrial fibrillation, or ventricular fibrillation.
Central Nervous System
Patients with central nervous system disturbances such as a subarachnoid hemorrhage, an intracranial bleeding problem, can present with EKG changes. These will be demonstrated by deeply inverted T waves. Bradycardia and U waves can also be present as well as prolongation of the QT interval (EKG changes associated with a subarachnoid hemorrhage).
EKG changes associated with a subarachnoid hemorrhage
A major pulmonary embolus, a blood clot in the lungs, can present with significant EKG changes. One of these is the S1Q3 pattern. In this abnormality, lead I demonstrates a significant S wave and lead III reveals a deep Q wave (EKG changes associated with pulmonary embolus). Another aspect of this may be the inclusion of an inverted T wave in lead III (S1Q3T3). The Q wave is differentiated from that of an AMI since it is found in only one lead and not contiguous leads associated with different parts of the cardiac anatomy. Other changes that might be present include indications of a right bundle branch block and right ventricular hypertrophy.
EKG changes associated with pulmonary embolus
Several different dysrhythmias can be present in a pulmonary embolus. The more common ones are sinus tachycardia and atrial fibrillation; though it is not uncommon for patients with large pulmonary emboli to have PVCs which will then progress to ventricular tachycardia or fibrillation. Patients who have smaller pulmonary emboli may only present with sinus tachycardia and this is a significant factor when people present with sudden onset of shortness of breath and chest or back pain that is sharp or pleuritic in nature. This tachycardia is not always extremely rapid. Rates of 110 to 120 should also be suspect.
Chronic Obstructive Pulmonary Disease
Patients with long standing chronic obstructive pulmonary disease (COPD) can have changes to their EKG tracing. COPD is divided into chronic obstructive bronchitis and emphysema. Changes within the thoracic cavity due to increases in the volume of the lung from alveolar air trapping, the change in the position of the diaphragm, and the subsequent change in orientation of the heart within the chest cavity can create the following changes in the emphysemic patient (EKG changes associated with chronic obstructive pulmonary disease):
- Low voltage
- Right axis deviation
- Poor R wave progression
Dysrhythmias that occur include both atrial and ventricular, but atrial fibrillation and flutter are common as well as multifocal atrial tachycardia. These dysrhythmias may occur due to the disease process or medications that are used to treat the patient.
EKG changes associated with chronic obstructive pulmonary disease
When patients experience right-sided heart failure as a consequence of pulmonary disease, it is known as cor pulmonale. P pulmonale is an EKG change associated with this disease process. This is an indication of right atrial enlargement and is expressed as an increase in the amplitude of the first upswing of the P wave in the inferior leads II, III, aVF.
Pericarditis is an inflammatory disease process of the heart. When this occurs, several EKG changes can be seen. These occur in the large majority of cases, but the early signs may not be seen if the patient has had the problem for several days (EKG Tracing in pericarditis). These changes are:
- Diffuse ST segment elevation
- T wave inversion (after ST segments have returned to the isoelectric line)
- T wave flattening and then return to normal
- Depressed PR interval
EKG Tracing in pericarditis
If an effusion (a collection of fluid) is present in the pericardial sac, low voltage would be seen in all leads. Electrical alternans, a change in the amplitude of successive QRS complexes, can be exhibited due to a rotation of the heart as fluid continues to fill the pericardial sac with the effusion.
These patients often appear to have large, extended infarctions on their EKG tracings due to the diffuse pattern of the ST segment elevation. Although it is imperative to prove that infarction has not occurred, the following changes can also provide clarity for the health care provider:
- More leads than would be associated with a localized area of infarction demonstrate the ST segment elevation.
- If a patient is in the process of myocardial infarction, the T wave inversion, indicating ischemia, would most likely lead the changes on the EKG rather than appear after the ST segment elevation.
- No Q waves occur with pericarditis.
- Left ventricular hypertrophy (larger R waves in leads that look at the left ventricle—V5 and V6—with V6 being greater than V5)
- Left axis deviation (lead I QRS positive with a negative QRS in aVF)
- Lateral and inferior Q waves (not associated with infarction)
Idiopathic Hypertrophic Subaortic Stenosis
Idiopathic hypertrophic subaortic stenosis (IHSS) is also known as hypertrophic obstructive cardiomyopathy (HOCM). This is a disease process seen very often in young people who are athletic. Sudden death can occur due to the enlargement and stiffness of heart muscle that does not allow for good filling and causes problems with ventricular outflow. Patients may also complain of lightheadedness, chest pain, or syncopal episodes. EKG changes that will be found on the 12-lead EKG are (EKG changes associated with IHSS):
EKG changes associated with IHSS
Some individuals who are athletic can have changes to their EKG simply due to the fact that they have been in training and their heart has made alterations that will maximize their efforts. This is especially true for runners. Some of these changes include dysrhythmias such as profound bradycardia, junctional rhythms, first-degree AV block, second-degree AV block (Wenckebach), or wandering atrial pacemaker. Other changes that might be seen are: ST segment elevations, T wave inversions, right and left ventricular hypertrophy, and right bundle branch block.
Brugada syndrome is an inherited autosomal dominant disease process that causes sudden death in otherwise healthy, younger male patients (age 30-50). Females can have this syndrome, but it is more common in men. It is also more common in Asian populations. Patients with this syndrome develop polymorphic ventricular tachycardia and subsequent ventricular fibrillation. EKG changes that are associated with this cardiac disturbance are right bundle branch block and ST segment elevation in precordial leads, V1, V2, and V3 not associated with an injury pattern (EKG changes associated with Brugada syndrome). The insertion of an automatic implantable cardioversion defibrillator is the treatment of choice at this time. Identifying these changes in the routine EKG can be life saving for these individuals.
EKG changes associated with Brugada syndrome
Wellens syndrome is another disease process that can cause sudden death in patients. In this abnormality, the left anterior descending artery (LAD) is stenosed and can be treated with angioplasty and placement of coronary stents. The EKG findings in this preinfarction disease state are T wave inversion in leads V2 and V3. Without treatment, these patients will progress to an anterior myocardial infarction. Patients will have chest pain with these specific EKG changes and no ST segment elevation or Q waves (EKG changes associated with Wellens syndrome).
EKG changes associated with Wellens syndrome
In general pacemakers are placed when heart rates are too slow such as bradycardia and AV blocks. When the patient’s heart does not generate an impulse, the pacemaker will take over to perform this function. Other reasons for pacemakers are tachydysrhythmias or sick sinus syndrome.
Electrodes are positioned within the heart and attached to a generator. In emergency situations a temporary pacemaker is placed. The leads that are used for pacemakers can be unipolar (a negative pole) or bipolar (both a negative and a positive pole). There are different kinds of pacemakers and each is programmed to assist the heart in the best manner available.
When patients have pacemakers, the EKG or cardiac monitor tracing will show a pacer spike or “blip.” On many cardiac monitors, this spike can be marked so that it shows up in a different color for easy recognition. Depending on the type of pacemaker placed, the spike or “blip” will appear prior to the P wave or the QRS. Atrial pacing will produce a pacer spike before the P wave and ventricular pacing will demonstrate a pacer spike before the QRS complex. Some pacemakers are called “AV sequential.” In this instance, there will be two pacer spikes for each complex—one before the P wave and one before the QRS. There are a variety of pacemakers and a number of ways in which they can be set specific for the patient’s underlying disease process. They are based on the chamber that is paced, the chamber that is sensing the stimulus, and the activity that occurs from that generated impulse. The ones listed above are the most common (Pacer spikes).
When pacemakers are in place, watch for failure to pace or failure to capture. Failure to pace is indicated when no pacing spikes are noted on the EKG tracing or cardiac monitor. This could mean that the battery needs to be changed or that there is some type of failure of the circuitry. This could be caused by a lead that has broken, has become disconnected, or that the amperage has been set too low. If this happens with a temporary pacemaker, the voltage or mA can be set higher until the pacer blip or spike is noted on the tracing or monitor.
Pacer failure to capture is identified when the pacer spike is seen but no atrial or ventricular waveforms are noted. Etiologies for this problem include incorrect lead positioning, deficient battery, faulty lead wires, a lead wire that has actually perforated through the myocardium, or disease processes such as electrolyte imbalances or hypoxia leading to acidotic conditions.
Pacemakers can also undersense and oversense. Undersensing causes the production of pacer spikes when they are not necessary, that is, the patient’s underlying rhythm is already producing a heart rate that is perfusing the body. These spikes can cause problems if they occur on the vulnerable portion of the T wave which can then cause ventricular fibrillation. Oversensing picks up other activity that is not cardiac in nature such as tremors or other muscular movements. At this point, the pacemaker will not fire in an attempt to correct the heart rate for the patient and the patient can become asystolic (Pacemaker malfunctions).
Some patients have a special pacemaker that is called a “Biventricular Pacemaker.” This was developed to assist patients who have heart failure. This is also known as cardiac resynchronization therapy and causes the ventricles to contract in a more synchronous fashion. There are three leads for this pacemaker—one that is placed in the right atrium, one in the right ventricle, and the last in the left ventricle.
Heart transplant patients can have changes on their EKG tracing and cardiac monitor. The most interesting of these is the presence of two P waves. Due to the manner in which the heart is attached to the existing piece of right atrium and thus maintains their own SA node, the patient will have both a “native P wave” and a “donor P wave” (Native and donor P waves). The native P wave, denoted as Pn, is not able to conduct the impulse beyond the sutured area. The donor P wave, denoted as Pd, becomes the dominant area of generated impulses and conducts the impulse through the myocardium. Other changes that may be seen with transplanted hearts are:
- An increase in the sinus rate
- Rotation of the axis
- A right bundle branch block
- Nonspecific ST-T wave changes
Native and donor P waves
Several medications can make changes on the EKG tracing or the cardiac monitor. Some of these have already been discussed throughout other chapters. The following table is a review of some of these changes that can occur with certain medications. Remember that many medications can create a prolonged QT interval which can then allow for the development of torsades de pointes (Some Medications Implicated in EKG Changes).
Some Medications Implicated in EKG Changes
Many medications can cause cardiac changes for the patient. Sometimes these changes occur due to the combined effects of two or more medications that the patient may be taking. Always take this into consideration when diagnosing and treating patients for EKG changes or dysrhythmias that are taking place.
Many processes can cause cardiac abnormalities for patients. These can be derived from a variety of sources and can impact the cardiac health of individuals in many unique ways. Body systems intertwine and it is important for the health care professional to understand the various adjustments that these systems make when disease processes or medication related events occur.
Some of the highlights from this chapter are:
- Hypokalemia is noted on the EKG by a flattened T wave, depressed ST segments, and the presence of U waves.
- Torsades de pointes can be caused by hypokalemia.
- Hyperkalemia will present with tall, peaked T waves.
- Ventricular fibrillation can be caused by hyperkalemia.
- Hypocalcemia causes a prolongation of the QT interval which can be a precursor to torsades de pointes.
- Hypercalcemia can cause the QT interval to shorten.
- Hypomagnesemia can look very similar to hypokalemia.
- Ventricular dysrhythmias can be caused by hypomagnesemia including torsades de pointes.
- Complete heart block can be caused by hypermagnesemia.
- The J wave (Osborne wave) is present with hypothermia.
- Intracranial events such as subarachnoid hemorrhage can produce deeply inverted T waves as well as bradycardia and prolongation of the QT interval.
- A pulmonary embolus has a special S1Q3 pattern. This can also include an inverted T wave in lead III (S1Q3T3).
- Tachycardia is a common dysrhythmia with pulmonary embolus.
- Patients with COPD will have low voltage, right axis deviation, and poor R wave progression on their EKG.
- Cor pulmonale is right-sided heart failure caused by an underlying pulmonary disease process.
- P pulmonale is the EKG change associated with cor pulmonale.
- Pericarditis appears with diffuse ST segment elevation across the EKG.
- T wave changes will also occur with pericarditis, but this will happen after the ST segment elevation, rather than before as with an acute myocardial infarction.
- An effusion can cause electrical alternans, a change in the amplitude of successive QRS complexes.
- Idiopathic hypertrophic subaortic stenosis (IHSS) can cause sudden death in young people, especially athletes.
- IHSS changes to the heart include left ventricular hypertrophy, left axis deviation, and Q waves in the inferior and lateral leads.
- Some athletic individuals can have some changes on their EKG and dysrhythmias which are considered to be “normal” for them.
- Many athletes will have a severe or profound bradycardia.
- Brugada syndrome is most common in Asian males and causes sudden death.
- The characteristic changes on the EKG for Brugada syndrome is a right bundle branch block and ST segment elevation in the precordial leads.
- Wellens syndrome is caused by a stenosed LAD.
- Wellens syndrome can be picked up on the 12-lead EKG as T wave inversion in V2 and V3.
- Patients with pacemakers will have a pacer spike or “blip” before captured QRS complexes.
- Pacemakers are usually used for bradycardias and AV blocks.
- Pacemakers can be atrial, ventricular, or AV sequential.
- Failure to pace, failure to capture, oversensing, and undersensing are complications that can occur with pacemakers.
- Undersensing can cause pacer spikes to appear throughout the EKG and these can fall on the vulnerable portion of the T wave causing ventricular fibrillation.
- Oversensing causes the pacemaker to fail to fire and the patient can become asystolic.
- Biventricular pacemakers are used to keep patients out of heart failure.
- Heart transplant patients will have two P waves—a native P wave (Pn) and a donor P wave (Pd).
- Many different medications can cause a variety of EKG changes including prolonged PR, QRS, or QT.