The ECG is the most widely used test examining electrical function of the heart. Although commonly used to assess myocardial ischemia and dysrhythmias, the ECG is also capable of detecting electrolyte abnormalities and fluid overload in critically ill patients. This case study describes the clinical presentation of an adult female with a complex medical history who presented to the ED for worsening fatigue and high ileostomy output. Her hospitalization was complicated by acute fluid overload—detected by ECG—after aggressive I.V. rehydration. This article provides a detailed description of the clinical case and a deeper understanding of the effects of fluid and electrolyte abnormalities on the ECG.
A 68-year-old female with a chief complaint of increasing fatigue, poor appetite, and increased ileostomy output over the last 2 weeks presented to the ED of a large academic medical center via ambulance. Concerned that she may be becoming extremely dehydrated and have a possible gastrointestinal (GI) infection, she attempted to visit her primary care provider but was unsuccessful in setting up an appointment, and decided to come to the ED instead.
She stated that the worsening fatigue lasted throughout the day and rated the severity as an 8 on a scale from 0 (none) to 10 (extremely severe). Her normal baseline fatigue was 2 out of 10. She described the fatigue as “extreme exhaustion” and “debilitating.” Her increased fatigue forced her to depend on family and neighbors for help with bathing and grooming, preparing meals, and completing other daily tasks.
Additionally, she reported an increasing amount of dilute output from her ileostomy for the last 2 weeks, which had been placed 7 years ago for ulcerative colitis. She reported 350 mL of ileostomy output every 2 to 3 hours, or a daily output of 2,800 mL that was clear and watery. Her normal output was 1,500 mL a day. She reported drinking about 1 liter a day of water and juice. She also reported a decrease in appetite over the last 2 weeks. In the last 24 hours, the patient consumed approximately 1,050 calories consisting of 1 banana, 1 coffee with creamer, 1 cup of cottage cheese, ½ cup of tuna with 1 slice of bread, and 2 nutritional supplement drinks. Her normal caloric intake was about 1,750 calories. She had been battling chronic weight loss and malnutrition due to her ulcerative colitis, which had been flaring up more recently in the last 6 months. During this ED presentation, she was still receiving treatment for a recent flare-up beginning 3 weeks prior. She reported a 1.8 kg weight loss in the last 2 weeks. The patient also complained of headache; lightheadedness upon standing; muscle cramps; and abdominal pain. She denied chest pain, palpitations, nausea, and vomiting at this time.
Her past medical history included depression, hypertension, past alcohol use disorder, and a 15-year history of ulcerative colitis resulting in the permanent placement of the ileostomy 7 years ago. Her last reported alcoholic drink was 6 months prior to this current hospital presentation, and her Clinical Institute Withdrawal Assessment for Alcohol, Revised (CIWA-Ar) score was 0.1 Current home medications included: lisinopril 40 mg P.O. daily for hypertension, chlorthalidone 12.5 mg P.O. daily for hypertension, mesalamine 800 mg P.O. three times daily before meals for ulcerative colitis, simethicone P.O. with meals and at bedtime PRN for symptoms of ulcerative colitis, and duloxetine 20 mg P.O. twice daily for depression. She was also taking prednisolone 40 mg P.O. daily due to an acute relapse of ulcerative colitis 3 weeks prior to this ED presentation. Significant family history included hypertension and cardiovascular disease in both parents. Both parents were deceased; the cause of death for the patient's mother was ischemic stroke and for the patient's father was myocardial infarction. The patient was single, having divorced her husband 20 years ago. She has one adult son but has not been in contact with him in more than 5 years. She lives alone in a ranch-style house.
The patient was weak but alert and oriented to person, place, and time. She appeared malnourished with significant muscle wasting on the temples, deltoids, and clavicles. She complained of abdominal pain with soft and deep palpation. Otherwise, the physical exam was normal at this time. Despite her fatigue, she was an excellent historian and advocate for herself describing her past medical history in detail. (See Vital signs recorded throughout hospital stay.)
Initial diagnostic assessment and therapeutic interventions
The NP ordered a comprehensive metabolic panel (CMP) and complete blood count (CBC). Notable findings from the blood work included severe hyponatremia, hypokalemia, hypocalcemia, and leukocytosis. (See Lab results.) The NP calculated a sodium deficit in hyponatremia of 440 mEq using a desired sodium of 135 mEq/L.2 Stool, urine, and blood cultures were also collected at this time to evaluate for potential infection.
Some differential diagnoses from most to least likely included: gastroenteritis, ulcerative colitis relapse, short bowel syndrome, cancer, and chronic fatigue syndrome. Gastroenteritis was most consistent with the patient's clinical presentation and past medical history. Gastroenteritis is associated with dehydration, abdominal pain, and diarrhea or, in this case, watery ileostomy output, and the elevated white blood cell count is suggestive of an acute infection. The resultant dehydration can be associated with fatigue and muscle cramps and corroborated by hypotension. The electrolyte abnormalities were consistent with dehydration and malnutrition. The patient is more vulnerable to acute gastroenteritis secondary to infection because of her significant past medical history of ulcerative colitis and ongoing corticosteroid use. Although most cases of gastroenteritis resolve within 1 to 2 weeks, given the patient's medical history, it is reasonable to assume the duration of her symptoms could be longer.
Based on this clinical reasoning, the NP diagnosed the patient with gastroenteritis and ordered the following interventions: regular diet to encourage nutrition, a nutrition consultation, and a 1,000 mL I.V. bolus of an isotonic I.V. solution containing 140 mEq of sodium, 5 mEq potassium, 3 mEq magnesium, 98 mEq chloride, 27 mEq acetate, and 23 mEq gluconate per liter (Plasma-Lyte) to be administered over 1 hour for fluid and electrolyte replacement.3 The I.V. infusion was started and the patient was transferred from the ED to the medical-surgical unit.
Diagnostic assessment of a new complication
Upon presentation to the medical-surgical unit, she reported new-onset chest pain and shortness of breath. Immediately, the NP examined the patient who now had 2+ pitting edema of the lower extremities with crackles in the lung bases bilaterally. Her breathing became more labored. A new set of vital signs revealed an oxygen saturation on room air of 92% with a respiratory rate of 26 breaths/minute. The NP placed the patient on 3 L of oxygen via nasal cannula with positive effect as the oxygen saturation rose to 96% and the respiratory rate decreased to 18 breaths/minute. Further, the patient's pulse dropped to 72 beats/minute. The patient's quick Sequential (Sepsis-related) Organ Function Assessment (qSOFA) score was 1 (lower risk of poor outcome) due to systolic BP of <100 mm Hg.4 Cardiac troponin, brain natriuretic peptide, CMP, and CBC as well as a 12-lead ECG were collected STAT. (See A resting 12-lead ECG at time of acute complication.) A chest X-ray and transthoracic echocardiogram were ordered afterward. (See Clinical case study timeline.)
The 12-lead ECG was obtained in a resting supine position. The calibration was standard, at 25 mm/s and 10 mm/mV. The ECG showed sinus rhythm at a rate of 72 beats/minute. The P wave axis was +66°, QRS axis was -14°, and the T wave axis was +59°, which are all within normal ranges. The PR interval was 156 ms, which is normal, and the QRS complex duration was 82 ms, which is normal.5 The QT interval was 436 ms and the corrected QT interval (QTc; Bazett formula) was 478 ms, which is prolonged.6 The QRS amplitudes were remarkably small throughout all 12 leads consistent with low voltage.7 Further, the P waves and T waves appeared short and flat.
Compared with a chest X-ray from a previous hospital admission, the chest X-ray showed new findings of pulmonary edema and pleural effusions at the lower bases bilaterally, and the echocardiogram showed a small pericardial effusion with a normal ejection fraction estimated to be 55%.
A result of low voltage on ECG can be due to several causes. The NP believed the low voltage warning and flat P and T waves for this patient were due to several factors: electrolyte imbalance, pleural effusion, pericardial effusion, and peripheral edema.7
Given the evidence from the ECG, chest X-ray, and echocardiogram as well as the timing of these findings coinciding with the fluid bolus, the NP concluded that the patient experienced fluid overload due to aggressive I.V. rehydration in the setting of albumin insufficiency. Although it is necessary to correct for fluid and electrolyte deficiencies, poor colloid osmotic pressure due to hypoalbuminemia resulted in deposition of the fluid into the pericardial, pleural, and interstitial spaces leading to pericardial and pleural effusions and peripheral edema.7 Ongoing corticosteroid therapy for the patient's ulcerative colitis may have exacerbated this process, as it is known to cause interstitial edema.7
The NP ordered the I.V. fluids to be stopped immediately until results of the chest X-ray and bedside echocardiography were reviewed. The patient had received about 750 mL of the fluid bolus. Once the diagnostic assessment was complete, the focus of treatment now included removing excess fluid, closely monitoring for electrolyte disturbances, and assessing for signs of worsening infection. Since this patient had other acute (possible infection, and required monitoring for sepsis) and chronic (ulcerative colitis) conditions, the patient was transferred to a progressive care unit. Furosemide 40 mg I.V. twice daily with spironolactone 100 mg P.O. twice daily was started promptly to remove excess fluid without excessive electrolyte loss. The patient continued receiving electrolyte replacements and small boluses of I.V. fluids to correct the initial hyponatremia, hypokalemia, and hypocalcemia. The speed of correction of fluid overload should be dependent on individual volume status, available treatment options, and an understanding of the underlying pathophysiology responsible for excess fluid.8 Caution is also needed to avoid overly rapid correction of hyponatremia to prevent its complications such as osmotic demyelination syndrome.2 The patient also received a one-time I.V. infusion of albumin 20% 250 mL. Although controversial, the albumin was given to improve the low albumin level and help increase colloid osmotic pressure to draw fluid into the intravascular space. Daily weights and input and output measurements were used to closely monitor fluid balance.8
A cardiology consult was necessary because the patient experienced a small pericardial effusion. Her troponins were elevated indicating myocardial injury and were trended to rule out type 2 myocardial infarction. The downward trend of the troponins was promising, suggesting no myocardial harm. Cardiology had no additional inputs on the plan of care other than a recommendation to hold lisinopril until her medical illness stabilized and BP increased. The cause of the rise in troponin was most likely related to the acute small pericardial effusion, and not ischemic injury.
Follow-up and outcomes
Over the course of 3 days in the progressive care unit, the patient was weaned off oxygen. The stool, urine, and blood cultures returned negative and the patient was not started on antibiotic therapy. She was diagnosed with viral gastroenteritis. The peripheral and central edema resolved with the furosemide and spironolactone, so they were stopped upon discharge. A final set of vital signs collected close to discharge was within normal limits. A repeat CMP and CBC count showed resolution of the electrolyte imbalances, though albumin remained at the low end of normal range at 3.5 g/dL. A dietitian recommended supplemental nutritional drinks to improve dietary protein intake and maintain albumin levels within normal limits. Her nutritional intake significantly improved with support from the nutritionist. A repeat chest X-ray and echocardiogram were obtained to assess for resolution of the pleural and pericardial effusions. Fluid was no longer seen on the X-ray and the echocardiogram showed complete resolution of the pericardial effusion with a normal ejection fraction estimated to be 63%. The patient reported improvement of symptoms and felt that the increased ileostomy output was resolving. Though the output was still higher than her usual baseline, there was a documented downward trend and the patient wished to manage it at home. The day before discharge, the patient restarted her home dose of lisinopril. The patient was discharged home and followed up with her primary care provider 7 days later.
The NP in this case ordered a 12-lead ECG when the patient developed shortness of breath on the medical-surgical unit. The ECG showed low voltage, which is an important warning sign requiring careful and methodical evaluation by the clinician to identify the probable cause. In this case, the NP correctly delineated the probable cause for the low voltage warning to be peripheral edema and pleural and pericardial effusions.
Low voltage is defined as a QRS amplitude of 5 mm (0.5 mV) or less in all of the frontal plane leads and 10 mm (1.0 mV) or less in the precordial leads.7,9 Low voltage can be caused by three main factors: cardiac voltage generation, extracardiac transmission, and equipment-related issues. Cardiac voltage generation refers to conditions that affect the electrical signaling of the heart, such as hypothyroidism, myocarditis, and dilated cardiomyopathy. Extracardiac transmission refers to difficulty for the ECG signal to be detected and transcribed due to increased space between the heart and the measuring electrode. Such conditions include obesity/epicardial fat, pericardial effusion, pleural effusion, and peripheral edema. Last, equipment malfunction or electrode misplacement can produce low voltage. Thus, low voltage requires further follow-up and clinical reasoning is necessary. When an ECG reads low voltage, potential mechanical issues should first be ruled out by repeating the ECG. If lead placement is verified, the cardiograph is in good-standing, and a similar result is produced, the clinician should consider the result valid and troubleshoot the potential etiology. Since low voltage can be associated with pathologic causes, the provider must have a clear understanding of the potential etiologies listed above. Although multiple factors may cause low voltage on the ECG, it is important to identify the leading cause and treat appropriately. Usoro and colleagues reported that among 6,440 participants from the Third National Health and Nutrition Examination Survey, low voltage was detected in 1.4% (n = 89) of participants, and the mortality rate among those individuals was almost twice that compared with those without low voltage (51.1 versus 23.5 events per 1,000 person-years, p < .01).10 A similar finding has been reported among hospitalized patients.11,12 Thus, low voltage is truly a warning sign for the clinician.
Fluid volume shifts causing edema and effusions are major causes of low voltage on the ECG.7,10,13 With greater fluid in the third spaces, the distance between the heart and the measuring ECG electrode increases, which affects extracardiac transmission.7,10,13 Given that the body serves as a volume conductor, increased volume in the form of peripheral edema leads to decreased electrical impedance and attenuated voltage; whereas, pleural effusions increase impendence in the chest, which acts as a conductor ultimately attenuating voltage.7 Thus, there is an inverse relationship between the strength of the electrical signal, best measured by the R wave, and the distance from the heart to the electrode.7,13 Fluid shifts can also be associated with local inflammation.7,13 Inflammation includes the release of mediators that cause vasodilation and increase microvascular permeability permitting increased flow into interstitial spaces.7 Such a pathophysiologic phenomenon with low voltage on the ECG has been described in cases of cardiac tamponade, pericardial effusion, and myocarditis.7,13 In addition, hypoalbuminemia causes edema leading to low voltage on the ECG.7 Interestingly, this patient received an albumin infusion to increase colloid osmotic pressure, which can help reduce edema and, thus, reverse the low voltage reading on the ECG.13,14 It is important to mention that randomized controlled trials studying the effect of albumin have been largely inconclusive among critically ill patients; however, some research suggests the use of albumin and furosemide is effective for managing complex patients with hypoalbuminemia who require diuresis.14-16
Electrolyte disturbances also cause ECG changes.7,17 This patient presented with hyponatremia, hypokalemia, and hypocalcemia. Although hyponatremia has no consistent effect on the ECG, hypokalemia and hypocalcemia do have consistent and measurable effects on the ECG. Hypokalemia is associated with prolongation of the QT interval and T waves that are lower in amplitude.17 In this patient, the T wave appears wide with a low amplitude, and the P wave is also dampened. T- and P-wave amplitudes are not reported automatically on the 12-lead ECG but can be beneficial for the NP to measure. Further, hypocalcemia can lead to lengthening of the QT interval; in this clinical case, the QTc interval is prolonged at 478 ms.5,6,17 Unlike T and P wave indices, the QT interval and QTc interval are automatically calculated on 12-lead ECG recordings.
In some complex cases, etiologies of low voltage may be due to multiple factors. In this clinical case, the peripheral edema and pericardial and pleural effusions in addition to the electrolyte imbalances were causes of low voltage on the 12-lead ECG. It is important to critically analyze the ECG and identify all possible causes for the warning. With that said, it should be noted that ECG is not commonly used to assess fluid volume shifts and electrolyte imbalances. For this reason, a 12-lead ECG at time of discharge was not available. Previous publications have shown a return to normal voltage from low voltage on the 12-lead ECG after extensive diuresis and return to normal electrolyte levels.13
A low-voltage ECG finding requires careful evaluation of the patient in order to clearly identify the probable cause or causes. Although low voltage is not specific to a particular condition, it is important to identify the causes because it is associated with potentially fatal conditions including pleural effusion, pericardial effusion, and myocarditis. In this specific patient case, low voltage was a result of multiple conditions including bilateral pleural effusions and a small pericardial effusion secondary to overly aggressive fluid resuscitation in the presence of hypoalbuminemia with electrolyte imbalances. With clinical reasoning and deductive thinking, the NP correctly evaluated the ECG, identified the likely causes of low voltage corroborated by evidence from imaging, and responded appropriately. The NP performed an assessment that was consistent with fluid overload (edema, crackles in lungs), stopped the ongoing fluid bolus, and transferred the patient to a unit with a higher level of care. Informed by the ECG, the NP expeditiously and appropriately managed the patient's care. As a result, the patient was able to make a full recovery and was discharged home.
The patient was grateful for the excellent care she received. Although her concerns were raised when developing secondary symptoms associated with the fluid resuscitation, she maintained trust in her medical team. At discharge, she was appreciative of the care she received.
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