A 64-year-old man was brought to the emergency department after an episode of dizziness followed by complete loss of consciousness. According to the patient’s daughter, he was resting at home when these symptoms occurred. He regained consciousness within 1 minute without any residual symptoms. There was no history of seizure activity, weakness, or numbness. He denied blurred vision, chest discomfort, and palpitation. His medical comorbidities were uncontrolled hypertension and chronic kidney disease. The medical regimen included metoprolol succinate, lisinopril, spironolactone, and furosemide. There was no significant family history noted. Upon arrival, vital signs were blood pressure of 123/75 mm Hg, heart rate of 37 bpm, respiratory rate of 16 breaths/min, and oxygenation of 95% on room air. The physical examination was notable for sinus bradycardia but otherwise unremarkable. The 12-lead ECG is shown in Figure 3.1.1. The laboratory data revealed potassium of 7.8 mEq/L and creatinine of 2.5 mg/dL. Imaging of the chest and head was negative. How would you manage this case?
This patient developed third-degree atrioventricular (AV) block or complete heart block (CHB) secondary to hyperkalemia. The patient has known chronic kidney disease and has been treated with medications including angiotensin-converting enzyme (ACE) inhibitors and mineralocorticoid antagonists, which are known to cause hyperkalemia. Treatment of the underlying cause, particularly hyperkalemia, is important and includes insulin with dextrose, β-adrenergic agonists, such as albuterol, and resin binders. Furthermore, stabilization of the cardiac membrane with intravenous calcium gluconate is a key step in the management of hyperkalemia.
Third-degree AV block or CHB should be considered as a differential diagnosis in the evaluation of syncope, especially in patients with underlying cardiac diseases. It occurs due to a defect in the AV conduction system that results in the inability of impulses to be conducted from the atria to the ventricles, thereby leading to dissociation of atrial and ventricular contraction. CHB can be due to many conditions, including electrolyte abnormalities such as hyperkalemia; hypoxia; ischemia/infarction; medications such as antiarrhythmic therapy; infiltrative diseases such as sarcoidosis, amyloidosis, multiple myeloma, and hemochromatosis; collagen vascular diseases such as systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis, and ankylosing spondylosis; infectious diseases such as Lyme disease, Chagas disease, rheumatic fever, and myocarditis; iatrogenic causes such as cardiac surgery; and congenital causes.
Symptoms of CHB include dizziness, loss of consciousness, chest pain, dyspnea, diaphoresis, and even sudden cardiac death. Occasionally, patients remain asymptomatic or have minimal symptoms. Physical examination findings may include hypotension, bradycardia, and elevated jugular venous pulsations with cannon a waves. These patients commonly present with acute heart failure symptoms.
The 12-lead ECG is characterized by bradycardia and regular P-P and R-R intervals; however, there is dissociation between P waves and QRS complexes. Evaluation of electrolyte abnormalities, toxicology screen, and workup for ischemic, infectious, and autoimmune etiologies should be performed based on suspicion. Transthoracic echocardiography can reveal underlying structural heart disease. Treatment of the underlying cause might reverse the CHB. The management depends on the hemodynamic status of the patient. Advanced cardiac life support measures and temporary pacing (transcutaneous or transvenous) are of utmost importance. Atropine can be also be used as a temporary measure. A permanent cardiac pacemaker should be implanted in stable patients once the offending agent has been discontinued.
Key Points
Treatment of the underlying cause of CHB and maintenance of hemodynamic stability are important in managing any type of symptomatic heart block.
Hemodynamically unstable patients with CHB can be treated with atropine.
Permanent pacemaker implantation is the definitive treatment for refractory CHB.
A 53-year-old man presented to the emergency department complaining of dizziness for 2 weeks. He reported a “room spinning” sensation, especially when standing up from a seated position. These episodes have been ongoing for the past 2 months but have lately worsened to the point where he is unable to get out of his bed. He denied experiencing nausea, vomiting, blurred vision, loss of consciousness, neurologic deficit, and palpitations. His medical conditions included uncontrolled diabetes mellitus with retinopathy, peripheral neuropathy, and chronic low back pain. There was no significant family or social history noted. Upon arrival, his vital signs showed a blood pressure of 110/90 mm Hg in the supine position and 90/78 mm Hg in the standing position and a pulse rate 82 bpm. The physical examination was unremarkable with the exception of decreased sensation in the bilateral lower extremities (sock-and-glove distribution). The 12-lead ECG demonstrated normal sinus rhythm without ST-T wave changes. Initial laboratory data revealed blood glucose of 240 mg/dL and normal blood cell counts, electrolytes, thyroid function, and liver enzymes. A CT scan of the head was negative. How would you manage this case?
This is a case of orthostasis caused by autonomic dysfunction secondary to uncontrolled diabetes mellitus. Assessment of orthostatic vital signs is a key step in the assessment of dizziness and syncope cases. These patients typically present with dizziness on changing positions (postural dizziness). Cardiac and neurologic causes should be excluded based on a detailed history and physical examination. Tight glycemic control is the cornerstone in management.
Orthostatic hypotension is defined as a decline in systolic blood pressure of 20 mm Hg or diastolic blood pressure of 10 mm Hg or greater within 3 minutes of changing position from the sitting or supine position to standing position. This occurs when the body’s normal regulatory mechanisms to maintain blood pressure are unable to compensate with postural changes. There are many causes for autonomic dysfunction, including volume depletion; endocrine disorders such as adrenal insufficiency, hypoglycemia, and uncontrolled diabetes mellitus; neurologic conditions such as Parkinson disease, idiopathic orthostatic hypotension, multisystem atrophy, and Lewy body dementia; and cardiac conditions such as arrhythmias, valvular heart disease, and heart failure. Other causes include drugs, pregnancy, or prolonged immobilization.
Symptoms of orthostatic hypertension include dizziness, loss of consciousness, generalized weakness, blurred vision, and diaphoresis.
Diagnosis and treatment of the underlying cause are recommended. Assessment of orthostatic vital signs should be performed and is considered high-value care. However, supportive laboratory tests to exclude other etiologies can be considered on a case-to-case basis. Routine testing includes blood cell counts and basic chemistry panel, 12-lead ECG, Holter monitoring, transthoracic echocardiography, and stress and tilt-table testing. Patients with suspicion of neurologic deficit should be evaluated using appropriate imaging studies. The most important part of management is identification of the cause. Hydration, glycemic control, medication reconciliation with avoidance of the offending medication, and use of compression stockings are a few management strategies. Avoidance of abrupt positional changes and use of safety positions should be advised. If conservative management remains unsuccessful, then medications such as midodrine and fludrocortisone can be used with caution. Some of the second-line medications for orthostatic hypotension include nonsteroidal anti-inflammatory drugs, caffeine, and epoetin alfa.
Key Points
Assessment of orthostatic vital signs is the best and most noninvasive method for the diagnosis.
Treatment of the underlying cause of orthostatic hypotension is key in management.
A 46-year-old man presented to the emergency department with complaints of intermittent dizziness for 2 weeks. He stated that he developed an abrupt onset of dizziness when sitting up and with quick changes in position. The dizziness was described as the “room spinning” around him and was associated with a nauseated feeling and vomiting. He had similar episodes in the past that resolved spontaneously, but this time, the dizziness remained persistent. He denied any hearing loss, tinnitus, focal neurologic deficits, or fever. His medical history was significant for uncontrolled hypertension, for which he takes amlodipine and losartan. There was no significant family history. He denied smoking and recreational drugs but drinks alcohol occasionally. He works as a parking lot attendant. Upon arrival, the vital signs were noted to be stable with negative orthostatic measurements. The physical examination demonstrated vertigo with head movements, especially when sitting up from the examination table and with horizontal nystagmus. The gait was normal. Other cerebellar signs were negative. Head CT scan did not show any acute findings. Initial laboratory data, including blood cell counts and electrolytes, were within normal limits. He was transferred to the telemetry floor for further evaluation. How would you manage this case?
This patient presented with intermittent vertigo of 2 weeks in duration. The history and physical examination suggest a positional component with horizontal nystagmus. Presence of intermittent episodes of postural dizziness, nauseated feelings, and negative neurologic signs are suggestive of peripheral vertigo. The management includes head repositioning by various maneuvers and vestibular rehabilitation. Although uncontrolled hypertension can be a cause of central vertigo, other components of the history are not consistent with the diagnosis.
Peripheral vertigo can be caused by benign paroxysmal positional vertigo (BPPV), vestibular neuronitis, Ménière disease, perilymphatic fistula, vestibular schwannoma, aminoglycoside toxicity, and migraine headache. BPPV is the most common cause and consists of positional dizziness due to an abnormality of the semicircular canals. The onset is usually sudden, lasting for days to weeks, but can sometimes extend for months. The positional vertigo triggers nystagmus when the head is turned to one side. Severity of the disease can vary from mild to severe dizziness even with minimal head movement, and severe disease can be associated with other symptoms such as a nauseated feeling and vomiting. These patients typically have symptom-free periods in between episodes.
Positional vertigo is the typical presentation in this condition. Nystagmus of limited duration is classic. Severe BPPV will have associated nausea and vomiting. The presence of additional clinical signs and symptoms should lead to further evaluation of other causes of vertigo.
Careful and focused clinical history is the key in the diagnostic approach. Diagnosis is made using the Dix-Hallpike maneuver, which produces nystagmus of limited duration. However, a negative test does not exclude BPPV. The remaining physical examination of these patients is usually normal. The Dix-Hallpike maneuver is performed by changing the patient’s head position rapidly from the sitting to the supine positon with head tilted to one side by 45 degrees. The patient is then seated again from the supine position and observed for nystagmus. The procedure is repeated on the opposite side and the patient observed for nystagmus. Other neurologic and otologic causes of vertigo need to be excluded because they can be present concomitantly with BPPV. The treatment of BPPV includes canalith repositioning using Epley maneuver and observation as this condition usually resolves by itself. Other treatment options include medications such as vestibular suppressants, rehabilitation, and surgery. Surgery is usually the last option for refractory symptoms and if the other options remain unsuccessful. Surgical options include labyrinthectomy, posterior canal occlusion, singular neurectomy, and vestibular nerve section.
Key Points
BPPV typically presents with a sudden onset of positional vertigo associated with nystagmus.
Vertigo is usually intermittent and precipitated by a specific position.
Diagnosis can be made using the Dix-Hallpike maneuver.
Treatment includes the Epley maneuver and observation as this is usually a self-resolving condition.
A 32-year-old man presented to the emergency department with complaints of intermittent palpitation and dizziness for 2 weeks. Additionally, he reported a brief episode of loss of consciousness 1 day ago. He was working but suddenly passed out and regained consciousness very quickly. There were no preceding events, and he never experienced similar symptoms in the past. He denied fever, seizure-like activity, postictal confusion, and any neurologic deficits. His medical history was significant for obesity and sickle cell trait. The medication history included chloroquine, which he recently began taking for antimalarial prophylaxis due to an upcoming trip to West Africa. The family history was negative for cardiac diseases. The social history was negative for any illicit alcohol or illicit drug use and smoking. Upon arrival, the vital signs were within normal range, and orthostatic measurements were also negative. The physical examination was completely unremarkable. The 12-lead ECG showed normal sinus rhythm without ST-T–wave changes and a QTc interval of 536 millisecond. The electrolytes were normal. Toxicology screen was negative. CT scan of the head was normal. The patient was admitted to the telemetry floor. What is the next step in management?
This case projects the importance of drug-induced arrhythmia (acquired prolonged QT interval) in a previous asymptomatic patient. With the exception of obesity, this is a young patient with no other risk factors for cardiac, neurologic, or vasovagal etiologies who presented with intermittent palpitation and syncope of new onset. The recent use of chloroquine, which is known for causing prolongation of the QTc interval, may lead to torsades de pointes and sudden cardiac death. Careful review of the medication history is the key in the diagnosis. Electrolyte assessment, transthoracic echocardiography, and telemetry monitoring should be performed.
Prolongation of the QT interval is estimated by the 12-lead ECG showing QTc >440 milliseconds in men and >460 milliseconds in women. A patients with a QTc interval >500 milliseconds is at greatest risk for sudden cardiac death. Acquired QT prolongation is separate from the inherited condition and is mainly caused by electrolyte imbalance or medications. Multiple medications are known to cause QT prolongation (Table 3.4.1). Congenital QT prolongation is seen in conditions such as Romano-Ward syndrome and Jervell and Lange-Nielsen syndrome. Other causes such as hypothyroidism, connective tissue disorders, and infections including HIV should be considered. The condition needs to be carefully addressed as it may lead to fatal arrhythmia such as torsades de pointes and sudden cardiac death.
| Antiarrhythmics | Quinidine, procainamide, disopyramide, flecainide, propafenone, amiodarone, sotalol, dronedarone, dofetilide, ibutilide |
| Antimalarials | Quinidine, artemether, chloroquine, halofantrine, lumefantrine |
| Antibacterials | Azithromycin, erythromycin, clarithromycin, roxithromycin, telithromycin, metronidazole, ciprofloxacin, gatifloxacin, levofloxacin, moxifloxacin, ofloxacin, telavancin |
| Antifungals | Fluconazole, itraconazole, ketoconazole, voriconazole |
| Antivirals | Efavirenz, lopinavir, ritonavir, saquinavir |
| Antipsychotics | Chlorpromazine, haloperidol, thioridazine, aripiprazole, asenapine, clozapine, olanzapine, paliperidone, perphenazine, quetiapine, risperidone, ziprasidone |
| Antidepressants | Tricyclic antidepressants, selective serotonin reuptake inhibitors, trazodone |
| Miscellaneous | Methadone, buprenorphine, loperamide, ondansetron, domperidone, metoclopramide, donepezil |
Symptoms include palpitation, dizziness, loss of consciousness, and sudden cardiac death.
The management mainly depends whether the patient is hemodynamically stable or unstable. The hemodynamically stable patient should be observed on a telemetry unit with serial 12-lead ECG testing after removal of the precipitating agent. Electrolyte imbalances (hypocalcemia, hypokalemia, and hypomagnesemia) should be corrected and drugs prolonging the QT interval discontinued or, if necessary, tapered under a monitored setting. Cardiac monitoring is essential until the QT prolongation is resolved. If the patient develops torsades de pointes but remains hemodynamically stable, intravenous magnesium is the drug of choice. Isoproterenol can be used if the arrhythmia is refractory to magnesium therapy.
In hemodynamically unstable or pulseless patients, the Advanced Cardiac Life Support (ACLS) protocol should be initiated, and unsynchronized cardioversion should be performed. Lidocaine (class Ib antiarrhythmic drug) shortens the QT interval and may be effective, especially for drug-induced torsades de pointes. Class Ia, Ic, and III antiarrhythmic agents should be avoided. Congenital long QT syndrome should be treated over the long term with β-adrenergic antagonists and an automatic implantable cardioverter-defibrillator (AICD) with pacemaker backup. Family members should be evaluated.
Key Points
Acquired prolonged QT interval should be evaluated with detailed history and medication review.
Inpatient admission and management with telemonitoring and serial 12-lead ECGs are needed because the patient is at risk for torsades de pointes and even sudden cardiac death.
Treatment of the underlying cause is of primary importance.
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