Sample Write Up #1

Grade:14/15

Grades Committee Member Comments: Pretty much everything was done really well! The data-gathering is complete, systematic and clearly indicates your ddx with pertinent +’s/-‘s mentioned. All of this and it’s not wordy or too long! The discussion shows excellent understanding of the issues and appropriate prioritization of them.

I wished you had covered more explicitly in your discussion one of the very likely causes of his atrial flutter – cardiomyopathy. I’m not sure why you think he had that and what you would do about it. I expect he needs evaluation of his coronary arteries and he certainly needs thyroid function tests.<

Chief Complaint: “My heart was beating fast.”

HPI: Mr. RY is a 57 year old African-American male with a history of hypertension and atrial septal defect repair (15 years old) that was in his normal state of health until two weeks ago (02/21/06) when he began developing intermittent palpitations, chest pain on exertion, and dyspnea on exertion. As they progressively worsened, he presented to his primary care physician with these complaints, and EKG revealed a heart rate between 130 and 150 beats per minute. Although at that time he was asymptomatic, he was referred to the Emergency Department for evaluation.

Before his first episode two weeks ago, he had never felt palpitations this badly before. He rates these palpitations as 10/10 in comparison to any other previous episode of tachycardia. He states that they occur two to three times per day. Each episode occurs suddenly, lasts approximately 5-10 minutes, and then subsides. Nothing specifically brings them on—no time of day, no activities, and no foods. Nothing exacerbates his symptoms, but nothing makes them better either. He did not take any OTC medications for his symptoms at any time. He does not experience any pain with episodes, has not had headaches or visual problems, but does feel some shortness of breath. He must sit down and rest while the palpitations occur, or else he feels lightheaded and slightly nauseous. However, he has never lost consciousness or vomited from any of these episodes.

In addition, he experiences shortness of breath and chest pain on exertion. The symptoms began suddenly around the same time as the palpitations began, with symptoms occurring with mild exertion. He states that he cannot walk up stairs without becoming very short of breath and diaphoretic. This dyspnea is accompanied by a feeling of chest “tightness and pressure,” without radiation into his arm or neck. Rest completely ameliorates these symptoms. He reports trouble sleeping at night if he lays flat, and episodes of paroxysmal nocturnal dyspnea have occurred several times over the past two weeks. He does not report any swelling in his extremities. He admits to a 40+ pack year smoking history. He has not had his flu shot this season. He has no history of rheumatic fever, TIA or stroke, asthma, COPD, MI, GERD, or PVD. He reports no subjective fevers, fatigue, chills, vomiting, headaches, cough, night sweats, weight loss, decreased appetite, sinus pain, ear pain, lymphadenopathy, sore throat, hemoptysis, diarrhea, constipation, joint pains, or numbness/tingling in the extremities.

PMH:

Hypertension, stage 2. Diagnosed in 1992, well controlled with hydrochlorothiazide according to PCP. No significant complications-no vision loss, no CHF, no aortic dissection, no kidney failure, no TIAs or strokes.
Chronic lower back pain-present since 2001, unknown etiology, worked up by both PCP and neurosurgery. Uncontrolled despite attempts with multiple modalities, including short term bed rest, NSAIDs, exercise, physical therapy, acupuncture, and muscle relaxants. He has not tried surgery. No severe complications-no neurologic deficits, minimal missed work, no reduced ambulation.
Methicillin resistant Staph. aureus (MRSA) infection-history of MRSA infection noted in note by PCP. The note failed to give a detailed history, so exact nature of infection unknown. Old records were unavailable and Mr. RY had no knowledge of MRSA.

PSH:

Pt had open heart surgery for repair of an atrial septal defect or patent foramen ovale when he was fifteen years old. He does not remember the exact details of what was done, only that he had a “hole” in his heart fixed. Records were unavailable.
Bilateral total knee replacement in 01/02.
Right inguinal hernia repair at 9 years of age.

Medications:

Skelaxin (metaxolone) 800 mg PO TID for chronic back pain
Ultram(tramadol) 50 mg PO Q4H PRN for chronic back pain
Aleve (naproxen) 350mg PO BID for chronic back pain
Motrin (ibuprofen) 400 mg PO TID for chronic back pain
HCTZ (hydrochlorothiazide) 12.5 mg PO QD for hypertension
1 multivitamin
No OTC medications taken.
No other supplements taken.

Allergies:NKDA

FH:

Mother-still living, age 87. Current problems include type 2 diabetes mellitus, hypertension, and COPD.
Father-passed away age 60 from MI, also had hypertension, kidney disease, and hyperlipidemia
Brother-cocaine abuse, passed away age 35 from MI.
Twin brother-age 57, still living. Type 2 diabetes mellitus.
Sister-age 60, still living. No major health problems.
Sister-age 55, still living. Mild mental retardation, CAD, hypertension.
Children-ages 30, 29. No major health problems.
Grandchildren-ages 2 ,3, and 6. No major health problems.
Extended Family-moderate history of type 2 diabetes mellitus, especially maternal.
Paternal family strongly positive for CAD and MI, including paternal grandfather and uncle.

SH: Pt. is currently divorced, but is engaged to be married again in six months. He is very happy with his current relationship, does not experience very much stress, and is content with his life. He gets along well with his ex-wife. He works as a custodian for a local high school, and enjoys interacting with young people as part of his job. He reports 40+ pack years of smoking, and does not wish to quit despite coaxing from his fiancé and primary care physician. He does not drink alcohol. He admits to recreational marijuana and cocaine use for a brief period of time in his twenties, but says he has not used illegal substances in the past 20 years. He does not exercise because his back bothers him. He tries to eat healthy by eating mostly chicken, fish, and vegetables. He enjoys watching baseball, attending high school sports games, and spending time with his grandchildren.

ROS

Constitutional: no tactile fever, no weight loss, + diaphoresis (see HPI), no chills, no night sweats, no fatigue.
Skin: no rashes, no pruritis, no new spots or pigmentation changes.
Heme/Lymph: no excessive bleeding, no easy bruising, no epistaxis, no otorrhea, no known lymph node enlargement or tenderness, no edema, no pallor, no bleeding from gums.
Head/Neck :no recent head injuries, no headaches, no neck stiffness or tenderness, no dizziness, no loss of balance, no recent loss of consciousness, no neck injuries.
Eyes :no loss of visual field, no blurry vision, no eye pain, no floaters, no light sensitivity, no trouble seeing, no excessive tearing, no dry eyes, no eye itching.
Ears:no loss of hearing, no ear pain, no tinnitus, no ear discharge.
Oropharynx: no dysphagia, no odynophagia, no post-nasal drip, no hoarseness, no mouth ulcers, no tooth pain, no sore throat.
Nose: no excessive discharge, no stuffiness, no loss of sense of smell, no sinus pain
Respiratory: + shortness of breath (see HPI), no cough, + dyspnea on exertion see (HPI), no wheezing, no sputum production, no pleuritic chest pain, no hemoptysis, no positive tuberculin skin test ever.
Cardiovascular: + palpitations (see HPI), + chest pain (see HPI), + orthopnea (see HPI), no claudication.
GI: no nausea, no vomiting, no hematemesis, no abdominal pain, no diarrhea, no constipation, no change in bowel movement frequency, consistency, color, or caliber, no bloating, no melena, no hematochezia, no change in appetite, no food intolerance, no heartburn after meals, no excess flatulence.
GU: no hematuria, no nocturia, no urinary frequency, no dysuria, no hesitancy, no flank pain, no polyuria, no genital ulcers, no urgency, no incontinence.
Neuro: no seizures, no weakness, no paralysis, no syncope, no numbness, no tingling , no tremors, no coordination or balance problems.
Psych: no memory loss, no disorientation, no depression, no suicidal tendencies, no mood changes, no problems with concentration, no excessive anxiety, no problems sleeping.
Musculoskeletal: no joint pain, stiffness, edema, or erythema, no loss of range of motion, no visible joint deformity, no joint trauma, no weakness.
Endocrine: no heat intolerance, no cold intolerance, no weight gain/loss, no polydipsia, no polyuria, no change in body fat distribution, no striae, no buffalo hump, no moon facies, no change in body hair distribution, no new growth of hands, feet, skull, or jaw.

OBJECTIVE

Vitals- T 36.6º P 130-150, irregular R 25 BP 133/89, R arm sitting Pain 0/10 Height 5’ 9” Weight 165 lbs BMI=24.4 kg/m² Orthostatic BP: Supine-132/90 Standing-132/88 O₂ Sat=100% RA

General- Calm, well groomed African-American male in his fifties sitting comfortably in bed. He is appropriately dressed and well groomed. Pt is awake, alert, oriented, and in no acute distress. He can complete full sentences without a problem, no slurred speech. No cyanosis. Good eye contact and appropriate answers throughout interview.

Skin-No pallor noted, skin moist, no excoriation, no visible rashes, no tenderness, no suspicious lesions noted, no digital clubbing noted.

Head/Neck-no visible cranial deformities, no visible cranial trauma, no tenderness to palpation, no visible lesions, no temporal tenderness or pulsations, neck supple, trachea midline, moves appropriately when swallowing, no visible masses, no tenderness to palpation, no sinus tenderness.

Thyoid -borders palpable, no thyromegaly, no nodules or masses noted, moves appropriately with swallowing, no tenderness to palpation.

Lymphatics-no enlargements seen, inguinal, axillary, supraclavicular, epitrochlear, neck nodes all nonpalpable and nontender.

Eyes-no tearing, no conjunctival erythema, no discharge, no lid lag, see neurological exam for visual function.

Ears-hearing intact bilaterally, no external lesions noted on auricles, no tenderness to palpation, minimal brown cerumen present bilaterally, tympanic membranes gray and translucent, no exudates or erythema present, light reflex and bony landmarks visualized bilaterally.

Nose-no obvious deformities, no tenderness to palpation, nares patent, septum midline, nasal mucosa pink and moist without erythema or exudates, no polyps.

Oropharynx-buccal mucosa moist and pink, no visible lesions, no erythema or exudates, uvula midline, no obvious tooth decay or abscesses, tongue midline.

Lungs-muscle and respiratory effort symmetric, no use of accessory muscles, inspiratory/expiratory symmetry noted, clear to auscultation bilaterally, no wheezes, rhonchi, or rales, tactile fremitus symmetric, percussion resonant in all lung fields, diaphragmatic excursion measured as 4 cm bilaterally, no egophany, no decreased breath sounds.

Cardiovascular-Non-visible, non palpable PMI. Large midsternal well healed scar noted. No palpable thrills. Irregular rhythm, tachycardia noted, S1 and S2 clearly auscultated without murmurs, rubs, or gallops. No pulse deficit-carotid, radial, femoral, popliteal, medial malleolar, and pedal pulses all palpated adequately. No bruits auscultated in carotid, renal, or abdominal arteries. No varicose veins seen. Jugular venous pulse assessed by placing patient supine with head elevated at 45º-no abnormally large pulsations or distended veins noted. Cycle of jugular venous pulsations within normal limits.

Abdominal-moderate distension, no abdominal scarring, no visible abdominal hernias or masses, bowel sounds normoactive in all four quadrants, no renal or abdominal bruits, no abdominal aorta pulsations, percussion dull in all four quadrants, no costovertebral angle tenderness, liver span measured by percussion as 5 cm. Liver, spleen, and kidney nonpalpable, no hepatosplenomegaly, no hepatojugular reflux, no palpable masses appreciated. DRE performed-no stool in rectal vault, no prostate enlargement, no mass palpated. Guaiac negative.

Extremities-Pink and warm to palpation, no edema, no erythema, no palpable cords or tenderness, no pulse deficits, no pallor or dependent rubor, negative Homan’s sign, capillary refill 2 seconds throughout.

Neurological- Mental Status: ANOX3, no change in mental status, mini-mental exam=30, sufficient object naming, concentration via serial 7’s, word recall (both immediate and extended), word repetition, 3 step command following, reading, and design copying.

Cranial Nerves- II: all visual fields intact. OD 20/20 OS 20/20, PERRLA. Both pupils constrict to light, consensual reflexes intact. Red reflex present bilaterally, optic fundi visualized, distinct borders bilaterally, no papilledema, no cherry red spots, no venous pulsations, no nicking or other lesions noted. III, IV, VI-Extraocular movements intact. No nystagmus. V-Corneal reflexes intact bilaterally, facial sensation intact and equal bilaterally in V1, V2, and V3. VII-no facial asymmetry or weakness. Eyebrow raise, eyelid close, smile all grossly within normal limits. VIII-hearing intact bilaterally. Oculocephalic reflex intact. IX ,X - palate elevates symmetrically, uvula midline. Gag reflex intact. XI-intact strength of sternocleidomastoid and trapezius. XII-tongue protrusion midline.

Sensation-Light touch, proprioception, temperature intact. No loss of vibratory sense in extremities. Pinprick testing revealed no sensory loss. Monofilament test negative. Negative Romberg test.

Motor-No spasticity or flacidity noted in extremities; normal muscle tone throughout. No pronator drift. Plantar reflexes toes downward, negative Hoffman and Tremner’s sign. No clonus present.

Muscle D B T WE WF HG IL Q

Left 5 5 5 5 5 5 5 5 5 5 5 5

Right 5 5 5 5 5 5 5 5 5 5 5 5 5 5

Reflexes: Normoreflexive throughout. triceps- 2/4 biceps- 2/4 brachioradialis- 2/4 patellar- 2/4 Achilles- 2/4 Jaw- 2/4

Coordination-no dysmetria, no dysdiadokinesia, heel to shin intact bilaterally

Gait-No instability, no difficulty initiating movement, normal stride length. Does not need support to ambulate.

Labs:

CBC- WBC 6.1, hemoglobin 14.3, hematocrit 41.4, MCV 92, platelet count 181, 000. Reticulocyte count was not requested, RDW value not reported.

Differential- N 66 L 25 M 8 E 1 B 0

BMP- Sodium 140, potassium 4.1, chloride 104, bicarbonate 27, BUN 21, creatinine 1.0, glucose 91, calcium 9.3 (no need for albumin correction), magnesium=2.1, phosphorus=3.0, anion gap=9.

LFTs-albumin 3.9, alkaline phosphatase 63, AST 56, ALT 55, total bilirubin 0.4, direct bilirubin ≤ 0.1

CK/Troponin-all cardiac enzymes WNL on admission, 6 hours after admission, and 12 hours after admission.

BNP-82, no previous value available for baseline evaluation.

ABG’s were not drawn

PFT’s were not done

Iron, ferritin studies were not done

Chest X-Ray- PA and lateral films read as: There are median sternotomy wires. The chest wall is otherwise unremarkable in appearance. The heart is enlarged. Mediastinal contours are otherwise normal in appearance. There are no pleural effusions or pneumothoraces. The lungs are clear. Impression: Cardiomegaly, otherwise no evidence for acute disease.

Thorax CT was not obtained

EKG-Rate=134 Rhythm=atrial flutter with 3:1 conduction Axis=-53º Normal QRS and QT intervals in all leads ( QRS<.12 and QT < .45). PR interval normal (<0.2) in impulses propagated through AV node. No signs of infarction-no inverted T waves, no Q waves, no ST segment elevation or depression. No U waves or delta waves noted. No signs of left or right bundle blocks present. No Poor R wave progression noted, left ventricular hypertrophy also noted.

Echo- Left Ventricle-normal in size, no thrombus, normal wall thickness, left ventricular systolic function is moderately to severely reduced, ejection fraction is 25-35%, severe septal hypokinesis, inferior wall akinesis. Right Ventricle-mild to moderately dilated, right ventricular systolic function is moderately to severely reduced. Atria-interatrial septum is intact with no evidence of atrial septal defect, left atrium is severely dilated, the right atrium is mildly dilated. Mitral valve-mild mitral stenosis. Tricuspid valve-mild tricuspid regurgitation. Aortic valve-trace aortic regurgitation. Pulmonic valve-trace pulmonic regurgitation.

PROBLEM LIST

Atrial flutter-the most likely cause of his major symptoms, including palpitations, dyspnea on exertion, poor exercise tolerance, and chest pain on exertion. Also responsible for major signs, including tachycardia and irregular heart beat.
Poor left ventricular systolic function-likely secondary to atrial flutter and contributory to CHF-like symptoms, including dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea.
EKG abnormalities-including left axis deviation, signs of left ventricular hypertrophy.
Other echocardiography abnormalities-including reduced right ventricular systolic function, severe septal hypokinesis, inferior wall akinesis, severe left atrial dilation, mild right atrium dilation, mild mitral stenosis, mild tricuspid regurgitation, trace aortic regurgitation, and trace pulmonic regurgitation.
Chest X-ray abnormalities-including sternotomy wires, cardiomegaly.
Hypertension-essential stage 2.
Chronic lower back pain-unknown etiology.
Tobacco dependence.
MRSA status-previous infection unknown.
Health maintenance-colonoscopy, flu shot

DISCUSSION

Mr. RY presents with many of the typical signs and symptoms of atrial flutter. These include intermittent palpitations, exertional dyspnea, chest pain, tachycardia, and irregular heart beat. Many different disease processes can cause atrial flutter (1), including cardiomyopathy, hypoxia, chronic obstructive pulmonary disease, thyrotoxicosis, pheochromocytoma, electrolyte imbalance, and alcohol consumption; however, the most common causes include idiopathic, coronary artery, and hypertensive heart disease. In fact, “approximately 30% of patients have no underlying cardiac disease, 30% have coronary artery heart disease, and 30% have hypertensive heart disease” (1). Since we know he has several cardiac problems, including a history of atrial septal defect and echocardiogram abnormalities, his flutter is most likely not idiopathic. Furthermore, Mr. RY has one of the major predisposing conditions for atrial flutter, hypertensive heart disease. He was diagnosed in 1992, which means that the disease process has been going on for at least fourteen years, maybe even longer. Despite the primary care physician’s indications that his hypertension is controlled, objective data indicates the contrary. For instance, he has noticeable cardiomegaly on chest X-ray and evidence of left ventricular hypertrophy on EKG. Surely, his hypertension played a role in development of atrial flutter, even if the echocardiogram did not confirm left ventricular hypertrophy. We do not know the status of his coronary arteries, since he has never undergone cardiac catheterization. The only indication that coronary artery disease may play a role include a decreased ejection fraction, septal hypokinesis, and inferior akinesis on echocardiogram. Indications of peripheral vascular disease often reflect the extent of atherosclerosis throughout the body, and consequently act as sentinel symptoms for coronary artery disease. Mr. RY has not had any signs or symptoms of significant peripheral vascular disease. He has had no claudication, no decrease in peripheral pulses, and no history of TIA or stroke. Since we have no direct data regarding the coronary arteries, and he has no other signs or symptoms of vascular disease, no definite conclusions can be made; however, wall motion abnormalities on echocardiogram provide enough evidence to hypothesize a probable role for ischemia in development of flutter.

Another possibility that could have contributed to the development of flutter in Mr. RY is Lutembacher syndrome. Lutembacher syndrome is the combination of mitral stenosis and a left-to-right shunt at the atrial level. Both can be either congenital or acquired. Since he has a history of congenital atrial septal defect, and mild mitral stenosis on echocardiography, his syndrome fits the definition of Lutembacher’s. In addition, Lutembacher’s syndrome is a known cause of dangerous arrhythmias, including atrial fibrillation and flutter. He denies any history of rheumatic heart disease, indicating possible congenital mitral stenosis, which is very rare (2). Since the vast majority of mitral stenoses are rheumatic in origin, it is possible that he had the disease without knowing it. Pathophysiology of Lutembacher’s syndrome involves increased blood flow through the atrial septal defect due to mitral stenosis, which leads to dilation of both atria and right sided fluid overload. Over time, this leads to right sided heart failure. Evidence that such a process has occurred in Mr. RY includes severely dilated left atria, mildly dilated right atria, and severely impaired right ventricular systolic function. Lutembacher’s syndrome also presents with symptoms similar to those of Mr. RY. They include palpitations, exercise intolerance, dyspnea, and fatigue. He did not, however, have any evidence of pulmonary edema or clinical signs of right sided heart failure. He had no jugular venous distension, no hepatomegaly, no heart murmurs, and no peripheral edema. In addition, if Lutembacher’s syndrome has contributed to his symptoms, it must have been present chronically. Since he had surgery to repair his atrial septal defect, at this time his surgeons would have noticed significant mitral stenosis, diagnosed Lutembacher’s, and repaired the disease valve as well. Lutembacher, however, remains a serious consideration in the patient, and should be ruled out before any attempting definitive treatment.

Regardless of whether Lutembacher’s syndrome has contributed, cardiac surgery itself is a risk factor for development of arrythmias, and could be the primary cause of his flutter. According to a recent article, dilation of the cardiac chambers after repair of an atrial septal defect induces a very high likelihood of developing flutter (3). Since Mr. RY has had previous open heart surgery, his atrial flutter may have different treatment options and prognosis than most types of flutter. Most patients with flutter have type I flutter, which activates either clockwise or counterclockwise around the tricuspid valve annulus, with an area of slow conduction between the tricuspid valve annulus and the coronary sinus ostium. In contrast, type II flutters, which emerge after open heart surgery, are less extensively studied, poorly electrically characterized, and have ill defined anatomic barriers. Consequently, they are much more difficult to treat and often recur after a period of sinus rhythm (1). Re-entry sites may arise in the surgical scar itself and often involve the mitral annulus. In addition, type II flutters have a higher atrial rate, lead to more severe cardiomyopathy, are more likely to become atrial fibrillation, and do not respond to pacing. If Mr. RY has a type II flutter, his prognosis is much worse. The only way to definitively distinguish between type I and type II flutters involves examination in an electrophysiology laboratory; however, Mr. RY most likely has a type I flutter, since it has been many years between his open heart surgery and onset of symptoms. In this case, his prognosis could depend on persistence of the arrhythmia. A recent study by Lickfett et al indicates that paroxysmal flutter is much more difficult to ablate than persistent variants (4). Type I flutters often respond to cardioversion, with ablation reserved for recurrent cases, while ablation is the treatment of choice for type II flutters. Regardless of the type of atrial flutter, Mr. RY is in danger of embolism and thromboembolic phenomenon; consequently, he needs to be rate controlled, anticoagulated, cardioverted, or ablated as soon as possible.

Another less likely cause of Mr. RY’s atrial flutter is chronic obstructive pulmonary disease. In general, pulmonary diseases that create pulmonary hypertension are known precipitants of dangerous cardiac arrythmias. He does have a 40+ pack year smoking history, which is a significant risk factor for COPD; however, key findings in patients with COPD are absent in Mr. RY. For instance, he has neither signs nor symptoms of being either a “blue bloater” or a “pink puffer.” He has no wheezing, cough, cyanosis, secondary polycythemia, or weight loss. He does not struggle to breathe at rest, and patients with COPD severe enough to cause arrythmias would most likely have more significant dyspnea than Mr. RY. He does not have hyperresonant percussion, increased expiratory phase, or abnormal breathe sounds on physical exam. His pulse oximetry reading is 100% on room air, an unlikely finding in a COPD patient. In addition, his chest X-ray shows no signs of significant hyperinflation or flattened diaphragms. Unfortunately, pulmonary function testing was not done, so an obstructive pattern can be neither ruled in nor ruled out; however, clinical examination reveals a low pretest probability for COPD. This diagnosis should not be discarded, but kept in mind if flutter is recurrent or if he develops more significant clinical signs and symptoms.

Hyperthyroidism is a definite possibility in this patient as well. Hyperthyroidism is also a well established cause of atrial arrhythmias. It can also cause similar symptoms, including palpitations, tachycardia, and dyspnea. Unfortunately, neither a TSH nor a free T₄was drawn in this patient. The most common cause of hyperthyroidism is Graves disease, which involves autoimmune activation of the thyroid TSH receptor. LATS levels were not drawn in this patient either, but Mr. RY probably does not have Graves disease. He lacks significant stigmata of the disease, including heat intolerance, weight loss, exopthalmos, and tremor. Subacute thyroiditis can cause a transient hyperthyroidism, but Mr. RY lacks typical findings of this syndrome. Usually subacute thyroiditis follows a viral illness. Mr. RY never had symptoms of a viral illness. In addition, this disease presents with a very tender thyroid, which Mr. RY never had either. Toxic multinodular goiter is the last most common cause of hyperthyroid, causing 15-20% of thyrotoxicoses (5). Mr. RY did not have multiple thyroid nodules; in fact, his thyroid did not even have one palpable nodule. Thyrotoxicosis can cause some of Mr. RY’s symptoms, but since he lacks many of the clinical findings of hyperthyroidism, it is lower on the differential diagnosis.

Pheochromocytoma is a definite possibility in Mr. RY, and is a diagnosis that should not be missed, since 10% are malignant. Pheochromocytoma is a catecholamine secreting tumor derived from chromaffin cells in the adrenal gland or in the organ of Zuckerkandl. Intermittent palpitations, atrial flutter, atrial fibrillation, and hypertension are extremely common symptoms in patients with pheochromocytoma, and Mr. RY presents with a series of symptoms that could easily result from catecholamine excess. Because Mr. RY’s symptoms lack certain characteristics of pheochromocytoma, this is a less likely cause of his problems. Pheochromocytoma usually also cause headaches, diaphoresis, anxiety, and a sense of impending doom. Mr. RY felt none of these symptoms. Pheochromocytomas are also very rare in African American patients, and cause hyperglycemia from increased glycogenolysis and gluconeogenesis. In order to make sure he does not have a pheochromocytoma, his urine should be screened for catecholamine breakdown products, including vanillylmandelic acid, and metanephrines . Should this test return negative, pheochromocytoma can effectively be ruled out in Mr. RY due to lack of clinical and laboratory findings. Should the test return positive, treatment with labetolol should be initiated until surgery is performed. Mr. RY most likely does not have a pheochromocytoma, but failure to consider this diagnosis could lead to disastrous consequences.

As a cause of pulmonary hypertension, pulmonary embolism could be behind Mr. RY’s symptoms. The two most common presenting symptoms of pulmonary embolism include tachypnea and tachycardia, both of which Mr. RY has. Dyspnea is a very common complaint, and new onset arrhythmias are common. Pulmonary embolism is a very dangerous condition and requires vigilance for diagnosis; hence, thorough consideration of pulmonary embolism is required for Mr. RY. Unfortunately, arterial blood gases were not drawn, so the presence of hypoxemia, hypercapnia, and respiratory alkalosis cannot be determined. He most likely does not have a pulmonary embolism. He has no fever, no rales, and no audible S₄. His pulse oximetry reads 100% on room air, which is unlikely during a pulmonary embolism. His EKG shows none of the typical patents associated with pulmonary embolism. He has no reason to be in a hypercoagulable state, he has had no vascular insult, and no prolonged stasis. In addition, he has no signs of a deep venous thrombosis. He has no lower extremity edema, no palpable cords, no erythema, and a negative Homan’s sign. Currently, his pretest probability for pulmonary embolism is very low. If it rises, then a spiral CT or a V/Q scan should be ordered to rule out this potentially disastrous condition.

Pericarditis is a known cause of atrial flutter as well. Pericarditis is part of the differential diagnosis for many common complaints, but usually it is low on the list unless classical symptoms are present. Therefore, a high index of suspicion is required for diagnosis, and is important because potential sequelae can be fatal. Pericarditis usually presents with dyspnea, fatigue, and chest pain with relief while leaning forward. Physical exam signs that indicate pericarditis include a friction rub, pulsus paradoxus, and congestive heart failure if constriction impedes diastolic filling. Mr. RY has some similar symptoms, but probably does not have pericarditis. First of all, he does not have a friction rub, his heart sounds are not faint, and his pain is not relieved by leaning forward. He has no predisposing factors for pericarditis, including tuberculosis, recent cardiac surgery, renal failure, infection, or radiation. Additionally, he is hypertensive, he has no pulsus paradoxus, and his EKG does not show signs of pericarditis, like electrical alternans, diffuse ST segment elevation, or low QRS voltage. Considering the lack of clinical symptoms and diagnostic test signs, pericarditis should remain low on the list, but should be kept in mind in hopes of avoiding dangerous sequelae.

Myocardial infarctions have been known to occasionally cause atrial flutter, and could be the underlying cause of his problems. Myocardial infarction associated with atrial flutter has a much graver prognosis. Recurrent atrial flutter after myocardial infarction would paint an even more dismal picture (6). Mr. RY, however, is unlikely to have had a myocardial infarction. First of all, he never felt any of the typical symptoms. He never had any crushing chest pain, no radiating pain, was never diaphoretic, dizzy, or nauseous. While clinically silent heart attacks are not unheard of, they do not usually occur in the general population. They usually occur in elderly diabetics whose neurons have infarcted, or heart transplant patients whose hearts are denervated. Additionally, serial cardiac injury enzymes were completely negative, he had no evidence of leukocytosis or inflammation, and electrocardiogram did not show any ST elevation or inverted T waves. A lack of both clinical symptoms and laboratory findings virtually rules out myocardial infarction as a cause of his symptoms. Regardless, serial cardiac enzymes for the first two days and daily EKGs should be done to make sure he has no infarct. If more evidence of an infarct arises, proper treatment for a myocardial infarction should be considered.

All in all, the most likely contributors to the development of atrial flutter in this patient include hypertensive heart disease, left ventricular systolic dysfunction, and history of previous open heart surgery. Other possible, but less likely causes of his condition include thyrotoxicosis, pheochromocytoma, chronic obstructive pulmonary disease, pulmonary embolism, pericarditis, and myocardial infarction. The best treatment includes adequate management of his hypertension, and cardioversion after exclusion of any contraindications. Transesophageal echocardiogram can determine the presence of thrombus in the left atrial appendage and is indicated as soon as possible. In the meantime, he should be anticoagulated to prevent thromboembolic phenomenon.

PLAN

Atrial flutter-Begin patient on Cardizem drip for rate control. Add B blocker if heart rate is still too high. Begin patient on Heparin for anticoagulation. Perform a transesophageal echocardiogram to make sure there are no thrombi in the atria, and cardiovert as soon as possible. If the flutter recurs or cardioversion is unsuccessful, consider ablation.
Hypertension-make sure the patient’s hypertension is controlled while in the hospital. Titrate hydrochlorothiazide until blood pressure remains in normal range, add ACE inhibitor if still uncontrolled. Add other blood pressure medications as needed.
Poor left ventricular function, chest X-ray, EKG, and echocardiogram abnormalities-adequate control of hypertension can minimize progression of these dangerous abnormalities. Order lipid panel to check for risk factors for coronary artery disease. Institute lipid lowering therapy if needed.
MRSA status-maintain contact precautions throughout hospital stay.
Chronic lower back pain-manage pain with pain medications as needed.
Tobacco dependence-discuss benefits of quitting and encourage. Prescribe nicotine replacement patch and Zyban if patient agrees to try and quit.
Health maintanence-inquire about most recent colonoscopy and flu shot. Encourage if any are not current.

WORKS CITED

1. http://www.emedicine.com/med/topic185.htm

2. http://www.emedicine.com/med/topic3424.htm

3. Lickfett et al. Clinical prediction of cavotricuspid isthmus dependence in patients referred for catheter ablation of "typical" atrial flutter. Journal of Cardiovascular Electrophysiology. 16(9):969-73, 2005 Sep.

4. Lucet et al. Arrhythmias after surgery for congenital heart disease. Archives des Maladies du Coeur et des Vaisseaux. 95(11):1035-9, 2002 Nov.

5. Agabegi, Steven S. Derby, Elizabeth A. Step Up to Medicine. Lippincott Williams & Wilkins, 2005. 351 West Camden Street; Baltimore, MD.

6. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1273025