Chest Pain+ Coughing Up Blood

28 year old man
Fever and chills x 6 days
Productive cough with greenish sputum + blood
Chest pain on inspiration
Smokes pk/day
Marijuana use ,drinks several beers/day

PE
Temp 102.5, Pulse 109, BP 128/76,Resp 23
Cardiac Pulse 110, harsh holosystolic murmur Left lower sternal border
that increases with inspiration
Forearms linear streaks of induration, hyperpigmentation, with nodules

LAB
WBC 17,500

Chest
Multiple peripheral ill defined nodules with cavitation

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Most likely diagnosis?

Infective endocarditis of tricuspic valve with setic pulmonary emboli

“Can’t Catch My Breathe”

72 year old male
Several weeks on increasing SOB
Chest pain on exertion
Hx of lighheadedness
Difficulty sleeping uses two pillows
Wakes up SOB
Bipedal edema
On no meds

PE
Pulse 86 Bp 115/92 Resp 16
Cardiac Normal s1, Normal S2 ,S3 present, systolic mumer at right upper sternal border
Chest rales at bases
2+ Pitting edema

DIAGNOSIS?

Congestive Heart Failure possibly due to Aortic stenosis

Other causes of CHF
Ischemia,hypertension,cocaine, ETOH,thyrotoxicosis, viral myocarditis,hemochromatosis, amylosidosis

LABS
BNP, CHEM 12,CBC,Thyroid levels, Tox Screen

X rays
Chest /Echocardiogram

Treatment
Diuretics, ACE and Beta Blockers

QUESTIONS
55 year oldmale has moderately severe CHF, shihc drug woul;d most likelu lower his risk of mortality

1)ACE
2)Thiazide diuretic
3)Low cholesterol diet
4)ASA

Most likely cause of CHF in patient above?
1)Diabetes
2)Atherosclerosis
3)Alcohol
4)Rheumatic heart Disease

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35 year old woman noted to have significant aortic stenosis. Which of the following would be the most important regarding this patient’s mortality risk

1)Systolic murmer
2)Angina
3)Syncope
4)CHF

“My Ribs Hurt”

A 42-year-old uninsured woman, who had not seen a doctor in 20 years, presented to the emergency department (ED) at 7:50 a.m., complaining of chest pain and trouble breathing. She was accompanied by her husband and her son, who helped interpret because English was her second language. The husband reported that his wife had been experiencing chest pain since 11:00 the prior evening, which she treated with aspirin. In the morning, she had sudden onset of severe chest pain and fainted on her bed.

The patient was first seen by the ED attending and then by a resident. Her initial vital signs were: HR:107, BP:146/99, RR:29. Her chest pain was documented as “sudden onset, right-sided, sharp, under the right breast, started while the patient was lying in bed and worse with inspiration, movement, and palpation.” The patient’s medical history was documented by the resident as: “fainting spells, no family history of coronary artery disease or clots, father suffered a stroke.”

At 8:00 a.m., the patient’s initial EKG evidenced changes, which the ED physicians interpreted as non-specific, possibly due to the rapid heart rate. A chest X-ray did not indicate acute cardiopulmonary process. The differential diagnoses included acute costochondritis, pulmonary embolus, and atypical cardiac chest pain. The patient received IV Toradol for pain, which was reduced within an hour. Her labs were significant for elevated glucose, which was noted as potentially stress-related or non-diagnosed diabetes. At 9:30, a second EKG showed continued tachycardia, HR:103; and improvement of the previous ST wave changes (but still some subtle abnormalities). The ED physicians interpreted the second EKG as reassuring.

At 10:30 a.m., while the patient was still being monitored, the son drove his father to his office so he could make arrangements to be with his wife. When the son returned to the ED at 11:00 a.m., his mother was being discharged with a diagnosis of rib pain, with instructions to follow up with a physician at a local clinic the next day, or to return to the ED for worsening symptoms. Her pre-discharge vital signs (documented at 10:15) were: HR:115 and RR:28. Her last recorded blood pressure (taken at 8:45 a.m.) was 140/99.

About four hours post-discharge, the patient’s family called for an ambulance because of worsening chest pain. The EKG taken en route to the hospital showed signs of ischemia. Paramedics were unable to auscultate a blood pressure, and the patient died in the ED.

Allegation
The patient’s estate file suit alleging that the ED resident and attending negligently failed to diagnose and treat the patient’s cardiac condition, resulting in her wrongful death.

Disposition
The case was settled for more than $1 million against the attending.

Analysis
Clinical Perspective
Because the patient did not present with classic symptoms of chest pain for ischemia and had no known cardiac risk factors, the subtle EKG changes were discounted.

The resident noted subtle changes in the first EKG, which the attending attributed to the patient’s rapid heart rate. The second EKG was interpreted as non-indicative of ischemia. Upon review, several medical experts noted that, while her chest pain was not classic for ischemia, the pain was also not classic for costochondritis. They also interpreted the EKG results as indicative of acute coronary syndrome. Since she remained tachycardic throughout her first ED stay, even after she appeared more comfortable, a safer approach would have been to admit the patient to rule out a cardiac cause of her chest pain.

Although the resident had listed atypical cardiac chest pain and pulmonary embolism in the differential diagnoses, these were not completely ruled out.
The appropriate tests to rule out a pulmonary embolism or myocardial infarction were not done. This emergency department had no clear chest pain protocol. Protocols for common ED presentations, such as chest pain and abdominal pain, help avoid missed opportunities. \

Family Perspective
We were marginalized.
The husband alleged that the ED doctors did not take the possibility of his wife having a heart problem seriously. The diagnostic process and care plan were unclear to the family. After the first series of tests, the son and husband expected that the patient would be in the hospital for a few days. Communication between the providers and the patient/family is vital to help providers glean clues from the previous medical history and history of present illness. And for the family and patient, being informed about the plan helps greatly to alleviate their anxiety.

We were treated different because we don’t have heath insurance.
The family expressed monetary considerations limited the care the patent received. The husband felt the need to tell the doctors, several times, “Please do everything you can; I will pay for it.” Patients and families in the midst of a traumatic medical situation need to be reassured-sometimes repeatedly-that the level of care being rendered is unrelated to their insurance situation.

Risk Management Perspective
A clinician’s narrow diagnostic focus of an atypical presentation led to a wrong decision.
The patient’s complaint, gender, and age were atypical for the presentation of ACS. The attending and resident felt that the clinical presentation and absence of risk factors did not warrant a full cardiac work-up. However, the abnormal EKG changes should have been reconciled.

Inadequate patient assessment led to premature discharge.
The EKGs were only read by the attending and resident prior to discharge. Although the EKG changes were subtle, it was an abnormal EKG in a patient with chest pain. A cardiac consult was not ordered, and providers failed to order cardiac enzymes to rule out an MI. The tachycardia was not really explained and was still present on discharge. Discharge occurred despite the fact that the vital signs were virtually unchanged from the time of initial presentation. In the face of ambiguous findings, the patient would have been better served by being admitted for observation and a cardiac workup.

An interpreter was needed to help this patient give a full account of her symptoms and history.
A patient who speaks and understands some English is a conundrum for emergency clinicians. But, when a patient’s medical history is unrecorded, or when subtle symptom information (e.g., the location, duration, or intensity of pain) is important, a trained interpreter reduces the risk of critical information being missed, or misunderstood. For example, during later testimony, the husband described his wife’s initial pain as starting on her left side and then moving to the center-typical for ischemia. Quite possibly, an interpreter might have clarified this information during the patient’s initial ED examination.

Lack of Documentation
The last set of vital signs was documented 35 minutes prior to discharge…and it was incomplete. The last recorded BP was more than two hours old. Even if a patient is on a monitor, it is important to document the vital signs in the chart, especially prior to discharge.

“My Cough Just Won’t Go Away”

A 50-year-old obese female patient was followed by the same practice for 12 years, beginning in 1992. During this time, the patient, a teacher who spends all day on her feet, was evaluated twice for leg pain and swelling. Ultrasounds both times to rule out DVT were normal.

In November 2003, six years after the last test for leg pain, the patient was seen by a covering physician for sore throat, runny nose, headache, and an ongoing cough of 10 days duration. She was a non-smoker who took oral contraceptives intermittently, and had recently completed a long airplane ride. The physician prescribed amoxicillin; 10 days later, the patient called to report no improvement. The covering physician prescribed another round of amoxicillin and bactrim for her cough. She was asked to come in if the symptoms did not resolve.

The patient did not return until January 9, 2004. She was seen in the office by a covering physician for complaints of cough, fever, chills, and shortness of breath, ongoing for the last few weeks. When evaluated, she had a temperature of 98.2 degrees, pulse 88, respirations 14, and blood pressure 120/80. She was diagnosed with bronchitis and prescribed zithromax, decongestants, steam and robitussin. She was asked to follow up in one week. Later that day the patient called the physician’s office to report that she was experiencing an episode of tachycardia at 120 beat per minute (per the school nurse where she worked). She was advised to start her medications, hydrate, and to get some rest.

On January 12, 2004 the patient returned to the office for follow up on her bronchitis and was seen by her PCP. She reported that her cough had not resolved. In the office, the patient’s respirations were 18 and her oxygen saturation was 88 percent. The patient was given a DuoNeb, which diminished her cough. The patient was also sent for chest X-ray, which was normal. The PCP diagnosed her with bronchitis with an asthmatic component. The patient was to continue with the zithromax, add a Medrol Dosepak, and an albulterol inhaler.

On January 16, 2004, the patient returned to the office with an ongoing complaint of shortness of breath and difficultly breathing. She was seen by her PCP and stated that she has had no improvement from any of her past medications, which included zithromax, guaifed, prednisone, Tessalon, Medrol Dosepak, and albulterol inhaler. During the patient’s workup, her blood pressure was 140/100, pulse 120, temperature 97.8 degrees, respirations 28, pulse oximetry was 96-97 percent on room air and her lungs appeared to be clear. The patient was diagnosed with subjective shortness of breath with probable bronchitis. She was advised to finish the Medrol Dosepak, use her albulterol inhaler prn, and start Advair. The patient was instructed to return to the office for follow up in four or five days.

She died the next day from a pulmonary embolism.

The physician never gave up on the initial diagnosis of bronchitis (only expanding it to include a possible asthmatic component). Several visits for the same problem, with no improvement after treatment and worsening vital signs, should call to mind an expanded differential diagnosis. Atypical presentation of a medical condition can contribute to a narrow diagnostic focus and thus to potential liability for failing to timely diagnose a serious condition. It is a time for seeking more information or considering a consult.

The patient had the following positive risk factors for pulmonary embolism: recent air travel, obesity, past problems with leg edema and pain, intermittent use of oral contraceptives and prolonged standing on her feet at her job; however, the patient was a non-smoker, with no prior DVT or surgery, and no family history for DVT or pulmonary emboli. Although a patient’s preexisting risk factors are mixed, applying them to the patient’s presentation should help raise the appropriate red flags for the physician. Being stuck on a predefined idea about what a condition must “look like,” can delay or obstruct the correct diagnosis. Malpractice cases often feature patients who did not fit the usual profile for their diagnosis, may not have had textbook symptoms, nor, in some cases, any predisposing factors.

Patient Perspective
The patient believed the providers were not keeping track of all the visits and treatments she had experienced over a short time for the same problem; she had been given Zithromax, Guaifed, Prednisone, Tessalon, a Medrol Dosepak, and an Albulterol inhaler to treat her upper respiratory complaints with no improvement over the course of seven days.Summarizing with the patient all that’s been attempted so far lets the patient know that a provider is focused on the patient’s problem and aware of the complexities. A participatory model of care that involves patients in the diagnosis of their own problems can be helpful when the solutions become less obvious. The clinician can openly share the frustration that patients have when a problem isn’t going away. An equally open discussion of alternative explanations can help the patient see the provider’s concern and diligence.

Risk Management Perspective
The patient’s record lacked a recent updated history and physical, though the chart featured multiple risk factors that could have pointed the physician in the direction of pulmonary embolism. Updating and documenting recent patient history can demonstrate that the care was comprehensive. More critically, the updated history can reveal vital clues—such as a recent long trip on an airplane—needed to properly diagnose the current problem. The patient history is not only a key factor in developing the initial differential diagnosis; returning to it and updating it can yield important information when the patient is not responding to a current treatment and the provider is looking for new directions.

As in any busy office practice, this patient was seen by numerous physicians over time. Patients can be seen for numerous episodic visits by whichever covering physician is currently available. This may ultimately impact an individual physician’s evaluation of symptoms, when he or she is not the one to initially treat the current problems or related previous conditions. Systems and practices should be established to allow multiple physicians working in the same office practice to easily document interactions and keep up to date with their patients who have been seen by colleagues.

Bradycardia in a Young Woman

A 53-year-old woman presented to an outpatient urgent care clinic with persistent nausea and vomiting. On the previous evening, she had had an acute onset of nausea that was followed by vomiting and light-headedness. The vomiting had occurred approximately every hour for 18 hours. She had mild discomfort in the chest and abdomen but reported no headache, fever, chills, diarrhea, shortness of breath, or diaphoresis.

These symptoms are nonspecific. The most likely cause is gastroenteritis or gastritis. Other gastrointestinal disorders – including hepatitis, cholecystitis, and pancreatitis – are possible, especially if she is febrile. The persistence of nausea and vomiting also raises the possibility of gastrointestinal obstruction. Knowledge of the quantity and quality of the emesis might help in differentiating the level, if obstruction is indeed the cause. A central nervous system process may cause nausea and vomiting; however, the patient did not have a headache or report other neurologic symptoms. I am concerned about an atypical presentation of an acute coronary syndrome. Women are more likely than men to present without classic chest pain; nausea and abdominal discomfort may be the primary presenting symptoms.

The patient had a history of the irritable bowel syndrome, attention-deficit disorder, hypercholesterolemia, and allergic rhinitis. Her medications included atorvastatin and methylphenidate. She had gone through menopause one year earlier and had been taking estrogen and medroxyprogesterone since that time. A brother had coronary artery disease with an onset before the age of 50 years. The patient had stopped smoking at the age of 40. She reported drinking a glass of wine occasionally, with no recent increase in alcohol consumption, and exercising for three hours per week.

A prescription medication, over-the-counter drug, herb, or supplement can induce gastritis or acute hepatitis or have a neurotoxic effect that might cause her symptoms. Of her medications, statins are associated with a mild increase in the aminotransferase level, but they very rarely induce symptomatic hepatitis. The patient should be asked specifically about the use of aspirin and nonsteroidal antiinflammatory drugs, which have gastric toxicity, and acetaminophen, in view of its hepatic toxicity. The patient’s postmenopausal status, her use of hormone-replacement medications for the previous year, and her brother’s premature coronary disease add to my concern about an acute ischemic event.

On physical examination,
Heart rate of 36 beats per minute, with a regular rhythm, and a supine blood pressure of 110/60 mm Hg. When sitting up, she had a heart rate of 38 beats per minute and a blood pressure of 90/50 mm Hg.
She was afebrile and had an oxygen saturation of 98 percent while breathing room air.
She had minimal tenderness in the right upper quadrant of the abdomen without guarding or rebound.
The cardiac examination revealed no murmurs, gallops, or rubs.
The patient’s lungs were clear on auscultation.
Her extremities were warm, with intact pulses and no edema.
She had no impairment of cognition or memory and no focal neurologic abnormalities.

With the patient’s history of vomiting and orthostasis, I am surprised she does not have tachycardia. Perhaps she has a gastrointestinal illness with an exaggerated vagal response. However, this would be an unusual cause of persistent bradycardia. I would wonder about an underlying conduction defect that predisposed her to an exaggerated vagal response. Although she engages in regular physical activity, it is unlikely that the amount of exercise she reports could account for this degree of bradycardia. Hypothyroidism might cause a sinus bradycardia, but even with increased vagal tone, her heart rate is extremely slow. It is possible that she has the sick sinus syndrome, but she is rather young for this disorder.

The patient might have an underlying infiltrative cardiomyopathy with a conduction defect, such as Lyme disease, sarcoid, or amyloidosis. Undiagnosed congenital heart disease or muscular dystrophy with heart block would be expected to present at a younger age.

I am still very concerned about an acute coronary syndrome, particularly an inferior-wall myocardial infarction with heart block. If this is not an exaggerated vagal response or active ischemia, then ingestion of a drug (such as a beta-blocker, a calcium-channel blocker, or digoxin) or other toxin that causes bradycardia needs to be considered, although the patient reports no such history. At this time, I would order an electrocardiogram, establish intravenous access, give her an aspirin, and call for an ambulance to transport her to the hospital.

The patient was transferred to the emergency department.
On arrival, she continued to have bradycardia, with a blood pressure of 100/50 mm Hg. An electrocardiogram revealed a marked sinus bradycardia at a rate of 36 beats per minute with nonspecific ST-T wave abnormalities . Her initial creatine kinase level was 247 U per liter (normal range, 27 to 218) with an MB fraction of 5.8 ng per milliliter (normal range, 0.0 to 5.0); troponin was 0.0 ng per milliliter. The serum potassium level was 5.2 mmol per liter, and the magnesium level was 1.6 mg per deciliter (0.7 mmol per liter); other electrolyte values were normal, as was the complete blood count. The serum urea nitrogen level was 12 mg per deciliter (4.3 mmol per liter), and the creatinine level was 0.9 mg per deciliter (79.6 micromol per liter). The calcium level was 8.6 mg per deciliter (2.2 mmol per liter), with a normal albumin level. The results of liver-function tests and measurements of amylase and lipase were within normal limits. Toxicologic screening of serum and urine was performed. The findings on a chest radiograph and an ultrasound of the right upper quadrant were normal. The patient was admitted to the hospital.
The electrocardiogram shows profound sinus bradycardia, diffuse ST-segment depressions in a “scooping” or “coving” pattern, and the presence of U waves. There are no Q waves to suggest prior myocardial infarction, and there is normal R-wave progression across the precordial leads.
The diffuse nature of the ST-segment depressions suggests a drug or electrolyte imbalance rather than ischemia. Also, the cardiac enzyme measurements obtained 12 to 24 hours after the onset of the patient’s symptoms are somewhat reassuring. Since she is symptomatic, serial electrocardiography, measurement of cardiac enzyme levels, and cardiac
monitoring are still appropriate, but attention should be focused on diagnoses other than cardiac ischemia.
I am surprised that the serum potassium level is slightly elevated in the setting of vomiting and normal renal function. However, the presence of U waves suggests that either intracellular potassium levels may be reduced or the initial laboratory value was an error. U waves can also be a toxic effect of medication (e.g., quinidine). The sinus bradycardia in conjunction with the concave pattern of the ST depressions also raises the suspicion of a toxic effect of digoxin; however, other drugs can have this effect as well.
The patient continued to have a heart rate in the 30s, with persistent nausea and occasional vomiting. She was given 0.5 mg of atropine intravenously, which was followed by a prompt increase in the heart rate to 70 beats per minute. Additional details of her history confirmed that she had not taken any unusual medications and that her most recent refills of medications did not appear to differ from her usual pills. She reported no recent travel, hiking, or tick bites. She said that she had consumed a salad with dandelion leaves from her partner’s inner-city garden two days before admission and again one day before admission.
With this additional information, a toxic ingestion seems most likely. Eating dandelion leaves is relatively safe, especially when they are eaten as part of a salad. The two most commonly reported side effects of ingesting dandelions are diuresis and an elevation in the blood glucose level.
What else might the patient have consumed or been exposed to that could cause this clinical picture? Her nausea, abdominal discomfort, and bradycardia might indicate organophosphate poisoning. However, the onset of symptoms from excessive acetylcholine activity can occur within 4 hours after pesticide exposure and routinely occurs within 12 hours, whereas this patient’s symptoms started more than a day after she first ate the salad. Also, she did not have some of the other classic symptoms of organophosphate poisoning, such as headache, abdominal cramping, diarrhea, blurred vision with small pupils, excessive sweating, and increased salivation.
Since her bradycardia responded to a small dose of atropine, there is no urgent indication for placement of a temporary pacemaker. If her hemodynamic status became compromised, advanced heart block developed, or she did not have a response to atropine, she then would be a candidate for a pacemaker.
The bradycardia and nonspecific electrocardiographic changes persisted for two days after admission. On the night of the second day, she had a syncopal episode with a five-second pause on telemetry after having a bowel movement (Figure 2). Serial cardiac enzyme measurements remained normal. Repeated tests of potassium and magnesium levels were normal. Toxicologic screening was negative. The level of thyrotropin was normal, and a serologic test for Lyme disease was negative. An echocardiogram showed normal left and right ventricular size and function, without wall-motion abnormalities and with structurally normal valves. An exercise stress test with perfusion imaging revealed no evidence of ischemia. Although the patient said that she had not taken digoxin, the persistent electrocardiographic findings and the absence of a clear cause of her condition prompted a test for serum digoxin on the third hospital day, which showed a level of 1.3 ng per milliliter.

Why does the patient have digoxin in her serum? Possibilities include surreptitious digoxin use by the patient, poisoning by someone else, or accidental ingestion of a cardiac glycoside from consumption of plants containing the compound. Other possibilities include laboratory error and a false positive test result due to the presence of endogenous digoxin-like immunoreactive factors, as has been described, for example, in patients with renal or hepatic disease or in those taking aldosterone inhibitors, such as spironolactone. However, the symptoms and signs that are consistent with digoxin toxicity argue strongly against a false positive test result.
Given the marked bradycardia and electrocardiographic changes with a serum digoxin concentration of only 1.3 ng per milliliter and normal renal function, other sources of glycoside-containing substances should be explored, including plants and herbal medications. Such glycosides may only partly cross-react or may not be detected at all in a standard digoxin serum assay. The serum digoxin level is only a rough indication of possible toxicity. A serum digitoxin level may correlate more closely with symptoms and cardiac manifestations of toxicity.
The patient and her partner reaffirmed that the patient had not taken digoxin. However, the patient’s partner reported that he was growing foxglove in his garden. The patient described where she had picked dandelion leaves for her salad, and he confirmed that this was the location where he was growing foxglove. The digitoxin level, measured on the third hospital day, was 43 ng per milliliter (therapeutic range, 10 to 32).
Digitoxin is the principal active agent in the foxglove leaf. Therefore, the patient’s digitoxin level is consistent with recent ingestion of foxglove. Digitoxin differs from digoxin in that digitoxin has a much higher gastrointestinal absorption, has a longer half-life (four to six days rather than two), is more protein-bound, and is cleared less by the kidneys and metabolized more in the liver. Because the effects of digitoxin are likely to persist longer than those of digoxin, the patient should be monitored in the hospital until her symptoms and bradycardia resolve.
Should the patient be treated with digoxin-specific-antibody Fab fragments? The generally accepted indications for this therapy are persistent hyperkalemia, life-threatening ventricular or supraventricular arrhythmias, hemodynamically significant bradycardia, high-degree heart block that is unresponsive to atropine, and cardiac arrest.
The patient’s nausea and light-headedness began to improve, but her heart rate remained slow, at an average of 40 beats per minute. By the seventh hospital day, her heart rate had increased to the high 40s. The patient’s partner brought in a sample of the foxglove, and the patient immediately recognized it as the plant she had eaten. Analysis of the plant confirmed the presence of digitoxin. The patient was well enough to go home on the ninth hospital day, with a resting heart rate in the 50s.
Commentary
Accidental digitalis toxicity associated with consumption of plants that contain cardiac glycosides is rare. [1] Although foxglove is indigenous to temperate climatic zones, few people consume it because of its bitter taste. [2] Exposure is more common among infants and children under six years of age than among adults. [1] Ingestion may also occur from consumption of contaminated field water near places where these plants grow, from homemade herbal preparations, and from homegrown gardens, as occurred in this case.
Toxicity due to consumption of leaves from the foxglove plant (Digitalis purpurea) produces clinical findings that are similar to those associated with an overdose of digoxin. Although some patients may present with typical side effects, such as gastrointestinal symptoms (nausea, vomiting, anorexia, or diarrhea), others may have central nervous system effects (fatigue, confusion, insomnia, or psychosis), visual effects (seeing yellow “halos” around lights, blurred or double vision, or photophobia), and cardiac effects (palpitations, light-headedness, or chest pain). Such diverse manifestations can mislead the clinician and delay the diagnosis, as occurred with this patient. It should be noted that symptoms associated with digitalis toxicity do not necessarily correspond to the serum digoxin concentration, and a person may have toxic effects at a level that is considered to be normal or therapeutic. [2]
In general, plant-derived cardiac glycosides have properties that affect the myocardium in a manner that is similar to that of digoxin. Cardiac glycosides enhance cardiac inotropy by inhibiting the cellular membrane Na(+))/K(+))-ATPase and ultimately increasing intracellular calcium within cardiomyocytes. [3,4] In addition, cardiac glycosides promote parasympathetic activity, thereby slowing the basal resting heart rate or the ventricular response to supraventricular tachycardia. This patient’s syncopal episode probably occurred because of the higher vagal state associated with having a bowel movement, coupled with the increased parasympathetic activity from foxglove-derived digitalis toxicity.
In addition to foxglove (Figure 3), several other plant and herbal sources of cardiac glycosides may be detected by serum immunoassays for digoxin or digitoxin (as in this case), including woolly foxglove (D. lanata), ornamental oleander (Nerium oleander), yellow oleander (Thevetia peruviana), squill or sea onion (Uriginea maritima), lily of the valley (Convallaria majalis), and ouabain (Strophanthus gratus). [2] Another source of cardiac glycosides is venom extracted from skin glands in certain species of toads (Bufo marinus and B. alvarius). This compound has turned up in some aphrodisiacs and Chinese medications (e.g., chan su). [5,6] Ingestion may cause symptoms and clinical findings similar to those of digitalis overdose, and deaths have been reported. [6]

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Chest Pain in a Pregnant Woman

A 36-year-old woman in her 34th week of pregnancy presented to the emergency department after the onset of severe substernal chest pain. The chest pain was sudden in onset and had awoken her from sleep in the early morning. She also noted diaphoresis and nausea. She did not have dyspnea, dizziness, syncope, hemoptysis, cough, or fever.
The fetal heart rate was approximately 150 beats per minute.

Hypotension and tachycardia may suggest a cardiovascular
condition as the cause of her chest pain,although these findings may also occur during normal pregnancy. Obtaining symmetric blood pressures from both arms would be important, since aortic dissection is possible. The absence of a rub during the examination of the heart sounds makes pericarditis less likely than other possible causes,
but it cannot be completely ruled out. The normal lung examination and oxygen saturation make pneumothorax and pneumonia improbable choices. Pulmonary thromboembolism remains a possibility, despite the normal oxygen saturation.

Electrocardiography showed sinus tachycardia with ST-segment elevation of 1 mm in leads II,III, and aVF

Chest radiography revealed a normal cardiac silhouette with no evidence of pneumothorax, consolidation, or effusion.

Initial laboratory studies revealed the following: hemoglobin, 9.0 g per deciliter; hematocrit, 27 percent; platelet count, 126,000 per cubic millimeter; whitecell count, 7000 per cubic millimeter; sodium,
134 mmol per liter; potassium, 3.6 mmol per liter; chloride, 104 mmol per liter; bicarbonate, 17 mmol per liter; blood urea nitrogen, 5 mg per deciliter (1.8 mmol per liter); and serum creatinine, 0.4 mg per deciliter (35.4 μmol per liter). The coagulation studies, including an activated partial-thromboplastin time (aPTT), were normal.

The results of electrocardiography are consistent with acute myocardial injury in the inferior wall, probably due to occlusion of the right coronary artery.Lateral changes and the ST-segment elevation of 1 mm in lead V1 suggest that the infarction involves the inferolateral wall and right ventricle, respectively. A right-sided electrocardiogram should be obtained.

Although rare, myocardial infarction is a well-described complication of pregnancy and is estimated to occur in 1 in 10,000 women during the peripartum period. Coronary atherosclerosis is
a frequent cause, but this patient has no risk factors for atherosclerosis. Other causes include thromboembolism, a spontaneous coronary-artery dissection, and severe coronary-artery vasospasm.
The normal chest radiograph essentially rules out pneumothorax and pneumonia. Pulmonary thromboembolism also appears less likely than other possibilities Chest pain in a pregnant woman may be the result of various conditions, ranging from benign to life-threatening diseases. Cardiovascular causes include a hypertensive crisis, an acute coronary syndrome, pericarditis, myocarditis, and aortic dissection. Possible
pulmonary disorders are pulmonary thromboembolism, spontaneous pneumothorax, and pneumonia. Peptic ulcer disease, gastroesophageal reflux disease, esophageal spasm, costochondritis, and even herpes zoster should also be considered.
The patient’s previous pregnancies had been complicated by preterm labor and a miscarriage. She had had an ectopic pregnancy two years earlier. Her current pregnancy was complicated by hyperemesis gravidarum, and she had required total parenteral nutrition support through a peripherally inserted central catheter for the past 12 weeks. Her only medication was famotidine. She did not smoke cigarettes or use alcohol. She said she did not use illicit drugs.
This woman’s history of preterm labor and spontaneous abortion suggests the possibility of the antiphospholipid-antibody syndrome. The antiphospholipid-antibody syndrome results in a hypercoaguable state and has been associated with myocardial infarction and pulmonary thromboembolism. It may also be associated with systemic
lupus erythematosus, rheumatoid arthritis, and Sjögren’s syndrome — all of which may cause pericarditis or pleuritis. An additional concern is the peripherally inserted central catheter, which might cause thromboembolism, although this is a rare occurrence.
Differential diagnosis remains broad and includes pulmonary thromboembolism, an acute coronary syndrome, aortic dissection, and pericarditis.
In the emergency department, the patient was alert and in distress from her chest pain. She was afebrile, with a blood pressure of 88/60 mm Hg, a pulse of 108 beats per minute, and a respiratory rate of 20 breaths per minute. Oxygen saturation as determined by pulse oximetry was 98 percent, with the patient breathing room air. An examination of the neck showed no jugular venous distention or carotid bruits, and auscultation of the chest revealed no wheezes or crackles. The heart sounds were normal, and there was no murmur, rub, or gallop. An abdominal examination revealed a gravid abdomen without tenderness. There was no cyanosis, clubbing, or edema of the arms or legs. A peripherally inserted central catheter in her left arm was functioning well. The fetal heart rate was approximately 150 beats per minute.

Hypotension and tachycardia may suggest a cardiovascular condition as the cause of her chest pain, although these findings may also occur during normal pregnancy. Obtaining symmetric blood pressures from both arms would be important, since aortic dissection is possible. The absence of a rub during the examination of the heart sounds makes pericarditis less likely than other possible causes, but it cannot be completely ruled out. The normal lung examination and oxygen saturation make pneumothorax and pneumonia improbable choices. Pulmonary thromboembolism remains a possibility, despite the normal oxygen saturation.

Electrocardiography showed sinus tachycardia with ST-segment elevation of 1 mm in leads II, III, and aVF .
Chest radiography revealed a normal cardiac silhouette with no evidence of pneumothorax, consolidation, or effusion.
Initial laboratory studies revealed the following: hemoglobin, 9.0 g per deciliter; hematocrit, 27 percent; platelet count, 126,000 per cubic millimeter; whitecell count, 7000 per cubic millimeter; sodium, 134 mmol per liter; potassium, 3.6 mmol per liter; chloride, 104 mmol per liter; bicarbonate, 17 mmolper liter; blood urea nitrogen, 5 mg per deciliter (1.8 mmol per liter); and serum creatinine, 0.4 mg per deciliter (35.4 μmol per liter). The coagulation studies, including an activated partial-thromboplastin time (aPTT), were normal.
The results of electrocardiography are consistent with acute myocardial injury in the inferior wall, probably due to occlusion of the right coronary artery. Lateral changes and the ST-segment elevation of 1 mm in lead V1 suggest that the infarction involves the inferolateral wall and right ventricle, respectively.

A right-sided electrocardiogram should be obtained. Although rare, myocardial infarction is a well-described complication of pregnancy and
is estimated to occur in 1 in 10,000 women during the peripartum period. Coronary atherosclerosis is a frequent cause, but this patient has no risk factors for atherosclerosis. Other causes include thromboembolism, a spontaneous coronary-artery dissection,
and severe coronary-artery vasospasm. The normal chest radiograph essentially rules out pneumothorax and pneumonia. Pulmonary thromboembolism also appears less likely than other possibilities
given the clinical presentation and the electrocardiogram, but it is not completely ruled out. Although a widened mediastinum would suggest
aortic dissection, chest radiography is insensitive for this condition. For a dissection to explain the electrocardiographic changes, the dissection
would have to extend into the right coronary artery.
Initial routine laboratory studies show anemia and a mild decrease in the platelet count, and coagulation studies were normal. These findings suggest that a diagnosis of the antiphospholipid-antibody syndrome is not as likely as some other choices. A transthoracic echocardiogram may be helpful at this point, because it can be obtained rapidly with no harm to the fetus and would confirm wallmotion abnormalities due to myocardial infarction. In addition, it might detect dilatation of the pulmonary artery, right ventricle, and right atrium or hypokinesis of the right ventricle, as may be seen with pulmonary thromboembolism. Although such an echocardiogram cannot be used to definitively rule out acute aortic dissection, it may detect an intimal flap in the proximal aorta. However, because “time is muscle,” additional studies should not
markedly delay decisions regarding immediate reperfusion therapy.

Owing to the lack of an on-site cardiac catheterization laboratory, the patient was transferred on an emergency basis to a nearby facility for cardiac catheterization with possible percutaneous coronary
intervention. Before she was transported, an aspirin was given, intravenous heparin and nitroglycerin were started, and a single 5-mg dose of intravenous metoprolol was given. A transient decrease
in blood pressure during transport responded to intravenous fluids and discontinuation of nitroglycerin. Although there is some debate about the relative benefits of transfer for emergency cardiac catheterization
and percutaneous coronary intervention in patients presenting with myocardial infarction with ST-segment elevation, in this case the decision is easier. The cause of this patient’s condition has not been established, and both the mother and fetus remain in jeopardy. Cardiac catheterization would help establish the diagnosis as well as offer
the possibility of definitive treatment. The risk to a third-trimester fetus associated with radiation from the procedure is considered negligible if proper shielding of the abdomen is used. Intravenous
fibrinolysis is an alternative for reperfusion and could be given immediately. However, it is rarely used in pregnancy because of limited data and the potential for bleeding. The precipitous drop in blood pressure with intravenous nitroglycerin suggests right ventricular
involvement, and further use of nitroglycerin should be avoided. Aggressive resuscitation with intravenous fluids is appropriate. Intravenous heparin probably has limited value in this setting and
may be detrimental, because acute aortic dissection with right coronary involvement has not been ruled out.
Transthoracic echocardiography, performed at the second hospital, revealed hypokinesis of the inferior wall and posterior wall, with an overall ejection fraction estimated at 50 percent. The right ventricle appeared to be normal in size and function. There were no other valvular abnormalities noted. The electrocardiogram shows a pattern of myocardial injury that involves the inferior and inferolateral walls with ST-segment elevation and Q waves present. There is also mild ST-segment elevation in V1, suggesting right ventricular involvement.

Electrocardiogram.
The electrocardiogram shows a pattern of myocardial injury that involves the inferior and inferolateral walls with ST-segment elevation
and Q waves present. There is also mild ST-segment elevation in V1, suggesting right ventricular involvement.

Cardiac catheterization on an emergency basis is needed. At this point, the potential benefits of the procedure in guiding management and allowing definitive therapy outweigh its risks, which include
bleeding complications, cardiac arrest, and prolonged arrhythmias
Cardiac catheterization was performed after shielding the patient’s abdomen with a lead apron. Coronary angiography showed a normal left main coronary artery, left anterior descending coronary artery, and left circumflex coronary artery. An injection of contrast medium into the right coronary artery revealed a total occlusion of the proximal
vessel, with contrast-medium staining suggestive of a dissection flap

The cause of a spontaneous dissection of a coronary artery during pregnancy is not well understood. The hormonal and hemodynamic alterations that take place during pregnancy may lead to morphologic
changes in the collagen of coronary arteries and weaken the media layer. Spontaneous coronary-artery dissection may also occur in patients with underlying atherosclerotic plaque, connective tissue
diseases, immunological diseases or Kawasaki’s disease. Regardless, the goal now should be immediate restoration of flow with percutaneous
coronary intervention. A temporary pacemaker was placed in the right
ventricle. Eptifibatide, an intravenous glycoprotein IIb/IIIa receptor blocker, and clopidogrel were given. The right coronary-artery occlusion was crossed and then dilated with balloon angioplasty
several times. Multiple intracoronary paclitaxel coated stents were deployed to tack up the dissection flap. The final angiography revealed no stenosis and normal intracoronary blood flow(The patient’s chest pain resolved, and repeated electrocardiography showed improvements
in ST-segment elevations. The fetal heart rate remained in the normal range throughout the procedure It would be ideal to have a full obstetrical team available if any hemodynamic compromise occurs in
such a case. The interventions performed were reasonable on the basis of clinical-trial evidence from patients who were not pregnant, although data are lacking in pregnancy.
Adjunctive therapy with a glycoprotein IIb/IIIa receptor blocker has been associated with improved clinical outcomes after percutaneous coronary intervention, but it may increase risk of bleeding as a result of inhibition of platelet aggregation; this is a particular concern if an emergency delivery is required. Dual antiplatelet therapy with aspirin and clopidogrel is recommended to prevent subacute stent thrombosis. Stenting —as opposed to traditional balloon angioplasty — is theoretically preferable when coronary-artery dissection occurs, in order to adequately tack down the dissection flap. The role of drug-eluting stents has not been established in this setting.

The patient’s hospital course was complicated by an episode of ventricular fibrillation one day after the percutaneous coronary intervention. She was treated with immediate cardioversion and did not
require cardiopulmonary resuscitation. Three days after this episode, still in her 34th week of gestation,labor was induced, and she delivered a healthy baby girl. After delivery, treatment with an angiotensin-
converting–enzyme inhibitor was begun,in addition to the aspirin, clopidogrel, and metoprolol she was taking already.
An implantable cardioverter–defibrillator was also placed before discharge. An angiotensin-converting–enzyme inhibitor may be beneficial for ventricular remodeling during theearly postinfarction period, but it may not be needed in the long term in the absence of coronary atherosclerosis.
Early use of statins is valuable in most patients with myocardial infarction, but their rolehere is uncertain. The use of an implantable cardioverter–defibrillator is highly controversial in this patient, especially as the episode occurred within 24 hours of her myocardial infarction and her ejectionfraction remained relatively preserved.
The optimal timing for delivery of the fetus after the mother has had a myocardial infarction is unknown. If possible, waiting for up to two to three weeks has been recommended in order to allow for
adequate myocardial healing. Earlier delivery may have been reasonable in this case, given the successful revascularization and the episode of ventricular fibrillation. Data are limited to guide the mode of delivery (vaginal or cesarean). Although an episode of spontaneous coronary-artery dissection is not considered an absolute contraindication
to future pregnancies, it may be best for the patientto avoid them. Of course, this decision requires an individualized approach, because data on the potential for recurrence are limited.Evaluating chest pain in pregnant women can bechallenging. Physicians need not only to distinguish between life-threatening and benign conditions,but also to quickly determine the best and safest treatment options for both the patient and the fetus.With the advent of fetal heart-rate monitoring
and improved antenatal testing, potential jeopardy to the fetus has emerged as both a medical and a legal consideration.However, it is important that maternal health remains the primary determining
factor in obstetrical treatment decisions. During emergency medical conditions, the tendency often is to “order first and think later.” This
is especially true when it comes to diagnostic imaging studies. Even though there is considered to be little risk to the fetus from radiation during the final trimester,the desire to avoid unnecessary exposure underscores the importance of the history,physical examination, and simple tests such as electrocardiography in assessing chest pain in
pregnant women. Fetal heart tones also should be quickly determined in any viable pregnancy, because a fetal status that was not reassuring might alter how the situation is managed. During normal pregnancy, left-axis deviation, ST-segment and T-wave abnormalities, and onsignificant
Q waves in leads III and avF may occur,but they are readily distinguishable in most casesfrom the more pronounced changes observed with acute coronary syndromes.Whereas other conditions
that were considered in this case (such as pulmonarythromboembolism) may produce ST-segment changes, the findings were highly suggestive
of myocardial infarction with ST-segment elevation.Furthermore, the echocardiogram confirmed the suspicion of myocardial infarction and justified the emergency cardiac catheterization. Spontaneous coronary-artery dissection is a rare but well-described cause of acute coronary syndromes. Its true incidence is unknown, since cases are often diagnosed post mortem. Most reported cases have been in young women during the peripartum period or in patients with coronary atherosclerosis.The clinical presentation of a patient with this condition is highly variable and depends primarily on the vessel involved and the rate and magnitude of the dissection. Patients may present with
chronic stable angina, acute coronary syndromes,cardiogenic shock, or sudden death from cardiac causes. Although the exact cause of spontaneous coronary dissection in pregnancy is unknown, it is
believed to relate to structural changes within the blood-vessel wall in response to hormonal changes associated with pregnancy, as well as to hemodynamic stress caused by increased coronary blood
flow during pregnancy. Autoimmune conditions, such as systemic lupus erythematosus and the antiphospholipid-antibody syndrome, have also been linked to coronary-artery dissections. Treatment includes medical therapies to reduce ischemia and revascularization performed on an
emergency basis when indicated. Aspirin, anticoagulantagents, and beta-blockers are safe and immediate options in most patients.
In this case, a decision was made to transfer the patient quickly to a
specialized center with the capability of performing emergency cardiac catheterization and percutaneous coronary intervention for reperfusion. As the discussant stated, fibrinolytic agents in this setting are relatively contraindicated because of the potential risk of maternal hemorrhage. Propagation of spontaneous coronary-artery dissection has
also been described with fibrinolysis. Although surgical revascularization has been used, it is typically reserved for cases that involve
multiple vessels or the left main coronary artery. Percutaneous
coronary intervention — and in particular, coronary stenting — has otherwise been successful at reestablishing flow and tacking down the
dissection flap. The role of drug-eluting stents is unknown in this setting. Drug-eluting stents dramatically reduce the rate of restenosis after deployment in patients with coronary-artery disease. However,
they have not been evaluated in patients with coronary-artery dissection or pregnancy. Paclitaxel has been used only rarely in pregnant women with advanced cancer as a systemic agent.
In this limited instance, the agent caused no apparent side effects in the fetus. The early delivery that occurred three days after treatment with this agent also minimized exposure of the fetus. Ventricular tachyarrrhythmias that occur soon after myocardial infarction are thought to be due primarily to electrical instability and increased sympathetic tone.
As mentioned by the discussant, the use of an implantable cardioverter–defibrillator is controversial in this setting, because in-hospital
ventricular tachyarrhythmias within 48 hours after myocardial infarction have not been consistently associated with long-term survival after discharge.

Lidocaine can be safely used during pregnancy to prevent recurrences of ventricular tachyarrhythmias; however, amiodarone should
not be given because of the potential association with neonatal thyroid dysfunction.

Chest Pain and SOB

Distended Abdomen, Chest Pain, Yellow-Tinged Eyes
By LISA SANDERS, M.D.

1. Symptoms
”I thought it was my smoking, and so I quit,” the patient said flatly. His bright blue eyes peered out of his thin, tanned face. ”But, you know, it didn’t make any difference.” He ran his hand through his graying hair. ”I felt like I was going to drop dead just walking to the TV.”
It started a while ago, he told the young resident in the E.R. He would be out of breath when he walked to the store or climbed the stairs. He had to take everything ”real slow.” Then, a couple of months ago he noticed that his abdomen and legs were swollen — that’s when he went to the emergency room the first time. He was in the hospital for a week and was sent home with diuretics but no answers. He was supposed to follow up with a cardiologist, for further evaluation, but he didn’t. He also stopped taking the medicines. He didn’t really like doctors. Until this started a couple of years ago, he hadn’t been sick since he had rheumatic fever as a child. He came back to the hospital this time only because he was scared and he was too winded to work. ”Hell, I can’t even walk.”
He’d worked as a painter, at least until recently. ”Houses or pictures?” the young physician asked. ”Both,” he answered with an unexpected smile. ”I paint murals.” He laughed at his own well-worn joke then stopped as he gasped for air. He quit smoking a year ago and quit drinking after his last hospital stay. On physical examination, he had an enormous abdomen that contrasted significantly with his well-muscled but slender upper body. His eyes, lively and attentive, made him appear younger than his 59 years. The whites, though, had a pale yellow tinge, and his skin was slightly jaundiced beneath his tan. His left lung sounded normal, but on the right, the resident couldn’t hear his breathing at all. His abdomen was tense and filled with fluid — a condition known as ascites. His liver, too, was large and seemed to throb in rhythm with his heart. His legs were swollen and ruddy. A chest X-ray revealed why the right lung was so quiet. The sack containing the lung was filled with fluid.

2. Investigation

The resident, Dr. Jaideep Talwalkar, carefully reviewed the patient’s chart from his first hospitalization. Though the patient had many tests done, the doctors who cared for him then had not been able to make a diagnosis. They thought that the cause of both the ascites and the shortness of breath would probably be found in either the heart or the lungs. The resident thought this was reasonable. Normally blood is pumped from the right side of the heart through the lungs into the left side of the heart, then out into the circulation. When something gets in the way of the smooth flow of blood, you get a backup. It’s like a construction site on a highway: cars have to slow to get past the workers, and that causes traffic to back up for miles before the obstruction. Same with the heart and lungs: if something blocks the forward flow of blood, it gets backed up and you get fluid accumulating in the heart, the lungs, the liver.
So where was the obstruction? Could it be in the lungs? The patient smoked two packs a day for more than 40 years, so severe emphysema was a real possibility. Just about any disease affecting the fragile lung tissue might produce these symptoms — if the damage was extensive enough. Pulmonary emboli — small clots blocking the flow of blood through the lungs — might give the same picture. Or could it be his heart? This patient did have rheumatic fever as a child. Doctors don’t see this much anymore, but before the widespread use of antibiotics, children who had untreated strep throat could develop heart-valve problems decades after the infection. Most commonly the valves became stiff and narrow, hampering blood flow. The resident thought that this was the most likely cause. So did the first set of doctors. They ordered an echocardiogram — a sonogram that looks at the heart in motion — to seek the suspected narrowed valve. They didn’t find it. The test did show that the heart wasn’t normal — the right side of the heart was stretched with backed-up blood to almost twice its normal size, but no blocked valve was found. Instead they saw a valve that was stuck open. Each beat of the heart sent only half the blood forward to the body, and the other half flowed back into the lungs.
Could this valve defect — known as mitral regurgitation — be the cause of his symptoms? The resident didn’t think so, and neither had the first team of doctors. Usually in mitral regurgitation, the squeezing part of the heart is stretched out and weakened by the constant forward and backward flow of blood. In this patient, both the echocardiogram and physical exam suggested that the heart’s ability to squeeze was unimpaired. Talwalkar ordered a CT scan of the lungs to look for either a clot or evidence of severe lung disease and restarted the diuretics to help the patient get rid of excess fluid.
The CT shed little light. There was no sign of a clot, and while the scan showed some lung destruction from his years of smoking, it wasn’t extensive enough to be the cause of the patient’s symptoms.
”I just don’t get it,” the resident said after outlining the case to the cardiologist he had called for help. Could all this be from the mitral regurgitation seen on the echocardiogram? But the patient’s symptoms didn’t fit the results of the echo. The cardiologist reviewed the fuzzy images from the last hospital stay. ”Get another echo,” he suggested. ”They didn’t get a good look at the valve.” A second echo was done. The reading was the same — mitral regurgitation.

3. Resolution

Despite the diuretics, the patient did not improve. The day after his echo he developed a rapid, irregular heart rhythm and chest pain. Blood tests showed that he hadn’t had a heart attack. Still, he couldn’t get out of bed without feeling the pain or the arrhythmia that left him dizzy and out of breath. Whatever he had, it was getting worse, and the resident was no closer to a diagnosis than the earlier doctors had been.
The cardiologist was undeterred by the second negative test. Everything about this case pointed to a blocked valve. The pumping part of the heart was working fine, and if this condition was a result of mitral regurgitation, that wouldn’t be the case. ”I still think the test is wrong,” the cardiologist told the resident. ”I’ve seen mitral stenosis, and I think that’s what he has. We should do it one more time.” The team decided to order a third echo. This time the resident made sure the technician knew what they were looking for. Finally, the test revealed what they had suspected all along. He had severe mitral valve stenosis — his valve was so blocked that the opening was a quarter of its normal size.
How could this happen? How could a test be wrong not once but twice? The cardiologist paused when I asked him this and then said briskly: ”Mistakes happen, but the bottom line was this: Everything pointed to mitral stenosis except for this test. Given that, most likely it was the test that was wrong.”
The patient listened eagerly as the resident relayed that surgery would be needed to repair his narrowed valve, though, he confessed later, he wasn’t sure he really understood what they were talking about. ”Whatever it takes,” he said gamely. ”Let’s just get this done.”
The next day, he was sent to a university hospital nearby for valve replacement. He got a new valve and was back home two weeks later. I called him recently to find out how he felt. ”I’ve never felt better,” he said. ”I went back to see my doctor not too long ago, and you know what he said? He told me to get the hell out of his office. I was too damn healthy to be there.”
Lisa Sanders is an internist and is on the faculty at the Yale University School of Medicine.

The Don’t Look Stupid Plan

http://applequack.com/2008/10/10/the-drcris-just-dont-look-stupid-study-plan/

have been reading a lot of med student blogs recently, so I am inspired to share my “Just Don’t Look Stupid” Study plan. I still use it regularly when planning my surgical study. I also browbeat any students I come across to try to make them into disciples of the plan. It is my main medical soapbox, so I am surprised it took me so long to share it.
Medical School Teaches Poor Priorities

Medical school is usually taught by clinical. Students get exposed to a wide variety of medical cases, and varied, interesting and rare cases get exposure. This is also a huge downfall of the system. “Unique learning opportunities” mean that bread and butter cases get de-emphasized – they are just not interesting enough.

When medical school is over, you suddenly have to deal with COPD, pneumonia, cardiac failure, and diverticulitis. The “exciting cases” happen maybe once a week or once a month, and will be treated by more senior doctors.

Your overall ability as a doctor will be based on your knowledge of simple every day cases. If you know them back to front, you will shine. If your seniors are busy, you should have the ability to initiate appropriate investigations and treatment for these common conditions. Failing to know details of histiocytosis X or Wilsons Syndrome will not lead to bad reports. But failing to know the best antibiotic for community acquired pneumonia will.
Just don’t look stupid
Stupidly common

Every time you start prep for a new rotation, list the 20 conditions that are most common, and therefore most important.

* Learn them back to front.
* If you are doing clinical rotations, see at least 5 cases for each. If you can’t find 5 cases, you have chosen the wrong 20 conditions.
* Learn all the details of the cases including meds and doses, even though that might not be required at your stage. For these common conditions, you need to know all algorithms without looking it up.

Stupidly important

Once you know those 20 topics back to front, then choose 5 conditions that are uncommon, but life-threatening or catastrophic, or easily misdiagnosed, and therefore important. Learn them back to front as well. See if you can find at least one case to see on each of these five. If you can’t find an inpatient case, then look up a historical patient and write a summary of their illness, and review their investigations.
The rest

Once you have your 25 conditions committed to memory, then you can select another 10, and work through them. These are extra-value. Try to avoid seeing rare cases on your own time as much as possible. The structure of med school will make sure you see enough of the rare stuff. Study to the beat of your own tendon-hammer and concentrate on the important.

If you are clever, you will end up studing most of the stuff you would have anyway, especially if you have multiple rotations in one discipline. This system simply makes sure you learn it in the right order, and you don’t miss something really important.
Selecting the stupidly common

It is not always easy to select the best topics to cover, and they will vary a bit depending on your location. I favour the survey approach.

* Survey all the consultants of your unit, and the registrars/residents you trust. They will each be unable to restrict their list to 20, but compile the suggestions anyway.
* Check the admission diagnoses in your ward for three consecutive mondays.
* Survey the ED presenting complaint lists for three days in a row, and pick any cases that relate to your current rotation.
* Compile all these lists and you should find lots of conditions on multiple lists.
* Choose the top 20.

Continue to avoid looking stupid

As you progress through training, the stupid cases will change. Interns who don’t know really common cases look stupid. Residents or registrars need to know less common conditions to avoid looking stupid, but they need to know them in more depth. Consultants or Fellows need to know really uncommon cases, but only in a very limited field.

This is how I plan my study, and you may not agree. However, you should choose whether you are studying to pass exams, or to be a good doctor. They are different purpose

Chest Pain Quickies

1)28 year old female presents with left sided chest pain at rest and exercise. What to do?

2)68 year old central retrosternal chest pain on exertion .Should you do

a)Exercise ECG
b)Coronary angiogram
c)Exercise Echo
d)Exercies thallium imaging
e)None

3)Most common cause of mitral regurg?
a)Rheumatic dx
b)MV prolapse
c)Endocarditis
d)HBP
e)None

4)Symptoms of aortic stenosis all except
a)Dyspnea
b)Syncope
c)Edema
d)Angina
e)Fatigue

5)27 year old female hx of SOB going up stairs and has palpitiations
PE regualr pulse, loud S1, apical diastolic murmur.DX
a)Aortic Stenosis
b)Mitral stenosis
c)Aortic regurg
d)Tricuspid stenosis
e)None