questions_c

Educational objective: Emphasize importance of hypomagnesemia for correction of hypokalemia.

Educational objective: Review risk factors for cardiovascular disease.

High HDL, which is defined as HDL cholesterol > or = 60 mg/dL, reduces risk of CHD by one and is known as a negative risk factor. Positive risk factors include: Male > or = 45 years, female > or = 55 years or premature menopause without estrogen replacement therapy, family history of premature CHD (male sibling or father who died of CHD before 55 years of age or female sibling or mother who died of CHD before 65 years of age), current cigarette smoking, hypertension (whether taking medications or not), diabetes mellitus and low HDL, which is defined as HDL< 35 mg/dL.

Educational objective: Review risk factors for DVT.

Obesity, malignancy, previous DVT, prolonged immobilization, trauma, estrogen therapy and surgery > 30 minutes are all significant risk factors for DVT.

Educational objective: Review side effects of amiodarone therapy.

Subclinical hypothyroidism evidenced by small increase in serum TSH and low T4 concentrations occurs in approximately 20% of patients treated with amiodarone. Some patients, particularly those with chronic autoimmune thyroiditis, may become overtly hypothyroid. Symptoms can develop from 2 weeks to as late as 39 months after the initiation of the amiodarone therapy.

About 3% of patients in the U.S. who are treated with amiodarone become hyperthyroid between 4 months and 3 years after initiation of therapy. It is more common in iodine deficient parts of the world (in about 10% of patients). It is important to note that symptoms may be attenuated by beta-blocking activity of the amiodarone. Serum TSH level is the best test to diagnose this complication.

Pulmonary disease occurs in 5-15% of patients and is the most common cause of death associated with amiodarone therapy. The pathologic changes include alveolar thickening and exudation associated with dense interstitial infiltrates and fibrosis. The mechanism for these changes is not understood. Symptoms may start as soon as 1 month and as late as 5 years after amiodarone is begun. There is a dose response relationship; in one study no cases were seen when maintenance dose was below 305 mg/day.

Amiodarone can directly cause sinus bradycardia and AV block due to its calcium channel blocking activity. However, of greater concern is the prolongation of repolarization and QT interval due to blockade of the potassium channels. Important to note – incidence of proarrhythmia is very low with amiodarone and incidence of torsade de pointes is below 1%.

A transient rise in serum aminotransferase level is commonly seen after amiodarone therapy initiation. Patients are usually asymptomatic, but the drug should be stopped if there is more than a two-fold elevation because of the potential for cirrhosis and liver failure.

The rest of the side effects include corneal microdeposits, photosensitivity and blue-gray discoloration of the skin, sterile epididymitis, etc.

It has been clearly shown that diabetics benefit from ACE-inhibitor therapy. It is indicated to start ACE-inhibitors in any diabetic with elevated blood pressure, and in the case of documented microalbuminuria, even if the blood pressure is within the normal range because ACE-inhibitors slow the deterioration of kidney function and delay the development of end stage renal disease.

Educational objective: Emphasize importance of exclusion of significant cardiac disease before start of levothyroxine supplementation.

Historically, treatment of patients with myxedema and heart disease, particularly coronary artery disease, was very difficult because levothyroxine replacement was frequently associated with exacerbation of angina, heart failure, or myocardial infarction. Today, when coronary angioplasty and coronary artery bypass surgery are widely available, patients with hypothyroidism and signs and symptoms of coronary artery disease should be first evaluated and treated for their cardiac condition, after which levothyroxine replacement is much better tolerated.

Treatment should be started with IV Heparin bolus followed by continuous infusion titrated to apt approximately twice the control value (in 5% of the patients thrombocytopenia develops). Heparin treatment should be maintained for at least 5-7 days. Low molecular weight heparin (4000-6000 Daltons) is reported to be as effective as or better than conventional unfractionated heparin in preventing extension or recurrence of venous thrombosis (therapy is administered subcutaneously in fixed doses once or twice a day). Warfarin may be administered as early as first day of the heparin therapy if the apt is therapeutic. It is important to overlap heparin treatment with oral anticoagulation therapy for 4-5 days because the full anticoagulant effect of warfarin is delayed. INR should be kept in 2.0 – 3.0 range.

Hemorrhagic diathesis represents a relative contraindication to anticoagulation. All of the other options are absolute contraindications.

In valvular aortic stenosis, the maximum intensity is appreciated over the right second interspace (a thrill may be palpable over the same area). This murmur radiates into the neck and over both carotid arteries. Atherosclerosis in elderly patients and congenital bicuspid valve are the most common causes of valvular aortic stenosis. Supravalvular stenosis has point of maximum intensity somewhat higher, and intensity of the radiating murmur may be more intense over the right carotid artery than over the left. In subvalvular left ventricular outflow obstruction (Hypertrophic cardiomyopathy) the maximum intensity of the murmur is usually located along lower left sternal border or over the cardiac apex. It radiates poorly to the base of the neck. Standing position increases intensity of the murmur of subvalvular left ventricular obstruction and decreases that of the valvular aortic stenosis.

Educational Objective: Review maneuvers for the differentiation of murmurs.

Amyl nitrite inhalation lowers systemic vascular resistance and arterial pressure. These effects will then decrease the severity of the regurgitation as well as the intensity of regurgitant murmurs. In aortic stenosis, the intensity of the ejection systolic murmur will increase due to increased flow across the stenotic aortic valve. In Hypertrophic cardiomyopathy, murmur intensity increases due to an accentuated left ventricular outflow obstruction.

Holosystolic, or pansystolic, murmurs are usually regurgitant murmurs and occur when blood flows from a chamber whose pressure throughout systole is higher than the pressure in the chamber receiving the flow. There are three causes of holosystolic murmurs: mitral regurgitation, tricuspid regurgitation, and ventricular septal defect.

Adverse effects of adenosine therapy occur in 40-60% of patients, but because adenosine’s half-life is short (5-10 seconds), both its intended and side effects are short lived. Caffeine and theophylline are used to counteract effects of adenosine.

The most common cardiovascular side effects of adenosine are facial flushing, chest pain, palpitations, and hypotension. The primary mechanism of action of adenosine is to decrease conduction through the AV node; it can therefore produce a transient first, second, or even higher degree of AV block.

While bradyarrhythmias and AV nodal prolongation are common, transient asystole is a rare complication of adenosine therapy. Patients who develop high-level block on one dose of adenosine should not receive additional doses. More serious arrhythmias may occur, including prolonged ventricular asystole, ventricular tachycardia, nonsustained polymorphic ventricular tachycardia or ventricular fibrillation. Adenosine should be used with caution in patients with a prolonged QT interval.

A few patients have been reported to develop atrial fibrillation after adenosine injection, and incidence may be as high as 12-17% in certain subgroups of patients.

The risk of developing alcoholic cardiomyopathy is related to both the mean daily alcohol intake and the duration of drinking. Most patients in whom alcoholic cardiomyopathy develops have been drinking more than 80 g of ethanol per day for more than 5 years. This corresponds to approximately one liter of wine, eight standard sized beers, or one-half pint of hard liquor each day. The risk is based upon the absolute amount of ethanol so that alcoholics who prefer less strong types of alcoholic beverage (such a beer) are not protected. However, individual susceptibility is important since many heavy drinkers do not develop either cardiomyopathy or liver disease.

The prevalence of alcoholic cardiomyopathy is similar in men and women with no significant differences in age or nutrition. However, when patients were matched for left ventricular ejection fraction, women consumed a significantly lower lifetime dose and lower daily dose of ethanol than men. Thus, women appear to have increased sensitivity for cardiac toxicity of ethanol.

Several studies have demonstrated that cardiac function and size of the left ventricle improve significantly in the majority of patients with alcoholic cardiomyopathy after total abstinence from alcohol. Improvement may be demonstrated as early as 3-12 weeks after the beginning of the abstinent period. However, a certain number of patients does not demonstrate any improvement in cardiac function after being abstinent even for prolonged periods of time, suggesting that the process becomes irreversible at some point. There is good evidence that this point occurs when a significant degree of the myocardial fibrosis develops.

If TEE can be performed, the following approach should be utilized: Administer heparin bolus and continuous drip (PTT 1.5-2.0 times control) and initiate oral warfarin. Obtain a biplane or multiplane TEE after anticoagulation with heparin is achieved to assess left atrial size and to check for the presence of left or right atrial thrombi or possible mitral stenosis. If an atrial thrombus is seen, the patient should receive a minimum of four weeks of therapeutic warfarin anticoagulation (INR 2.0-3.0) and follow-up TEE to document thrombus resolution prior to attempted cardioversion. Patients with thrombi should not be cardioverted. It is probably best to be conservative if severe spontaneous echo contrast is present, the left atrial appendage cannot be adequately evaluated for technical reasons, or TEE is contraindicated. These patients should receive a full 3 weeks of warfarin anticoagulation prior to cardioversion. Among the patients without TEE evidence of thrombus, anticoagulation should be continued to the time of cardioversion, and then continued for 4 weeks after cardioversion in all patients regardless of cardioversion method.

Antibiotic prophylaxis for infective endocarditis when undergoing dental, GI, or GU procedures is only indicated in patients with MVP who have a systolic murmur and/or echocardiographic evidence of mitral regurgitation. Cefoxitin is indicated for certain GI operations for prevention of infection in the operative site. Amoxicillin, erythromycin and clindamycin are all acceptable alternatives for endocarditis prophylaxis in patients with MVP if necessary.

The most common complication of MVP is mitral regurgitation. Bacterial endocarditis is 3-8 times more common in people with MVP than in the general population. The risk of TIA and stroke secondary to embolic phenomena by fibrin and platelet thrombi in a young patient with MVP is <0.05% per year. Of the cardiac arrhythmias complicating MVP, supraventricular arrhythmias are the most common, although in the rare instances of sudden death in patients with MVP, ventricular arrhythmias are most frequently implicated. The incidence of complications in MVP is very low (<1% per year) and generally associated with an increase in mitral leaflet thickness to >5 mm. Young patients (age<45 years) with absence of mitral systolic murmur or mitral regurgitation on Doppler echocardiography are at low risk for any complications.

Congenital stenosis of the aorta, idiopathic calcification of aortic valve, Rheumatic inflammation of the valve, and progressive stenosis of the bicuspid valve are all established etiologic mechanisms of aortic stenosis. Syphilitic involvement of the aortic root usually results in the dilatation of the aortic root, resulting in aortic insufficiency and the development of an aneurysm of the ascending part of the aortic arch.

Educational objective: Review cardiac effects of hypothyroidism. The major cardiovascular changes that occur in hypothyroidism include a decrease in cardiac contractility and mass, a reduction in heart rate, and an increase in peripheral vascular resistance. Symptoms and signs of cardiovascular dysfunction are not common or prominent in patients with hypothyroidism. Exertional dyspnea and exercise intolerance are typical, although these symptoms are probably due to decreased activity or muscle dysfunction in most cases. Bradycardia is the most common rhythm disturbance, but premature ventricular beats are seen, and--rarely--ventricular tachycardia with a long QT interval (torsade de pointes). Approximately 20-40% of patients with hypothyroidism have hypertension, even though cardiac output is reduced. A few patients have a pericardial effusion, which is rarely hemodynamically important. Periorbital edema and nonpitting edema of the hands and feet are characteristic features of hypothyroidism and are due to interstitial accumulation of glycosaminoglycans, with associated water retention.

Educational objective: Emphasizing danger of beta-blockers in patients with bronchospastic disease. Of the offered options only the first two are situations where side effects of beta-blockers may be expected. The other three are situations in which use of the beta-blockers are legitimate. - Beta blockade with nonselective agents may also block bronchodilatation due to bronchial beta-2 receptors. This can lead to increased airways resistance in patients with bronchospastic disease (asthma, COPD). This problem is less likely to occur with compounds with intrinsic sympaticomimetic activity (pindolol and acebutolol) or beta-1 selectivity (atenolol and metoprolol). However, in higher doses selectivity is not absolute and all beta-blockers should generally be avoided in all susceptible patients (also many of these patients are treated with beta-agonists) Administration of carvedilol to patients with CHF caused aggravation of symptoms in only 6% of patients.

Educational objective: Emphasize usefulness of low molecular weight heparin for outpatient treatment of DVT.

Low molecular weight heparin (Enoxaparin) has been repeatedly shown to be safe and effective for treatment of patients with DVT. Enoxaparin 1mg/kg every 12 hrs and Dalteparin 200U/kg daily have been used in clinical trials. Subcutaneous Heparin in prophylactic doses would be insufficient to prevent a recurrent thrombosis in this patient. Aspirin has not been shown to be effective in DVT.

Educational objective: Review diagnostic studies required for evaluation of atrial fibrillation.

Although ischemic events may be associated with atrial fibrillation, they are not an etiology of chronic atrial fibrillation. Over-the-counter medications like pseudoephedrine may precipitate paroxysmal atrial fibrillation, as may alcohol and caffeine, valvular heart disease, and hyperthyroidism.

Educational objective: Review indications for elective cardioversion of atrial fibrillation.

Conditions considered risks for failure of cardioversion include duration of illness greater than one year, cardiomyopathy, uncorrected mitral valve disease, COPD, CHF, LAE, and prior failure to cardioversion.

This patient presents with the clinical picture and EKG presentation of acute inferior myocardial infarction. Different types of rhythm disturbances may occur in this setting. Most commonly seen is sinus bradycardia (40% of patients within first 2 hours, decreasing to 20% by the end of the first day). First degree AV block may also occur and is usually due to occlusion of RCA supplying AV node and is commonly transient, generally resolving in 5-7 days with no therapy. Second degree AV block in inferior myocardial infarction is typically the more benign Wenckebach type (Mobitz type 1). This block is usually transient, resolving in most cases within 5 days. Mobitz type II is uncommon in this setting and occurs more commonly with anterior MI.

Complete heart block with inferior MI generally results from intranodal lesion, and it is associated with narrow QRS complex and develops in a progressive fashion from first to second to third degree block. It often results in an asymptomatic bradycardia (40-60 beats per minute) and is usually transient, resolving within five to seven days.

Any high degree AV block associated with inferior MI is located above the HIS bundle in 90% of patients. For this reason, complete heart blocks often result in only a modest, usually transient bradycardia with junctional or escape rhythms with rates above 40 beats per minute. It is not uncommon for the junctional pacemaker that controls the ventricles to accelerate to more than 60 beats per minute. The QRS complex is narrow in this setting and is associated with a low mortality.

High degree AV block that is located below the AV node is associated with anterior MI; it is usually symptomatic and has been associated with mortality rate approaching 80% (this is mostly due to big losses of functioning myocardium).

Patient in question was able to reach the emergency room very early after onset of the chest pain. So early that cardiac enzymes did not have enough time to rise and allow diagnosis. However, his ECG is suggestive of acute anterior myocardial infarction. The hyperacute phase of the myocardial infarction is characterized with ST-T elevation and increased positivity of T-waves over the affected area of myocardium (high peaked T-waves). In the EKG from this question there is slight elevation of ST-T segment and high peaked T-waves in V2-V4 precordial leads. Repeated cardiac enzymes assays confirmed myocardial injury, and EKG obtained only 30 minutes after the first one revealed marked elevation of ST-T segment in V2-V4 leads.

Massive rhabdomyolysis may cause marked increase in serum potassium level and thus cause peaked T waves in EKG, but this patient has peaked T waves only over the infarcted area, and his K and myoglobin levels are within normal limits. All of this makes rhabdomyolysis very unlikely.

Heat stroke does not present with chest pain, but with hyperthermia, confusion, dehydration, etc.

Spontaneous pneumothorax may present with substernal chest pain, and may be so small that it is hard to diagnose it from the chest radiograph; however this is unusual, and it should not produce changes in EKG.

Esophageal spasm may be very hard to distinguish from anginal pain, but it should resolve on nitroglycerin therapy and should not produce changes in EKG.

The ECG of the patient reveals irregular tachyarrythmia caused by atrial fibrillation. The average rate is about 148 beats per minute. Patient has symptoms of shortness of breath, which may be alleviated by control of the ventricular rate and by administration of oxygen. Control of the ventricular rate by pharmacologic means may be accomplished by the use of calcium channel blockers, by diminishing sympathetic tone using beta-blockers, by increase in parasympathetic tone with vagotonic drugs (digitalis), and by combination of the above drugs. Digoxin is the drug most commonly used in the U.S. for ventricular rate control in patients with atrial fibrillation and acts by vagotonic inhibition of AV nodal conduction. Although digoxin is used most commonly, it is less effective than beta-blockers or calcium channel blockers and has little ability to terminate atrial fibrillation. It is commonly used in combination and should not be used as first-line therapy.

Diltiazem and verapamil are calcium channel blockers used to control the rate in atrial fibrillation. Diltiazem has a less pronounced negative inotropic effect than verapamil, and it can be used intravenously for acute control of the ventricular rate.

Esmolol is a rapid acting beta-blocker that is given intravenously to control the ventricular rate alone or in combination with digoxin. Metoprolol and propranolol can also be given intravenously but have a much longer half-life than esmolol. Oral beta-blockers are widely used as primary therapy for rate control in chronic atrial fibrillation. These medications decrease the resting ventricular rate as well as the heart rate response to exercise.

Theophylline has never been used for any aspect of treatment in atrial fibrillation and in fact has been implicated as one of the causes of atrial fibrillation.

This rhythm is atrial flutter, and it is characterized by the absence of P waves and presence of biphasic “saw tooth” waves (F or flutter waves) at the rate of about 300 beats per minute (range 240-340 per minute). These waves are fairly regular and do not have isoelectric intervals between them. The ventricular response to this atrial activity is usually one half the rate of atrial frequency (this is in absence of atrioventricular (AV) nodal disease or medications that slow AV nodal conduction). That is known as 2:1 nodal conduction and usually results in a ventricular rate of approximately 150 per minute. This is so common that atrial flutter should be considered whenever the rate is 150 beats per minute. The QRS complex is usually narrow (in absence of preexcitation or bundle branch block). In this case AV conduction is not constant and varies from 2:1 to 4:1, which gives a degree of irregular arrhythmia, but typical “saw tooth” atrial activity is clearly visible.

In atrial fibrillation “irregularly irregular” arrhythmia is present, but atrial activity is very irregular and does not follow any pattern. Ventricular response may be very variable.

In atrio-ventricular dissociation there is regular atrial activity (P waves are clearly visible) and regular ventricular activity that is faster than atrial activity (there is not any constant temporal relationship between P waves and QRS complex). In complete heart block there is no relation between atrial and ventricular activity, but in this condition ventricular rate is slower than atrial. This also cannot be normal sinus rhythm since there are no P waves.

The ECG shows a rate of about 62 beats per minute. The P waves are flat but can be seen occasionally. Most important feature seen in this ECG is convex deflection of the J point (point of junction between QRS complex and ST segment). These changes appear to prolong QRS complex and are, in this case, best visible in leads II, aVR, and aVF. This deflection of J point is also called Osborn wave and is seen in severe hypothermia. Mechanism by which this occurs is not known, and this phenomenon resolves with rewarming of the body. In cardiac tamponade ECG may show low voltage, but there are no specific ECG changes seen in this condition.

Pericarditis is characterized with low voltage and diffuse (over all leads) elevation of ST-T segment, and has no effect on length of QRS complex. Hyperthermia is usually manifested as a sinus tachycardia in ECG. Long standing cardiomyopathy has no any specific ECG presentation.

Acute pericarditis is characterized by elevation of ST segment in many leads (usually all leads because of diffuse nature of inflammation), depression of ST segment may be seen in V1 precordial lead, and PR segment depression which, however, is not seen in all patients (50-60%). Low voltage ECG also may be seen. The ST segment elevation is caused because inflammation involves the most superficial layer of myocardium and causes injury. When pericarditis is localized over part of the myocardium (rare occurrence) it may be very difficult to distinguish between acute pericarditis and acute transmural ischemia. The ECG shown in this question has very subtle diffuse elevation of ST segment, low voltage QRS complex and no definite PR segment depression.

ST segment elevation does not resolve completely during the acute phase of MI. This most commonly occurs with anterior infarcts. The features seen on this ECG are associated with the development of a ventricular aneurysm. Marked aneurysm dilatation may preclude effective systolic emptying of the left ventricle by expanding with the increase in intraventricular pressure during the systole. This leads to diminished stroke volume, cardiac output, pulmonary congestion, exercise intolerance, etc.

Confirmation of the diagnosis is most effectively made by echocardiography. Radionuclide ventriculography, Thallium imaging, and cardiac catheterization also have the ability to demonstrate aneurysms, but these methods are slower and more invasive; ventriculography and Thallium imaging may only be able to detect large abnormalities.

This patient presents with clinical signs of hyperkalemia. This is suggested even more by his high potassium level two days ago, prior to the hemodialysis. Finally, his EKG demonstrates marked prolongation of the QRS complex and high peaked T-waves. Hyperkalemia causing such changes on EKG is a medical emergency and should be treated without waiting for laboratory confirmation of hyperkalemia.

The first drug to be administered in this situation is calcium (for the stabilization of the electrical properties of the cell membranes). Calcium may be given as gluconate or chloride. Chloride has three times the relative calcium content per volume as calcium-gluconate.

After calcium is given, patient should receive one vial of 50% dextrose (50 ml) intravenously followed by a bolus of regular insulin. This results in a shift of the extracellular potassium into the cells and temporarily relieves hyperkalemia (improvement in the EKG changes should be observed).

All of these actions do not diminish total body potassium stores, and to accomplish this in this patient, urgent hemodialysis is indicated (due to EKG changes). In cases with no such changes, a slower method, administration of sodium polystyrene (cation exchange resin) by mouth or as enema may be used.

Sodium bicarbonate also may be used, but not in the solution containing calcium because of precipitation.

Educational objective: Emphasize cough as an important side effect of all ACE inhibitors.

All angiotensin-converting enzyme (ACE) inhibitors cause dry cough in patients taking them (6-25% of all patients). All of them are equal in ability to produce dry cough, and substituting one for another has no place in dealing with this side effect. However, in mild cases the medication may be continued. In more severe cases change to another antihypertensive agent may be advisable. Angiotensin II receptor inhibitors are considered the best replacement drug in patients with diabetes in whom the protective effect on proteinuria and renal failure is of great importance.

This patient has no history of coronary artery disease, and his normal physical examination and EKG finding make anginal equivalent unlikely as a cause for his cough. This patient also has no risk for recurrent aspiration, and has a normal examination of the lung, as well as a normal chest x-ray.

There are no signs of congestive heart failure (peripheral edema, shortness of breath, S3, crackles or rales on lung auscultation, etc.) or infection (fever, sore throat, productive cough, etc.).

Ref: Simon SR, Black HR, Moser M at all. Cough and ACE inhibitors Arch Intern Med 1992: 152(8), 1698-700.

Educational Objective: Review a common problem in differential diagnosis of ascites.

Both cirrhosis and heart failure produce ascites as a result of portal hypertension, and the serum-ascites albumin gradient will be >1.1 in both. The ascitic protein level in cirrhosis is typically <2.5 g/dl but in heart failure is >2.5 g/dl.

Educational Objective: Illustrate hepatotoxic effect of amiodarone.

Twenty to thirty percent of patients on amiodarone will have a transient elevation of their aminotransferase levels. If it is prolonged or about twice normal levels they should have the drug discontinued or undergo a liver biopsy looking for progressive non-alcoholic steatohepatitis which may progress to micronodular cirrhosis.

Pregnancy is a relative contraindication, all of the others are absolute.

On the boards, ALWAYS look for the young innocent patient to have either an STD or some illicit drug activity. The serum toxicology will show cocaine.

Wolff-Parkinson-White syndrome is demonstrated in this ECG. Catheter ablation is the best approach to treatment.

Caused by the closing of the mitral valve. Decreased in AR, calcified mitral valve, and long PR interval Increased in Mitral stenosis, short PR interval

Persistently split S2 (widened S2) is due to pulmonic stenosis, PE, and RBBB (all cause delayed function of right ventricle.)

An aortic dissection is an intimal tear in the aorta resulting in hematoma formation. Accumulating blood in false lumen of arterial wall leads to propagation of the dissection. A CT or MRI can quickly provide the diagnosis.