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Anterior wall myocardial infarctions are associated with an increased risk of arterial thromboembolism. Therefore, these patients require full doses of heparin when they are hospitalized, followed by 3 months of warfarin therapy. Other indications for chronic anticoagulation in the setting of acute MI are the presence of a mural thrombus, atrial fibrillation, history of systemic embolization, congestive heart failure, and severe LV dysfunction. This thrombus can occasionally embolize to the extremities. The onset is usually sudden and associated with a cold leg without any pulses. The lesion is usually identified by angiogram. The best treatment for this patient is an embolectomy, which can be performed under local anesthesia. Anticoagulation must be continued with heparin. Distal pulses must routinely be checked in all patients who suffer an MI The role of fibrinolytic therapy for embolic disease has been disappointing. This therapy can be associated with significant bleeding and has to be administered over a period of several hours. The therapy does not always work and may delay resolution of symptoms. Embolectomy is a quick procedure and has immediate results. Recently, intra-arterial thrombolysis has become an alternative to surgical embolectomy. The choice depends on several factors. If the patient has a clot in the proximal arteries, such as bifurcation of the common femoral artery, embolectomy is better, whereas, for embolus in distal arteries such as the tibial artery, intra-arterial thrombolysis may be a good alternative. (Choice B) In general, intravenous heparin should be started immediately in all patients with a high index of suspicion for embolism. However, it is not the definitive therapy. Patients who have arterial occlusive disease generally hang their legs over the side of the bed. Patients who suffer an MI and develop a cold leg need an echocardiogram. The thrombus is generally found on the left ventricular wall. Patients with an MI can also develop a left ventricular aneurysm, mitral regurgitation or ventricular septal perforation. Echocardiography is diagnostic for these complications. It also determines the left ventricular ejection fraction and the presence of pericardial effusions, if any. However, in a patient with a cold leg, with a confirmed angiogram, an embolectomy carries a higher priority. The majority of left ventricular thrombus after an MI will resolve with anticoagulation therapy. Echocardiography is required to follow these patients. Age-dependant idiopathic sclerocalcific changes are the most frequent cause of isolated aortic stenosis in elderly patients. These changes are common and usually have minimal hemodynamic significance, but sometimes may be severe. In patients who present with stable angina and hypertension, a betablocker is the drug of choice. Question ---------------------------------------------------------------------A 65-year-old white female, with chronic congestive heart failure, was admitted for community-acquired pneumonia. She is receiving aspirin, digoxin, furosemide, levofloxacin, and oral simvastatin. She is feeling better and her pneumonia is resolving. While planning for discharge she developed recurrent sustained ventricular tachycardia with stable vital signs during the nighttime. The patient has recieved amiodarone and now is stable in sinus rhythm. A recent echocardiogram showed an ejection fraction (EF) of 35%. What is the most important next step in the management at this stage? A.Add beta blocker B.Add spiranolactone C.Measure serum electrolytes D.Stop simvastatin E.Discharge the patient Normal Labs Explanation: When someone is having recurrent VT, first thing to do after stabilizing the patient is to search for underlying cause. This patient, most likely, has an electrolyte imbalance due to diuretics. Furosemide commonly causes hypokalemia, which may lead to digoxin toxicity. Therefore, ordering serum electrolytes and serum digoxin level is the most reasonable approach. Adding a beta-blocker is a good thing for chronic heart failure but not the next step in this case. Spironolactone is a potassium sparing diuretic that is not indicated at this stage. The most probable diagnosis in this patient is situational syncope related to micturition. The scenario described (middle age or older male with prostatic hypertrophy, who lost his consciousness after awakening and voiding at night) is typical for this type of syncope. The pathophysiologic mechanism underlying the situational syncope includes autonomic dysregulation, which can be partially explained by straining and rapid bladder emptying. Cardioinhibitory and/or vasodepressor mechanisms may be involved. Cardiovascular causes like arrhythmia (Choice A) are less likely because there are no signs of a structural heart disease on the physical examination and the ECG. Situational syncope should be considered in the differential diagnosis of syncopal episodes. The typical scenario would include a middle age or older male, who loses his consciousness immediately after urination, or a man who loses his consciousness during coughing fits. Always suspect malignant hypertension in patients with very high blood pressure (>/= 200/140 mmHg). Presence of papilledema on ophthalmoscopy confirms the diagnosis. The pathologic change responsible for end-organ damage in malignant hypertension is fibrinoid necrosis of small arterioles. papilledema should be present in order to make a diagnosis of malignant hypertension. Renal failure with elevated creatinine level (Choice B) and oliguria (Choice D) can develop rapidly in this case without treatment, but its presence is not required to diagnose malignant hypertension. Left ventricular hypertrophy on ECG (Choice A) is not a diagnostic criterion for malignant hypertension. The presence of a left to right shunt, with an oxygen step up at the level of the right ventricle, will confirm the diagnosis of ventricular septal rupture. Presence of a left to right shunt differentiates ventricular septal rupture from other mechanical complications of acute MI particularly acute MR, which can also produce a pansystolic murmur. ‘V’ waves in the pulmonary capillary wedge pressure tracing may be present in MR but not in ventricular septal rupture. The diagnosis of ventricular septal rupture can be made if there is evidence of left to right shunting on Swan-Ganz catheter readings, when a 2D-echo is not available. Viral or idiopathic myocarditis is most commonly seen following Coxsackie B infection. Viral myocarditis is seen in about 3.5-5 % of patients infected with Coxsackie B virus. Other viruses implicated are adenovirus, cytomegalovirus, echovirus, hepatitis C, influenza virus, parvovirus B-19, and Epstein-Barr virus. The diagnosis is made by echocardiogram, which typically shows dilated ventricles with diffuse hypokinesia resulting in low ejection fraction (systolic dysfunction). Viral myocarditis can cause dilated cardiomyopathy by direct viral damage, as well as sequel of humoral or cellular immune responses to persistent viral infection. Eccentric hypertrophy of the heart is seen following chronic volume overload, as seen in valvular regurgitation Hypokinesia of the inferior wall would be seen in case of inferior wall myocardial infarction Procainamide is a class I A drug used to treat atrial and ventricular arrhythmias. it has few side effects including: nausea, lupus like syndrome, agranulocytosis and prolonged QT. It does not cause lung fibrosis. Quinidine is a class I A anti arrhythmic agent used in the treatment of atrial arrhythmias. It does have a few well-known side effects including: diarrhea, tinnitus, prolonged QT, torsades, hemolytic anemia and thrombocytopenia. It does not cause lung fibrosis. Lidocaine is a Class I B anti arrhythmic agent used in the treatment of ventricular arrhythmias. High doses can cause: confusion, seizures, and respiratory depression. It does not cause lung fibrosis. Please remember the 5 common side effects of the amiodarone class III: It is an excellent drug for both atrial and ventricular arrhythmias but the multiple side effects limits its long-term use. 1- Pulmonary toxicity: Pulmonary toxicity is associated with total cumulative dose rather than the serum drug levels. Longer the use of amiodarone, the higher the chance that patient develops pulmonary fibrosis. “Three months later he returns with dyspnea on exertion, and chest-x ray reveals bilateral lung fibrosis. All cultures are negative and a lung biopsy reveals lipoid pneumonitis”. 2- Thyroid dysfunction: It can also cause thyroid dysfunction including both hypothyroidism (most common, 85%) and hyperthyroidism (15%). Since, the thyroid dysfunction is so common with the amiodarone, patients should have TSH level checked before starting treatment and every 3-4 month intervals. 3- Hepatotoxicity: Transient elevation of aminotransferases occurs in upto 25% of patients. These patients are usually asymptomatic; however, the drug should be stopped if there is more than 2 fold elevation of aminotransferases. 4- Corneal deposits: Corneal deposits occur in most patient’s receiving amiodarone because the drug is secreted by lacrimal gland. Most patients do well without problems with visual acuity. Presence of corneal deposits is not a contraindication. 5- Skin reactions: Skin reactions, specifically a bluish-slate gray discoloration of the skin (usually most prominent on the face) is also seen. In cases of restrictive cardiomyopathy: chest x-ray shows only mild or no enlargement of the cardiac silhouette. Echocardiography shows a symmetrically thickened ventricular wall, a normal or slightly reduced ventricular cavity size, and a normal or near normal systolic function. Regarding the cause of restrictive cardiomyopathy in this patient, the appearance of ‘speckled pattern’ suggests the diagnosis of cardiac amyloidosis. This patient is most likely suffering from a combination of primary amyloidosis and myeloma suggested by the combination of bone pain, hypercalcemia, and renal failure. Isolated systolic hypertension (ISH) is an important cause of hypertension in elderly patients. The pathophysiologic mechanism leading to ISH is believed to be decreased elasticity of the arterial wall, which leads to an increased systolic blood pressure, without concurrent increase (and even decrease) in diastolic blood pressure. Normally during systole, the heart ejects the blood under a certain pressure that is dumped by elastic properties of the aorta and major arteries. Then, this elastic recoil of the arterial wall contributes the diastolic flow of the blood and diastolic pressure. When elastic properties of the arterial wall diminish and arteries become more rigid, this ‘dumping’ of pressure changes during the cardiac cycle also decreases. As a result of increased arterial rigidity, patients with ISH have a widened pulse pressure (the difference between systolic and diastolic pressure). Widened pulse pressure was recently recognized as an important cardiovascular risk factor. Therefore, ISH should be treated appropriately, in spite of the fact that diastolic pressure is not elevated. The initial drug of choice, for these patients, is a low-dose thiazide diuretic. Long acting dihydropyridine calcium channel blockers are an acceptable alternative, but they are more expensive. An increased cardiac output can be a cause of systolic hypertension in hyperdynamic states, such as in hyperthyroidism. There is no sign of hyperdynamic circulation in this case. Whenever a patient of chronic aortic regurgitation develops symptoms of LV dysfunction, he should undergo aortic valve replacement after his congestive symptoms are relieved by intense medical treatment with digoxin, diuretics, and vasodilators (ACE inhibitors). Acute aortic regurgitation is an emergency and requires emergent surgery. Sodium nitroprusside or inotropes like dopamine or dobutamine are used to stabilize this condition before emergent surgery can take place. Jervell-Lange-Nielson syndrome: is one of the congenital ‘QT’ prolongation syndromes caused by molecular defects in ion channels. It is an autosomal recessive disease characterized by congenital deafness and QT interval prolongation on EKG (torsades de pointes= polymorphic ventricular tachycardia, is often selfterminating but may degenerate into frank ventricular tachycardia and cause syncopal episodes and sudden death. The clues to the correct diagnosis in this patient are a syncopal episode without following disorientation (post-episode confusion is more characteristic for a seizure), hearing impairment and family history. The most commonly used treatment modality for these patients is a beta-blocker like propranolol. * If the patinet is asymptomatic, or does not have a clearly documented syncope, beta blocker alone is sufficient. * If the patient is symptomatic, or has a documented episode of syncope, the treatment will be beta-blocker plus a DDD pacemaker. NOTE; Quinidine is an anti-arrhythmic agent that prolongs QT interval; therefore it is contraindicated in this case. Hypertrophic cardiomyopathy is the most common cause of sudden cardiac death (SCD) in young athletes. Congenital anomalies of coronary arteries, arrhythmogenic right ventricular dysplasia, atrial septal defect, and Ebstein’s anomaly are all important causes of SCD in young athletes but they are far less frequent than hypertrophic cardiomyopathy. Patients with artificial pacemakers and defibrillators do not require prophylaxis for infective endocarditis. The presence of hyponatremia indicates that the heart failure is severe: Water retention and the associated reduction in the plasma sodium concentration parallel the severity of the heart disease; they reflect the degree of neurohumoral activation in patients with heart failure. Low serum sodium level is associated with high levels of renin, aldosterone, vasopressin, and norepinephrine. As a result, a patient's survival is significantly reduced if the serum sodium level is below 137 mg/dL. Decreasing the intake of water, not increasing sodium intake , can help to control the electrolyte abnormalities. The American Heart Association recommends that all school and collegiate athletes be offered pre-participation screening, by a skilled healthcare worker. Noninvasive investigations like 12 lead EKG, echocardiography, and exercise testing have a low sensitivity (many false positives) in this low risk population and are not cost effective. Therefore, they are not recommended for routine screening of such a large population. A detailed medical history and physical examination is the most effective way to screen a low risk population for the presence of underlying cardiac disease. A 52-year-old white male presents to emergency room for palpitations and light-headedness. His vitals are, BP: 110/76 mm of Hg; HR: 170/min; RR: 28/min=> determisn: supra or ven? Look at the narrow complex QRS morphology => This patient has classic supraventricular tachycardia. SVT is usually recognized by a HR of >140/min, regular, loss of ‘P’ waves and narrow QRS complex. * if the patient is stable=> 1) vagal maneuvers should be attempted initially. If these fail to convert him to normal sinus rhythm=> 2) IV adenosine push is the drug of choice. Verapamil is no longer the drug of choice for this purpose but can be used as a second line drug. Clinical features of right ventricular infarction include jugular venous distension, Kussmaul’s sign, hepatomegaly, and hypotension in the presence of clear lung fields. Sometimes tricuspid regurgitation is also present. Along with inferior or inferoposterior MI (ST elevation), EKG shows ST segment elevation in right-sided leads (V4R, V6R), especially in V4R, which is indicative of acute right ventricular injury. Greater elevation of ST in lead III than lead II also suggests the diagnosis of right ventricular infarct. The underlying mechanism for the clinical findings of a right ventricular infarct lies in the fact that the right ventricle becomes less compliant resulting in: decreased filling and stroke volumes of the right ventricle with a resulting elevated central venous pressure. Right ventricle also becomes dilated and tricuspid regurgitation may develop. As a result of the decreased right-sided stroke volume, there is decreased filling of the left ventricle and hence decreased contraction and cardiac output. Left sided filling pressures are low, as well, and pressures in the right atrium are high, thus the lungs are clear. The right ventricle is normally thinner than the left, as its workload is much less. Therefore loss of its diastolic, not systolic, function gives rise to the symptoms of right ventricular infarction. Prinzmetal's angina. She presented with a classic picture of this disease, with absence of risk factors of coronary artery disease, night pain waking her up from sleep, transient ST elevation on the EKG, absence of Q waves and negative cardiac enzymes. The study of choice for diagnosis and follow-up of abdominal aortic aneurysms is an abdominal ultrasound. It allows for the measurement of the size of the aneurysm, as well as it can show the presence of an associated thrombus. In patients with hyperthyroidism-related tachysystolic atrial fibrillation, a beta-blocker is the drug of choice. Dipyridamole can be used during myocardial perfusion scanning to reveal the areas of restricted myocardial perfusion. The redistribution of the coronary blood flow to ‘non-diseased’ segments induced by this drug is called coronary steal phenomenon. Mitral valve prolapse is the most common cause of mitral regurgitation in USA. acute cardiac tamponade secondary to a rupture of the free left ventricular wall. The presence of pulsus paradoxus and pulseless electrical activity are important diagnostic clues.” neck veins are distended and measurement of blood pressure shows an 18 mm drop of systolic blood pressure with inspiration, The EKG monitor shows sinus tachycardia” Sometimes heart sounds become inaudible due to the accumulation of blood within the pericardial cavity. Free wall rupture usually occurs in the first week after MI. Risk factors include advanced age, large Q wave infarct, a history of HTN, and no prior history of angina pectoris. In HCM (AD on 14): Valsalva maneuver and standing after squatting are two maneuvers that intensifying the associated systolic murmur. On handgrip increases the systemic arterial resistance and thus decreases the gradient and associated systolic murmur. Phenylephrine also decreases the murmur by increasing systemic arterial pressure. Leg elevation increases the left ventricular volume and thus decreases the gradient and the associated murmur. in HOCM it is the systolic anterior motion of mitral valve leaflet that causes mitral regurgitation. First-degree heart block is a completely benign arrhythmia and requires no treatment. If the edema is significant, the drug should be discontinued. The clues to the correct diagnosis in this case are the therapy with a dihydropyridine Ca-channel antagonist, amlodipine initiated recently, and normal physical examination with normal laboratory findings. Thus any patient who has atrial fibrillation and heart failure will benefit from digoxin; it should be considered over before beta-blockers or calcium channel blockers. IV dobutamine is used when a patient is in cardiogenic shock. Norepinephrine is a powerful vasoconstrictor and can lead to decreased blood supply to both the lower and upper extremity. Norepinephrine is a powerful pressor drug and frequently used to revive patients in shock. In addition to decreasing blood supply to the digits, other organs like the kidneys can also be affected. For this reason, the use of this vasoconstrictor is limited in the ICU. Thrombosis of the forearm vessels may be seen in Buerger’s disease. Buerger’s disease is seen in young males who are heavy smokers. Digital ischemia and gangrene are common features. MVP: Auscultation of the precordium reveals mid systolic click with late systolic crescendo-decrescendo murmur. Click and murmur occurs earlier with Valsalva maneuver and it disappears with squatting Beta blockers are used to treat chest pain, palpitations, and autonomic symptoms of MVP. Thiazide diuretics are the initial antihypertensive of choice in patients with Osteoporosis LV aneurysm can cause CHF in a patient who sustained an anterior wall MI in the past. A double apical beat and persistent elevation of the ST segment are important diagnostic clues. Complete heart block is a dangerous condition These patients are at very high risk for sudden cardiac death and they should be admitted in ICU and permanent pacemaker should be placed as soon as possible. Atropine should always be made available at the bedside. Chaga’s disease is a condition caused by insect-borne protozoan called Trypanosoma cruzi, which is a common form of myocarditis in Central and South America. Major clinical manifestations may appear after a latent period of more than a decade. At this stage, patients usually present with cardiomyopathy, conduction abnormalities, and certain death. This patient has classic features of cardiomyopathy. Almost all these patients will have a have a history megacolon or mega-esophagus. In both constrictive pericarditis and pericardial tamponade, right and left sided diastolic pressures are equal and elevated (external compression) Dressler’s syndrome, an autoimmune pericarditis, is a late complication of acute MI that usually develops between the second and tenth weeks post MI. AR: LVH, LVF: dyspnea, breathlessness at rest. She also had episodes of paroxysmal nocturnal dyspnea. Auscultation of lungs shows bilateral crepitations. RVF; She noticed bilateral ankle swelling a week ago that became progressively worse. Examination shows jugular venous distension, - BP is 140/66 mmHg, rapidly rising carotid pulse with a sudden collapse and bilateral ankle edema. Her apical impulse is heaving and displaced inferolaterally. Cardiac auscultation shows an S3 gallop as well as a high-pitched, blowing, early diastolic decrescendo murmur heard best in the left third intercostal space. Leaning forward and holding the breath in expiration intensifies the murmur. dilated cardiomyopathy secondary to alcoholism. Findings of thrombocytopenia, macrocytosis, and elevated transaminases are all suggestive of alcoholism in this patient Tapping apex beat and malar flush are important physical findings of mitral stenosis. Pulsus paradoxus and hypotension point toward the diagnosis of pericardial tamponade. Pulsus paradoxus is uncommon in constrictive pericarditis unless an effusion is present. It may also be present in severe airway obstruction and superior vena cava obstruction The treatment of ventricular fibrillation is STAT defibrillation with 200-360 joules. If defibrillation fails, lidocaine or amiodarone (drug of choice) can be loaded and the patient shocked again. Epinephrine can sensitize the heart and lower the threshold for conversion. It has been found that prevention of recurrent attacks of rheumatic fever may slow down the progression of mitral stenosis. Therefore, penicillin prophylaxis with monthly IM injection of benzathine penicillin is recommended in adolescent patients in whom the recurrence risk is high. Patients with, or without, carditis need penicillin prophylaxis, although the recommended duration of prophylaxis is 10 years in the former and 5 years in the latter. Patients with mitral stenosis are also at high risk for thromboembolism. Anticoagulation is indicated if they have a history of an embolic event or they have intermittent or chronic atrial fibrillation. Antihypertensive management should be the first step in patients with aortic dissection with hypertension. (Don’t measure enzymes if it is ST Depression). only ACE inhibitors, aspirin, and beta-blockers have been shown to reduce mortality after acute MI ST segment depression, T wave inversion and first degree AV block can occur at therapeutic levels of digoxin and they do not represent digitalis toxicity and therefore there is no need for discontinuation of the drug. Atrial tachycardia along with variable degree of AV block is the most important EKG finding of digitalis toxicity and it has a high specificity for digitalis toxicity Severe diastolic dysfunction is present in restrictive cardiomyopathy due to rigid and stiff ventricle wall. Systolic function is preserved in this condition. Severe systolic dysfunction and increased left ventricle size are features of dilated cardiomyopathy. Supernormal ejection fraction is present in hypertrophic cardiomyopathy as is dynamic outflow obstruction. Diastolic dysfunction is present in HCM, due to the stiff, hypertrophied ventricle wall. T6 + T20-31 --------------T7 In patients presenting with significant peripheral vascular disease, calcium channel blockers are preferred as anti-hypertensive Doxazosin is an alpha-blocker with a favorable metabolic profile. It is not considered as a first-line drug in the treatment of hypertension, because the long-term effects of alpha-blocker therapy are not clear. Moreover, some side effects of the alpha-blocker therapy may be disturbing (e.g., orthostatic hypotension). A 65-year-old American male is brought to the emergency room for the sudden onset of severe substernal chest pain associated with severe shortness of breath that started 40 minutes ago. He says that the pain radiates to his left arm. He had 2 episodes of vomiting at home and is diaphoretic. His pain is not relieved with 4 baby aspirins and 5-sublingual nitroglycerine tablets. His initial EKG has shown diffuse ST elevation in the inferior and lateral leads. He is started on IV Morphine and oxygen 4L/minute. His exam shows muffled S 1, S2 and the presence of S3. Bilateral crackles are heard halfway up to the lungs. There is obvious jugular venous distension and 2+ pedal edema bilaterally. Stool hem test is (FOBT) is negative. His vitals are BP: 110/70 mm Hg; PR: 56/min; RR: 32/min; Temperature: 36.9(98.4F). His oxygen saturation is 91% on 4L oxygen. The patient receives t-PA and IV heparin. Which of the following is the most beneficial next step in the management of this patient? A.IV metoprolol B.IV digoxin C.IV furosemide D.Low dose enalapril E.IV normal saline Normal Labs Explanation: This patient has acute heart failure resulting in pulmonary edema in the setting of an acute infero-lateral MI. Even though IV betablockers improve mortality in acute MI, they are contraindicated in the presence of pulmonary edema. Furthermore, the patient's pulse rate is only 56/minute, which is not uncommon in inferior infarctions. Other absolute contraindications to their use include asthma, hypotension, severe bradycardia and heart block greater than first degree. Diuretics are the drugs of choice in this patient. The most commonly used agent is furosemide. They rapidly relieve the pulmonary edema by decreasing the preload and pulmonary capillary pressure. Furosemide causes venodilation that occurs earlier than the diuresis and this helps to decrease preload rapidly. Digoxin is useful in the setting of chronic congestive heart failure and it is not useful for the treatment of acute cardiogenic pulmonary edema. Therapy with digoxin, in the setting of chronic congestive heart failure, does not improve survival but it provides a symptomatic benefit for patients with systolic dysfunction and sinus rhythm. It is also used to control ventricular rate in patients with heart failure who have atrial fibrillation. IV fluids should not be used in this patient, as they will worsen the heart failure by increasing the preload. IV fluids are used in the setting of a right ventricular infarct that can be associated with an inferior wall MI. ACE inhibitors have been shown to improve survival in patients with MI and therefore, are used routinely. They produce their beneficial effect by decreasing the ventricular remodeling and thus prevent the worsening of the left ventricular dysfunction. Contraindications to their use include allergy to ACE inhibitors, renal failure (Cr of>2.5-3.0), bilateral renal artery stenosis, hypotension, and previous failure of ACE inhibitors. The above patient has hypotension and therefore ACE inhibitors are contraindicated. They improve survival in patients with congestive heart failure but they are not useful in the acute setting of pulmonary edema. Educational Objective: Know how to treat acute pulmonary edema in the setting of an acute MI. Loop diuretics should be given to treat pulmonary edema. left ventricular aneurysm is a late complication of an acute MI. It usually occurs after an anterior wall MI and may be: either asymptomatic, or it may present with congestive heart failure, an arterial embolism, or sustained ventricular arrhythmias. Precordial examination may show a double apical beat. Auscultation of the heart may reveal an additional S3 or S4 and sometimes a murmur of mitral regurgitation is present due to papillary muscle dysfunction, annular dilatation, or abnormal left ventricular geometry. Chest x-ray usually shows a characteristic prominence of the left border of the heart. The EKG shows persistent ST segment elevation. Thrombolytic therapy is indicated when the chest pain is suggestive of MI and there is ‘ST’ segment elevation greater than 1 mm in two contiguous leads after sublingual nitroglycerin administration to rule out coronary vasospasm If the PVC complexes have the same morphology, they are referred to as "unifocal"; if of different morphologies, "multifocal". When they are frequent, as shown in this strip, they may alternate with a sinus beat and the rhythm is then called bigeminy The presence of a tapping apex beat, a loud first heart sound, and a mid-diastolic rumble at the apex suggest the diagnosis of mitral stenosis in this patient Non Pharmacologic Tx for HTN: cessation of cigarette smoking is strongly encouraged in patients suffering from HTN but only to reduce the risk of cardiovascular disease and not to reduce high blood pressure. Weight reduction in obese patients leads to a significant fall in blood pressure. A clear association has been found between excessive alcohol intake and development of hypertension. If average alcohol intake is greater than 2 drinks/day, risk of development of hypertension increases by 1.5-2 times compared to the general population and the risk increases substantially if the average alcohol intake is greater than 5 drinks/day. On the other hand moderation of alcohol intake to 1-2 drinks per days also has been shown to have a cardioprotective effect. Nitrates are contraindicated when a patient is continuously or intermittently taking sildenafil (Viagra). In such settings nitrates may cause syncope, MI, or sudden death when a patient has an acute coronary syndrome. It is recommended not to use nitrates within 24 hours of the last dose of sildenafil. The reason for the dangerous interaction between nitrates and sildenafil is that both induce nitric oxide mediated vasodilatation. Atrial myxoma: presents with systemic symptoms, exertional dyspnea and auscultatory findings similar to MS, but there is no opening snap. The murmur of atrial myxoma changes with position. These patients are at high risk for systemic embolization. clinical syndrome in which sinus node dysfunction produces symptomatic bradyarrhythmias, including sinus bradycardia, sinoatrial block and sinus arrest either singly or in combination. Symptoms may range from syncope, dizziness, confusion, and congestive heart failure. Management of sick sinus syndrome involves elimination of significant bradycardia as well as suppression of any associated atrial tachycardias. This is easily done by utilizing a single lead ventricular pacemaker. Once the ventricle rate is under control, the atrial tachyarrhythmias can be controlled with type 1 anti arrhythmic drugs (When a patient with sick sinus syndrome develops symptoms, treatment is necessary. There is little place for vagolytic therapy (atropine) or isoproterenol in the management of this condition. These agents are transient and are not the solution in long-term management of symptomatic patients. )Provocative stress testing plays a role in the diagnosis of sick sinus syndrome, but once the diagnosis is established, stress testing is redundant. Treadmill testing can be used to delineate the range of sinus node responses to exercise. The failure of sinus rate to increase with exercise is abnormal, however this lack of response does not establish the sick sinus syndrome as the cause of symptoms. Aortic dissection is a medical emergency and should be diagnosed and treated. If hypertension is present it should be treated aggressively before any diagnostic studies are done. A 65-year-old Caucasian male presents with a chief complaint of exertional substernal chest pain radiating to the let arm. Pain is usually relieved within 5 minutes of rest or within 5 minutes of single sublingual nitroglycerine. His other medical problems include type II DM and hypertension. He is a non-smoker and drinks alcohol occasionally. His medications include metoprolol, lisinopril, glyburide, and sublingual nitrates as needed. He is doing well on his anti-ischemic medications. Which of the following investigations is the most appropriate next step in the management of this patient? A.Exercise stress testing B.Pharmacological stress testing C.Coronary angiography D.2D-echocardiography E.Resting electrocardiogram F.No testing required unstable angina (USA) is defined as angina of recent onset, angina at rest, accelerated angina, post-infarct angina, and post-revascularization angina. A change in the character, severity, duration of previous stable angina, or failure to resolve with increasing doses of sublingual nitroglycerin also represents unstable angina. In unstable angina, EKG may show either ‘ST’ depression, ‘T’ wave inversion, or many times no changes. All patients with unstable angina should be hospitalized and treated with aspirin, IV heparin, and IV nitroglycerin. Once the patient is free of chest pain, an angiography can be performed nonemergently. constrictive pericarditis are idiopathic (42% in USA), post radiotherapy (31% in USA), post surgical (11%), connective tissue disorders, neoplasm, uremia, sarcoidosis, etc. Sharp 'x' and 'y' descent on central venous tracing is characteristic of constrictive pericarditis as is the presence of pericardial knock (early heart sound heard after S2). Benzodiazepines are the first-line medication, along with aspirin, and nitrates in the treatment of cocaine-related cardiac ischemia. The first line medication for HTN in the general population is either a thiazide diuretic or betablocker. spontaneous mediastinal hemorrhage due to coagulation abnormality caused by warfarin. The blood accumulated in the mediastinum causes compression of the surrounding structures leading to cardio-vascular compromise i.e. mediastinal tamponade. It can also spread towards the neck causing ecchymoses. Equalization of right and left cardiac filling pressures may be present in severe cases. Pericardial tamponade can give the same clinical picture and pressure equalization but it is excluded by the ultrasound. Nitroglycerine is not used in AS, because it will reduce cardiac output by decreasing LV filling pressures and it may result in hemodynamic collapse. All patients have no BP at the onset of ventricular fibrillation and the most immediate step is to defibrillate as soon as possible. The energy required may be 200-360 joules. More than a few minutes of delay can lead to permanent brain injury and death. Lidocaine is an excellent agent for ventricular arrhythmias. In the presence of ventricular fibrillation, cardioversion is the first modality of therapy. If cardioversion does not initially work, patients may require a lidocaine bolus followed by a second shock. C.Amoxicillin (dental, can take the drug orally) A.Ampicillin(dental, can’t take the drug orally) E.Clindamycin, or mactrolide(dental, sens to PCN) B.Ampicillin and gentamicin(lower GI/GU, not sens to PCN) D.Vancomycin and gentamicin (lower GI/GU, sens to PCN) The EKG findings that may be present in pericardial tamponade include sinus tachycardia, low voltage QRS complexes, and electrical alternans. Electrical alternans is characterized by alternating amplitudes of QRS complexes. It occurs in pericardial tamponade due to swinging of heart within the pericardium and beat-to-beat change of the QRS axis. Presence of this finding with the associated hypotension, distended neck veins, and muffled heart sounds represent the diagnostic criteria for cardiac tamponade. Electrical alternans may also be present in cases of severe cardiomegaly. Pulmonary thromboembolism doesn’t present with pulmonary edema. Overhydration is one of the most common causes of perioperative pulmonary edema. Diastolic and continuous murmurs as well as loud systolic murmurs revealed on cardiac auscultation should always be investigated using transthoracic Doppler echocardiography. Midsystolic soft murmurs (grade I-II/IV)-MVP- in an asymptomatic young patient are usually benign and need no further work-up. ischemic symptoms are most likely due his anemia and a blood transfusion is most likely to be helpful in this patient. I.V atropine is the drug of first choice in patients with symptomatic bradycardia. Transcutaneous pacing is the next step after atropine. If the patient has severe bradycardia with hypotension then epinephrine is the drug of choice; however, it should not be administered if the patient is hemodynamically stable. Statin intolerance should be suspected if the patient develops myalgias and elevated serum transaminases(within few weeks to few months of starting statin therapy). CPK elevation greater than 10 times normal in the presence of myalgias defines statin induced muscle injury. Rhabdomyolysis resulting in acute renal failure is an extremely rare side effect of statins and occurs only when other risk factors are present. Concomitant use of drugs like gemfibrozil, niacin and cyclosporine increases the risk for the development of myopathy. Other risk factors include hypothyroidism and hepatobiliary disease. A possible explanation of statin induced muscle damage is reduction of CoQ10 production by statins and CoQ10 is required for energy production by muscle cells. Statin intolerance is treated by discontinuation of the drug and symptoms resolve with return of CPK to baseline within a few days to a few weeks after discontinuation. Supportive care for rhabdomyolysis is the only treatment needed. When a patient who is taking a statin develops clinical significant myopathy, statins should be stopped otherwise his condition may worsen. Clinical trials demonstrated that prophylactic lidocaine decreases the frequency of VPBs and diminishes the risk of ventricular fibrillation, but the overall prognosis is unaffected (Choice B). The problem is that lidocaine can increase the risk of asystole in these patients In VFib Epinephrine can sensitize the heart and lower the threshold for conversion. New onset of RBBB indicates PE. The primary mechanism responsible for the effect of nitroglycerin in patients with anginal pain is dilation of veins (capacitance vessels). Increased venous capacitance and venous pooling of the blood lead to significant decrease in ventricular preload and decrease in heart size. Decreased tolerance to glucose is a well-known side effect of thiazide diuretic therapy. Thiazide diuretics can also unfavorably affect lipid metabolism by increased LDL cholesterol and plasma triglycerides IN Diabetics, SBP<130 Acute atrial flutter with stable hemodynamics can be treated with cardioversion or can be managed with rate control. Chronic stable atrial flutter is best treated with rate control, which is best achieved with either calcium channel blockers or beta-blockers. vasovagal syncope (common faint). This is also known as neurally mediated or neurocardiogenic syncope. The clinical scenario described is very typical for this condition including prodrome (lightheadedness, weakness, and blurred vision), provocation by an emotional situation, and rapid recovery of consciousness. Vasovagal syncope is frequently recurrent. In this case, upright tilt table testing with or without pharmacologic provocation (isoproterenol) may be indicated to confirm the diagnosis (although there is no orthostatic hypotension). Out of all the above medications, only beta-blockers have been shown to decrease perioperative mortality, probably by decreasing intraoperative myocardial ischemia. This has been proven in several clinical trials. Their routine use perioperatively in patients with CAD or at risk of CAD is under consideration. Calcium channel blockers are associated with a slightly increased risk. They may cause postoperative bleeding due to platelet inhibition. ACE inhibitors may cause prolonged hypotension postoperatively. Patients on chronic diuretic therapy may have hypokalemia and hypovolemia intraoperatively. Abrupt withdrawal from centrally acting sympatholytics may cause severe rebound HTN. These are not first line drugs for treating hypertension in any setting. In a young male who presents with an aneurysm of the descending aorta, the most likely cause is a history of prior blunt chest trauma. elderly patients very poorly tolerate even what seems to be an insignificant loss of fluid. The second point is that mild hypovolemia may predispose an individual (especially elderly) to orthostatic syncope after bed rest (like nighttime sleep) because it takes time for the body to adjust to the sudden change in the body position. This is caused by getting up from the bed. Increased BUN/creatinine ratio is a sensitive indicator of the patient’s hydration status, although it is not very specific discontinue OCP in HTN (they cause it). High dose nicotine is giving to increase HDL => it may cause pruritis+flushing (PGlandines dilate vessels) <= ASA