Internal Med MKSAP Cardiology – Flashcards

Volume expansion is the primary supportive treatment for the hemodynamic abnormalities of a right ventricular myocardial infarction. Although ischemia of the right ventricle may occur in a high percentage of patients with inferior ST-elevation myocardial infarction (STEMI), only 10% to 15% develop right ventricular myocardial infarction with hemodynamic abnormalities. These patients have a significantly higher in-hospital mortality rate (25%-30%) compared with patients with inferior STEMI without right ventricular infarction, and thus these patients should receive reperfusion therapy. The physical examination findings of hypotension, clear lung fields, and elevated estimated central venous pressure represent the classic triad of right ventricular myocardial infarction. However, the most predictive finding is ST-segment elevation on right-sided electrocardiographic lead V4R. Therefore, all patients with an inferior STEMI should have a right-sided electrocardiogram performed at the time of presentation. This patient's electrocardiogram shows ST-segment elevation in frontal inferior leads II, III, and aVF and 1-mm ST-segment elevation in right-sided precordial lead V4R. These findings indicate inferior and right ventricular injury in the setting of an inferior STEMI, likely related to a right coronary artery occlusion. In the setting of right ventricular myocardial infarction, right ventricular contractility is reduced, resulting in higher right ventricular diastolic pressure, lower right ventricular systolic pressure, and reduced preload or filling of the left ventricle. Volume expansion improves the hemodynamic abnormalities of right ventricular myocardial infarction because the gradient of pressure from the right atrium to the left atrium maintains filling of the left ventricle. In addition to reperfusion therapy for STEMI, the acute treatment of right ventricular myocardial infarction is supportive. Inotropic support, specifically using intravenous dobutamine, is appropriate treatment in patients with right ventricular myocardial infarction whose hypotension is not corrected after 1 L of saline infusion. However, volume expansion should be tried before giving inotropic agents.

CABG is recommended for pts with DM and multivessel disease

stenosis of the left main coronary artery and multivessel coronary artery disease with mildly reduced left ventricular systolic function. Coronary artery bypass grafting is indicated in patients with left main coronary artery disease, severe three-vessel disease with reduced left ventricular systolic function, and severe three-vessel disease with involvement of the proximal left anterior descending artery. In addition, patients with diabetes mellitus and multivessel disease also derive benefit from coronary artery bypass graft surgery. DM2 pts also have a mortality benefit.

This patient has symptomatic mitral stenosis with pulmonary hypertension, and intervention is now necessary. Given that moderate regurgitation is present in this patient, valve replacement surgery, rather than balloon valvuloplasty, is indicated. Clinical markers consistent with severe mitral stenosis are transmitral pressure gradients greater than 10 mm Hg, enlargement of the left atrium, mitral valve area less than 1.5 cm2, and pulmonary pressures greater than 50 mm Hg. Clinical outcome in asymptomatic or minimally symptomatic patients with mitral stenosis is excellent (>80% survival at 10 years), but once patients are symptomatic, 10-year survival is less than 15%. Morbidity associated with untreated mitral stenosis includes pulmonary hypertension, right-sided heart failure, systemic embolism from atrial fibrillation, and valve infection. In symptomatic patients, percutaneous valvuloplasty is the preferred intervention if valve anatomy is amenable. Valvuloplasty is less invasive than surgical intervention and avoids the need for lifelong anticoagulation. Major complications of percutaneous valvuloplasty include severe mitral regurgitation (1%-8%), systemic embolization (1%-3%), and tamponade (1%-2%). Procedural mortality rate is 1%. Valve characteristics that favor successful valvuloplasty include pliable mitral valve leaflets, minimal commissural fusion, and minimal valvular/subvalvular calcification, as evaluated by echocardiography. However, percutaneous valvuloplasty should not be performed if there is moderate or severe mitral regurgitation, as the procedure would likely worsen any mitral regurgitation already present. In patients under consideration for valvuloplasty, transesophageal echocardiography is necessary to definitively exclude a left atrial thrombus because of the risk of thrombus dislodgement and embolization during the procedure.

Peripartum cardiomyopathy is defined as heart failure with a left ventricular ejection fraction less than 45% that is diagnosed between 3 months before and 6 months after delivery in the absence of an identifiable cause. It is usually diagnosed during the first month postpartum. This patient presents with clinical features consistent with peripartum cardiomyopathy, including timing of onset, evidence of left ventricular dilation (displaced and diffuse apical impulse), and typical signs of heart failure. Risk factors for peripartum cardiomyopathy in this patient include her age (>30 years at the time of the pregnancy), race (black, African, Haitian), and the presence of gestational hypertension. With a maternal mortality rate of approximately 10%, peripartum cardiomyopathy is the major cause of pregnancy-related death in North America. In women suspected of having peripartum cardiomyopathy, urgent confirmation of global ventricular systolic dysfunction by transthoracic echocardiography and institution of treatment with standard heart failure therapy are critical. Improvement in left ventricular function occurs in about 50% of women with peripartum cardiomyopathy within 6 months after delivery. Intravenous immune globulin and pentoxifylline have been shown to improve outcomes in some studies. Anticoagulation is recommended for thromboembolic prophylaxis when left ventricular ejection fraction is less than 35%.

NYHA class III or IV heart failure, an ejection fraction less than or equal to 35%, and a QRS width greater than 120 msec. Approximately 70% of patients who undergo biventricular device placement obtain a symptomatic benefit, thought to result from mechanical "resynchronization" of the timing of right and left ventricular contraction. These devices have been shown to improve ejection fraction, quality of life, and functional status, as well as to decrease heart failure hospitalizations and mortality.

The jugular venous pulse contour demonstrates a prominent a wave. A right ventricular lift and systolic thrill are present. An ejection click is noted and is close to the S1, suggesting severe pulmonary valve stenosis. This sound decreases in intensity during inspiration (the only right-sided sound that decreases during inspiration). An early systolic murmur is noted over the pulmonary area. The electrocardiogram demonstrates right ventricular hypertrophy and right axis deviation. The chest radiograph demonstrates pulmonary artery dilatation. The diagnosis can be confirmed by echocardiography.

classic symptoms of aortic stenosis include dyspnea, angina, and exertional syncope. Aortic stenosis is characterized by small and late carotid pulsations, a late-peaking systolic murmur loudest in the second right intercostal space, absent splitting of S2, and a sustained apical impulse. The murmur characteristically radiates to one or both carotid arteries.

fixed splitting of the S2. Equal a and v waves may be noted on jugular venous assessment. A right ventricular impulse is present. An ejection click may be audible if the pulmonary artery is enlarged but is less common than in patients with pulmonary stenosis. A pulmonary midsystolic murmur and a tricuspid diastolic flow rumble may be heard owing to increased flow through the valves from the left-to-right shunt. A systolic thrill, loud systolic murmur, and post-stenotic dilation of the pulmonary artery would not be expected in a patient with an isolated atrial septal defect.

holosystolic murmur at the apex that radiates to the axilla without respiratory variation. Mitral valve regurgitation may cause secondary pulmonary hypertension, but an ejection click and a loud early systolic murmur would not be expected with mitral valve regurgitation, even in the presence of pulmonary hypertension.

holosystolic murmur noted at the left sternal border. This characteristically increases with inspiration. The jugular venous pulse contour demonstrates a prominent v wave with tricuspid regurgitation, rather than a prominent a wave.

Surgical septal myectomy should be considered in patients with outflow obstruction who are NYHA functional class III or IV and whose symptoms are refractory to medical therapy. Septal myectomy has been beneficial in improving symptoms of heart failure and may lead to a better prognosis. Thus, this patient who is refractory to medical therapy with no significant comorbidities should undergo surgical septal myectomy.

TIMI risk score consists of the sum of four historical and three presentation characteristics. This patient's age, elevated troponin, ST-segment deviation, recent history of angina, recent use of aspirin, and presence of three traditional cardiovascular risk factors (family history, diabetes mellitus, hypertension) give him a TIMI risk score of 6, which places him at high risk of death or nonfatal myocardial infarction over the next 14 days. Patients with high TIMI risk scores benefit from aggressive medical therapy and referral for early coronary angiography (early invasive approach).

present in 50% of pts at 5 years - presents atypically, syncope, arryhtmias, DOE, SOB, new heart failure prognosis is poor once symptomatic -consider new heart transplant

NYHA class 2-3 heart failure ischemic or non-ischemic cardiomyopathy EF<35%

ACE and Beta-blocker for everyone Amlodipine is only Ca channel blocker ok for htn, neutral effect in PRAISE trial Digoxin is indicated for moderately to severely symptomatic heart failure patients (NYHA class III-IV) or for rate control in patients with atrial fibrillation. Digoxin improves symptoms and reduces hospitalizations, but does not affect survival. Spironolactone is indicated only for treatment of moderate to severe (NYHA class III-IV) heart failure; in this setting, its use is associated with a 30% reduction in mortality. This patient, however, is only minimally symptomatic (NYHA class II), and treatment with either medication is not indicated.

ACE/ARD teratogens Atenolol class D, metop is class C adenosine class C Diltiazem class C

In asymptomatic patients, repair is indicated for aneurysms with a transverse diameter of 5.5 cm or larger, or those demonstrating an expansion rate of more than 0.5 cm/year. From 4-5.5cm can do f/u US Q6months

Key Point * Glycoprotein IIb/IIIa inhibitors should be added to standard anti-anginal and antithrombotic therapy in patients with unstable angina or non-ST-elevation myocardial infarction with ongoing anginal symptoms.

Echocardiography shows a left atrial mass with features consistent with a tumor, as evidenced by attachment to the atrial septum, echogenic texture, mobility, and protrusion into the mitral valve orifice obstructing inflow. This mass is most likely a left atrial myxoma, the most common tumor type of the left atrium. A left atrial myxoma does not metastasize to other organs, but it has significant associated morbidity. Left atrial myxoma causes fever, night sweats, and weight loss, and may embolize to the brain or other organs such as the kidney, as seen in this patient. Cardiac surgery to remove the left atrial mass is the best treatment and would be curative if the mass is a benign tumor.

* Patients presenting late with an ST-elevation myocardial infarction (>12 hours after symptoms onset) and ongoing chest pain should be treated with primary percutaneous coronary intervention as opposed to thrombolytic therapy.

The goal LDL cholesterol level for a patient with two or more risk factors for CAD is dependent on the 10-year risk for a CAD event based upon the Framingham risk equation. In patients with two or more risk factors and with an intermediate (10%-20%) 10-year risk, the goal LDL cholesterol level is below 130 mg/dL (3.4 mmol/L). However, in patients with two or more risk factors and a high risk (>20%) of a CAD event, the goal LDL cholesterol level is below 100 mg/dL (2.6 mmol/L). A statin is the first-line treatment for cholesterol reduction.

Transthoracic echocardiography is indicated when a grade 3/6 or greater systolic murmur is heard on examination, in the presence of any diastolic or continuous murmur, or if a new murmur is diagnosed in the interval since a normal prior physical examination. Midsystolic murmurs grade 2/6 or less are considered innocent murmurs, especially when they are short in duration, associated with a physiologically split (normal) S2, and are not accompanied by any other abnormal cardiac sounds or murmurs. The most common etiology of this type of murmur in persons older than 65 years is minor valvular abnormalities due to aortic sclerosis.

Acute viral pericarditis is typically characterized by pleuritic chest pain, fever, pericardial friction rub, lymphocytosis, and ST-segment elevation, occ elevations in troponins and CK

Post-myocardial infarction patients with reduced ejection fraction are not candidates for implantable cardioverter-defibrillator placement until 40 days after infarction.

The implantable loop recorder has been shown to have the greatest diagnostic yield and cost-effectiveness for the evaluation of infrequent syncope in the setting of a structurally normal heart relative to ambulatory external monitoring for infrequent events

Patients who have sustained a non-ST-elevation myocardial infarction benefit from the addition of clopidogrel to aspirin regardless of whether percutaneous coronary intervention was performed.

There is jugular venous distention to her jaw line while sitting upright. Cardiac auscultation demonstrates an irregularly irregular rhythm, a loud S1, normal S2, and an opening snap. A grade 2/6 holosystolic murmur is heard at the cardiac apex radiating to the axilla, and a low-pitched diastolic murmur is heard following the opening snap. Bibasilar crackles are present. MOst frequently caused by rheumatic heart disease, can be asymptomatic but gets worse with additional stress like pregnancy Acute decompensation is with IV B-blocker therapy, diuretics, consider anticoagulation

Colchicine then high dose aspirin, NSAIDs Steroids are third line

tx with vasodilators like nitro

A bicuspid aortic valve is present in more than 50% of patients with aortic coarctation. Other associations include ventricular septal defect, patent ductus arteriosus, aortic stenosis (valvular, subvalvular, or supravalvular), and mitral stenosis. This patient has physical findings consistent with severe aortic valve regurgitation, including a wide pulse pressure, rapidly collapsing pulse, pulsating nailbeds, a brief systolic and long diastolic murmur, and features of left ventricular enlargement. The displaced apical impulse suggests left ventricular dilation and the presence of chronic aortic regurgitation. Need monitoring for aortic stenosis and aortic valve regurgitation

pseudoclaudication. The discomfort of spinal stenosis may be very similar to that of peripheral arterial disease. However, whereas the pain of peripheral arterial disease is precipitated by a predictable degree of exertion and relieved by rest and is unaffected by lumbar flexion or extension, that of spinal stenosis is provoked by prolonged standing and is relieved by sitting, lying down, or flexing at the waist. In addition, the pain of spinal stenosis may occur with walking, especially downhill (lumbar extension). Deep tendon reflexes are reduced at the ankle in about half of patients with spinal stenosis; reduced reflexes at the knee are less common. MRI of the lumbosacral spine would be the most useful first test in confirming the clinical suspicion of spinal stenosis.

severe aortic stenosis based on clinical and echocardiographic examination findings. An absent aortic component of S2, a long and late-peaking systolic murmur, and a sustained apical impulse are all associated with severe aortic stenosis with likelihood ratios between 4.1 and 4.5. The primary indication for valve replacement in aortic stenosis is the presence of cardiopulmonary symptoms (angina, syncope, exertional dyspnea, heart failure). Aortic valve replacement is indicated in any symptomatic patient, regardless of age, because of the substantial improvements in long-term survival and quality of life. Aortic valve replacement is not performed in asymptomatic patients because of the increased surgical risk incurred, with potential complications including thromboembolism, bleeding from anticoagulation, prosthetic valve dysfunction, and endocarditis.

if CVA unclear source diver with AMS, concern for embolic event TTE is study of choice with bubbles

Lytics best <1hr if 3-12h since onset symptoms consider transfer if can get PCI within 90 minutes. Clear benefit up to 12 hrs, and lytics less good after 3 hours

The physical examination is notable for findings of right heart failure (jugular venous distention, peripheral edema) in the absence of left heart failure (clear lung fields, absence of gallop). The most important physical examination findings are a Kussmaul sign (accentuated jugular venous pressure during inspiration) and an early diastolic sound (pericardial knock). These findings help to confirm constrictive pericarditis as the most likely diagnosis.

OK to watch for 3 months If persists then consider pericardiocentesis, curative in 50%, and may help with diagnosis, prevent cardiac tamponade

some data on safety, but CT is much preferred, US or plain radiography

fixed splitting of the S2, a parasternal impulse due to right-sided chamber enlargement, and tricuspid diastolic and pulmonary systolic murmurs related to the increased right heart volume from the left-to-right shunt. The right-sided murmurs increase with inspiration due to the increased systemic venous return. The chest radiograph demonstrates right heart and pulmonary artery enlargement, consistent with long-standing right-to-left shunt. The test of choice for confirming the diagnosis of atrial septal defect suspected on physical examination is transthoracic echocardiography.

Acute pericarditis post MI, weeks to months after STEMI - ASA preferred to NSAIDs for Tx pleuritic chest pain, pericardial friction rub, fever, leukocytosis, and, sometimes, pleural effusion or pulmonary infiltrates. This is distinguished from infarction pericarditis, which is characterized by a pericardial friction rub with or without chest pain and typically occurs within 1 to 2 days of the myocardial infarction. Anti-inflammatory therapy is the mainstay of treatment for pericarditis. Treatment with aspirin is preferred over NSAIDs if an acute myocardial infarction is the cause of acute pericarditis because its antiplatelet effects are beneficial and because of a prevailing concern that NSAIDs may promote ventricular rupture by impairing myocardial scar formation. Although animal data support this proposition, no definite proof for this concern exists in humans

Adenosine and dipyridamole are contraindicated in patients with hypotension, sick sinus syndrome, high-degree atrioventricular block, and bronchospastic disease. These agents may cause dyspnea and reduced FEV1 in persons with chronic obstructive pulmonary disease. For these reasons, dobutamine is the preferred pharmacologic agent for stress testing in the presence of underlying bronchospastic lung disease.

For patients intolerant of angiotensin-converting enzyme inhibitors due to hyperkalemia or renal insufficiency, the combination of hydralazine and a nitrate is a suitable alternative. Leads to vasodilation and afterload reduction.

The most common cause of sudden death in patients with heart failure is arrhythmia, including both ventricular tachyarrhythmia and bradyarrhythmia. Current guidelines recommend implantable cardioverter-defibrillator (ICD) placement in patients with ischemic or nonischemic cardiomyopathy and an ejection fraction of less than or equal to 35%. ICD placement is, therefore, indicated in this setting (primary prevention), regardless of symptoms or functional status. This patient does not meet current criteria for implantation of a biventricular pacemaker in addition to ICD implantation. This patient is asymptomatic (New York Heart Association [NYHA] class I) and does not have a prolonged QRS complex on electrocardiogram. Current criteria for biventricular pacemaker implantation include left ventricular ejection fraction less than or equal to 35%, QRS duration greater than or equal to 120 msec, sinus rhythm, and NYHA class III or IV symptoms (that is, symptoms with mild activity or at rest) on optimal medical therapy for heart failure.

The jugular venous pulse contour in pulmonary stenosis demonstrates a prominent a wave. A right ventricular lift is frequently present. An early systolic click is common, and increased proximity of the click to the S1 suggests increased severity of pulmonary stenosis. A systolic murmur with a delayed pulmonic component of the S2 is noted. In patients with severe valvular pulmonary stenosis, the pulmonic component of the S2 and ejection click disappear due to reduced pliability of the valve. Right ventricular hypertrophy and right axis deviation are noted on the electrocardiogram. The diagnosis of pulmonary valve stenosis is confirmed by transthoracic echocardiography. Echocardiography with Doppler evaluation determines the severity of pulmonary stenosis and the degree of right ventricular hypertrophy. Intervention is recommended when the gradient is greater than 50 mm Hg or when right ventricular hypertrophy is present. Systolic doming of the pulmonary valve noted on two-dimensional echocardiography suggests that the valve is likely amenable to percutaneous intervention. The treatment of choice for pulmonary valve stenosis is pulmonary balloon valvuloplasty.

Loop recorders, as opposed to hand-held event monitors, continuously record data but only save when the patient manually activates the monitor because of symptoms. Rhythm data are saved preceding and following activation, usually for a period of 1 to 2 minutes. The advantages of loop recorders include a longer period of monitoring time (up to 1 month) compared with 24-hour ambulatory monitoring and continuous monitoring in patients with transient loss of consciousness.

(delayed distal pulses, a radiating systolic murmur, and a single S2 due to delayed closure of the calcified aortic valve). Aortic stenosis is a slowly progressive disease process, and asymptomatic patients can remain event-free for prolonged time periods. As a consequence, prophylactic valve replacement is not performed in asymptomatic patients. In patients with significant aortic stenosis but with good preoperative exercise tolerance, surgical procedures are generally well tolerated. Percutaneous aortic balloon valvuloplasty is generally not performed for calcific aortic stenosis because serious complications, including aortic regurgitation and embolic stroke, occur in more than 10% of procedures, and restenosis occurs within a year in most patients.

the finding of a diastolic murmur consistent with pulmonic regurgitation and right ventricular enlargement requires further evaluation because these findings would not be present if the pulmonic valve was still competent after surgical repair. In adults with repaired tetralogy of Fallot, the most common long-term adverse outcome is severe pulmonic regurgitation leading to right ventricular dilation and systolic dysfunction. Cardiac magnetic resonance imaging is the most accurate method for quantitation of right ventricular volumes and ejection fraction, and can also provide quantitative measures of pulmonic regurgitant severity. Repeat pulmonic valve surgery will eventually be needed in this patient to prevent progressive right heart dysfunction.

only indicated if symptomatic and sever Beta-blockers are best 1st choice - if refractory to meds, consider ablation Premature ventricular complexes are spontaneous depolarizations originating from the ventricles. A premature complex can be single, in pairs (couplets), or alternating with sinus beats in a specific multiple, such as in bigeminy, in which premature ventricular complexes and sinus beats alternate in a 1:1 ratio. These beats are usually followed by a compensatory pause, and patients may feel as if their heart is stopping. In the absence of structural heart disease, the prognosis is benign, and treatment is based on ameliorating significant symptoms, which may include palpitations, fatigue, and lightheadedness. β-Blockers, such as metoprolol, are reasonably effective at suppressing premature ventricular complexes. This prognosis is in contrast to patients with heart failure, hypertension, or left ventricular hypertrophy; in all of these groups, ventricular ectopy has been described as a marker of increased risk of cardiovascular events.

Digoxin is indicated in patients with NYHA class II to IV heart failure and left ventricular systolic dysfunction (ejection fraction <40%) despite optimal medical treatment with an angiotensin-converting enzyme (ACE) inhibitor and a β-blocker. Digoxin has been shown to alleviate symptoms and decrease hospitalizations in patients with heart failure but does not improve survival.

The addition of hydralazine and isosorbide dinitrate to standard medical therapy is indicated for treatment of black patients with systolic heart failure and New York Heart Association functional class III or IV symptoms. Hydralazine and nitrates together provide afterload reduction in patients with left ventricular dysfunction. Hydralazine and isosorbide dinitrate have been shown to reduce mortality by 40% in black patients when added to standard medical therapy (angiotensin-converting enzyme inhibitor, β-blocker).

In patients with atrial fibrillation, it is important to correlate symptoms with episodes of arrhythmia and assess rate control to determine whether symptoms are caused by rapid heart rate or by the atrial fibrillation itself. - 24 hr ambulatory monitoring would be best way to evaluate

CT with contrast OK, but watch Cr TEE benefit of doing at bedside, eval aorta, valve, and pericardial space Physical examination findings typical of acute aortic dissection include severe aortic pain, blood pressure or pulse differential between the arms, and a widened mediastinum on chest radiograph. The positive likelihood ratio of aortic dissection in a patient with one of these findings is 0.5, with two of these findings, 5.3; and with all three of these findings, 66. The recent use of cocaine increases the risks for aortic dissection acutely around the time of use.

An atrial septal defect should be closed if there is evidence of a left-to-right shunt with a pulmonary flow to systemic flow ratio that is greater than or equal to 1.5:1.0, volume overload of right-sided cardiac chambers, or symptoms related to the defect.

For patients with low or moderate (<20%) 10-year risk of a coronary artery disease event by Framingham Risk, lifestyle modifications are recommended initially, with follow-up in 3 to 6 months.

manifesting with flu-like systemic symptoms, chest pain, elevated troponin level, and reduced systolic function. The presentation of myocarditis is quite variable, ranging from asymptomatic to cardiogenic shock. Electrocardiographic findings may be variable as well, including findings mimicking acute coronary syndrome or myocardial infarction. Atrial or ventricular arrhythmias may be seen as well. Echocardiographic findings may show either global hypokinesis or regional wall motion abnormalities, the latter mimicking acute myocardial infarction. There is no specific treatment for idiopathic (also called lymphocytic) myocarditis other than supportive care and standard therapy for heart failure; thus, therapy with an angiotensin-converting enzyme (ACE) inhibitor such as captopril and a β-blocker such as carvedilol would be appropriate to start at this time.

Clopidogrel should be continued for at least 1 year following placement of a drug-eluting stent and for at least 1 month following placement of a bare metal stent.

In patients with unstable angina who have contraindications to β-blockers, calcium channel blockers should be used. Such as COPD, FEV1<30

The ductus arteriosus connects the aorta and pulmonary artery during fetal life. Persistence of the ductus arteriosus after birth is associated with maternal rubella infection. Patients with a moderately sized patent ductus arteriosus may present with symptoms of heart failure, with enlarged heart chambers on the left side. The patient has features of a large left-to-right shunt with associated left heart enlargement characterized by a displaced left apical impulse. These findings suggest that the shunt is beyond the atrial level and rules out an atrial septal defect. The systolic and diastolic (continuous) murmur is most consistent with a patent ductus arteriosus. - DONT see cyanosis

Ventricular septal defect may cause left ventricular volume overload, as is suggested in this patient; however, patients with a ventricular septal defect characteristically have a systolic murmur associated with a thrill that obliterates the S2, whereas a diastolic component is minimal or absent. A large ventricular septal defect causing volume overload may be associated with a displaced left ventricular impulse and mitral diastolic flow rumble.

90% from 3 gene mutations often misdiagnosed as a seizure disorder Abnl if >440 in men, 460 in women 1-recurrent syncope trigger by activity 2-emotional arousal, exercise, loud noises 3-long QT, events during sleep

carries a high risk of sudden cardiac death. The syndrome is characterized by an autosomal dominant pattern of inheritance, a short QT interval (<300 msec), atrial fibrillation occurring at a young age, and an increased risk of death due to ventricular fibrillation.

characterized by ventricular preexcitation (short PR interval and delta wave) and symptomatic tachycardia. Owing to the rapid conduction properties of some accessory pathways, atrial fibrillation can be a life-threatening arrhythmia in these patients due to rapidly conducting atrial fibrillation degenerating to ventricular fibrillation. Although patients with Wolff-Parkinson-White syndrome have an increased risk of sudden cardiac death, it is very unusual for this to be the first symptomatic manifestation of the syndrome.

Although endomyocardial biopsy is generally not indicated in the evaluation of heart disease, it may prove critical in diagnosing unusual conditions, such as giant cell myocarditis, in which a histologic diagnosis dictates management. Endomyocardial biopsy is recommended in patients with new-onset heart failure (<2 weeks) with hemodynamic compromise and in those with new-onset heart failure of 2 weeks' to 3 months' duration associated with a dilated left ventricle and new ventricular arrhythmias, Mobitz type II second- or third-degree atrioventricular heart block, or failure to respond to usual care within 1 to 2 weeks. Giant cell myocarditis is a rare, idiopathic cause of fulminant or subacute-onset heart failure. Most patients with giant cell myocarditis present with heart failure (75%), but a substantial minority may present with ventricular arrhythmia (14%) or heart block (5%). Diagnosis is made by endomyocardial biopsy and is characterized by the presence of multinucleated giant cells with eosinophils and myocyte necrosis. Prognosis is very poor, and urgent evaluation for cardiac transplantation is recommended, although giant cell myocarditis can recur in the transplanted heart.

closure of the mitral valve (and tricuspid valve)

aortic valve closure (and pulmonic, slightly delayed) inspiration, A2 and P2 split, prolongs ejection of blood from right ventricle heard best in 2nd intercostal space on L

rapid deceleration of blood on ventricular wall common in young adults may represent pathologic change of compliance of ventricles in older adults, CHF, volume overload of a ventricle = gallop of 3 heart sounds, like "Kentucky"

marks atrial contraction immediately precedes S1, also represents change in ventricular compliance - listen with the bell hypertensive heart disease, CAD, aortic stenosis, CM if S3 and S4 = summation gallop

heard best at apex

Left lower sternal border

Usually 2-3rd intercostal space on L, but sometimes higher or lower on L

can be from apex to RUSB

suggests pulmonary HTN

Increase murmur of HOCM Decrease murmur of aortic stenosis

decrease murmur of HOCM Increase murmur of aortic stenosis

pulmonic stenosis and delayed closing, or RBBB Or early closure of aortic valve in mitral regurg

Usually from mitral valve prolapse, intensity often decreases with inspiration often followed by a late systolic murmur from mitral regurg could be from bicuspid aortic valve

usually from mitral valve stenosis medial to apex, LLB

tricuspid regurg

mitral regurgitation murmur

VSD blood flows from LV to RV

Aortic stenosis can also see aortic sclerosis, bicuspid aortic valve

HOCM Maneuvers that increase preload (stand-to-squat and passive leg lift) decrease the murmurs of hypertrophic cardiomyopathy and mitral valve prolapse. The Valsalva maneuver and the squat-to-stand maneuver transiently decrease venous return, with the septum and anterior mitral leaflet brought closer together. Turbulent flow—and the murmur—are increased. Handgrip exercise increases afterload and decreases the relative pressure gradient across the left ventricular outflow tract, so murmur intensity for hypertrophic cardiomyopathy is decreased.

Pulmonic stenosis increases RV afterload

Aortic Regurg volume overload on LV

Mitral Stenosis

PDA

Valve replacement surgery is recommended for asymptomatic patients with a bicuspid aortic valve and severe aortic regurgitation when the left ventricular end-systolic diameter reaches 55 mm or the left ventricular ejection fraction is less than 60%.

young patient with systemic HTN pulse delay between the upper and lower extremities (radial artery to femoral artery delay). The blood pressure in the lower extremities, when measured, will be lower than the blood pressure noted in the upper extremities. The patient also has an ejection click and an early systolic murmur consistent with a bicuspid aortic valve, which is present in more than 50% of patients with aortic coarctation. The systolic and diastolic murmurs noted over the back are related to collateral vessels, which also cause the sign of rib notching, seen on this patient's chest radiograph on the inferior surface of the posterior upper thoracic ribs bilaterally.

This patient has tricuspid regurgitation and significant pulmonary hypertension with evidence of pressure overload on the right ventricle. Pulmonary hypertension with right ventricular enlargement and tricuspid valve annular dilation can lead to significant regurgitation of an otherwise normal tricuspid valve. Pulmonary hypertension may occur when abnormalities in left heart valvular or myocardial function (systolic or diastolic) cause pulmonary venous hypertension. Additional causes of pulmonary hypertension include chronic hypoxic pulmonary disorders (such as chronic obstructive pulmonary disease, interstitial lung disease, or sleep apnea) and chronic thromboembolic disease. Pulmonary hypertension may occur in association with anorectic drug use, HIV infection, chronic liver disease, or collagen vascular disease. In the absence of identifiable risk factors, pulmonary hypertension may be idiopathic. A diagnosis of idiopathic primary pulmonary arterial hypertension requires exclusion of secondary and associated causes of pulmonary hypertension. Additionally, right heart catheterization is also needed in order to demonstrate elevated pulmonary vascular resistance. Numerous diagnostic tests may be used to evaluate a patient with suspected pulmonary hypertension. Pulmonary function tests are needed to identify and characterize underlying lung disease. Ventilation-perfusion scanning is used to evaluate patients for chronic thromboembolic disease. A normal scan has greater than 90% sensitivity in excluding chronic thromboembolic disease and a similarly high specificity. Although helpful in the evaluation of acute pulmonary embolism, CT angiography is not known to be sufficiently sensitive for detection of chronic thromboembolism. Blood tests are performed to evaluate potential liver disease, HIV infection, or collagen vascular disease. A right heart catheterization confirms the presence of pulmonary hypertension and allows for calculation of pulmonary vascular resistance. Some patients require left heart catheterization as well.

Pulmonary arterial hypertension (PAH) carries a very high risk of death during pregnancy, with an estimated maternal mortality rate of 30% to 50%. Thus, pregnancy is contraindicated in patients with severe PAH, even when asymptomatic. This patient should be counseled to avoid pregnancy because of PAH; if an unplanned pregnancy occurs, termination is recommended

Carotid endarterectomy is beneficial for symptomatic patients with recent nondisabling carotid artery ischemic events and ipsilateral 70% to 99% carotid artery stenosis. It may be considered in patients with stenosis of 50% to 69% if the patient is likely to live for 5 years or longer. Carotid endarterectomy has not demonstrated benefit for patients with stenosis of less than 50%.

The presence of an ascending aortic atheroma of 4 mm or greater in diameter increases the risk of recurrent stroke. There is debate as to whether warfarin or antiplatelet monotherapy is superior for risk reduction, and as no direct comparative study has been completed, either choice would be appropriate. While intensive lipid-lowering therapy has not been studied specifically in patients with cerebrovascular events and aortic atheroma, treatment with 40 mg/d of pravastatin in the CARE trial was associated with a clinically significant reduction in the risk for stroke.

Controversial Warfarin is best answer at this time LMWH is a possibility Both need close monitoring Warfarin has a low molecular weight and crosses the placenta, causing fetal anticoagulation. Thus, the risk of spontaneous abortion, prematurity, embryopathy, stillbirth, and fetal intracranial hemorrhage are increased. Warfarin use throughout pregnancy until near term, however, does provide the lowest risk for maternal complications and death and is the primary treatment used in most countries outside of the United States. Warfarin embryopathy is a concern when warfarin is administered during the first trimester; however, when the dose of warfarin is less than 5 mg daily, the risk of embryopathy decreases to below 10%. There is controversy regarding the best anticoagulation regimen for the pregnant patient with a mechanical valve prosthesis, balancing the safety to mother and fetus. No single agent has been demonstrated to be the agent of choice. Meticulous monitoring and dose adjustment of all anticoagulation regimens is required during pregnancy

BNP often low in obese pts, so could be a false negative test for heart failure if symptoms present

The primary indication for valve replacement in aortic stenosis is onset of cardiac signs and symptoms, such as angina, syncope, exertional dyspnea, or heart failure. Age is not a contrainidcation.

granulomas on biopsy black patient major risk of sudden cardiac death Sudden death accounts for up to 65% of deaths due to cardiac sarcoidosis, presumably caused by ventricular tachyarrhythmias or conduction block. Symptomatic or electrocardiographically evident arrhythmias or conduction abnormalities typically become evident prior to sudden cardiac death. This patient's history of recurrent syncope, ventricular tachycardia, conduction abnormalities, and family history of sudden death place her at high risk for sudden death. The most appropriate management for this patient is placement of an implantable cardioverter-defibrillator (ICD), which has defibrillation and pacing capabilities for treatment of ventricular tachyarrhythmias and bradyarrhythmias, respectively.

The presence of the characteristic skin rash, erythema migrans, with or without a history of tick bite in an endemic region, has a probability greater than 80% of being caused by Borrelia burgdorferi infection, and is sufficient to support a decision to treat Lyme disease empirically without laboratory confirmation. Although antibiotics have not been shown to improve resolution of cardiac symptoms, it is recommended that patients with cardiac symptoms or advanced heart block be admitted for monitoring and antibiotic therapy. The preferred antibiotic regimen is intravenous ceftriaxone until the heart block resolves, followed by a 21-day course of oral therapy. The discovery of Lyme disease in any stage should prompt antibiotic treatment since early phases may regress spontaneously but leave patients at risk for later (neurologic or rheumatic) stages. The recommended 3-week course of treatment seems to reduce the chance of disease progression dramatically. Lyme carditis is manifested by acute-onset, high-grade atrioventricular conduction defects that may occasionally be associated with myocarditis. Carditis occurs in 5% to 10% of patients with Lyme disease, usually within a few weeks to months after infection. Cardiac involvement can occur in isolation or with other symptoms of the disease. Atrioventricular block can present in any degree, and progression to complete heart block is often rapid. Prognosis is good, with usual resolution of atrioventricular block within days to weeks. This patient has complete heart block, as evidenced by a faster sinus rate than the escape rhythm, and no relationship between the atrial and ventricular electrical activity. In some patients, heart block is the first and only manifestation of Lyme disease, but the diagnosis can be confirmed by a positive IgM and IgG antibody response to B. burgdorferi. Lyme serologic testing should be considered in any patient with unexplained high-grade atrioventricular block, particularly in patients with potential tick exposure living in endemic areas.

If this patient were taking a β-blocker for hypertension control, it would need to be withheld prior to the stress test because a stress test requires that the patient achieve 85% of maximum predicted heart rate to be diagnostic.

A supervised program of regular, repeated exercise to the point of near-maximal pain significantly increases pain-free walking time and walking distance in patients with symptomatic peripheral arterial disease. Additionally, for infrapopliteal disease, a supervised exercise program is more effective over the long-term than percutaneous revascularization and is less expensive. Patients with severe ischemic heart disease, severe valvular heart disease, or known large aortic aneurysms must be considered carefully and individually before prescription of exercise, but there are no other vascular contraindications in patients without threatened limb loss. Consider surgery if there is pain at rest, ABI<0.4, ischemic ulceration or gangrene

Relative contraindications to thrombolytic therapy include pregnancy, poorly controlled hypertension, prior ischemic stroke more than 3 months ago, prolonged cardiopulmonary resuscitation within 3 weeks, recent (within 2 to 4 weeks) internal bleeding, active peptic ulcer disease, and current use of anticoagulants (warfarin). Absolute contraindications include any prior intracerebral hemorrhage, known cerebrovascular lesion (arteriovenous malformation), ischemic stroke within 3 months, suspected aortic dissection, active bleeding (excluding menses), and significant closed head or facial trauma within 3 months.

Spironolactone is indicated for treatment of severe (NYHA functional class III or IV) systolic heart failure in addition to standard therapy with angiotensin-converting enzyme (ACE) inhibitors, β-blockers, and diuretics as needed. The addition of spironolactone is associated with a 30% relative reduction in mortality.

Positive inotropic agents such as dobutamine or milrinone can be used to correct low cardiac output and improve perfusion in patients with cardiogenic shock.

In patients with class I acute limb ischemia (moderate to severe claudication but no rest pain, audible venous and arterial Doppler signals), antiplatelet therapy along with systemic anticoagulation with heparin is indicated. Patients with transient sensory deficits and no motor weakness are typically considered for intra-arterial thrombolytic therapy. This patient has marked motor and sensory deficits and his limb is immediately threatened; he needs emergency surgical revascularization. Acute arterial occlusion is manifested by the "five P's"— pain, paresthesia, absent pulses, paralysis, and pallor; the viability of an acutely threatened limb is determined by the severity of these clinical characteristics. Improvement in pain, as occurred in this patient, should not be taken as a reassuring sign, but rather as a sign of progressive neurologic deficit due to ischemia. This patient has an immediately threatened limb as demonstrated by marked motor and sensory deficits and the absence of arterial Doppler signals, but with the presence of intact venous signals and some residual motor function (class IIb acute ischemia). Emergency surgical revascularization is necessary if the limb is to be saved. Patients with anesthesia, paralysis, and loss of vascular flow signals (class III ischemia) have irreversible ischemia and prompt amputation is required. Patients with less dense sensorimotor defects and intact venous flow signals (class IIb ischemia) may obtain limb salvage, but only with immediate revascularization. Patients without sensorimotor loss and with evidence of intact vascular flow (class IIa ischemia) are more likely to obtain limb salvage, but only with prompt vascular intervention.

Symptomatic sinus node dysfunction is an indication for pacemaker placement, even if the bradycardia occurs as a consequence of drug therapy, if there is no acceptable alternative. SSS comprises a collection of pathologic findings that result in bradycardia. These include sinus arrest, sinus exit block, and sinus bradycardia. Approximately 50% of patients with SSS also have associated supraventricular tachycardia, most often atrial fibrillation or atrial flutter. The tachycardia-bradycardia syndrome is characterized by rapid ventricular conduction during episodes of atrial fibrillation, but resting bradycardia between episodes. This combination makes management of intermittent tachycardia difficult without pacemaker backup. SSS is common in the elderly, and because symptoms can be intermittent or nonspecific, misdiagnosis can occur.

consistent with heart failure with preserved systolic function; that is, she has symptoms of heart failure in the setting of normal systolic function and no valvular abnormalities. She has hypertension, which predisposes to the development of left ventricular hypertrophy and impaired ventricular relaxation. The primary treatment goals in diastolic heart failure are to treat the underlying cause and to manage any potentially exacerbating factors, which commonly include tachycardia, hypertension, and ischemia. This patient's blood pressure is still not optimally controlled, and adding candesartan would be appropriate at this time. Blockade of neurohormonal activation, including the renin-angiotensin-aldosterone system, in heart failure with preserved systolic function is beneficial in reducing salt and water retention, as well as ameliorating adverse cardiac remodeling, cellular fibrosis, and hypertrophy. One of the few large, randomized prospective trials examining treatments for heart failure with preserved systolic function demonstrated that the angiotensin receptor blocker candesartan reduced heart failure-related hospitalizations but not mortality in patients with heart failure with preserved systolic function.

Usually happens 2-7 days after STEMI Late complications following STEMI include cardiogenic shock, ventricular septal defect, mitral regurgitation, free wall rupture, and left ventricular thrombus. A ventricular septal defect following an ST-elevation myocardial infarction results in a new systolic murmur and a "step-up" in oxygen saturation from the right atrium to the right ventricle. Although treatment for a ventricular septal defect is emergent surgery, in-hospital mortality remains high at approximately 60%.

Atrioventricular nodal (junctional) ablation with pacemaker placement is a safe and effective nonpharmacologic rate control option in patients with rapidly conducted atrial fibrillation. Maze procedure and radiofrequency ablation are second line options

tetralogy of Fallot with previous repair, which usually involves placement of a transannular pulmonary outflow tract patch. This causes severe pulmonary valve regurgitation, which is confirmed by the presence of a diastolic murmur that increases with inspiration, a parasternal impulse (right ventricular enlargement), and elevated central venous pressure. The holosystolic murmur at the left lower sternal border is characteristic of tricuspid regurgitation. Long-standing pulmonary valve regurgitation causes right ventricular enlargement and tricuspid annular dilatation with resultant regurgitation. The tricuspid regurgitation causes right atrial enlargement and increases the risk of atrial arrhythmias. The chest radiograph demonstrates features of right heart enlargement with a prominent right heart border (right atrium) and absence of the retrosternal air space (right ventricular enlargement). A right-sided aortic arch is also noted, which is present in 25% of patients with tetralogy of Fallot. Tetralogy of Fallot is the most common form of cyanotic congenital heart disease, accounting for approximately 10% of all congenital defects. Although these defects have been successfully repaired for more than 50 years, most patients with repaired tetralogy of Fallot have cardiac residua that may manifest with symptoms of dyspnea, heart failure, or arrhythmias years after repair. Life-long informed surveillance is recommended for patients with repaired tetralogy of Fallot. Patients with repaired tetralogy of Fallot are at increased risk of developing atrial arrhythmias due to atrial enlargement and prior atrial surgical incisions. These patients are also at risk of developing ventricular arrhythmias, which result primarily from dilatation and dysfunction of the right ventricle. Arrhythmias are a major cause of morbidity and mortality in patients with repaired tetralogy of Fallot.

Low-risk patients with mechanical valves (aortic prosthesis and no history of prior thromboembolism) undergoing noncardiac surgery can have warfarin discontinued without a heparin bridge 5 days prior to surgery.