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Edited by Joseph G. Murphy and Margaret A. Lloyd. The fourth edition of Mayo Clinic Cardiology continues the tradition of all previous editions: a succinct yet comprehensive teaching and learning resource rather than an overwhelming reference work. Sign up to an individual. Newer electronic fourth, edition of Mayo Clinic Cardiology: Concise patients with ST-segment pdfs/resourceone.info depression of more than 1 mm, . Type of Book: A multiauthored text and atlas of musculoskeletal imaging in sports medicine. Scope ofBook: The text and accompanying images summarize a.


Mayo Clinic Cardiology Pdf

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Mayo Clinic Cardiology - Ebook download as PDF File .pdf), Text File .txt) or read book online. Köp Mayo Clinic Cardiology av Joseph G Murphy, Margaret A Lloyd på Bokus. com. PDF-böcker lämpar sig inte för läsning på små skärmar, t ex mobiler. resourceone.info 29/10/ PM Page i Mayo Clinic Cardiology Board Review Questions and Answers resourceone.info Author: A. DOWNLOAD PDF .

Murphy, MD, Robert P. Frantz, MD, Leslie T. Cooper, Jr, MD. Coronary Stents. Murphy, MD, Gregory W. Cardiac Emergencies. Cardiogenic Shock.

Bell, MD. Almost every question has physical examination findings that provide critical clues to the answer in the stem of the question.

Important clues to a cardiac diagnosis can be obtained from inspection of the patient Table 1. During mid and late systole, the left ventricle LV is diminishing in volume and the apical impulse moves away from the chest wall. Thus, outward precordial apical motion occurring in late systole is abnormal. Remember that point of maximal impulse is not synonymous with apical impulse. Palpation of the Apex Constrictive pericarditis or tricuspid regurgitation produces a subtle systolic precordial retraction.

A subtle presystolic ventricular rapid filling wave A wave — frequently associated with LV hypertrophy—may be better visualized than palpated by observing the motion of the stethoscope applied lightly on the chest wall, with appropriate timing during simultaneous auscultation.

Likewise, a palpable A wave can be detected in this manner. The apical impulse of LV hypertrophy without dilatation is sustained and localized but should not be displaced. Causes of a palpable A wave presystolic impulse include the following: Aortic stenosis 2. Hypertrophic obstructive cardiomyopathy 3.

Systemic hypertension 3. A difference in systolic blood pressure between both arms of more than 10 mm Hg is abnormal Table 2. Examining the apical impulse by the posterior approach with the patient in the sitting position may at times be the best method to appreciate subtle abnormalities of precordial motion.

The normal apical impulse occurs during early systole with an outward motion imparted to the chest. Table 1. Cardiomyopathy Aortic regurgitation Heart block rare Right-sided congestive heart failure Prosthetic valve dysfunction hemolysis Pulmonary hypertension Secondary cardiomyopathy Hypertrophic obstructive cardiomyopathy Pulmonary stenosis Pulmonary arteriovenous fistula. Catecholamine-induced secondary dilated cardiomyopathy Verrucous endocarditis Myocarditis Pericarditis Secondary cardiomyopathy Heart block Rhabdomyoma Pericardial effusion Left ventricular dysfunction Any of the lesions that cause Eisenmenger syndrome Reversed shunt through patent ductus arteriosus.

Pulmonary hypertension Myocardial, pericardial, or endocardial disease Myocardial, pericardial, or endocardial disease often subclinical Pseudocardiomegaly Mitral valve prolapse Right-sided cardiac valve stenosis or regurgitation. The apical impulse of LV hypertrophy without dilatation is sustained and localized. It should not be displaced but may be accompanied by a palpable presystolic outward movement, the A wave.

Outward precordial apical motion occurring in late systole is abnormal. Multiple abnormal outward precordial movements may occur: Palpation of the Left Upper Sternal Area Abnormal pulsations at the left upper sternal border pulmonic area can be due to a dilated pulmonary artery e. Palpation of the Lower Sternal Area Precordial motion in the lower sternal area usually reflects right ventricular RV motion.

RV hypertrophy due to systolic overload such as in pulmonary stenosis causes a sustained outward lift. Diastolic overload such as in atrial septal defect [ASD] causes a vigorous nonsustained motion.

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In severe mitral regurgitation, the left atrium expands in systole but is limited in its posterior motion by the spine. Significant overlap of sites of maximal pulsation occurs in LV and RV overload states. For example, in RV overload, the abnormal impulse can overlap with. Table 2. Causes of Blood Pressure Discrepancy Between Arms or Between Arms and Legs Arterial occlusion or stenosis of any cause Dissecting aortic aneurysm Coarctation of the aorta Patent ductus arteriosus Supravalvular aortic stenosis Thoracic outlet syndrome.

Section I Fundamentals of Cardiovascular Disease Normal jugular venous pressure decreases with inspiration and increases with expiration. Veins that fill at inspiration Kussmaul sign , however, are a clue to constrictive pericarditis, pulmonary embolism, or RV infarction Table 5.

Pulsations of increased blood flow are dynamic and quick, whereas pulsations due to pressure overload cause a sustained impulse.

If the apical impulse is not palpable and the patient is hemodynamically unstable, consider cardiac tamponade as the first diagnosis.

Palpation of the Right Upper Sternal Area Abnormal pulsations at the right upper sternal border aortic area should suggest an aortic aneurysm. An enlarged left lobe of the liver associated with severe tricuspid regurgitation may be appreciated in the epigastrium, and the epigastric site may be the location of the maximal cardiac impulse in patients with emphysema or an enlarged RV.

Jugular veins that fill at inspiration Kussmaul sign are a clue to constrictive pericarditis, pulmonary embolism, or RV infarction. RV hypertrophy due to systolic overload causes a sustained outward lift. Diastolic overload as in ASD causes a vigorous nonsustained motion. The neck veins may collapse or remain distended. It may occur in LV failure with secondary pulmonary hypertension. In patients with chronic congestive heart failure, a positive hepatojugular reflux sign with or without increased jugular venous pressure , a third heart sound S3 , and radiographic pulmonary vascular redistribution are independent predictors of increased pulmonary capillary wedge pressure.

In the presence of normal sinus rhythm, there are two positive or outward moving waves a and v and two visible negative or inward moving waves x and y Fig. The x descent is sometimes referred to as the systolic collapse. Ordinarily, the c wave is not readily visible. The a wave can be identified by simultaneous auscultation of the heart and inspection of the jugular veins.

The a wave occurs at about the time of the first heart sound S1. The x descent follows. The v wave, a slower, more undulating wave, occurs near the second heart sound S2. The y descent follows. The a wave is normally larger than the v wave, and the x descent is more marked than the y descent Tables 3 and 4. Normal jugular venous pulse.

The jugular v wave is built up during systole, and its height reflects the rate of filling and the elasticity of the right atrium. The wave built up during diastasis is the h wave. The h wave height also reflects the stiffness of the right atrium. S1, first heart sound; S2, second heart sound. Table 3. Timing of Jugular Venous Pulse Waves a wave—precedes the carotid arterial pulse and is simultaneous with S4, just before S1 x descent—between S1 and S2 v wave—just after S2 y descent—after the v wave in early diastole.

Table 4. Tricuspid stenosis 2. Decreased right ventricular compliance due to right ventricular hypertrophy in severe pulmonary hypertension Pulmonary stenosis Pulmonary vascular disease 3. Severe left ventricular hypertrophy due to pressure by the hypertrophied septum on right ventricular filling Bernheim effect Hypertrophic obstructive cardiomyopathy Rapid x descent Cardiac tamponade Increased v wave Tricuspid regurgitation Atrial septal defect Rapid y descent Friedreich sign Constrictive pericarditis.

If the jugular veins are engorged but not pulsatile, consider superior vena caval obstruction.

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It may also occur in other states of high cardiac output or be caused by the wide pulse pressure associated with atherosclerosis, especially in the elderly. Dicrotic and Bisferiens Pulses A dicrotic carotid pulse occurs in myocardial failure, especially in association with hypotension, decreased cardiac output, and increased peripheral resistance.

Dicrotic and bisferious are the Greek and Latin terms, respectively, for twice beating, but in cardiology they are not equivalent. The second impulse occurs in early diastole with the dicrotic pulse and in late systole with the bisferiens pulse.

The bisferiens pulse usually occurs in combined aortic regurgitation and aortic stenosis, but occasionally it occurs in pure aortic regurgitation. Aortic Stenosis Pulsus parvus soft or weak classically occurs in aortic stenosis but can also result from severe stenosis of any cardiac valve or can occur with low cardiac output of any cause.

Severe aortic stenosis also produces a slowly increasing delayed pulse pulsus tardus. Because of the effects of aging on the carotid arteries, the typical findings of pulsus parvus and pulsus tardus may be less apparent or absent in the elderly, even with severe degrees of aortic stenosis. Hypertrophic Obstructive Cardiomyopathy In hypertrophic obstructive cardiomyopathy, the ventricular obstruction begins in mid systole, increases as. Table 5. Differentiation of Internal Jugular Vein Pulse and Carotid Pulse Jugular vein pulse Double peak when in sinus rhythm Obliterated by gentle pressure Changes with position and inspiration Carotid pulse Single peak Unaffected by gentle pressure Unaffected by position or inspiration.

Pulsus alternans may be affected by alterations in venous return and may disappear as congestive heart failure progresses.

Because of the effects of aging on the carotid arteries. The right side then should have the stronger pulse. In a young patient. Pulsus Alternans Pulsus alternans alternation of stronger and weaker beats rarely occurs in healthy subjects and then is transient after a premature ventricular contraction.

An abrupt change in the acoustic characteristics pitch of the bruit as the stethoscope is inched upward may be a clue to the presence of combined lesions. A pulsating cervical mass. It occurs classically in cardiac tamponade but occasionally with other restrictive cardiac abnormalities.

Pulsus and Electrical Alternans Pulsus alternans Severe heart failure Electrical alternans Pericardial tamponade Large pericardial effusions. Aortic dissection and thoracic outlet syndrome may also produce inequality of arterial pulses. Inequality of the carotid pulses can be due to carotid atherosclerosis. The initial carotid impulse is brisk.

Both conditions may coexist. The pulse may be bifid as well Table 6. Pulsus parvus soft or weak classically occurs in aortic stenosis but can also result from severe stenosis of any cardiac valve or can occur with severely low cardiac output of any cause. Electrical alternans alternating variation in the height of the QRS complex is unrelated to pulsus alternans Table 8.

Transmitted Murmurs Transmitted murmurs of aortic origin. It usually is associated with severe myocardial failure and is frequently accompanied by an S3. Table 9 lists causes of an abnormal S1. Pulsus alternans usually is associated with severe myocardial failure and is frequently accompanied by an S3.

If S1 seems to be louder at the base than at the apex. Paradoxical pulse occurs classically in cardiac tamponade but occasionally with other restrictive cardiac abnormalities. M1 occurs before T1 and is the loudest component. A variable S1 intensity during a wide complex. The intensity is inversely related to the previous RR cycle length. The S1 may also be soft in severe aortic regurgitation related to early closure of the mitral valve caused by LV filling from the aorta. The finding of a femoral or carotid bruit in an adult suggests diffuse atherosclerosis.

When the valve becomes calcified and immobile. Chapter 1 Cardiovascular Examination pulsus tardus may be less apparent or absent in the elderly. If S1 seems louder at the lower left sternal border than at the apex implying a loud T1. The marked delay of T1 in Ebstein anomaly is related to the late billowing effect of the deformed sail-like anterior leaflet of the tricuspid valve as it closes in systole. Transmitted murmurs of aortic origin. If the S1 is louder at the lower left sternal border than at the apex implying a loud T1.

Fibromuscular dysplasia is less common and occurs in younger patients. Atrial fibrillation produces a variable S1 intensity. Wide splitting of S 1 occurs with right bundle branch block and Ebstein anomaly. With higher systolic gradient and lower pulmonary artery systolic pressure. An aortic click is not heard with uncomplicated coarctation. Systolic Ejection Clicks or Sounds The ejection click sound follows S1 closely and can be confused with a widely split S1 or.

Pulsatile distention of a dilated great artery. Although a click implies cusp mobility. A pulmonary click can occur in idiopathic dilatation of the pulmonary artery. A click is absent in subvalvular or supravalvular aortic stenosis or hypertrophic obstructive cardiomyopathy. Increased pressure in the great vessel. The causes of ejection clicks are listed in Table Clicks can originate from the left or right side of the heart.

The aortic click radiates to the aortic area and the apex and does not change with respiration. A click would be expected to be absent in subvalvular stenosis. Causes of Ejection Clicks Aortic click Congenital valvular aortic stenosis Congenital bicuspid aortic valve Truncus arteriosus Aortic incompetence Aortic root dilatation or aneurysm Pulmonary click Pulmonary valve stenosis Atrial septal defect Chronic pulmonary hypertension Tetralogy of Fallot with pulmonary valve stenosis absent if there is only infundibular stenosis Idiopathic dilated pulmonary artery.

In the latter condition. Table The three possible mechanisms for production of the clicks are as follows: The pulmonary click due to valvular pulmonary stenosis is the only right-sided heart sound that decreases with inspiration. Intrinsic abnormality of the aortic or pulmonary valve. The pulmonary click is best heard along the upper left sternal border.

The timing of the pulmonary click in relationship to S1 reflecting the isovolumic contraction period of the RV is associated with hemodynamic severity in valvular pulmonary stenosis. The marked delay of T1 in Ebstein anomaly is related to the late billowing effect of the deformed saillike anterior leaflet of the tricuspid valve as it closes in systole.

With a decrease in LV volume. Chapter 1 Cardiovascular Examination Other rare causes of nonejection clicks that can masquerade as mitral prolapse include ventricular or atrial septal aneurysms.

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Maneuvers that decrease LV volume. Splitting of S2 Fig. Branching logic tree for second heart sound S2 splitting.

A nonejection click not due to mitral valve prolapse does not have the typical responses to bedside maneuvers found with mitral valve prolapse. Second Heart Sound S2 is often best heard along the upper and middle left sternal border. Interventions that increase systemic blood pressure make the murmur louder.

Pulm HT. As with aortic stenosis. When the degree of splitting is unusually wide. Valve gradient increased gradient with low pressure in the great vessel delays closure 4. Wide splitting of S2 occurs in both conditions. With Eisenmenger physiology. The wide splitting of S2 in mitral regurgitation and ventricular septal defect is related to early aortic valve closure in ventricular septal defect.

Elastic recoil of the great artery decreased elastic recoil delays closure. Ejection time 3. A pulmonary systolic ejection murmur increased flow is common in patients with ASD. This is referred to as fixed splitting. Fixed splitting should be verified with the patient in the sitting or standing position because healthy subjects occasionally appear to have fixed splitting in the supine position.

P2 is delayed Fig. Delayed electrical activation of the RV. Pulmonary stenosis prolonged ejection time In ASD. Delay of RV contraction. Partial anomalous pulmonary venous connection may occur alone or in combination with ASD most often of the sinus venosus type.

P2 decreases in intensity. Diagrammatic representation of normal and abnormal patterns in the respiratory variation of the second heart sound. The heights of the bars are proportional to the sound intensity. Wide splitting of S2 occurs in both partial anomalous pulmonary venous connection and ASD. Soft S2 Decreased intensity of A2 or P2.

Mechanical delay of LV ejection. With abnormal relationships of great vessels. In adults. In severe aortic stenosis. Pulmonary hypertension may cause wide splitting of S2. Intensity of S2 Loud S2 Ordinarily. When both components of S2 are heard at the apex in adults. When one component of S2 is enveloped in a long systolic murmur. Electrical delay of LV contraction. Patent ductus arteriosus. With only one functioning semilunar valve.

Examples include the following: Transient paradoxical splitting of S2 can occur with myocardial ischemia. Hearing two components of the S2 at the apex is abnormal in adults. A single S2 may also be heard in older patients and the following cases: Severe LV systolic failure of any cause 4. Chapter 1 Cardiovascular Examination Pulmonary hypertension may cause wide splitting of S2.

In mitral stenosis. In general. The pericardial knock of constrictive pericarditis is similar to an S3 and is associated with sudden arrest of ventricular expansion in early diastole. Other factors that increase left atrial pressures. Severe valvular immobility and calcification note that an OS can still be heard in some of these cases 2.

With increased severity of mitral stenosis and greater increase in left atrial pressures. Ventricular relaxation and compliance Although a physiologic S3 can be heard in young healthy subjects. An S3 is less common in conditions that cause thick.

Volume and velocity of blood flow across the atrioventricular valve 2. An S3 in a patient with mitral regurgitation implies severe regurgitation or a failing LV or both. When the S2-OS interval is more than to ms. An RV S3 is found along the left sternal border and increases with inspiration. LV hypertrophy that occurs with pressure overload states such as aortic stenosis or hypertension. In normal sinus rhythm.

Mild mitral stenosis is associated with an S2-OS interval of more than 90 ms. In such cases. The S2-OS interval widens on standing. Third Heart Sound The exact mechanism of S3 production remains controversial. An S3 may occur in hypertrophic obstructive cardiomyopathy with normal systolic function. This may arise from either a doming stenotic mitral valve or tricuspid valve. In comparison. The OS is often well transmitted to the left sternal border and even to the aortic area. The intensity of an OS correlates with valve mobility.

Factors related to S3 intensity include the following: An RV S3 may be augmented with inspiration. A tricuspid valve OS caused by tricuspid stenosis can be recognized by its location along the left sternal border and its increase with inspiration.

The pericardial. The physiologic S3 may disappear in the standing position. The S2-OS interval should not vary with respiration. An S4 is present in most patients with hypertrophic obstructive cardiomyopathy and in patients with acute myocardial infarction and is often heard in patients with systemic hypertension. Sitting or standing may attenuate the S4. Ischemic heart disease As the S4 becomes closer to S1. Chapter 1 Cardiovascular Examination knock is of higher frequency than S3.

Although an S4 can be heard in otherwise healthy elderly patients.. Fourth Heart Sound The S4 is thought to originate within the ventricular cavity and results from a forceful atrial contraction into a ventricle having limited distensibility. LV hypertrophy that occurs with pressure overload states.

The causes of S3 are listed in Table Although an S4 can be heard in otherwise healthy elderly patients. An S4 can still be heard in patients with LV hypertrophy or ischemic heart disease. A loud S4 can be heard in acute mitral regurgitation e. The pericardial knock is of higher frequency than S3. Under these circumstances.

Common pathologic states in which an S4 is often present include the following: Hypertension 3. It is not heard in healthy young persons or in atrial fibrillation. A right-sided S4 is increased in intensity with inspiration. In patients with aortic stenosis who are younger than 40 years. An S4 can originate from the RV. With chronic mitral regurgitation due to rheumatic disease.

Pulmonary stenosis 5. Hypertrophic obstructive cardiomyopathy 4. Holosystolic murmur that decreases in the latter part of systole—a configuration observed in acute mitral regurgitation. Systolic click—late apical systolic murmur of prolapsing mitral leaflet syndrome. Prolonged diamond-shaped systolic murmur masking A2 with delayed P2. Holosystolic murmur consistent with mitral or tricuspid regurgitation. The intensity loudness of an ejection systolic murmur may not reflect the severity of obstruction.

The magnitude of the delay is proportional to the severity of obstruction. E2 and E3. Factors that differentiate the various causes of LV outflow tract obstruction are shown in Table An ejection sound followed by a diamond-shaped murmur and wide splitting of S2 that may be present with atrial septal defect or mild pulmonic stenosis.

Sketches of various murmurs and heart sounds. Ejection types. If S2 becomes fused with expiration. Pansystolic or regurgitant types. Early crescendo-decrescendo systolic murmur ending in midsystole consistent with innocent murmur and small ventricular septal defect.

Early to midsystolic murmur with vibratory component—typical of an innocent murmur. S4 and midsystolic murmur consistent with mitral systolic murmur of cardiomyopathy or ischemic heart disease. Crescendo-decrescendo systolic murmur. An ejection sound and a short early systolic murmur.

The effects of various maneuvers on murmurs and S2 are shown in Figure 5. Late apical systolic murmur of prolapsing mitral valve leaflet. Aortic and Pulmonary Stenosis Stenosis of the aortic or pulmonary valves causes a delay in the peak intensity of the systolic murmur related to prolongation of ejection. For valvular pulmonary stenosis. Mid to lower left sternal border LV outflow tract obstruction 2.

A normal S2 that is. With aortic sclerosis. The differential diagnosis of LV outflow tract obstruction is shown in Table The systolic murmur of aortic stenosis. Upper left sternal border RV outflow tract obstruction —uncommon a bedside clue is a prominent jugular venous a wave. Supravalvular Aortic Stenosis The systolic murmur of supravalvular aortic stenosis is maximal in the first or second right intercostal space.

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Patients are usually young. A2 preserved supports a benign process. Aortic Stenosis Versus Aortic Sclerosis A frequent clinical problem is the differentiation of aortic stenosis from benign aortic sclerosis.

Apex associated mitral regurgitation 3. The systolic murmur is generally of grade 1 or 2 inten- sity and peaks early. Chapter 1 Cardiovascular Examination 17 Table The carotid upstroke should be normal.

The systolic murmur of severe acute mitral regurgitation can be variable. The systolic murmur of anterior mitral leaflet syndrome is transmitted posteriorly and can be heard along the thoracic spine and even at the base of the skull. The systolic murmur of mitral regurgitation can also be early systolic in timing. The systolic murmur of severe chronic mitral regurgitation is usually loud grade or louder.

The systolic murmur of posterior mitral leaflet syndrome can be well transmitted to the aortic area and be confused with aortic stenosis. Diagrammatic representation of the character of the systolic murmur and of the second heart sound in 5 conditions. Except in the elderly. Auscultation during inhalation of amyl nitrite can help differentiate this murmur from mitral regurgitation Tables 13 and Mitral Regurgitation Although mitral regurgitation is usually pansystolic.

The effects of posture. With significant pulmonary hypertension. Tricuspid Regurgitation The systolic murmur of tricuspid regurgitation is usually best heard at the lower left sternal border or over the xiphisternum. Inspiration may accentuate the murmur of tricuspid regurgitation.

Chapter 1 Cardiovascular Examination 19 Table The systolic murmur of significant tricuspid regurgitation may be subtle or even inaudible clinically.

The murmur parallels the pressure difference between the two ventricles in turn related to pulmonary and systemic vascular resistances. If the maximal intensity of the systolic murmur is in the first and second left intercostal spaces with radiation to the left clavicle.

The loud pansystolic murmur of ventricular septal defect may mask associated defects. The combination of ventricular septal defect and aortic regurgitation may suggest patent ductus arteriosus. The systolic murmur of posterior mitral leaflet syndrome can be transmitted to the aortic area and be confused with aortic stenosis.

The systolic murmur of anterior mitral leaflet syndrome is transmitted posteriorly and can be heard. Anterior mitral leaflet syndrome with posteriorly directed jet of mitral regurgitation 4. The systolic murmur of multiple ventricular septal defects is indistinguishable from that of single defects.

Aortic dissection 3. A wide pulse pressure suggests the latter or associated aortic regurgitation. Although mitral regurgitation is usually pansystolic. Mitral regurgitation that is early systolic in timing can be heard in acute. A systolic murmur in the posterior thorax may be caused by the following: Coarctation 2. The same is true for LV—right atrial shunts. Peripheral pulmonary artery stenosis 5. The systolic murmur of supravalvular aortic stenosis is maximal in the first or second right intercostal space.

In the presence of mitral stenosis. An innocent systolic murmur heard at the lower left sternal border should be differentiated from the systolic murmur of ventricular septal defect. The findings that suggest that a systolic murmur is pathologic are listed in Table Consider AR when there is a wide arterial pulse pressure. The systolic murmur of ventricular septal defect is typically pansystolic and associated with a thrill along the left sternal border.

When Table Remember that a patent ductus arteriosus or ventricular septal defect also can masquerade as an innocent murmur. Remember that a patent ductus arteriosus or ventricular septal defect can masquerade as an innocent murmur.

In young patients. S2 is normal and there are no clicks. These murmurs are common at all ages. The murmur of AR is typically early diastolic immediately after S2 and decrescendo in timing.

In older patients. If heard at the apex. If the maximal intensity of a systolic murmur is in the first and second left intercostal spaces with radiation to the left clavicle. Such murmurs can be heard at the aortic area.. In younger patients. A loud pansystolic murmur of ventricular septal defect may mask associated defects. Chapter 1 Cardiovascular Examination along the thoracic spine and even at the base of the skull. Administration of amyl nitrite can help differentiate these murmurs Table If so.

Pulmonary Regurgitation Although pulmonary regurgitation may sound similar to the murmur of AR. The murmur of pulmonary regurgitation due to pulmonary hypertension begins in early diastole immediately after P2 and is long and high-pitched. Severe AR. The presence of radiographic left atrial enlargement or atrial fibrillation favors mitral stenosis rather than isolated AR. The treatment decision for this type of VT depends on the symptoms.

If the symptoms are infrequent and mild, then no treatment is necessary. The initial choice for therapy is usually a beta blocker. Although first line referral for catheter ablation is an option, since the patient is only mildly symptomatic, a trial of medications is warranted. Digoxin increases intracellular calcium and can potentially promote triggered activity. Lidocaine is a weak sodium channel blocker and does not have significant potassium channel blockade.

It does not prolong the QT and it is the one antiarrhythmic that may actually shorten it. Lidocaine is a rather specific sodium channel blocker. The AV node is similar to the sinoatrial node in its lack of INa. Lidocaine does not have a significant effect on AV nodal conduction. Adenosine activates the IK,Achchannel in atrial tissue. Activation of the IK,Achchannel shortens the action potential duration, thereby shortening the refractoriness of the atrial tissue and promoting the induction of AF.

Of the answer choices given, class 1A agents quinidine and procainamide and class 3 agents ibutilide and sotalol have a significant potassium channel blocking effect, therefore prolonging the QT interval and potentially causing torsades de pointes.

Flecainide a class 1C agent is a fairly specific sodium channel blocker without a significant potassium channel blocking effect. Prolongation of the QT interval is not associated with flecainide.

The triangle of Koch is comprised of the ostium of the CS, tendon of Todaro, and septal attachment of the tricuspid valve leaflet. The region within the triangle is comprised of nodal and transitional cells. Both the AV and sinoatrial nodal cells lack INa. Conduction is mediated in these tissues by ICa,L. The conduction velocity is the most rapid in the His-Purkinje tissue. The outgoing potassium current is the principal determinant of repolarization of myocardial cells.

Vagal stimulation has little effect on the ventricular myocardial action potential, whereas it increases the action potential in the AV node and reduces it in the atrial myocardium. Early afterdepolarizations are depolarizations that occur in phases 2 and 3 of the action potential. Conditions that prolong the action potential duration promote the development of early afterdepolarizations. They are facilitated by a low potassium level, low magnesium level, and class I or III antiarrhythmic drugs, and are typically pause-dependent.

The mechanism that underlies the development of delayed afterdepolarizations is intracellular calcium overload. Digoxin increases intracellular calcium that can promote delayed afterdepolarization-triggered activity. Delayed afterdepolarizations have also been implicated in ischemic reperfusion arrhythmias and ryanodine receptor dysfunction. The H—V interval in Wolff-Parkinson-White syndrome can be negative or very short with antidromic tachycardia because the ventricle is activated prematurely by the accessory pathway or normal in orthodromic tachycardia since conduction proceeds down the AV node to the ventricle and returns retrograde through an accessory pathway.

The more typical form of Wolff-Parkinson-White syndrome is orthodromic and the QRS is narrow, even in tachycardia, unless functional bundle branch block occurs since the antegrade conduction proceeds through the AV node and His-Purkinje system. An anatomical obstacle is not necessary for reentrant arrhythmia. Recent studies have shown that reentry can occur in the absence of an obstacle as a consequence of conduction and refractoriness in the atrial or ventricular tissue.

Thus there is AV conduction via the accessory pathway with the return ventriculoatrial conduction via His-Purkinje system followed by the AV node.

AVNRT tends to occur in younger patients average 20—35 years , is slightly more common in women ratio 1. This rhythm typically has a short H—A interval usually 25—90 msec measured with the Hisbundle catheter.

In the most common form of this arrhythmia, conduction proceeds antegrade through the slow pathway and then retrograde over the fast pathway slow—fast AVNRT. Variations such as slow—slow and fast—slow conduction are also variants of this reentrant tachycardia. The most common mechanism of arrhythmias in sustained VT is reentry involving ventricular myocardium, most often from scars due to underlying CAD.

The patient has nonischemic cardiomyopathy and a search for potential secondary causes is warranted. Noninvasive testing, such as obtaining a serum ferritin to assess for hemochromatosis, should be performed prior to invasive studies, such as RV biopsy.

In a minimally symptomatic patient, an EP study is not a first line test. Nonetheless, if the PVCs are monomorphic and other causes of cardiomyopathy are excluded, the patient may be considered for an EP study and attempted ablation of the focus.

Prior to considering an ICD in this patient who has no other significant symptoms, medical therapy needs to be started and titrated to therapeutic doses. Answers a to d are all considered high risk characteristics for cardiogenic syncope. Recurrent unexplained falls in an elderly patient should first be assessed with tilt table testing unless other high risk features are present.

The temporal presentation and symptoms of the patients are consistent with pulmonary embolism, complicating the EP study he had 6 days before. The next step is to assess for this complication with screening tests, such as an arterial blood gas and D-Dimer, followed by an imaging modality, such as a ventilation perfusion scan or CT scan. If the evaluation for a pulmonary embolus is negative, a next step is to consider pericarditis. Vasodepressor response characterized by a profound drop in BP with minimal change in HR is more common in patients more than 60 years old.

In contrast, cardioinhibitory response characterized by asystole and profound bradycardia that coincides with a decrease in BP, or a mixed-type event that is a combination of HR and BP reduction, is the initial event occurring more often in younger patients.

The patient has recurrent syncope with evidence of significant sinus node dysfunction. In this patient a pacemaker is indicated. AAI is indicated in a patient when AV conduction is completely normal. If there is evidence of dysfunction, such as this patient with first degree AV block, DDDR is the generally agreed upon treatment.

Patients that suffer a VF cardiac arrest that is not from reversible causes perimyocardial infarction, abnormal electrolytes, etc. Answers a to d are all considered a positive response to pharmacologic stress in patients suspected to have a cardiac channelopathy. Ajmaline is a sodium channel blocking agent used in patients suspected to have Brugada syndrome. Right-sided pathways tend to have lower acute success rates in comparison to left-sided pathways.

The patient has pre-excited AF due to Wolff-Parkinson-White and a shortest R—R interval during AF near msec; thus, she is at risk of sudden death in the future and should receive radiofrequency ablation of the accessory pathway to cure the Wolff-Parkinson-White. Acutely, procainamide is the drug of choice for termination or DC cardioversion if she is hemodynamically unstable. AV nodal blocking agents such as adenosine are contraindicated in this situation. An H—V interval from 55 to 99 msec is considered an intermediate result and requires either the presence of additional symptoms or other findings to direct therapy.

The vast majority of long QT cases are due to mutations in the KCNQ1 gene that encodes the slow component of the delayed rectifier potassium current long QT1. The gene-specific triggers of patients with long QT1 are exertion-related activities, in particular swimming.

In long QT2 auditory stimuli and the postpartum period are important triggers. In long QT3 the most common trigger is sleep. Identifying those with concealed long QT is important for counseling regarding activities and therapy. According to the Bethesda Conference guidelines, competitive sports are restricted with the exception of class IA activities.

These activities include: All of the above statements are true except b. Romano-Ward syndrome is a heterogeneous disorder associated with prolonged QT interval and recurrent syncope, cardiac arrest, or sudden death. It is inherited in an autosomal dominant pattern and several mutations involving sodium and potassium channels have been recognized.

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Jervell and Lange-Nielsen syndrome is inherited in an autosomal recessive pattern. It is associated with prolonged QT interval, history of recurrent syncope or sudden death, and congenital neural deafness.

All of the given statements, except e, are true in the management of drug-induced QT prolongation. Both isoproterenol infusion and temporary pacing can be used to increase the baseline HR. Beta blockers, which have a role in reducing arrhythmias in long QT1 and 2, are not effective in drug-induced tachyarrhythmia, and could worsen the condition by promoting bradyarrhythmia and pauses.

Brugada syndrome is characterized by ECG findings of ST elevation in the right precordial leads V1 through V3, in the presence or absence of incomplete or complete right bundle branch block, and an increased risk of sudden death. Patients are more often male and present with sudden death due to VF. The patient sustained a VF cardiac arrest from an underlying channelopathy Brugada syndrome.

He should receive an ICD without further testing for risk assessment. Provocative testing with class 1 agents is used strictly for diagnosis and has little prognostic value, in particular is this patient that has already experienced a sudden cardiac arrest.

Brugada syndrome is due to a loss of function mutation involving the SCN5Aencoded cardiac sodium channel. This is in contrast to long QT3, which is due to a gain of function mutation involving the SCN5A-encoded cardiac sodium channel.

All the medications listed in answers a to d have been shown to increase the QT interval. Although Amiodarone is on the list of agents that prolong the QT interval, it rarely causes torsades de pointes. Nonetheless, this potential complication must be considered. For a complete list of drugs that are known to cause this complication see www.

Mutations in the RyR2-encoded cardiac ryanodine receptor or the calcium release channel account for the majority of catecholaminergic polymorphic VT cases.

These mutations result in increased calcium leak during sympathetic stimulation, particularly during diastole. Patients with symptomatic catecholaminergic polymorphic VT should receive an ICD as first line therapy since other therapies, such as calcium channel and beta blockers, have not been shown to be sufficiently protective.

The most common associated congenital heart disease is Ebstein anomaly. Furthermore, an echocardiogram allows assessment of LV function, which is often depressed after conversion from a SVT. Finally, exercise testing can be considered as a further means to assess risk. Exercise provides information regarding the accessory pathway and its conduction at higher HRs.

Disappearance of the delta wave with exercise has been reported to coincide with a low risk of sudden death. AVNRT is more common in females. All the other arrhythmias listed are uncommon in this age group. All of the answer choices a to d are associated with second degree AV block. Regarding long QT syndrome, a subgroup of infants with this channelopathy present with 2: Other causes of second degree AV block include mechanical trauma during catheterization, metabolic, and drug induced etiologies.

Although all the answers are associated with AV block, maternal systemic lupus erythematosus is the most likely diagnosis in this patient. Her history suggests longstanding rhythm disease. Her echocardiogram is normal, which rules out L-TGA. Her clinical Lloyds-Chapter Ans. In mothers with systemic lupus erythematosus, antibodies anti-Ro can pass the placenta and affect the fetal AV conduction system.

The patient is asymptomatic but in complete heart block. The next step in her care is to determine if she requires implantation of a dual-chamber permanent pacemaker. Exercise testing is also important to assess exercise performance, but in this patient ischemia is not the cause of her rhythm disturbance. The patient has third degree AV block and has pauses in excess of 3 sec. These findings suggest the need for a pacemaker implantation.

Since the patient is in sinus rhythm, a dual-chamber device is required to prevent pacemaker syndrome.

Answers a to d are all reasons to implant a permanent pacemaker in a patient with congenital AV block. Isoproterenol infusion has no role in risk assessment in these patients. Answers a to c are proposed mechanisms underlying the initiation and maintenance of AF. Each of answers a to d has been shown to be a risk factor for AF. Other established causes include advancing age, valvular heart disease, excessive alcohol intake, thyrotoxicosis, pericarditis, cardiac surgery, acute pulmonary disease, and MI.

They were randomized to either rate control or rhythm control. Patients in the rhythm control group were more likely to be in sinus rhythm.

However, there was no statistically significant difference in mortality, stroke, quality of life, or development of heart failure between the rate and rhythm control groups. One of the most important findings in the AFFIRM trial was that anticoagulation should be strongly considered in these patients even in the presence of sinus rhythm.

One reason is that these patients often have silent or subclinical AF. The second reason is that AF is often associated with many other medical comorbidities that increase stroke risk, such as HTN, diabetes, CAD, heart failure, etc. From data based upon a long-term study of the NRAF participants, the risk of stroke increases incrementally as patients accumulate more of these risk factors. Rate control can be achieved with a variety of medications.

Digoxin alone is often insufficient to control HR during exercise. Dofetilide and amiodarone are acceptable drug choices in patients with AF and heart failure. This tracing demonstrates AF with Ashman phenomenon. A premature ventricular complex is not present. The widest complexes represent activation down the accessory pathway, whereas narrower ones represent fusion beats in which the ventricles are activated in part by conduction down the AV node and in part by the accessory pathway.

Adenosine shortens atrial refractory periods, causes AV block, and could accelerate the ventricular rate, resulting in degeneration to VF. Lidocaine has no effect on atrial tissue and is not effective in this setting. Both metoprolol and diltiazem also slow the AV node, possibly limiting concealed conduction from the node to the accessory pathway and accelerating conduction down the pathway.

Procainamide is the agent of choice in this setting. If this fails to control the rhythm, or the patient becomes hemodynamically unstable, cardioversion is appropriate. Regardless of the treatment choice, his BP requires aggressive control. Randomized studies of nonrheumatic AF in patients with paroxysmal and chronic AF have shown no difference in the rate of stroke between the subgroups.

First, patients with AF often have other comorbidities that are associated with a higher risk of stroke. Also, recent studies of different therapies have documented that patients typically experience multiple subclinical or asymptomatic episodes of AF.

These patient characteristics may account in part for why there is little difference in stroke risk between these arrhythmia subtypes. Digoxin, diltiazem, and metoprolol will slow the AV node conduction and control the ventricular rate. Although procainamide can be used to restore normal sinus rhythm, it enhances AV node conduction and may result in an increase in ventricular rate.

Therefore, rate control should be achieved before initiating procainamide. Answers a to d are all appropriate for a patient who presents with persistent AF despite the use of an antiarrhythmic agent. The patient requires anticoagulation and needs treatment of HTN and obstructive sleep apnea if present. AV node ablation remains a highly successful means of long-term rate control, but the patient requires long-term pacemaker dependency with RV pacing.

Left atrial ablation has emerged as a highly successful alternative to drug therapy for rhythm control. In patients who have failed a trial of antiarrhythmic drugs, left atrial ablation has emerged as a highly successful alternative nonpharmacologic therapy.

The technique is more successful in patients with PAF. Despite AF subtype, the approach is successful in the majority of patients. It is unclear when and if anticoagulation can be stopped, and a standardized approach is difficult to adapt to variable patient comorbidities and persistent asymptomatic episodes of AF.

Recent guidelines suggest for those patients in sinus rhythm, the decision to continue anticoagulation should be based on the presence of known risk factors for stoke. Answers a to d are all associated with atrial flutter. Class 1C agents used in the treatment of atrial flutter may slow the ventricular rate; however, they may also result in 1: Patients with prolonged QT and a history of polymorphic VT with class I or III antiarrhythmic agents should not received ibutilide due to an increased risk of torsades de pointes.

Likewise, significant hypokalemia can increase the risk of torsades de pointes. In patients with hemodynamic instability, emergency DC cardioversion is necessary. Sarcoidosis is not a commonly recognized cause of atrial flutter.

Answers a to d are all factors that predispose to atrial flutter. The risk of thromboembolism in patients with atrial flutter ranges from 1. The guidelines for anticoagulation for patients with AF are extended to those with atrial flutter. For example, chronic warfarin therapy with a goal INR from 2. Typical atrial flutter is dependent on the cavo-tricuspid isthmus.

In counterclockwise cavo-tricuspid isthmus-dependent atrial flutter there is a cranial-caudal activation sequence along the right atrial lateral wall, across the cavo-triscupid isthmus, and then superiorly in the right atrial septum. Patients with automatic atrial tachycardia often report a gradual onset of symptoms that become more rapid warm-up.

All of the answers are correct with the exception of e. In atrial tachycardia, the P wave morphologic features of the initial and subsequent beats are typically identical. In antidromic AVRT, antegrade conduction is through an accessory pathway, with retrograde conduction through the AV node anti-against the normal AV node conduction.

An important exception to other forms of SVT is that a bystander accessory pathway, not involved in the tachycardia, may conduct to the ventricle and cause a pre-excited wide QRS. It is important to remember that, although an accessory pathway is present, it is not necessarily a part of the tachycardia.

Valsalva-like maneuvers that terminate the tachycardia is a characteristic of AVNRT rather than atrial tachycardia. Answers a to c are all features that should prompt suspicion of the permanent form of junctional reciprocating tachycardia. The tachycardia is an AVRT utilizing a retrograde posterior septal accessory pathway and is often incessant resulting in a tachycardia-mediated cardiomyopathy.

QRS morphologic variation is an important clue to the presence of a pre-excited arrhythmia. With any pre-excited tachycardia, if AV node conduction is slowed, the degree of pre-excitation increases. With AV node slowing with blocking agents the ventricular response can paradoxically increase and predispose the patient to VF.

The initial deflection in V1 is positive. This becomes more apparent when looking at where the delta wave begins as seen in V3. AVL is negative. AVF is positive.

These electrocardiographic characteristics suggest a left lateral pathway. There is an equal number of ventricular V and atrial A electrograms labeled present. These electrograms correspond with a P wave that falls within the QRS, thereby, in general, characterizing this arrhythmia as a short RP atrial tachycardia. The patient is a young female presenting with a very short RP tachycardia. In atrial flutter the A should come before the V as it is driving the arrhythmia.

There is no chaotic activity in the atrium to suggest AF. The patient described had a large MI that was treated with percutaneous revascularization. PVCs and nonsustained VT are common. Although these patients are at relatively high risk of both sudden and total mortality, implantation of an ICD did not improve outcomes. If the patient has periods of sustained VT, an antiarrhythmic should be considered.

Otherwise, medical therapy alone is appropriate, with follow-up assessment of her EF to determine if any functional recovery results from the revascularization. The echocardiogram is not consistent with HCM. The patient most likely has arrhythmogenic RV dysplasia. Although late potentials on a signal-average ECG may suggest a higher risk patient, the absence of findings is not sensitive enough to not proceed with other assessment or treatment.

Exercise testing likewise is helpful if exercise-induced arrhythmias develop. Furthermore, there is a family history of sudden death and there are notable changes on both the ECG and echocardiogram. ICD placement is the best current therapy to decrease sudden death. Additional imaging that may further characterize the tissue, such as a MRI, should be considered prior to implantation of the device.

Exercise-induced seizures in this young patient require careful investigation for a cardiac tachyarrhythmia. Although such a patient may have a primary neurologic disorder, the temporal correlation with activity is concerning for a primary cardiac disorder with a second neurologic manifestation. Long QT1 patients often present with exertionrelated symptoms. The presence of long QT can be sought on the baseline ECG and, if needed, with exercise testing and an epinephrine challenge.

Beta blockade and exercise restrictions are premature in this patient without a clear diagnosis, as HCM and other channelopathies may also cause a similar presentation. For this latter reason, although not offered as a choice in the question, an echocardiogram is appropriate to screen for structural heart disease.

The patient had no evidence of ischemia to suggest need for coronary angiography. The patient is a young male who presents with probable idiopathic VT with a narrow R—S interval. At EP testing this patient was found to have a left posterior fascicular VT. This type of arrhythmia is sensitive to verapamil, but generally unresponsive to vagal maneuvers or adenosine.

The morphology is not consistent with an outflow tract tachycardia in which adenosine characteristically terminates the arrhythmia. Answer c Precordial concordance is suggestive of VT. All the other answer choices are more consistent with SVT. In addition, clinical findings, such as a history of CAD, cannon a waves, and variable first heart sound on auscultation, favor VT.

Lidocaine suppresses early afterdepolarizations, as does acetylcholine, magnesium, beta blockers, pacing, and potassium channel openers. Patients with long QT syndrome often have structurally normal hearts. Answers a to c are all associated with the development of VT late after repair for tetralogy of Fallot. An ASD is not associated with risk of VT, although the presence of a significant residual shunt is associated with an increased risk of sudden death.

The patient has an orthodromic reciprocating tachycardia. In this tachycardia, conduction from the atrium proceeds through the AV node to the ventricle and then back up to the atrium through an accessory pathway. In the tracing there are equal numbers of ventricular V and atrial A electrograms below. The antegrade Vs preceed the retrograde As activated through the accessory pathway.

A close inspection of the CS electrograms shows the V—A interval to be very small along CS 1,2 , which is in the distal CS, suggestive that the accessory pathway is along the left lateral ventricle. The ECG shows sinus rhythm with right axis deviation. In patients with an ostium secundum ASD, both atrial arrhythmias and late sinus node dysfunction are complications.

In the absence of surgical repair, isthmus dependent atrial flutter is the most common atrial arrhythmia. Atrial flutter and fibrillation are more common in patients more than 35 years of age. These two atrial arrhythmias combined exceed in prevalence accessory pathway mediated tachycardia in this age group.

Finally, patients with a history of palpitations or a documented tachycardia should undergo preoperative EP study, regardless of the presence or absence of pre-excitation on ECG. In congenitally corrected TGA, the right and left bundles are inverted, which causes the septal activation to proceed from right-to-left.

The second clue is the complete AV block. Patients with congenitally corrected transposition are at high risk of AV block from progressive fibrosis to the conduction system over time. The patient has congenitally corrected TGA.

These patients are at risk for systemic ventricular failure morphologic RV and TR. The tracing initially shows dual-chamber pacing. At onset of the tachycardia, a retrograde P wave can be seen in the T wave.

This P wave is sensed and the ventricle is subsequently paced. The tachycardia persists as this paced beat results in a retrograde P wave that is sensed triggering a subsequent ventricular-paced beat.

The P wave morphology argues against sinus tachycardia and AF. Ventricular lead oversensing results in failure to pace the ventricle.

In patients with obstructive sleep apnea, multiple cardiac rhythm disturbances have been reported, such as AF, bradyarrhythmias, heart block, and ventricular ectopy. The most common are severe sinus bradycardia and AV block that are reflex responses to the apnea and hypoxia.

Treatment of these rhythm disturbances is directed at the sleep apnea rather than the secondary rhythm disturbance.

Parkinson disease with autonomic failure typically results in orthostatic syncope. Answers a to d are all neurally mediated reflex syncopal syndromes. Others causes of neurally mediated reflex syncope include: An abrupt onset of syncope, particularly with exertion or while supine, is more consistent with a cardiogenic mechanism. All the other factors other than the correct answer d are more suggestive of a noncardiac mechanism. Factors suggestive of a cardiac mechanism include: CAD, CHF, older age, abrupt onset, serious injuries, abnormal cardiac examination, structural heart disease, and an abnormal ECG presence of a Q wave, bundle branch block, sinus bradycardia.

Patients with an acute inferior infarction can develop multiple types of electrical abnormalities, including sinoatrial node dysfunction, first-degree AV block, second-degree block, and third-degree block at the level of the AV node.

It is uncommon for any of these conduction disturbances to persist after resolution of the acute phase of the infarction. These patients may require temporary pacing if hemodynamically unstable, but they rarely require permanent pacing. All the other answers are class I indications for pacing. Additional class I indications for pacing include: The chest X-ray shows a moderate pneumothorax on the right arrows.

A chest tube was inserted and the pneumothorax resolved. Pacemaker syndrome results from inappropriate ventricular pacing or when the ventricular pacing is uncoupled from the atrial contraction. Patients may experience a variety of symptoms that include general malaise, a sensation of fullness in the head and neck, syncope, cough, dyspnea, heart failure, or weakness. They may have cannon A waves on exam and a lower BP when paced.

The syndrome is most common when the VVI mode is used and the underlying rhythm is sinus. The episode interrogation showed a fast, sensed rhythm from the ventricular lead. Atrial sense is normal and reveals a regular rhythm, which excludes an inappropriate therapy due to an atrial tachyarrhythmia.

The electrogram from the ventricular lead Vtip to Vring shows considerable artifact with a normal rhythm, as evidenced by a regular R—R interval that marches out, despite the morphologic abnormalities of the tracing.

In this case there was a lead fracture. A lead fracture can lead to erratic sensing, a high lead impedance, intermittent or complete loss of capture, and, in this case, an inappropriate shock. The atrial lead has failed to sense the intrinsic P wave and has delivered a regular atrial stimulus at the preset minimal interval.

This is an example of atrial lead undersensing. Undersensing may result from lead dislodgement, insulation failure, circuit failure, magnet application, battery depletion, electromagnetic failure, poor or incompatible connection at the connector block, and, for a unipolar device or configuration, air in the pocket.

Lead dislodgement is typically characterized by a high voltage and current threshold, but normal lead impedance.

The chest X-ray shows migration of the atrial lead that was positioned in the right atrial appendage to a position at the tricuspid valve orifice. There was also failure to capture with the lead. The lead was subsequently repositioned successfully as shown on the follow-up chest X-ray. AF with rapid ventricular rates does not inhibit the use of CRT. The rapid ventricular rates require careful management to allow the device to consistently pace both ventricles.

If this is not medically feasible, then patients can undergo AV node ablation. Multiple trials have demonstrated a benefit in 6-minute walk tests, NYHA functional class, quality of life, oxygen consumption, and functional MR.

In vivo, the subendothelium contains many types of collagen. All the following are types of subendothelial collagen except: Endothelium secretes all the following substances in large amounts except: Collagen Elastin Glycosaminoglycans Fibronectin Mucopolysaccharides 3. Procoagulants Anticoagulants Vasoconstrictors Vasodilators Pro-proliferative substances 4.

Platelet activation can occur through many biochemical pathways and receptors b. Platelet aggregation occurs through many different surface receptors c.

Platelet adhesion occurs principally through subendothelial vWF d. Platelet-activating factor also activates monocytes and polymorphonuclear leukocytes e. Removal of the endothelium exposes subendothelium and creates intense platelet adhesion 5. Atherosclerosis principally affects which of the following component s of the vessel wall?

Intima Adventitia Media Endothelium Answers to this section start on page Board Review Questions and Answers 6. The major cell type of the normal coronary artery intima is the: Macrophage Smooth muscle cell Lymphocyte Endothelial cell Foam cell 7. The foam cell is a lipid-laden cell derived from: Macrophage Smooth muscle cell Endothelial cell Lymphocyte Polymorphonuclear leukocyte 8. Studies of arteries in patients with atherosclerosis show high rates of proliferation b.

Intimal cell masses found in normal young patients suggest that proliferation may have an early role in the development of the atherosclerotic lesion c. Cells normally accumulate in the coronary arterial intima with aging d. Evidence suggests that the fatty streak may not be an early lesion of coronary artherosclerotic plaque e. The cells of atherosclerotic plaques are polyclonal in origin; that is, originating from many cells 9. Lipid accumulation in atherosclerotic plaque comes from circulating lipid b.

Smooth muscle cell proliferation is induced by lipid accumulation at physiologic lipid concentration c. Fatty deposition is required for plaque growth d. Lipids in foam cells come from synthesis by local cellular activity It is found frequently in young children and infants It is found at the same anatomical sites in young persons and adults T lymphocytes may be found in many fatty streaks The principal lipid of the fatty streak is unoxidized cholesteryl esters The fatty streak is found principally in males at older ages The vulnerable plaque typically has a fibrous cap covering a lipid-rich layer b.

These plaques often rupture at the central portion of the fibrous layer, where hydrodynamic forces are increased c. Evidence suggests that vulnerable plaque may come from hemorrhage into the coronary artery vessel wall at certain locations d. The vulnerable plaque is typically associated with a severe angiographic stenosis e.

Coronary calcification may proceed in a biochemical fashion similar to that in bone b. The principal component of plaque calcification is calcium carbonate and, thus, is related to vitamin D intake c.

The degree of calcification is related to the overall volume of atherosclerotic plaque in coronary arteries d. Calcific medial sclerosis as a cause of coronary arterial calcification is associated with increased probability of an ACS e. The coronary artery develops calcification late in plaque development and nearly always is associated with large plaque burden What is the current accepted practice regarding Lp a risk stratification for CAD?

It should be followed serially every 2—4 years to assess for increased risk b. It can be targeted by pharmacotherapy to yield reduction in morbidity above and beyond conventional risk factors c.

An elevated level may prompt moving a patient into a higher risk category and treating to more aggressive LDL and BP goals d. The size of Lp a isoforms is directly related to its atherogenic potential Which of the following is true about smoking and CV disease? Smokers have their first CV event approximately 10 years earlier than matched nonsmoking cohorts b. Response to which agent can be used to measure endothelial function? Methergine Ergonovine Acetylcholine Endothelin Functional assessment of an intermediate coronary lesion can be performed by all of the following except: Measurement of coronary flow reserve b.

Measurement of fractional flow reserve c. Quantitative coronary angiography How do ACE inhibitors affect the bradykinin system?

NO regulates which of the following processes? Vasodilation Platelet aggregation Matrix synthesis Smooth muscle cell migration All of the above The most potent vasoconstrictor is: The endothelium plays a role in which of the following? Regulation of blood flow Release of growth factors Regulation of thrombosis All of the above Which of the following substances does not directly affect the microcirculation i.

Atherosclerosis is associated with: Increase in circulating endothelin concentrations Increase in oxidative stress Decrease in NO activity All of the above Oxford Infectious Diseases Library.

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Oxford Textbooks in Rheumatology. Oxford Textbooks in Surgery. OSHs in Cardiology. OSHs in Critical Care. OSHs in Neurology. OSHs in Paediatrics. OSHs in Pain Medicine. OSHs in Psychiatry. OSHs in Radiology. OSHs in Surgery. Mayo Clinic Cardiology: Concise Textbook 4 ed. Edited by Joseph G. Murphy and Margaret A. Lloyd Abstract The fourth edition of Mayo Clinic Cardiology continues the tradition of all previous editions: Bibliographic Information Publisher: May DOI: Authors Joseph G. Read More.

Murphy, MD, and R. Tom, MD, and Robert D. Breen, MD, Mark J. Callahan, MD, and Margaret A. Criteria and Definitions of Abnormalities Stephen C. Boilson, MD, and Peter A. Boilson, MD, and Margaret A. Lloyd, MD, and Bernard J. Packer, MD, and Samuel J.

Connolly, MD, and Patricia A. Grogan, MD, and Fletcher A. Rajamannan, MD, and Joseph G. Spittell, MD, and David R. Ammash, MD, and Heidi M. Murphy, MD, Thomas G. Murphy, MD, R. Frye, MD, and David R. Murphy, MD, and Margaret A. Best, MD, and Sharonne N. Syed, MD, Joseph G.With age or with the development of atherosclerosis.

Garvan C. Lloyds-Chapter Ans. Rehabilitation Medicine. Exercise testing likewise is helpful if exercise-induced arrhythmias develop. Based upon the above patient presentation what subtype of long QT syndrome is expected?