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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. 29/10/ PM Page i Mayo Clinic Cardiology Board Review Questions and Answers Author: A. DOWNLOAD PDF .

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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/ 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.

Calcium channel blockers Beta blockers Amiodarone Lidocaine Sotalol Branching logic tree for second heart sound S2 splitting. Frantz, MD. What treatment should be considered for this patient? His clinical focus will include echocardiography and pulmonary vascular diseases.

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.

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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.

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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 Coronary endothelial dysfunction is associated with: Which of the following substances is not an endothelium-dependent dilator?

Nitroprusside is an endothelial independent vasodilator. False Lloyds-Chapter Qns. All the following are obligate coronary vasodilators except: The risk of plaque disruption depends primarily on all of the following factors except: Severity of angiographic stenosis Plaque morphology Lipid content of the plaque Endothelial function Plasma endothelin concentrations are increased in the following states: NO endothelium-derived relaxant factor mediates its vasorelaxation effect through: Specific receptor on the endothelium Specific receptors on smooth muscle cells Direct effect on smooth muscle cells Decrease in intracellular calcium Endothelin exerts its vasoconstriction through: Endothelial dysfunction is characterized by: Vasoconstriction to endothelial-dependent vasodilator substances Possible occurrence without significant CAD Possible causal link to smoking All of the above Endothelial dysfunction may be reversed by: Which of the following is not considered a CAD risk equivalent?

If two risk factors are present without CAD or equivalent, a patient can still be treated as a risk equivalent if their year risk is greater than: Which of the following drugs would be first-line therapy for a patient without documented heart disease who has the following lipid profile: A year-old man presents for risk evaluation.

His target LDL is: A year-old male lawyer is evaluated because of chest pain for the past 3 mos. He is trying to follow a low-fat diet and to lose weight but has not had his cholesterol level rechecked.

His family history is unremarkable. He does not report any previous history of chest discomfort or MI. The discomfort has never forced him to stop a courtroom argument or to interrupt his tennis game. In fact, he notes that it frequently resolved while he continued his activity. The discomfort sometimes lasts for an hour or more after he stops playing tennis. He has never taken NTG for this discomfort. All of the following statements regarding plasma homocysteine are true except: Elevated levels increase the risk of atherosclerotic vascular disease Interventions to lower homocysteine levels reduce mortality from CAD Vitamin B12 deficiency tends to raise levels Vitamin B6 and folic acid treatment lowers levels In a cigarette smoker with a history of intermittent claudication and newly diagnosed HTN, a doubling of the serum creatinine concentration immediately after the addition of an ACE inhibitor suggests: You are asked to see a year-old female dietitian in consultation for HTN.

She adopted a vegetarian lifestyle. Despite these measures, her BP remained above normal and her health care provider prescribed several medication regimens. Her medications include: The absence of an abdominal bruit excludes renovascular HTN as the underlying diagnosis c. The next step should be US assessment of renal arterial flow Her BP is now mmHg systolic. Laboratory results include: Normal Creatinine: LVH by voltage criteria Chest X-ray: Normal The most likely secondary form of HTN in this setting is: Primary aldosteronism Renovascular stenosis Phenochromocytoma Chronic renal failure In the patient in Question 43, the diagnosis of primary aldosteronism requires each of the following except: Alcohol Natural licorice Diuretic Premarin Which of the following antihypertensive agents is contraindicated in women who are pregnant?

All of the following are associated with the syndrome of familial hypercholesterolemia except: A year-old previously athletic man presents with history of anterior wall MI, poorly controlled HTN, and daytime somnolence.

A modifiable risk factor for ischemic heart disease that should be further evaluated in this patient is: The diet that has shown to decrease the risk for future CV events or death in patients after MI is: A year-old female presents for evaluation of chest pain.

The discomfort is accompanied by shortness of breath and is relieved within a few minutes by leaving the classroom or by rest. She denies any chest pain at rest or at night. She has never used NTG. She smokes one pack per day of cigarettes. She feels that she is overweight and is trying to follow a low-fat diet and to lose weight. Her cholesterol has never been checked. Her father died of an AMI at age Her cardiac exam is normal. Her resting ECG is normal. A year-old male presents with a min episode of central chest tightness with diaphoresis while watching TV, now resolved in the ED.

His family history is significant for a brother with MI at age He is sedentary and is a former smoker discontinued tobacco 6 months ago. He gained 15 pounds after quitting. Troponin T: Low b. Intermediate c. High A year-old man who received a living-related donor kidney transplant 2 yrs ago is referred to you after an inferior MI that was successfully treated with thrombolysis. He currently has no limitation of his daily activities. His lipid profile is as follows: Total cholesterol: Which of the following drugs is the best choice for this patient?

Simvastatin Atorvastatin Niacin Pravastatin Fluvastatin In the patient in Question 55, what would the target LDL cholesterol level be? The patient in Question 55 undergoes exercise stress testing with contrast MPI. He completes stage 2 of a Bruce protocol limited by typical angina and fatigue. Perfusion imaging demonstrates a large area of anterior and anterolateral ischemia and an inferior infarct. The combination of hypertension. In mild AR. With severe. It can be primarily transmitted down the right sternal border.

The murmur of AR is often best heard along the left sternal border. These pressures will decrease the gradient between the aorta and the LV in diastole.

A short. A patient with severe AR due to infective endocarditis may present in this way. When the AR is of valvular origin. Pulmonary regurgitation. The murmur of AR.

The murmur characteristics depend on the cause. Tricuspid Stenosis The bedside differentiation of tricuspid and mitral stenosis includes the following: Large jugular venous a wave with a slow y descent—suggestive of tricuspid stenosis other causes of large a waves. Consider mitral stenosis when atrial fibrillation is found in association with any of the following clinical scenarios: The duration of the diastolic murmur is related to the severity of mitral stenosis.

Very mild mitral stenosis 3. Other provocative maneuvers that increase flow across the mitral valve. Response to inspiration—murmur of tricuspid stenosis increases 2. Even in the apparent absence of a murmur.

Improper auscultation most commonly 2. The associated OS. The usual reasons for silent mitral stenosis are as follows: Rarely in mitral stenosis.

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Frequency—tricuspid stenosis is higher in frequency and begins earlier in diastole than mitral stenosis these differences may be difficult to appreciate at the bedside 4. Location—the diastolic murmur of tricuspid stenosis is best heard at the left sternal border.

Chapter 1 Cardiovascular Examination heard at the left sternal border is more likely to be AR than pulmonary regurgitation.

With the patient in the left lateral decubitus position. Other causes of RV inflow obstruction. The presence of a loud S1 or an OS should prompt a careful search for this easily overlooked diastolic murmur.

Abnormal chest wall configuration limiting auscultation. If the murmur is not audible. Stroke or other systemic or peripheral embolus an atrial myxoma may also present in this way 2. A decrease in flow rates across the mitral valve. The murmur may crescendo in late diastole presystolic accentuation. After the release of the Valsalva maneuver. During the active strain phase. When a continuous murmur is loudest in the posterior thorax.

The murmur of mitral valve prolapse may get longer and possibly louder. The murmur of hypertrophic obstructive cardiomyopathy typically gets louder. There are two important exceptions to this rule: In cases of severe RV failure. In AR. The clinical finding of left-sided valve lesions often overshadows the tricuspid involvement.

Valsalva Maneuver The Valsalva maneuver is useful for differentiating right-sided from left-sided murmurs. Murmurs due to dilated bronchial. Almost any condition that increases flow across atrioventricular valves such as mitral regurgitation. In patients with rheumatic heart disease. Mid-Diastolic Flow Murmurs Almost any condition that increases flow across atrioventricular valves such as mitral regurgitation. Pulmonary arteriovenous fistula 3. The murmur may begin after a prominent S3 and does not show presystolic accentuation.

The clinical finding of left-sided valve lesions often overshadow the tricuspid involvement. Continuous murmurs should be differentiated from to-and-fro murmurs such as occur in combined aortic stenosis and AR.

Murmurs caused by coronary arteriovenous fistula. Respiration The effect of normal respiration is also useful for distinguishing right-sided and left-sided murmurs. Continuous Murmurs Continuous murmurs should be differentiated from toand-fro murmurs such as occur in combined aortic stenosis and AR. Handgrip Isometric exercise such as handgrip. Systolic ejection murmurs such as with aortic or pulmonary stenosis increase after a long cycle length.

Squatting Prompt squatting causes a rapid transient increase in venous return and a sustained increase in peripheral resistance. The diastolic murmur of AR diminishes.

Amyl nitrite causes all stenotic murmurs. Innocent venous hums are loudest in the neck but can be transmitted to the precordium and be mistaken for patent ductus arteriosus or atrioventricular fistula.

Amyl nitrite causes acute systemic vasodilation. Because LV volume and peripheral resistance increase. AR decrease and pulmonary regurgitation increase 5.

The murmur of mitral regurgitation usually decreases because of the decrease in LV afterload during the vasodilation phase. Motion of the neck or jugular vein compression affects the intensity of the murmur. The latter may augment the murmurs of mitral and aortic regurgitation.

A small ventricular septal defect murmur decreases and pulmonary stenosis murmur increases 2. All stenotic murmurs. The systolic murmur of mitral prolapse may become longer as LV volume decreases initially but not necessarily louder. Amyl Nitrite Administration of amyl nitrite is simple. Aortic stenosis increase and mitral regurgitation decrease 3.

The venous hum is loudest in the sitting or standing position. AR decrease and mitral stenosis increase 4.

Chapter 1 Cardiovascular Examination RR Cycle Length Varying RR cycle length such as in atrial fibrillation or with frequent premature ventricular contractions affects murmurs in specific ways that can be of diagnostic value at the bedside. It can be obliterated by pressure with the examining finger next to the stethoscope.

The major usefulness of amyl nitrite is to differentiate within the following pairs Tables 13 and The systolic murmur of hypertrophic obstructive cardiomyopathy is augmented with the increased contractility of a post—premature ventricular contraction beat.

The serous pericardium is a delicate mesothelial layer that lines the inner aspect of the fibrous pericardium parietal pericardium and the outer surface of the heart and intrapericardial great vessels visceral pericardium. An aberrant retroesophageal right subclavian artery indents the esophagus posteriorly and may cause dysphagia.

Giuliani ER. The ascending aorta. Modified from Edwards WD. Hemopericardium results from perforation of either the heart or the intrapericardial great vessels. Applied anatomy of the heart. The fibrous pericardium forms a tough outer sac. Gersh BJ. McGoon MD. Mayo Clinic practice of cardiology. Scott Wright. In obese subjects. Mediastinal neoplasms can compress the atria. By permission of Mayo Foundation.

Enlargement of a cardiac chamber or great vessel may displace or compress an adjacent noncardiac structure. Cardiac enlargement or chronic pericardial effusions.

The visceral pericardium. The fibrous pericardium cannot stretch acutely. An enlarged left atrium may displace the left bronchus superiorly and the esophagus rightward. St Louis: The fibrous pericardium is inelastic and limits the diastolic distention of the heart during exercise. In the setting of constrictive pericarditis.

After cardiac surgery. Densely fibrotic adhesions. Focal adhesions are usually unimportant. Thick and roughened surfaces associated with fibrinous pericarditis lead to an auscultatory friction rub.

Superior Vena Cava The right internal jugular vein. A persistent left superior vena cava occupies the expected site of the ligament of Marshall. See Appendix at end of chapter for abbreviations. The pericardium is thickened in subjects with chronic constriction but may be of normal thickness in persons with constriction that develops relatively rapidly.

The latter then join to form the superior vena cava or superior caval vein Fig. Most postoperative pericardial adhesions are usually functionally unimportant. Between the great arteries aorta and pulmonary artery and the atria is a tunnel-like transverse sinus. Int iliac Ext iliac Fig. Systemic veins. Between the parietal and visceral layers of the serous pericardium is the pericardial cavity. A sequential saphenous vein bypass graft to the left coronary system may be positioned posteriorly through the transverse sinus.

Inferior Vena Cava The inferior vena cava receives systemic venous drainage from the legs and retroperitoneal viscera and. Hepatocellular carcinomas often involve the hepatic veins and occasionally may enter the suprahepatic inferior vena cava or right atrium. The superior and inferior pulmonary veins from each lung enter the left atrium. An interatrial communication must also be present. The proximal 1 to 3 cm of the pulmonary veins contain cardiac muscle within the media and may thereby function like sphincters during atrial systole as well as when significant mitral valve disease exists..

The inferior vena cava. Connection of the right pulmonary veins to the right atrium commonly accompanies sinus venosus atrial septal defects. Mediastinal neoplasms. The thin-walled and low-pressure pulmonary veins may be compressed extrinsically by mediastinal neoplasms or fibrosis. A fenestrated membranous or muscular shelf subdivides the left atrium into a posterosuperior chamber.

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Chapter 2 Applied Anatomy of the Heart and Great Vessels endomyocardial bioptome across the tricuspid valve and into the right ventricular apex to obtain a cardiac biopsy specimen. In partial anomalous pulmonary venous connection.

The inferior vena cava may become trapped and compressed between the vertebral column posteriorly and either an adjacent retroperitoneal structure or an intraperitoneal structure and thereby produce the inferior vena cava syndrome.

Connection of one usually the upper or both right pulmonary veins to the right atrium commonly accompanies sinus venosus atrial septal defects. Venous thrombi in the lower extremities may extend into the inferior vena cava or may become dislodged and embolize to the right heart and pulmonary circulation.

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Cor Triatriatum Cor triatriatum sinistrum results when the junction between the common pulmonary vein and the left atrium is stenotic. Anomalous Venous Connection In total anomalous pulmonary venous connection. Pulmonary vein stenosis is a rare complication of electrophysiology radiofrequency ablation.

Catheters and pacemakers within the innominate veins and superior vena cava become partially coated with thrombus and may be associated with thrombotic venous obstruction. Renal cell carcinomas may extend intravascularly within the renal veins and inferior vena cava and may even form tethered intracavitary right-sided cardiac masses.

The thin-walled. Atrial dilatation stimulates the release of natriuretic peptide. The thickness of the right atrial free wall varies considerably. The atrial wall between the pectinate muscles is paper-thin and can be perforated by a stiff catheter. Atrial anatomy with tricuspid and mitral valves in profile. The ostium of the inferior vena cava is bordered anteriorly by a crescentic eustachian valve. The right atrial appendage abuts the right aortic sinus and overlies the proximal right coronary artery.

An atrial pacing lead can be inserted into the muscle bundles within the appendage. The atrioventricular septum is anterior to the interatrial septum and posterior to the interventricular septum. Through a patent foramen ovale. The interatrial portion contains the fossa ovalis or oval fossa.

In some subjects. If right atrial pressure exceeds left atrial pressure. With atrial enlargement and blood flow stasis. The coronary sinus ostium is partly shielded by a fenestrated thebesian valve. The foramen ovale or oval foramen. The origin of the normal tricuspid valve is below that of the mitral valve.. As a result. Indwelling cardiac catheters or pacemaker wires tend to injure the endocardium at the cavoatrial junction and are often associated with shallow linear mural thrombi.

Four-chamber view from year-old boy. Atrial Septum The atrial septum has interatrial and atrioventricular components Fig. The right atrium receives the systemic venous return from the superior and inferior venae cavae and receives most of the coronary venous return via the coronary sinus and numerous small thebesian veins.

Such paradoxical emboli may be thrombotic e. The right atrium free wall has a smooth-walled posterior portion. In the remaining third.. Separating the two regions is a prominent C-shaped muscle bundle.

Pronounced atrial dilatation may so stretch the atrial septum that the limbus no longer covers the ostium secundum in the valve of the fossa ovalis. Position of atrioventricular node triangle of Koch. With chronic obstruction to left atrial emptying e. Comparison of Atria The right atrial free wall contains a crista terminalis and pectinate muscles. Tendon of Todaro The tendon of Todaro is a subendocardial fibrous cord that extends from the eustachian-thebesian valvular commissure to the anteroseptal tricuspid commissure at the membranous septum.

The membranous septum generally is less than 1 mm thick. Triangle of Koch The atrioventricular septum corresponds to the triangle of Koch.. The esophagus and descending thoracic aorta abut the left atrial wall. The body of the left atrium does not contribute to the frontal cardiac silhouette.

The valve of the fossa ovalis is a paper-thin translucent membrane at birth but becomes more fibrotic with time and may achieve a thickness of 1 to 2 mm. Left Atrium The left atrium. The atrioventricular component of the atrial septum. Thin wall of foramen ovale transilluminated.

The limbus of the fossa ovalis ranges from 4 to 8 mm in thickness. The muscular atrioventricular septum forms the summit of the ventricular septum and may range from 5 to 10 mm in thickness. The thickness of the atrial septum varies considerably. In contrast to left atrial mural thrombi. Normally the appendage. Mural thrombi often develop within the atrial appendage or. In subjects in whom the foramen ovale is anatomically sealed.

The right atrial appendage is large and pyramidal. Even postnatally. Owing to hemodynamic streaming within the right atrium during intrauterine life. Superior vena caval blood is directed toward the tricuspid orifice.

It is crescent-shaped in short-axis and triangular-shaped when viewed in long-axis Fig. In contrast.

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A primum atrial septal defect involves the atrioventricular septum and represents a malformation of the endocardial cushions. Atrial Septal Defect A secundum atrial septal defect involves the fossa ovalis region of the interatrial septum. A coronary sinus atrial septal defect is usually associated with an absent coronary sinus and connection of the left superior vena cava to the left atrium.

Normal atria. A coronary sinus atrial septal defect is usually associated with an absent unroofed coronary sinus and connection of the left superior vena cava to the left atrium. Right atrial hemodynamic streaming. A secundum atrial septal defect involves the fossa ovalis region of the interatrial septum. Right Ventricle The right ventricle does not contribute to the borders of the frontal cardiac silhouette radiographically. A sinus venosus atrial septal defect involves the posterior aspect of the atrial septum and is usually associated with an anomalous right atrial connection of the right pulmonary veins.

Opened right atrium from year-old man. When permanent transvenous pacemaker electrodes are inserted into the right ventricle. Volume Overload Disorders that impose a volume overload on the left ventricle. Although the heart weight may double or triple. Like the right ventricle. It is circular in 33 short-axis views and is approximated in three dimensions by a truncated ellipsoid. During right ventricular endomyocardial biopsy.

A complex meshwork of muscle bundles characterizes the anteroapical trabecular region. Along the outflow tract. They thereby produce a globoid heart with increased base-apex and short-axis dimensions. Right ventricle. The inlet region receives the tricuspid valve and its cordal and papillary muscle attachments. The term volume hypertrophy is favored in this situation.

In extreme cases. Tissue is more often procured from the meshwork of apical trabeculations than from the septal surface per se. Pressure Overload Conditions such as aortic stenosis and chronic hypertension. The right ventricular chamber consists of three regions—inlet. The arch consists of a parietal band. Left Ventricle The left ventricle forms the left border of the frontal cardiac silhouette radiographically.

During vigorous cardiopulmonary resuscitation in which ribs are fractured. The inlet receives the mitral valve apparatus. Although the short-axis chamber diameter does not increase significantly. Left ventricle with thin-walled membranous septum transilluminated. For comparison. Each level is then further divided into segments. For practical purposes. Cardiac amyloid may mimic hypertrophic cardiomyopathy.

The anterior mitral leaflet is also in direct contact. Regional analysis of the left ventricle. Left ventricular trabeculae carneae are small. Hypertrophic cardiomyopathy is characterized by asymmetric nonconcentric left ventricular hypertrophy that disproportionately involves the septum. In the normal elderly heart. Inflow and outflow tracts are separated by the anterior mitral leaflet. With advancing age. Short-axis views show the recommended segment system.

In short-axis. A defect of the atrioventricular septum is considered to be an atrioventricular canal defect. Left ventricle free wall and septum with mitral valve and papillary muscles on free wall. Muscular defects involve the muscular septum and can be solitary or multiple so-called Swiss cheese septum. When left ventricular endomyocardial biopsy is performed.

Tetralogy of Fallot Within the spectrum of cyanotic congenital heart disease is a group of anomalies that share in common a maldevelopment of the conotruncal septum. When the pulmonary valve is atretic. By two-dimensional echocardiography. Whereas the tricuspid and pulmonary valves are separated from one another. Ventricular Septal Defect The most common ventricular septal defect. Transposition of the Great Arteries Complete transposition of the great arteries is associated with abnormal conotruncal septation and parallel rather than intertwined great arteries.

Comparison of Ventricles Normally. Tetralogy of Fallot. A malalignment ventricular septal defect occurs when one of the great arteries overrides the septum and attains biventricular origin. The right ventricular apex is much more heavily trabeculated than the left. An infundibular also called outlet.

In some persons. Chapter 2 Applied Anatomy of the Heart and Great Vessels arteries or with complete transposition of the great arteries and a previous Mustard or Senning operation. Acute myocardial ischemia is characterized by intense sarcoplasmic staining with eosin dyes.

They are exquisitely sensitive to oxygen deprivation. Chordae Tendineae The chordae tendineae are strong. Valve Leaflet The valve leaflets are delicate fibrous tissue flaps that close the anatomical valvular orifice during ventricular systole Fig. Hypertrophy of cardiac muscle cells is accompanied by degenerative changes.

Because myocardial cells have a very limited ability to replicate. Myocyte Response to Injury Myocardial cells are by volume one-half contractile elements and one-third mitochondria. Since the tricuspid anulus is an incomplete fibrous ring. The closing edge. Truncus Arteriosus Truncus arteriosus implies absent conotruncal septation and is characterized by a single arterial trunk from which the aorta.

Necrosis is the histologic hallmark of lethal cellular injury. They restrict excessive valvular excursion during ventricular systole and thereby prevent valvular. The mitral anulus. Adaptive responses include hypertrophy and dilatation. Valve Anulus The anulus of each atrioventricular valve is saddleshaped. In dilated hearts. Double-Outlet Right Ventricle Double-outlet right ventricle is characterized by the origin of both great arteries from the right ventricle.

When the valve closes. The heart has only a limited response to stress or injury. Each leaflet comprises two major layers—namely. Other injurious agents include viruses. Necrotic myocardium elicits an inflammatory infiltrate of neutrophils and macrophages. As part of the fibrous cardiac skeleton at the base of the heart. Nuclei fade away karyolysis or fragment karyorrhexis. When ischemic cells are irreversibly injured. The leading edge of each leaflet is its free edge. Along the free wall. The septal medial leaflet lies parallel to the ventricular septum.

Because of their position directly beneath a commissure. Tricuspid Valve The plane of the tricuspid anulus faces toward the right ventricular apex. In living subjects.

Leaflets become thicker.

Contributing to the latter is a decrease in ventricular base-apex length. Each commissure C separates two leaflets and overlies a papillary muscle Pap M.

In the elderly. Components of an atrioventricular valve from the mitral valve of an 8-year-old girl. The three tricuspid leaflets are not always well separated from one another.

Papillary Muscles The papillary muscles. Most tendinous cords branch one or more times. Each leaflet has a large clear zone CZ and a smaller rough zone RZ between its free edge arrow and closing edge dashed line. Mitral valve papillary muscles short-axis. The reduction in area is due to contraction of the underlying basal right ventricular myocardium. By virtue of these numerous cordal insertions.

Tricuspid stenosis involves commissural and cordal fusion and may occur in rheumatic or carcinoid heart disease. In normal hearts. Valvular incompetence also may be observed in conditions that limit leaflet and cordal excursion.

Because of differences in leaflet size and cordal length. Four valves at base of heart. Mitral Leaflets The mitral leaflets form a continuous funnel-shaped veil with two prominent indentations. Right atrial dilatation alone. Secondary left atrial dilatation may contribute to the progression of preexisting mitral incompetence by displacing the posterior leaflet and its anulus and thereby hindering the excursion of this taut leaflet Fig.

Although the two commissures do not extend entirely to the anulus. The orifice changes shape during the cardiac cycle. Valve fibrosis in rheumatic mitral stenosis. Mitral anular calcification almost invariably involves only the posterior mitral leaflet and forms a C-shaped ring of anular and subanular calcium which may impede basal ventricular contraction and thereby produce mitral regurgitation. In contrast to the aspect of the right ventricular free wall. In the setting of anular dilatation.

Because the tricuspid anulus is incomplete. At midleaflet level. In hypertrophic cardiomyopathy. Two particularly prominent cords insert along each half of the ventricular surface of the anterior mitral leaflet.

In the setting of infective endocarditis. Mitral valve leaflets and cords short-axis. Two prominent muscles originate from the anterolateral and posteromedial inferomedial free wall. The total mitral leaflet surface area is 10 cm2. The myxomatous or floppy mitral valve is characterized by anular dilatation. The anterolateral muscle is generally larger and extends closer to the anulus than the postero- Fig.

In chronic aortic insufficiency. Trabeculations not only anchor the papillary muscles but also may form a muscle bridge between the two papillary groups and thereby contribute to valve closure. Rheumatic mitral stenosis is characterized by cordal and commissural fusions. Cordal rupture may occur in a myxomatous floppy valve. Mitral valve leaflets and anulus short-axis. The mitral papillary muscles occupy the middle third of the left ventricular base-apex length.

Cordal length is generally 1 to 2 cm. The leading edge of each cusp is its free edge. The closing edges become thickened and. They consist of anulus. Behind each cusp is an outpouching of the arterial root. Secondary left atrial dilatation may contribute to the progression of preexisting mitral incompetence.

Chronic postinfarction mitral incompetence is associated with papillary muscle atrophy and scarring. They are nonplanar structures. Semilunar Valves The right pulmonary and left aortic semilunar valves. Clinical Cytogenetics and Molecular Genetics. Medical Microbiology and Virology. Caring for Others. Complementary and Alternative Medicine. Molecular Biology and Genetics. Reproduction, Growth and Development. Addiction Medicine. Child and Adolescent Psychiatry. Forensic Psychiatry.

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