The cardiology intensive board review question book pdf

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Download the Medical Book: Cardiology Intensive Board Review PDF For Free. Questions: An Interventional Cardiology Board Review 3rd Edition pdf. Mayo Clinic Cardiology: Board Review Questions and Answers. Pages· · The Only EKG Book You'll Ever Need, 5th Edition - Ace your cardiovascular medicine certification or recertification exam with The Cardiology Intensive Board Review PDF Question Book – the.

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Overflows shall forth countermand. Download book "The Cardiology Intensive. Board Review Question Book" by Leslie Cho,. Eric J. Topol, Brian P. Griffin. PDF . Ace your cardiovascular medicine certification or recertification exam with The Cardiology Intensive Board Review Question Book – the bestselling exam prep. Read "Cardiology Intensive Board Review" by Leslie Cho available from Rakuten Kobo. board (and MOC) review text consists of hundreds of questions created by Textbook of Clinical Electrocardiography ebook by Antonio Bayés de Luna.

Two weeks following implantation he presented to the ED with sustained palpitations, dyspnea, and lightheadedness. Answers a to c are proposed mechanisms underlying the initiation and maintenance of AF. Structural heart disease After the device was implanted the following chest X-ray was obtained. Mayo Clinic. The serum potassium concentration of 3. He also reports intermittent palpitations with presyncope that occur 1 to 2 times a month and last 2 to 4 minutes.

Accessory pathway mediated tachycardia is the most common atrial arrhythmia c. Atrial flutter and fibrillation are common after the age of 35 years d. Patients without a history of Wolff-Parkinson-White do not require a preoperative EP study to assess for an accessory pathway A year-old female with a history of congenital heart disease presents with a history of progressive weakness and fatigue. The patient in Question is at high risk for which complication?

A year-old male with a history of symptomatic sinus node dysfunction recently underwent dual-chamber permanent pacemaker implantation. Two weeks following implantation he presented to the ED with sustained palpitations, dyspnea, and lightheadedness. The following telemetry strip was obtained in the ED. A year-old obese male is referred for a formal sleep study due to a history of severe snoring with daytime somnolence and fatigue. He reports no history of palpitations, lightheadedness, or syncope.

He is taking no medications. The following tracing is obtained during the sleep study. Courtesy of Dr. Apoor S.

Gami and Dr. Sean M. Caples What is the next step in his care? Continuous positive airway pressure Dual-chamber permanent pacemaker implantation Single-chamber permanent pacemaker implantation EP study to further assess the sinus and AV node function All of the following are neurally mediated reflex syncopal syndromes except: Vasovagal Postmicturition Gastrointestinal stimulation swallow, defecation, visceral pain Carotid sinus Parkinson disease with autonomic failure The following factors are associated with noncardiogenic syncope except: All of the following are class I indications for pacing except: Symptomatic acquired complete third degree and advanced second degree AV block b.

Complete third degree AV block in a patient with an acute inferior MI d. Symptomatic sinus bradycardia secondary to drug treatment only for which there is no acceptable alternative Lloyds-Chapter Qns. A year-old male received a dual chamber permanent pacemaker for complete heart block. Shortly after the new system was placed on the right he noted chest pain, palpitations, and dyspnea. The following chest X-ray was obtained. Chest X-ray courtesy of Dr. Gami What is the most likely diagnosis for his symptoms?

Pacemaker syndrome is a hemodynamic abnormality that results from which of the following abnormalities? The delay between the right and LV pacing leads is too long to allow a synchronous contraction b.

Ventricular pacing is uncoupled from the atrial contraction c. Cross talk that results in inappropriate inhibition of the pacing stimulus d. Endless-loop tachycardia that results from retrograde P waves that trigger another ventricular stimulation A year-old female with a history of ischemic dilated cardiomyopathy presents after receiving a shock from her ICD. This was her first shock and she had no symptoms prior to the therapy.

The ICD was implanted 3 years ago due to her reduced LV function with underlying ischemic heart disease. The device was interrogated and the following information obtained. The following stored electrogram was obtained from a permanent pacemaker in a patient that presented with general malaise. Atrial lead oversensing Atrial lead undersensing Ventricular lead oversensing Ventricular lead undersensing Pacemaker syndrome Which of the following statements is incorrect regarding the intraoperative assessment of a pacing system?

Wire fracture: Insulation break: Lead dislodgement: Exit block: A year-old female underwent dual-chamber ICD implantation. After the device was implanted the following chest X-ray was obtained. What is the complication with this device implantation?

Lead dislodgement Pneumothorax Cardiac perforation Lead fracture Poor connection at the connector block The following statements regarding CRT are true except: It improves distance in 6-minute walk tests c. In general, it improves NYHA functional class and quality of life d.

It reduces death and hospitalization for any cause e. Answer e. The most likely diagnosis is long QT syndrome. Although both Brugada syndrome and idiopathic VF present with sudden death, the clinical circumstance surrounding the arrest, gender of the patient, and ECG make these diseases less likely. RVOT tachycardia is typically not associated with sudden death. HCM often presents with exertional symptoms.

Table Point system for the diagnosis of congential long QT syndrome Circulation ; Board Review Questions and Answers 2. Answer b. The most likely genotype for the presented phenotype is long QT2 syndrome. This is supported by the family gender and the auditory stimuli. Exertion related triggers are more common with long QT1 syndrome.

Sleep-related events are more common in long QT3 syndrome. Jervell and Lange-Nielsen long QT syndrome is rare, autosomal recessive, and associated with congenital deafness. Timothy syndrome long QT8 syndrome is associated with other phenotypic manifestations, such as syndactyly, and significant learning disabilities.

Answer d. The patient suffered an aborted sudden death and thereby has a class I indication for an ICD. There is little role for a permanent pacemaker. If pacing is required, the implantation of a dual-chamber ICD should be considered.

Amiodarone often further prolongs the QT interval. Left cardiac sympathetic denervation can be considered in patients with recurrent appropriate ICD shocks. Beta blockers preferably nadolol or propranolol should be considered as standard therapy in all patients with long QT1 or 2 syndromes.

Answer c. Although amiodarone often prolongs the QT interval, it rarely causes torsades de pointes. It is also responsible for the rapid terminal repolarization in phase 3. Ventricular myocytes have high densities of these channels and their activation accounts for the ST elevation on the ECG seen during a MI. The sinus node is predominantly characterized by its phase 4 depolarization, which accounts for the pacemaker activities.

There are few sodium channels and the upstroke is primarily mediated by ICa,L. There is no discernible phase 1. The lack of IK1, which is active in phase 3, accounts for the relative depolarized state of the tissue.

Answer a. The arrhythmia is catecholamine-sensitive with calcium-mediated triggered activity from delayed depolarizations. Lloyds-Chapter Ans. 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.

The Cardiology Intensive Board Review Question Book

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.

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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. 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.

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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.

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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.

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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.

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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 next step would be to: Add a beta blocker Add nitrate therapy Initiate intensive glycemic control Order coronary arteriography Increases of the serum fibrinogen value have been associated with an increased risk for development of CAD in some studies.

Which of the commonly available lipid-lowering drugs has been consistently shown to lower the serum fibrinogen level? Ensure highly targeted, high-yield preparation with content areas covered in the same proportion as those on the actual exam. Supplement gaps in your knowledge by exploring complete discussions of why each answer is correct or incorrect, with references to the literature for further study. Assess your mastery of the latest topics with abundant new questions on cardiac catheterization, electrophysiology, congenital heart disease, hypertension, and much more.

Prepare efficiently and effectively thanks to a user-friendly full-color design, filled with images and tables comparable to those used on the boards. Now with the print edition, enjoy the bundled interactive eBook edition, offering tablet, smartphone, or online access to: User Reviews In general the questions are good, but a lot of them are based on outdated guidelines like bicuspid valve surgery with aortic aneurysms recommended at 5 cm rather than 5.

Keeping that in mind though, the majority of the questions are still good and the explanations are helpful in teaching concepts. This should NOT be your only source of review questions however. Great Edition I recommend it. Table of Contents Cardiology Intensive Board Review pdf 3rd edition includes the following units and chapters: Download Book Disclaimer: Please enter your comment!