Cardiovascular disease

13 Cardiovascular disease



Questions




Question 1


What is the Bernheim effect and the reverse Bernheim effect?



Question 2


Kindly explain why the left side of the heart is more prone to disease.



Question 3



1. Is it always necessary to examine the cardiovascular system of a patient in the 45° incline of the head end? Other than convenience for examining the jugular venous pressure (JVP), does this position have any other advantage?

2. If the JVP is not visible when the patient is in the upright position, can one presume it is not raised?


Question 4


The mitral area (of auscultation) normally corresponds with the apex beat. When the heart is dilated and the apex beat is shifted laterally, will the mitral area follow the apex beat to its new location or remain at the place where the apex beat is normally situated?



Question 5


Please explain in detail how to measure the pulsus paradoxus using a sphygmomanometer.



Question 6


What is the difference between dicrotic pulse and pulsus bisferiens?



Question 7



1. Why does the radial pulse become more prominent when the hand is lifted overhead?

2. Please explain the mechanism of a collapsing pulse. Which is the best artery to elicit it: radial, brachial or carotid?


Question 8


What is the mechanism of Durozier’s sign?



Question 9


What effects do aortic stenosis, aortic regurgitation and coarctation of the aorta have on systolic and diastolic blood pressure, and why do they produce these effects?



Question 10


In the section headed ‘Pulsus bisferiens’ (K&C 7e, p. 691) what do ‘percussion wave’ and ‘tidal wave’ mean? An illustration here would be helpful.



Question 11


When examining a patient’s carotid pulse, why should we not palpate both carotids at once? Is it because it might block the blood supply to the brain?



Question 12


How can I differentiate between jugular and arterial pulsation in the neck practically?



Question 13


Can you please help me with this: ‘Thrusting due to mitral or aortic regurgitation. Heaving due to aortic stenosis and systemic hypertension. There is often confusion about the terms thrusting and heaving’.


Another book I read considers aortic stenosis and hypertension for thrusting and mitral/aortic regurgitation for heaving. Who should I go with? Thank you.



Question 14


Where is the best place on the precordium to auscultate a split-second heart sound?



Question 15


What is the mechanism by which murmurs of mitral valve prolapse (MVP) and hypertrophic cardiomyopathy (HC) are accentuated by standing or the Valsalva manoeuvre?



Question 16


What is the correct procedure for a fluoroscopy and why is this essential for the insertion of cardiac catheter, pacemaker and prosthetic valve?



Question 17


What is the role of amiodarone in the acute management of asystole or pulseless electrical activity (PEA)?



Question 18



1. Is there any contraindication to the use of microwaves or mobile phones in patients with pacemakers?

2. What, if any, appliances should be avoided in a patient with a pacemaker?


Question 19



1. What is tachy-brady arrhythmia in the sick sinus syndrome?

2. How can it be managed?


Question 20


Practically, how can we differentiate between a second-degree atrioventricular (AV) block Mobitz I and Mobitz II? What is the meaning of first-degree block? What is the difference between heart asystole, heart arrest and third-degree AV block?



Question 21


How can a complete atrioventricular (AV) block be diagnosed on an electrocardiogram (ECG)?



Question 22


Usually, we look for an R’SR pattern for bundle branch block in the chest leads. What does it mean if there is an R SR pattern in the limb leads?



Question 23


What is Wolff-Parkinson-White syndrome?



Question 24


In management of atrial fibrillation (AF), is the priority to control ventricular rate or to restore cardiac rhythm?



Question 25


Can digoxin be given in paroxysmal atrial fibrillation?



Question 26


In a patient with atrial fibrillation and bronchial asthma, what is the recommended treatment and do beta-blockers make the condition worse?



Question 27


What is the difference between atrial flutter and atrial tachycardia?



Question 28


What are the possible causes of atrial extrasystoles, in a patient with a normal echo, which last for several days and then disappear spontaneously? Is treatment with anxiolytics recommended?



Question 29


In the treatment of ventricular tachycardia, could lidocaine be used in the absence of any other drug? How effective is lidocaine?



Question 30


Why is an extremely low level of potassium in the blood sometimes a cause of ventricular fibrillation?



Question 31


How often does verapamil cause impotence and inhibit ejaculation?



Question 32


Why does a patient with congestive cardiac failure have excessive sweating?



Question 33


What is cardiac asthma?



Question 34


In a book, under the title ‘Heart failure’ I have seen the following phrase: ‘Cardiac failure occurs when, despite normal venous pressures, the heart is unable to maintain sufficient cardiac output…’. Is it correct to say ‘normal venous pressures’? All protective and compensatory mechanisms raise the venous pressure to maintain a sufficient cardiac output – according to Frank-Starling law – and this is the case in heart failure, so I think it was meant to say: ‘…despite high venous pressures…’.



Question 35


I wanted to ask whether a third heart sound is present, or should be present, in all cases of heart failure, whatever the underlying cause.



Question 36


Why can left heart failure lead to right heart failure but not vice versa? What is the physiology involved in this transition?



Question 37


Could you explain the fetal gene program, activated in heart failure?



Question 38


How safe is it to stop administration of carvedilol to a patient with heart failure? Can the drug be tapered off? What are the effects/dangers of stopping carvedilol suddenly? What, if any, are the reasons for discontinuing carvedilol in patients with heart failure?



Question 39


What are the advantages and disadvantages of furosemide in the treatment of cardiac failure?



Question 40


In heart failure, can furosemide be given once daily?



Question 41


What are the clinical features of a ruptured sinus of Valsalva?



Question 42


Does dobutamine (dose range 2.5-10μg/kg/min) cause significant tachycardia?



Question 43


Are beta-blockers indicated in heart failure; if yes, in all cases or in selected cases?



Question 44


Why does long-term treatment by digitalis cause gynaecomastia?



Question 45


Why do toxic doses of digoxin (which cause a decrease in excitability of cardiac tissue) cause arrhythmias, whereas therapeutic levels of digoxin (which cause increase in excitability) cause no arrhythmias?



Question 46


Hypokalaemia is one of the complications of digitalis. In treatment we give K+. How does the hyperkalaemia enhance the digitalis toxicity?



Question 47


Why should we measure serum potassium before we start digoxin?



Question 48


The intravenous administration of loop diuretics such as furosemide relieves pulmonary oedema rapidly. Is this due to arteriolar vasodilatation reducing afterload which is an action that is independent of its diuretic effect? I ask this because I have been told that this drug has no effect on arterioles (except on efferent arterioles of the kidney), but rather a venodilatatory effect. What could be the cause of such different opinions?



Question 49


There have been a number of recent publications concerning aspirin versus warfarin trials. Would you recommend prescribing warfarin for secondary prevention of coronary heart disease in patients suffering from their first myocardial infarction (MI)?



Question 50


Is it true that in future the ApoA:ApoB ratio will be used to predict the risk of coronary artery disease more efficiently than low-density lipoprotein (LDL)?



Question 51


What is the exact link between C-reactive protein (CRP) and coronary artery disease?



Question 52


In angina pectoris, why does the chest pain get radiated to the left side, i.e. left arm and back?



Question 53


Please explain why thrombolytic therapy is not indicated in cases of unstable angina and non-ST-segment elevation myocardial infarctions (nSTE-MI) despite the fact that both nSTE-MI and ST-elevated MI (STEMI) are caused by a thrombus for which thrombolytic therapy is highly indicated? Could it be true that, in the case of unstable angina and nSTE-MI has a higher incidence of intracranial haemorrhage than in the case of ST-segment elevation MI?



Question 54


Doesn’t the term ‘acute coronary syndrome’ include unstable angina, non-ST-segment elevation myocardial infarctions and ST-elevated MI (STEMI)?



Question 55


Kindly mention the indications for clopidogrel in acute coronary syndrome (ACS). Should it be used along with aspirin or alone if the latter is contraindicated? Are there any studies that combine both with either low-molecular-weight heparin (LMWH) or unfractionated heparin? How long should clopidogrel be continued?



Question 56


What role do IV fluids play in the management of acute inferior wall myocardial infarction?



Question 57


Is there any benefit in combining aspirin with clopidogrel in post-MI angina and ischaemic stroke? A MATCH trial showed this combination not to be of benefit – would you therefore recommend we stop using this combination in our hospital unit?



Question 58


In a patient with the typical chest pain of myocardial infarction (MI) and no other criteria for thrombolysis would highly elevated cardiac enzymes indicate thrombolysis?



Question 59


I cannot figure out the role of an acetylcholinesterase inhibitor in post-myocardial infarction from Conn’s Current Therapy and Swanson’s Family Practice. Can you help?



Question 60


Can thrombolytic therapy for myocardial infarction (MI) be started in patients who have cardiac pain and raised cardiac markers? Can streptokinase be given irrespective of electrocardiogram (ECG) changes (according to some books, ST elevation has to be present)?



Question 61


Can carvedilol be used in an elderly patient who developed left ventricular failure after a very recent myocardial infarction, or should it wait until the condition becomes stable?



Question 62


I have seen some patients with chronic rheumatic heart disease with no obvious evidence of rheumatic fever (i.e. they could not recall if there was an episode of severe infection with subsequent fever and joint pain). So, actually, how is chronic rheumatic heart disease diagnosed?



Question 63


If a young patient presents with hemiparesis and rheumatic atrial fibrillation and is already on oral anticoagulant, with an international normalized ratio (INR) = 3 and a normal computed tomography (CT) scan done 2 hours after onset, should he receive heparin for prophylaxis against further embolism? Should aspirin be combined with oral anticoagulant later, or should target INR be increased?



Question 64


When treating mitral stenosis using a balloon valvotomy, how come no thrombus develops at the site of the atrial septum or at the separated commissure of the valve leaflets?



Question 65


Why does a mitral stenosis produce a loud S1?



Question 66


Why is the mitral valve more affected than any other valve in the heart in most valvular diseases?



Question 67


What is William’s syndrome (supravalvular obstruction)? Why does hypercalcaemia occur with this syndrome?



Question 68


Kindly tell me all the causes postulated for the collapsing pulse seen in aortic regurgitation.



Question 69


Does pulmonary stenosis cause pulmonary hypertension?



Question 70


Under what conditions would a pulsatile liver be found and what is its clinical significance?



Question 71


Can we use warfarin during pregnancy or during menstruation in a patient with a prosthetic valve? Is anticoagulation necessary in a patient with a corrected ventricular septal defect (VSD) or corrected coarctation of aorta?



Question 72


I want to ask about Duke criteria in diagnosing infective endocarditis.



Question 73


Is Staphylococcus aureus the most frequent causative agent of acute bacterial endocarditis? And is this typical of acute bacterial endocarditis?



Question 74


Please explain the mechanism of the mycotic aneurysm in infective endocarditis.



Question 75


Why are the right valves more commonly affected in infective endocarditis when the microbes enter through the IV route, for example with IV drug users?



Question 76


You have said that in IV drug users the microbes go directly to the right ventricle, thus causing endocarditis in the right heart. But in dental xCardiovascular disease procedures the microbes also go through the veins to the right heart first, so why are the left heart valves more commonly affected?



Question 77


What causes splenomegaly in infective endocarditis?



Question 78


We know that Janeway lesions appear with infective endocarditis, but is there any other disease that can cause it?



Question 79


Patent ductus arteriosus (PDA) is also called duct-dependent circulation. What is the meaning of this phrase and do any other conditions present with a similar condition? What is the implication of this condition to the human body?



Question 80


What is the recommended treatment for a child with both congenital and valvular heart disease?



Question 81


Can you describe a few instances that might cause a case of tetralogy of Fallot to go into congestive cardiac failure, even though this is an unlikely occurrence? Please explain how this happens.



Question 82


Is a single ventricle disease associated with any syndrome? If so, what is its name and what are its characteristics?



Question 83


What is the cause of splitting of the second sound in breathing and why is it wide and fixed in atrial septal defect (ASD)?



Question 84


Why are deep-sea divers considered a ‘high-risk’ group if they have an atrial septal defect (ASD)?



Question 85


Is it prognostically beneficial to start treatment of impending cor pulmonale in a case of chronic obstructive pulmonary disease (COPD) with no symptoms of failing heart but with investigational evidence (electrocardiogram and chest X-rays)?



Question 86


What would be the ideal investigation for a suspected pulmonary embolism according to the protocol in a UK hospital?



Question 87


Can the apical pulsation in right ventricular enlargement be hyperdynamic?



Question 88


Please explain concentric and eccentric left ventricular hypertrophy. When the hypertrophied ventricle dilates and the wall thins out, is it still called a hypertrophied ventricle?



Question 89


What is viral pericarditis?



Question 90


I want to know why thrombolytic therapy is contraindicated in acute pericarditis.



Question 91


Why would sitting bring pain relief to, and lying aggravate, a patient with acute pericarditis?



Question 92


How do you determine whether a patient is in a ‘hypertensive condition’? And what is wide pulse pressure?



Question 93


I have a question about hypertension. Every textbook that I’ve come across places the greatest emphasis on the systolic blood pressure; it seems that diastolic pressure is often a figure that ‘just happens to be there’. My question is: What is the clinical importance of a diastolic pressure? And what problems might arise if a patient has a too high/low diastolic blood pressure?



Question 94


What causes hypertension in children?



Question 95


Is haemochromatosis a cause of hypertension?



Question 96


What are the most recent advancements in management of hypertensive crisis? Is there any new approach or method under trial?



Question 97


Why does hypertension not cause headache, and why does only the accelerated hypertension cause headaches. You say in ‘coarctation of aorta’ that there is headache and epistaxis from hypertension.



Question 98


Why is a headache one of the signs and symptoms of hypertension?



Question 99


In a hypertensive hypercholesterolaemic patient, is it contraindicated to use a bisoprolol-hydrochlorothiazide combination to control the patient’s hypertension if it is not controlled on bisoprolol alone?



Question 100


Should a hypertensive patient with recurrent ischaemic strokes, a total cholesterol of 200mg/dL (5.2mmol/L), low-density lipoprotein (LDL) cholesterol of 120mg/dL (3.12mmol/L) and high-density lipoprotein (HDL) cholesterol of 35mg/dL (1mmol/L), have a statin therapy?



Question 101


Has Tenormin any advantage over other beta-blockers in the control of hypertension?



Question 102


Is the use of sublingual captopril 25mg/h, in combination with IV furosemide 40mg/h to a maximum of 120mg, safe to lower greatly elevated blood pressure?



Question 103


Is ACEI superior to calcium channel blockers in the treatment of hypertension, in terms of prognosis and of the prevention of complications?



Question 104


Are angiotensin-converting enzyme (ACE) inhibitors more effective than beta-blockers in reducing the risk of stroke in hypertensive patients?



Question 105


Do non-steroidal anti-inflammatory drugs (NSAIDs) affect the antihypertensive effect of angiotensin-converting enzyme (ACE) inhibitors? If so, how?



Question 106


What antihypertensive is recommended for a patient with aortic stenosis (AS) and hypertension, as a mono- and combination therapy?



Question 107


Impotence is a common side-effect of antihypertensive drugs. How can I solve this problem in young hypertensive patients?



Question 108


In the treatment of hypertension, is it recommended to commence treatment with two drugs containing a thiazide (if elderly) or a beta-blocker (if young)?



Question 109



1. Following a stroke, both haemorrhagic and ischaemic, in previously hypertensive and normotensive patients, can you explain precise blood pressure control and the desired blood pressure levels?

2. In the case of a hypertensive emergency, with a blood pressure of 220/130 with acute myocardial infarction, what immediate measures should be taken?


Question 110


On lowering blood pressure, to what extent can heart failure secondary to chronic hypertensive heart disease be reversible?



Question 111


Is the use of amlodipine or furosemide recommended to normalize blood pressure in a case of hypertensive heart failure? If so, which is most effective?



Question 112


How can diabetes cause endothelial dysfunction? What are the roles of ACE inhibitors in the kinin-kallikrein system? What are the mechanisms by which a decrease in the level of nitric oxide causes endothelial dysfunction?



Question 113


Can sublingual nifedipine be given to a patient with malignant hypertension/accelerated hypertension? It seems to be a controversial issue with some favouring it and some against it.



Question 114


Is the diagnosis of malignant hypertension based only on the basis of the retinopathy (even in the presence of a normotensive state)? Labetalol, parenterally, is suggested as a treatment for malignant hypertension. What other more readily available preparations (besides sodium nitroprusside) are recommended in addition to this drug? Parental labetalol is not available in Pakistan!



Question 115


Patients at medium risk of DVT and pulmonary embolism are usually given specific prophylaxis with low-dose heparin at a dose of 5000 units subcutaneously every 8-12 hours until the patient is ambulatory. Is the first dose given immediately after, say, extensive varicose vein surgery of small and great saphenous veins?

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Dec 4, 2016 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on Cardiovascular disease

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