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101 Cardiology Questions Home Page

Cardiology Questions and Answers Brain Dump

A guide to the management of common cardiological scenarios, this questions and answers offers the response of leading experts in each field to the more common, and often poorly dealt with problems of cardiology. It is a very useful 'how-to' guide, based on sound evidence.

Interactive Anatomy of the Brain

An interactive study guide to the structures and functions of the brain.

After reviewing the study section of this interactive tutorial, the learner will be able to do the following:
Name or list the structures of the brain
Describe the functions of various brain regions
Name the cranial nerves

Interactive Anatomy of the Brain

(Click on the above link for Interactive Anatomy of the Brain)

Which factors predict cardiac risk from general surgery?

Cardiology Questions and Answers Brain Dump Which factors predict cardiac risk from general surgery and what is the magnitude of the risks associated with each factor?

Mangano and colleagues reported an in-hospital adverse cardiac event rate of 17.5% among patients undergoing major noncardiac surgery. Four factors require consideration:

1 Clinical predictors
2 Functional status
3 Surgical magnitude
4 Results of non-invasive investigations.

Clinical risk factors have been integrated into clinical risk scores, of which the best known are the Goldman, Detsky and Eagle scores (Table 101.1). Detsky and colleagues have reported the likelihood of post-testing adverse cardiac events for these scores (Table 101.2). The American Heart Association has classified clinical risk factors into three categories (Table 101.3), based on the conclusions of a consensus conference. This index retains the greatest clinical utility.

Functional capacity determines the need for non-invasive testing in the presence of intermediate or minor clinical predictors. Daily activities can be scored according to estimated energy expenditure (Table 101.4). The magnitude of the surgical procedure also influences risk (Table 101.5). High surgical risk combined with intermediate clinical risk factors or minor clinical risk factors plus low functional capacity dictate the need for noninvasive testing.

It is vital to understand that the positive and negative predictive value of non-invasive tests (e.g. thallium scans and dobutamine stress echocardiography) depend critically on the underlying prevalence of cardiac disease in the population. Very low or very high levels of ischaemic heart disease diminish the value of these tests, which are most useful in groups with intermediate levels of disease.

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Which patients should undergo preoperative non-invasive investigations or coronary angiography?

Cardiology Questions and Answers Brain Dump Which patients should undergo preoperative non-invasive investigations or coronary angiography?

Non-invasive testing refers to investigations other than angiography such as dipyridamole thallium scanning or dobutamine stress echocardiography. The literature on this question is overwhelming. It is best approached by nine simple steps. These are based on the recommendations of the joint consensus conference of the American College of Cardiology and the American Heart Association. Clinical predictors, functional capacity and magnitude of surgical risk can be assessed from Tables 101.3, 101.4 and 101.5 in the next question.

Step 1 What is the urgency of surgery?

If absolute emergency proceed to surgery, otherwise proceed to step 2.

Step 2 Has the patient undergone coronary revascularisation in the last five years?

If so and symptoms are stable, proceed to surgery. If not, or symptoms are unstable go to step 3.

Step 3 Has there been a coronary evaluation in the past two years?

If so and there are no changes or new symptoms proceed to surgery. If not, or there have been changes go to step 4.

Step 4 Is there an unstable coronary syndrome or major clinical predictor of risk?

If so proceed direct to angiography. If not go to step 5.

Step 5 Are there intermediate clinical predictors of risk?

If so go to step 6. If not go to step 7.

Step 6 What is the functional capacity and magnitude of surgical risk?

If there are intermediate clinical predictors, then order noninvasive investigations if there is either poor function or high surgical risk. Otherwise go to surgery.

Step 7 Are there minor clinical predictors?

If so go to step 8. If not proceed to surgery.

Step 8 What is the functional capacity and magnitude of surgical risk?

If there are minor clinical predictors, then order non-invasive investigations if there are both poor function and high surgical risk.

Step 9

All patients have now been assigned to surgery, angiography or non-invasive testing. The results of non-invasive tests must incorporate both the absolute result (positive or negative) and quantification of the result (e.g. magnitude and regional location of ischaemic area). These results will determine which patients should proceed to angiography. Significant abnormalities require further assessment by angiography. Minor and intermediate abnormalities only require further assessment in the presence of low functional capacity or major surgical risk.

It should be noted that, at least in high-risk patients undergoing vascular surgery, beta blockade is the only medical intervention proven to have major impact on outcome.

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Which patients should receive antibiotic prophylaxis for endocarditis, and which procedures should be covered in this way?

Cardiology Questions and Answers Brain Dump Which patients should receive antibiotic prophylaxis for endocarditis, and which procedures should be covered in this way?

There is little firm scientific evidence for present advice on antibiotic prophylaxis for endocarditis, mainly because of the rarity of the disease. Only 10% of cases are related to bacteraemia caused by invasive procedures. Prevention of endocarditis in patients with abnormal heart valves can be achieved by many general measures, for example, regular dental care. The convention for the use of antibiotics in the prevention of endocarditis derives from animal models and clinical experience. Although dental extraction results in a bacteraemia of about 100cfu/mL, no obvious relationship has been found between the number of circulating bacteria and the likelihood of developing endocarditis.

In man, case-control studies suggest 17% of cases might be prevented if prophylaxis is given for all procedures in patients with abnormal valves. Individual cases of endocarditis following dental or urological procedures have been reported but the risk of developing endocarditis must be very low. Underlying cardiac abnormalities greatly increase the risk of endocarditis, e.g. patent ductus arteriosus, prosthetic valves, hypertrophic cardiomyopathy, aortic valve disease or previous endocarditis. Mitral valve prolapse is common but merits antibiotic prophylaxis if it causes a murmur.

Procedures causing gingival bleeding should be covered by prophylaxis as should tonsillectomy, adenoidectomy and dental work. Other procedures in which prophylaxis should be used include oesophageal dilatation or surgery or endoscopic laser procedures, sclerosis of oesophageal varices, abdominal surgery, instrumentation of ureter or kidney, surgery of prostate or urinary tract. Flexible bronchoscopy with biopsy, cardiac catheterisation, endoscopy with biopsy, liver biopsy, endotracheal intubation and urethral catheterisation in the absence of infection do not need prophylaxis. Patients having colonoscopy or sigmoidoscopy probably do not require prophylaxis unless there is a prosthetic valve or previous endocarditis or unless biopsy is likely to be performed. Recommendations for prophylaxis in patients undergoing obstetric or gynaecological procedures are required for patients with prosthetic valves, or who have previously had endocarditis.

Recommendations for prophylaxis vary between countries. Dental (causing gingival bleeding), oropharyngeal, gastrointestinal and urological procedures are usually considered a risk. The use of antibiotic prophylaxis is routine during cardiac surgery, flucloxacillin, plus an aminoglycoside, or a cephalosporin being common choices.

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What percentage of blood cultures will be positive in endocarditis?

Cardiology Questions and Answers Brain Dump What percentage of blood cultures will be positive in endocarditis?

The great majority of patients with endocarditis have positive blood cultures within a few days of incubation and only a few cases will become positive on further incubation for 1–2 weeks. The proportion of culture-negative cases depends on the volume of blood and method of culture but a common estimate is 5% with a range from 2.5% to 31%. Most cases of culture-negative endocarditis are related to use of antibiotics within the preceding two weeks and probably represent infections with staphylococci, streptococci or enterococci. If antibiotics have been given, withdrawal of treatment for four days and serial blood cultures will usually demonstrate the pathogen.

A number of organisms may grow only if incubated under the correct conditions. Nutritionally-deficient streptococci may fail to grow in ordinary media and yet are part of the normal mouth flora and can cause endocarditis. The HACEK organisms are slow growing and easily missed. Coxiella burnetti, Chlamydia spp. and Mycoplasma spp. are rare causes of endocarditis and are difficult to grow, diagnosis requiring biopsy or serology. Bartonella spp. are now known to cause endocarditis in homeless patients and diagnosis is difficult by conventional methods.

Three sets of blood cultures will demonstrate at least 95% of culturable organisms causing endocarditis. After four negative cultures there is only a 1% chance of an organism being identified by later culture. Contamination as the result of poor collection technique makes interpretation difficult and is a greater risk when repeated sets of culture are collected.

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What is the morbidity and mortality of endocarditis with modern day management?

Cardiology Questions and Answers Brain Dump What is the morbidity and mortality of endocarditis with modern day management (and how many relapse)?

Despite progress in management, morbidity and mortality remain major problems for the patient with endocarditis, both during the acute phase and as the result of long term complications after a bacteriological cure. Improvements in microbiological diagnosis, types of antibiotic treatment and timing of surgical intervention have improved the outlook for some patients but the impact has been minor with some of the more invasive pathogens. The infection can relapse and vegetations can be reinfected. Healed vegetations may leave valvular function so compromised that surgery is required.

In 140 patients with acute infective endocarditis, 48 (34%) required valve replacement during treatment. Heart failure occurred in 46 patients. During the active disease, 22 patients (16%) died. Medical treatment alone cured 80 patients. Relapse occurred in 3 (2.7%) of 112 patients all within one month of discharge. Recurrence was observed in 5 (4%) patients between 4 months and 15 years after the first episode. In the follow up period, another 16 patients died of cardiac causes, most within five years. Of 34 patients with late prosthetic valve endocarditis, 27 (79%) survived their hospital admission but 11 had further surgery during the next five years, usually following cardiac failure. In another study, 91 (70%) of 130 patients survived hospitalisation for native valve endocarditis and 17 of 60 initially treated medically required surgery during a mean 9 year follow up. During follow up, 29 (22%) patients died, 13 from cardiac causes.

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What are the indications for surgical management of endocarditis?

Cardiology Questions and Answers Brain Dump What are the indications for surgical management of endocarditis?

The indications for surgical management of endocarditis fall into six categories.

1. Congestive heart failure

Patients with moderate-to-severe heart failure require urgent surgical intervention. With mitral regurgitation, afterload reduction and diuretic therapy can improve symptoms and may make it possible to postpone surgical repair until a full course of antibiotic therapy has been completed. In contrast, acute aortic regurgitation progresses rapidly despite an initial favourable response to medical therapy, and early surgical intervention is imperative.

2. Persistent sepsis

This is defined as failure to achieve bloodstream sterility after 3–5
days of appropriate antibiotic therapy or a lack of clinical
improvement after one week.

3. Recognised virulence of the infecting organism

• With native valve endocarditis, streptococcal infections can be cured with medical therapy in 90%. However, S. aureus and gram negative bacteria are more aggressive, requiring transoesophageal echocardiography to rule out deep tissue invasion or subtle valvular dysfunction. Fungal infections invariably require surgical intervention
• With prosthetic valve endocarditis, streptococcal tissue valve infections involving only the leaflets can be cleared in 80% with antibiotic therapy alone; however, mechanical or tissue valve infections involving the sewing ring generally require valve replacement. If echocardiography demonstrates a perivalvular leak, annular extension, or a large vegetation, early operation is necessary

4. Extravalvular extension

Annular abscesses are more common with aortic (25-50%) than mitral (1-5%) infections; in either case, surgical intervention is preferred (survival: 25% medical, 60-80% surgical). Conduction disturbances are a typical manifestation.

5. Peripheral embolisation

This is common (30-40%), but the incidence falls dramatically following initiation of antibiotic therapy. Medical therapy is appropriate for asymptomatic aortic or small vegetations. Surgical therapy is indicated for recurrent or multiple embolisation, large mobile mitral vegetations or vegetations that increase in size despite appropriate medical therapy.

6. Cerebral embolisation

Operation within 24 hours of an infarct carries a 50% exacerbation and 67% mortality rate, but the risk falls after two weeks (exacerbation less than 10%, mortality less than 20%).Following a bland infarct, it is ideal to wait 2–3 weeks unless haemodynamic compromise obligates early surgical intervention. Following a haemorrhagic infarct, operation should be postponed as long as possible (4–6 weeks).

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How should the anticoagulation of a patient with a mechanical heart valve be managed for elective surgery?

Cardiology Questions and Answers Brain Dump How should the anticoagulation of a patient with a mechanical heart valve be managed for elective surgery?

Mechanical heart valves are associated with an annual risk of arterial thromboembolism of less than 8%. Although warfarin greatly reduces the risk, it is at the expense of an INR-related risk of serious haemorrhage. This constitutes an unacceptable risk for patients undergoing major surgery, and it is necessary to temporarily institute alternative anticoagulant measures.

The anticoagulant effect of oral warfarin is prolonged (half life 36 hours) and it can take 3–5 days for a therapeutic INR to fall to less than 1.5. It is also dependent on the half life of the vitamin K dependent clotting factors (particularly factors X and II, with half lives of 36 and 72 hours respectively). The surgical procedure must therefore be planned with this in mind. A “safe” INR depends on the surgery being undertaken. An INR <1.5 is usually suitable, although this should be <1.2 for neurosurgical and ophthalmic procedures.

Four days prior to surgery warfarin should be stopped. Once the INR falls below a therapeutic level heparin should be started. Unfractionated heparin (UFH) should be administered as an intravenous infusion. It has a short lasting effect (half life 2 to 4 hours) and is monitored using daily measurements of the APTT ratio (aim for APTT 1.5–2.5 times greater than control APTT). Alternatively, a weight-adjusted dose of low molecular weight heparin (LMWH) is given subcutaneously once daily with predictable anticoagulant effect, although data are limited. The night prior to surgery the INR should be checked and if it is inappropriately high then surgery should be delayed. If surgery cannot be delayed, the effect of warfarin can be reversed by fresh frozen plasma (2–4 units) or a small dose of intravenous vitamin K (0.5–2mg). Six hours prior to surgery heparin should be stopped to allow the APTT to fall to normal.

Recommencing intravenous heparin in the immediate postoperative period may increase the risk of haemorrhage to greater levels than the risk of thromboembolism with no anticoagulation. Heparin is usually restarted 12–24 hours after surgery, depending on the type of surgery and the cardiac reason for warfarin. Each case must be considered individually. Warfarin should be restarted as soon as the patient is able to tolerate oral medication. Prophylactic heparin should be stopped once an INR greater than 2.0 is established.

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A patient is on life-long warfarin and wishes to become pregnant. How should she be managed?

Cardiology Questions and Answers Brain Dump A patient is on life-long warfarin and wishes to become pregnant. How should she be managed?

All anticoagulant options during pregnancy are associated with potential risks to the mother and fetus. Any woman on warfarin who wishes to become pregnant should ideally be seen for prepregnancy counselling and should be involved in the anticoagulation decision as much as possible. Potential risks to the fetus need to be balanced against the increased maternal thrombotic risk during pregnancy. Anticoagulation for mechanical heart valves in pregnancy remains an area of some controversy.

The use of warfarin during pregnancy is associated with a low risk of maternal complications but it readily crosses the placenta and embryopathy can follow exposure between 6–12 weeks’ gestation, the true incidence of which is unknown. A single study has reported that a maternal warfarin dose 5mg is without this embryopathy risk. As pregnancy progresses, the immature vitamin K metabolism of the fetus can result in intracranial haemorrhage even when the maternal INR is well controlled. In addition, a direct CNS effect of warfarin has been described, resulting in structural abnormalities. Conversion to heparin in the final few weeks of pregnancy is recommended to prevent the delivery of, what is in effect, an anticoagulated fetus.

In contrast, unfractionated heparin (UFH) is free from direct fetal harm but it has varied pharmacokinetic and anticoagulant effects and adequate maternal anticoagulation can be difficult to achieve. The use of UFH in women with mechanical valve replacements during pregnancy has been associated with increased maternal thrombosis and bleeding. Studies have been criticised for the use of inadequate heparin dosing and/or inadequate therapeutic ranges although a recent prospective study which used heparin in the first trimester and in the final weeks of pregnancy reported fatal valve thromboses despite adequate anticoagulation. Long term heparin use risks osteoporosis and heparin-induced thrombocytopenia (HIT). Intensive monitoring is required in pregnancy and the use of anti-Xa assays may be necessary.

Low molecular weight heparins (LMWH) have a more reliable anticoagulant effect. The dose is adjusted according to anti-Xa levels. Use in pregnancy is mainly for thromboprophylaxis rather than full anticoagulation but experience is increasing. Indeed, case reports are starting to emerge where LMWH has been used for mechanical valve replacements. Compared with UFH the risk of HIT and osteoporosis are reduced and these heparins may hold the future for anticoagulation in pregnancy.

Management

Women who do not wish to continue warfarin throughout pregnancy can be reassured that conceiving on warfarin appears safe but conversion to heparin, to avoid the risk of embryopathy, needs to be carried out by 6 weeks. Breast-feeding on either warfarin or heparin is safe. Possible regimes include:

• Warfarin throughout pregnancy until near term and then conversion to unfractionated heparin.
• Unfractionated heparin for the first trimester. Warfarin until near term and then resumption of heparin.

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Which cardiac patients should never get pregnant? Which cardiac patients should undergo elective Caesarean section?

Cardiology Questions and Answers Brain Dump Which cardiac patients should never get pregnant? Which cardiac patients should undergo elective Caesarean section?

Which women should never get pregnant?

1 Those with significant pulmonary hypertension (pulmonary vascular resistance >2/3 of systemic), especially cyanotic patients and those with Eisenmenger reaction (maternal mortality ~50%) and those with residual pulmonary hypertension after e.g. VSD closure. NB: Even women with modest pulmonary vascular disease ~1/2 systemic are at risk of death.
2 Those with grade 4 systemic ventricular function (EF <20%). style="font-weight: bold;">Which women should not get pregnant until operated upon?

1 Marfan’s syndrome patients with aortic aneurysm/dilated aortic root.
2 Those with severe left sided obstructive lesions (AS, MS, coarctation).

Which women should undergo elective Caesarean section?

1 Those with independent obstetric indications.
2 Caesarean section should be strongly considered for the following women:
• Those with mechanical valves, especially tilting disc in the mitral position. The key here is to leave the mother off warfarin for the minimum time possible. An elective section is performed at 38 weeks’ gestation, replacing the warfarin with unfractionated heparin for the minimum time possible
• Severe aortic or mitral stenosis.

If the mother’s life is at risk, section followed by valve replacement may be necessary.

Controversy remains over whether the following patients should undergo elective Caesarean section:

1 Cyanotic congenital heart disease with impaired fetal growth. Section may help to avoid further fetal hypoxaemia, but at the expense of excessive maternal haemorrhage to which cyanotic patients are prone.
2 Pulmonary hypertension. See comments above.

A balance has to be made between a spontaneous vaginal delivery with the mother in the lateral decubitus position to attenuate haemodynamic fluctuations, forceps assistance and the smaller volume of blood lost during this type of delivery, and the controlled timing of an elective section. Probably more important than the route of delivery is peri-partum planning and teamwork: delivery must be planned in advance, and the patient intensively monitored, kept well hydrated and not allowed to drop her systemic vascular resistance. Consultant obstetric and anaesthetic staff experienced in these conditions should be present, and the cardiologist readily available.

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How do I manage the pregnant woman with valve disease?

Cardiology Questions and Answers Brain Dump How do I manage the pregnant woman with valve disease?

Native or tissue valves

In general, regurgitant lesions are well tolerated during pregnancy, whereas left sided stenotic lesions are not (increased circulating volume and cardiac output lead to a rise in left atrial pressure). Tissue valves can deteriorate rapidly during pregnancy.

Management of patients with significant mitral and aortic stenosis

1 Bedrest:
• Reduced heart rate allows time for LV filling and ejection
• Reduced venous return due to IVC compression by the uterus reduces LA pressure (also increases risk of thrombosis: patients must be heparinised).
2 Dyspnoea and angina: slow the heart rate with beta blockers or digoxin. Nitrates may be useful, but should be used with caution in those with aortic stenosis.
3 Intractable pulmonary oedema:
• Balloon valvotomy
• Closed mitral valvotomy (advantage as no cardiopulmonary bypass, but few surgeons nowadays have experience)
• If valvotomy not possible, then deliver fetus by Caesarean section followed by cardiopulmonary bypass and valve replacement.

Mechanical valves

Anticoagulation is the issue here: in particular, the risk of warfarin embryopathy vs risk of valve thrombosis.

The choice lies between:

1 Warfarin throughout pregnancy, stopping it for a minimal
length of time for delivery
2 Convert to heparin during the first trimester with hospital
admission and meticulous control of APTT. Return to warfarin
for the second trimester and reinstate heparin at ~34/40.

Note:

1 Mitral tilting disc prostheses at particular risk: fatal thrombotic occlusion of these valves in pregnant women described despite well-controlled heparin anticoagulation
2 Risk of significant warfarin embryopathy not as high as previously thought, especially if the mother achieves adequate anticoagulation on less than 5mg warfarin
3 No data on low molecular weight heparin in this situation, so its use cannot be recommended.

The patient must be fully informed, and involved in deciding her mode of anticoagulation (medicolegal implications).

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How do I manage the pregnant woman with dilated cardiomyopathy?

Cardiology Questions and Answers Brain Dump How do I manage the pregnant woman with dilated cardiomyopathy?

The management of a pregnant woman with dilated cardiomyopathy should be considered in terms of maternal risk, and risk to the fetus.

Maternal risk

This relates to the degree of ventricular dysfunction and the ability to adapt to altered haemodynamics. Risk and management can therefore be discussed in relation to New York Heart Association (NYHA) functional class:

NYHA I-II

• Should manage pregnancy without difficulty (maternal mortality 0.4%)
• May require admission for rest and diuretic therapy
• Venous thrombosis prophylaxis with heparin for patients on bedrest

NYHA III

• At significant risk (maternal mortality for NYHA III-IV 6.8%)
• Planned hospital admission for rest, treatment of heart failure and monitoring
• Risk of deterioration in ventricular function which may not improve post-partum.
• Early delivery if heart failure progressive despite optimal inpatient management

NYHA IV

• Should be advised not to become pregnant. Therapeutic abortion should be considered.

Fetal risk

Fetal risk should be considered in terms of two factors:

1 Factors which put the mother at risk
2 Adverse effects from maternal drugs:
• ACE inhibitors should be discontinued prior to conception because of the risk of embryopathy
• Limited or unfavourable data on fetal effects of many antiarryhthmics
• Beta blockers may be associated with maternal hypotension, and hence reduce placental perfusion. They may thus contribute to premature labour
• Warfarin – see Q93 and Q95 .

Note that digoxin and verapamil are safe to use.

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What do I do if an ICD keeps discharging?

Cardiology Questions and Answers Brain Dump What do I do if an ICD keeps discharging?

Most patients who experience a single ICD shock do so for successful conversion of a malignant ventricular arrhythmia. However, it must be remembered that the default programming in an ICD is designed to maximise sensitivity at the expense of specificity. Consequently, a significant number of ICD shocks can be inappropriate. For example, multiple shocks in quick succession may indicate inappropriate therapy for an atrial arrhythmia or a problem with the rate sensing lead. For this reason, it is important to retrieve the stored data from the device using the appropriate programmer even after a single shock. Evaluation of events stored in the ICD memory shows intracardiac electrograms, far field electrograms and recorded intervals as well as the onset and stability of the tachycardia to determine appropriate or inappropriate therapy. Frequent episodes of ventricular arrhythmia will require antiarrhythmic drugs for suppression; sotalol is often effective as a first line drug in this situation.

The more common reason for multiple ICD shocks is recurrent ventricular arrhythmia. Patients experiencing “storms” of shocks should be adequately sedated, and monitored in a coronary care setting. Intravenous antiarrhythmic drugs should be used for rapid arrhythmia suppression. Electrolyte abnormalities should be sought and promptly corrected. Myocardial ischaemia has to be a serious consideration when recurrent ventricular fibrillation or polymorphic ventricular tachycardia is responsible for shocks. Most episodes of repetitive ventricular tachycardia respond to intravenous drugs such as lidocaine, procainamide or amiodarone allowing for oral loading with an antiarrhythmic agent in a more controlled fashion.

If it becomes apparent that shocks are being delivered inappropriately (e.g. atrial fibrillation with rapid ventricular rates or shocks with no apparent arrhythmia signifying a lead fracture) suppression of ICD function can be achieved by applying a magnet over the ICD generator. Unless specifically programmed to the contrary, one can temporarily disable the sensing circuit of most ICDs during the period that a magnet is held over the ICD generator and prevent unnecessary shock while awaiting availability of appropriate equipment for definitive ICD programming changes.

Other causes of inappropriate therapy include:

• Sinus tachycardia
• Lead fracture
• Diaphragmatic muscle sensing
• Electromagnetic interference.

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How do I follow up the patient with the implantable cardioverter defibrillator?

Cardiology Questions and Answers Brain Dump How do I follow up the patient with the implantable cardioverter defibrillator?

Follow up of the patient with an implantable cardioverter defibrillator (ICD) demands an integrated team approach. The cardiologist, technical staff and nurses involved should have a wide experience and knowledge of pacemakers and general cardiac electrophysiology. Current generation ICDs do not just shock the heart but provide complex regimens of tachycardia discrimination and anti-tachycardia pacing (ATP) as well as single and dual chamber bradycardia therapy.

Routine follow up may occur in a tertiary centre or a local hospital as long as the expert staff and necessary equipment such as programmers and cardiac arrest kit are available. Follow up should start before the device is implanted with an educational programme and support for the patient and immediate family members. Videos, information booklets and meeting other patients with ICDs may be of benefit.

No consensus exists as to the interval between routine follow ups. Previously the patient had to return every month or two to have a capacitor reform. This is not now necessary, as all modern ICDs will undertake this automatically. With most current devices a 3 to 6 month interval is usual but treat each patient according to their individual circumstances.

Good management of the ICD should aim to achieve the following objectives:

1 Monitor the performance of the therapy delivered by the device, look at the success and failure of the programmed regimes and any acceleration of arrhythmias. Use this information to optimise clinical effectiveness of the programming.
2 Measure necessary parameters of the ICD and leads to ensure correct function. These should include lead impedance, shock coil impedance (if possible non-invasively), battery voltage, charge time, R and P wave amplitudes as well as pacing thresholds.
3 Review the intracardiac electrograms to ensure no inadvertent sensing of noise or other interference.
4 Maximise device longevity by safe and effective reprogramming of parameters.
5 Minimise the risk of complications occurring both from inappropriate therapy delivered to the patient and those associated with wound and pocket infection.
6 Anticipate the elective replacement of the device and plan for this eventuality.
7 Provide a support structure for the patient and their family including advice, counselling and education. Some centres provide a formal patient support group; there are both positive and negative views on this practice.

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How do I manage the patient with an ICD?

Cardiology Questions and Answers Brain Dump How do I manage the patient with an ICD?

An implantable cardioverter defibrillator (ICD) serves as prophylaxis against sudden collapse and death from rapid ventricular arrhythmias. In general, all ICDs sense the heart rate and provide anti-tachycardia pacing or deliver synchronised (cardioversion) or unsynchronised (defibrillation) shocks. Some of the modern ICDs also incorporate dedicated pacing function; patients with heart block or sinus node disease may be dependent on these devices just like any patient with an implanted cardiac pacemaker.

Like pacemakers, ICDs have to be checked by telemetric interrogation at periodic intervals to confirm integrity of the lead systems and proper function of ICD components including adequacy of battery voltage. Reprogramming of the various parameters that govern pacing, arrhythmia detection and therapy may be necessary from time to time. Such routine follow up, usually undertaken at established arrhythmia centres, should occur at 3 to 6 monthly intervals in the absence of major intercurrent events. Some issues specific to this group of patients can be summarised as follows:

1. Avoid rapid heart rates

In its basic form, arrhythmia detection algorithms of ICDs rely on a programmed heart rate threshold. Once this is exceeded for a defined period of time, the device may deliver therapy irrespective of whether the arrhythmia is of ventricular or supraventricular origin. In a ventricular-based ICD, the shock energy vector is designed primarily to encompass the ventricles. Consequently, atrial arrhythmias may fail to convert such that multiple inappropriate ICD shocks may result. Further, if antitachycardia pacing is delivered in the ventricle for an atrial arrhythmia, ventricular arrhythmias may be provoked creating a pro-arrhythmic situation. The newer ICDs incorporate atrial sensing to improve arrhythmia discrimination but it must be remembered that any algorithm that improves specificity for ventricular arrhythmia will entail some loss of sensitivity. Cognisant of the above, it is imperative that atrial arrhythmias are adequately treated in these patients, particularly the paroxysmal form of atrial fibrillation that is commonly associated with rapid rates at its onset. Occasionally, RF ablation of the AV node is necessary. Beta adrenergic blockers should be an integral part of therapy in most ICD patients.

2. Recognise ICD—drug interactions

Antiarrhythmic drugs have the potential for interacting with an ICD in several ways. Drugs such as flecainide and amiodarone can increase pacing and defibrillation thresholds. In patients with a low margin of safety for these parameters, use of these drugs may result in failure of pacing or defibrillation. Secondly, these drugs can slow the rate of ventricular tachycardia below the programmed rate threshold for detection by the ICD; failure of arrhythmia detection can result. Some rarer interactions include alteration of the T wave voltage by drugs or hyperkalaemia resulting in double counting and inappropriate shocks.

3. ICD wound management

As an implanted device, the system is susceptible to infections. Pain and inflammation of the skin over the ICD may herald an infective process. Similarly, unexplained fever, particularly staphylococcal septicaemia may indicate endocarditis involving the leads and/or tricuspid valve.

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What are the indications for implantable cardioverter defibrillator (ICD) implantation and what are the survival benefits?

Cardiology Questions and Answers Brain Dump What are the indications for implantable cardioverter defibrillator (ICD) implantation and what are the survival benefits?

Studies in the early 1980s showed that recurrence rates were high for patients presenting with a malignant arrhythmia unrelated to myocardial ischaemia or infarction. Survivors of cardiac arrest, those presenting with sustained monomorphic VT and unexplained syncope in the presence of heart disease clearly are patients at high risk for sudden cardiac death. A series of clinical trials completed in the recent past have confirmed the uniform survival benefit from ICD therapy in such patients (AVID, CASH, CIDS) when compared to therapy with amiodarone or sotalol. In the largest prospective randomised trial (Antiarrhythmics versus Implantable Defibrillators Trial – AVID trial), the ICD reduced mortality by 39% at 1 year and 31% at 3 years. Most patients randomised to the antiarrhythmic arm of the trial were treated with amiodarone.

With remarkable improvements in ICD technology allowing easier implantation, the ICD is being embraced increasingly and earlier in the course of cardiac disease. Attention has now turned to primary prevention of sudden death. For patients with asymptomatic non-sustained VT, there appears to be a clear survival benefit from ICD in the presence of a remote myocardial infarction, LVEF <40%, and inducible VT at electrophysiological study (MADIT, MUSTT). Interestingly, this benefit cannot be extrapolated to patients without nonsustained VT or inducible VT. The CABG patch trial that randomised patients with LVEF <36% and positive signal averaged ECG to ICD or not during elective bypass surgery failed to show a survival benefit. The role of the ICD in primary prevention of sudden death in non-ischaemic dilated cardiomyopathy is also unclear at this time. Clinical trials are in progress.

The benefit from an ICD appears to be greatest for patients with severe LV function and additive to conventional therapy with ACE inhibitors and beta adrenergic blockers. In the AVID trial for example, survival benefit with ICD was observed only when LVEF was less than 35%. Similarly, in the primary prevention trials, the mean LVEF was 30%. One could advance the argument that the ICD should be reserved for those with the worst LV function. Unfortunately, such patients have competing causes for mortality such as pump failure and electromechanical dissociation that are responsible for 50% of deaths. On the other hand, patients with little or no impairment of LV function and a single tachyarrhythmic event usually have late and rare recurrence leading to sudden death. An ICD can potentially restore them to near normal life expectancy in the absence of ongoing myopathic process. The long term studies requiring more than one life span of an ICD are not available to define the true value of ICD therapy in such patients.

Although the ability of the implantable cardioverter defibrillator (ICD) to terminate potentially lethal ventricular arrhythmias is well acknowledged there is less consensus as to whom should receive an ICD. A good place to start is the American College of Cardiology/American Heart Association Practice Guidelines for Arrhythmia Devices. There are three classes of indications: class one, where there is evidence and/or general agreement that the treatment is beneficial, useful and effective; class two, where there is conflicting evidence or a divergence of opinion; and class three, where there is evidence and general agreement that a treatment is not useful or effective.

The class one indications for ICD implantation are:

1 Cardiac arrest due to VF or VT not due to a transient or reversible cause.
2 Spontaneous sustained VT.
3 Syncope of undetermined origin with clinically relevant, haemodynamically significant sustained VT or VF induced at electrophysiological study when drug therapy is ineffective, not tolerated or not preferred.
4 Non-sustained VT with coronary disease, prior MI, LV dysfunction, and inducible VF or sustained VT at electrophysiological study that is not suppressible by a class I antiarrhythmic drug.

The class two indications for ICD implantation are:

1 Cardiac arrest presumed to be due to VF when electrophysiological testing is precluded by other medical conditions.
2 Severe symptoms attributable to sustained ventricular arrhythmias while awaiting cardiac transplantation.
3 Familial or inherited conditions with a high risk for lifethreatening ventricular tachyarrhythmia such as long QT syndrome or hypertrophic cardiomyopathy.
4 Non-sustained VT with coronary artery disease, prior MI, and LV dysfunction, and inducible sustained VT or VF at electrophysiological study.
5 Recurrent syncope of undetermined aetiology in the presence of ventricular dysfunction and inducible ventricular arrhythmias at electrophysiological study when other causes of syncope have been excluded.

The size of the risk reduction to patients and the degree of life prolongation are only moderate in the trials showing benefit of ICD over antiarrhythmic therapy. The cost per life year saved is also wildly different in these trials giving us conflicting information, e.g. $22,800 (MADIT) and $114,917 (AVID).

There is a wide variation in implant rates across the world (Table 87.1).

The UK has one of the lowest implant rates in Western Europe and it is not clear if this is reflective of a conservative approach by UK cardiologists, tight budgetary constraints or a lack of clear clinical trial data. The recently published NICE guidelines, if implemented, will result in an increase in the ICD implantation rate to 50 per million.

In conclusion, a patient who has survived an out of hospital cardiac arrest unrelated to a transient or reversible cause should receive a device irrespective of inducibility at EP study. If this patient has an EF < 35% the case for this is stronger. Patients who have repeated hospital admissions for symptomatic sustained ventricular tachycardia that are not amenable to RF ablation are also clear beneficiaries as well as providing a long term cost saving to the health care system. Other patients must be dealt with on a case by case basis weighing up all the individual circumstances.

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Who should have a VT stimulation study? What are the risks and benefits?

Cardiology Questions and Answers Brain Dump Who should have a VT stimulation study? What are the risks and benefits?

Contrary to conventional wisdom, a significant number of sudden arrhythmic deaths result from re-entrant ventricular tachycardia that occurs in patients with chronic heart disease in the absence of acute infarction. These arrhythmias can be safely studied in a controlled setting using electrophysiological testing. Programmed electrical stimulation of the ventricle (also termed VT stimulation studies) has a remarkable sensitivity for reproducing monomorphic ventricular tachycardia associated with infarct related myocardial scars and offers a fairly reliable means of identifying patients at risk for sudden death. Patients with LV dysfunction (LV ejection fraction <40%) who are inducible for monomorphic VT have a risk of sudden cardiac death of approximately 30% over the ensuing year.

The patients at highest risk for sudden death include those who have survived a cardiac arrest not occurring in the context of an acute infarction, and those presenting with sustained VT. These patients are best treated with implantable cardiac defibrillators. The role of VT stimulation studies in such patients is primarily to confirm the diagnosis and exclude focal ventricular arrhythmias or unusual supraventricular arrhythmias indistinguishable from VT that are amenable to RF ablation. Occasionally, suppression of VT inducibility with drugs such as amiodarone and sotalol may be an acceptable alternative to implantable cardioverter defibrillator (ICD) implant.

VT stimulation studies are more valuable for patients with severe heart disease and unexplained syncope. Such patients may have had a self-limiting arrhythmia causing their syncope. Inducibility of monomorphic VT is a fairly specific finding in this patient population especially if their heart disease is based on coronary artery disease. In addition, electrophysiological studies can unmask severe His-Purkinje conduction disease requiring pacemaker implantation. One major drawback of VT stimulation studies is the low sensitivity for ventricular arrhythmia in nonischaemic dilated cardiomyopathy. In these patients, if the clinical suspicion is high, a negative study may well represent a false negative. A second problem with VT studies is the uncertain reliability of induced polymorphic VT or ventricular fibrillation as end points. Recent data from subgroup analysis of the Multicenter Unsustained Tachycardia Trial (MUSTT) suggests that such arrhythmias may be just as important as monomorphic VT for predicting mortality in the face of severe LV dysfunction.

Perhaps the most important role of VT study is in primary prevention of sudden death. Two recent randomised trials have demonstrated conclusively that patients with depressed LV function and non-sustained VT (defined as three or more beats of VT at a rate >120bpm) will benefit from ICD implantation if they are inducible for sustained VT. Clinical trials are in progress to determine if ICD implantation would benefit patients with low LVEF and heart failure alone without resorting to an EP study. Pending their results, patients with LV dysfunction who manifest non-sustained VT should undergo VT stimulation studies to see if they would benefit from an ICD. This strategy appears to be cost effective.

The risks of invasive electrophysiological studies are related to venous (and rarely arterial) cannulation and from the arrhythmias induced. Injury to the vascular structures and venous thrombosis occurs rarely (less than 2%). Cardiac perforation from catheter placement is equally rare (0.4%); death from the procedure occurred in 0.12% in one study and underlines the importance of trained personnel and well equipped laboratories for these studies.

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How do I assess thyroid function in someone on amiodarone therapy?

Cardiology Questions and Answers Brain Dump What percentage of patients will suffer the complications of amiodarone therapy, and how reversible are the eye, lung, and liver changes? How do I assess thyroid function in someone on amiodarone therapy?

Amiodarone therapy is associated with a number of serious toxicities which primarily involve the lung, heart, liver or thyroid gland. The drug is also associated with a wide array of other side effects involving the skin, eye, gastrointestinal tract and neurologic system. Drug discontinuance rates with amiodarone are closely related to its daily dose. The table summarises the cumulative incidence of adverse reactions reported in two separate meta-analyses.

Eye, lung, and liver toxicity are all potentially reversible if amiodarone is discontinued early after the development of toxicity. However, cases of permanent blindness, death from liver failure and death from respiratory failure have been rarely reported with amiodarone.

There are no adequate predictors of pulmonary toxicity, and serial lung function studies are usually not helpful. Dose and duration of treatment are no guide to risk. Clinical suspicion must remain high, especially in the elderly or those with co-existent pulmonary disease.

Amiodarone has been implicated as a cause of both hyperthyroidism and hypothyroidism. Hypothyroidism is a predictable response to the iodide load presented by amiodarone. Two types of hyperthyroidism have been reported to occur with amiodarone. Type I amiodarone-induced hyperthyroidism occurs in patients with underlying thyroid disease such as Graves disease. The iodide load in these patients accelerates thyroid hormone synthesis. Type II amiodarone-induced hyperthyroidism occurs in patients with normal thyroids. Hyperthyroidism results from a direct toxic effect of amiodarone causing a subacute destructive thyroiditis with release of preformed thyroid hormone. Patients receiving amiodarone should have thyroid function evaluated at periodic intervals. A low TSH is indicative of hyperthyroidism, but does not distinguish between Type 1 and Type 2 hyperthyroidism. Radioactive iodine uptake may be low normal or elevated in Type 1 hyperthyroidism but is very low or absent in Type 2 hyperthyroidism. Interleukin-6 levels are normal or moderately increased in Type 1, but markedly increased in Type 2 amiodarone-induced hyperthyroidism. In addition, colour flow Doppler ultrasound shows an absence of vascularity in Type 2 amiodarone-induced hyperthyroidism.

Amiodarone-induced hypothyroidism is characterised by an elevated TSH. Treatment of amiodarone-induced hypothyroidism is indicated if the free T4 is low or low normal and the TSH is greater than 20 microIU/ml.

As a complication of therapy, hyperthyroidism is more common where dietary iodine intake is low, whilst the reverse is true in areas of high intake. In patients with hyperthyroidism in whom amiodarone therapy is still warranted, thought should be given to concomitant treatment with carbimazole.

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How do I investigate the relatives of a patient with sudden cardiac death?

Cardiology Questions and Answers Brain Dump How do I investigate the relatives of a patient with sudden cardiac death?

In patients aged over 30 years by far the commonest cause of sudden cardiac death is coronary disease (80%). In patients younger than this, inherited disorders play a major role, with hypertrophic cardiomyopathy accounting for approximately 50% of these deaths. Although perhaps not entirely representative of the general population, the most systematically collected data on sudden death in young people comes from athletes. Common causes of sudden death in young athletes are shown in table 84.1. Aortic root dissection and arrhythmias due to accessory pathways and long QT syndromes may also be causative. A specific diagnosis in the deceased should be pursued by means of expert examination of the postmortem heart if available and attempts to obtain antemortem electrocardiograms and other investigations.

In general first-degree relatives should undergo history, physical examination, 12-lead electrocardiography and 2-D echocardiography. Other investigations may also be performed depending on the suspected cause of death, such as exercise testing in suspected long QT syndrome. In the case of a suspected inherited condition, if both parents of the deceased can be evaluated and found to be free of abnormalities, the condition causing death is likely to have been sporadic and the chances of siblings being affected are low. However, this inference must be tempered by the realisation that some inherited conditions (including hypertrophic cardiomyopathy) may be associated with incomplete penetrance. Extended pedigree analyses have demonstrated that occasionally apparently unaffected individuals, termed “obligate carriers”, carry the mutation. A follow up strategy after an initial negative evaluation is empirical, and depends on the age of the person, the level of anxiety and the nature of the suspected condition.

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How do I assess the patient with long QT? Should I screen relatives, and how? How do I treat them?

Cardiology Questions and Answers Brain Dump How do I assess the patient with long QT? Should I screen relatives, and how? How do I treat them?

Patients affected by the congenital long QT syndrome (LQT) are often first assessed when syncope, documented ventricular arrhythmia or aborted cardiac arrest affects them or a family member. The diagnostic cut-offs (<100%>0.46 sec (children <16>0.45 sec (adult males), and >0.47 sec (adult females), after drug induced QT prolongation has been excluded. T wave morphology should also be carefully examined, in particular for high takeoff, late onset, broad base, bifid morphology with humps, and beat-by-beat alternating polarity (T wave alternans). In several LQT variants, sinus bradycardia is an additional common feature. Holter monitoring should be performed to exclude repetitive ventricular arrhythmias of the torsade de pointes type. Family screening by 12-lead ECG of all first-degree relatives is mandatory in order to have a definite diagnosis of hereditary LQT. In Romano-Ward syndrome (1/20,000 births: autosomal dominant transmission with >90% penetrance), 50% of offspring of one affected parent are predicted to be similarly affected.

Six associated genetic loci (on chromosomes 3, 4, 7, 11, 21, 22) have been identified, of which four relate to genes that encode cardiac ion-channel proteins. Several mutations have been described for each gene. Although only 50% of all LQT affected families can be linked to one of these genes, genetic screening is 100% accurate amongst these, and can provide a definite diagnosis in phenotypically borderline cases.

Medical therapy should be promptly started in symptomatic LQT patients, and beta blockers are currently the first choice, with the occasional need for pacemaker implantation. However, recent evidence suggests that in symptomatic cases with aborted cardiac arrest, automatic implantable cardiac defibrillator (ICD) implantation, in addition to beta blocker therapy, is probably indicated. In patients who do not respond to the abovementioned measures, high cervicothoracic sympathectomy might be beneficial. Currently, there is no consensus regarding the need for therapy in asymptomatic patients, unless their phenotype is exceedingly abnormal. Gene-specific medical therapy is currently being investigated.

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How do I treat torsade de pointes at a cardiac arrest?

Cardiology Questions and Answers Brain Dump How do I treat torsade de pointes at a cardiac arrest?

Consideration of the electrophysiological disturbances predisposing to the development of torsade de pointes provides a logical approach to management. Experimental and clinical evidence implicates abnormal prolongation of cardiac action potential as a critical factor. Under these conditions early after-depolarisations may occur and lead to repetitive discharges (“triggered activity”).

Drugs that prolong cardiac action potential and are associated with torsade include antiarrhythmic agents of class Ia and III, tricyclic antidepressants, phenothiazines, macrolide antibiotics, certain antihistamines and cisapride. Hypokalaemia and hypomagnesaemia are well recognised causes of torsade although the evidence for hypocalcaemia is less convincing. Bradycardia – either sinus or due to atrioventricular block – is an important contributory factor.

In the setting of cardiac arrest torsade should be managed with synchronised DC cardioversion which is almost always successful in restoring sinus rhythm. However, additional measures will be necessary to prevent recurrence. These measures are aimed at shortening cardiac action potential duration. The heart rate should be increased. Atropine has the advantage of rapid availability and ease of administration. Where the bradycardia is due to atrioventricular block atropine is unlikely to increase the ventricular rate. Transvenous ventricular pacing should be established rapidly although it is almost certainly wise to stabilise the patient first with an isoprenaline infusion (at a rate of 1-10micrograms/min, titrated against the heart rate) or external cardiac pacing. There is experimental and clinical evidence to support the use of intravenous magnesium in the acute treatment of torsade. A dose of 8mmol (administered over 10-15 minutes) has been shown to abolish torsade in the majority of patients although a second dose may be necessary. There is no evidence to support the use of either intravenous potassium or calcium. The serum concentration of these electrolytes is frequently disturbed as a result of cardiac arrest per se and a reasonable strategy would be to obtain a formal laboratory measurement after a period of haemodynamic stability and to correct as necessary. Ventricular pacing should be maintained and the ECG monitored while the factors predisposing to the development of torsade are considered and corrected. There is no role for conventional antiarrhythmic drugs in the management of torsade de pointes: on the contrary many antiarrhythmics may aggravate the situation.

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What do I do about non-sustained ventricular tachycardia on a 24 hour tape?

Cardiology Questions and Answers Brain Dump What do I do about non-sustained ventricular tachycardia on a 24 hour tape?

The term non-sustained ventricular tachycardia (VT) is used conventionally to describe salvos lasting a minimum of four consecutive ventricular beats and a maximum of 30 seconds in the absence of intervention. The concerns are that the non-sustained VT may itself cause symptoms of palpitation, presyncope or syncope and that the arrhythmia may persist or degenerate into ventricular fibrillation. The finding of non-sustained VT on a 24 hour tape should prompt the following questions: firstly, is there evidence of underlying heart disease; secondly, what is the morphology of the VT; thirdly, what are the patient’s symptoms?

An arrhythmia is usually although not invariably a sign of underlying heart disease. This is an important consideration because treatment of the underlying condition, where possible, is likely to be more effective than antiarrhythmic drug therapy both in terms of preventing the arrhythmia and improving prognosis. Conversely, if treatable underlying heart disease remains untreated then antiarrhythmic drug therapy is unlikely to be successful.

The morphology of the VT may help to guide management: for example if torsade de pointes is observed then management will focus on adjustment of drug regimes and treatment of electrolyte deficiencies and bradycardia. The finding of monomorphic VT might suggest the presence of a re-entrant circuit or automatic focus that may be amenable to mapping and modification or ablation. Non-torsade polymorphic VT is typically seen in the context of heart failure and is seldom reliably induced by electrophysiological study or amenable to radiofrequency ablation.

There is little evidence that antiarrhythmic drug therapy alters prognosis in patients with non-sustained VT. This may reflect a lack of efficacy and/or toxicity of currently available antiarrhythmic agents. Another explanation is that non-sustained VT is frequently a marker of underlying heart disease, which itself determines prognosis. There is evidence that implantable cardioverter-defibrillators (ICDs) may improve the prognosis of patients with poor left ventricular function, asymptomatic nonsustained VT and inducible, non-suppressible VT following myocardial infarction. However, many important questions remain about the prophylactic implantation of ICDs in such patients. The decision to implant is easier if there is a history of presyncope or syncope.

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101 Cardiology Questions Home Page

Interactive Anatomy of the Brain

Which factors predict cardiac risk from general surgery?

Which patients should undergo preoperative non-invasive investigations or coronary angiography?

Which patients should receive antibiotic prophylaxis for endocarditis, and which procedures should be covered in this way?

What percentage of blood cultures will be positive in endocarditis?

What is the morbidity and mortality of endocarditis with modern day management?

What are the indications for surgical management of endocarditis?

How should the anticoagulation of a patient with a mechanical heart valve be managed for elective surgery?

A patient is on life-long warfarin and wishes to become pregnant. How should she be managed?

Which cardiac patients should never get pregnant? Which cardiac patients should undergo elective Caesarean section?

How do I manage the pregnant woman with valve disease?

How do I manage the pregnant woman with dilated cardiomyopathy?

What do I do if an ICD keeps discharging?

How do I follow up the patient with the implantable cardioverter defibrillator?

How do I manage the patient with an ICD?

What are the indications for implantable cardioverter defibrillator (ICD) implantation and what are the survival benefits?

Who should have a VT stimulation study? What are the risks and benefits?

How do I assess thyroid function in someone on amiodarone therapy?

How do I investigate the relatives of a patient with sudden cardiac death?

How do I assess the patient with long QT? Should I screen relatives, and how? How do I treat them?

How do I treat torsade de pointes at a cardiac arrest?

What do I do about non-sustained ventricular tachycardia on a 24 hour tape?

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