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Showing posts with label Internal Medicine. Show all posts
Showing posts with label Internal Medicine. Show all posts

What is the pathology in Ebstein's anomaly ?

What is the pathology in Ebstein's anomaly ? 

The tricuspid leaflets are abnormal and are displaced into the body of the right ventricle.

The septal leaflet is variably deficient or even absent.

The posterior leaflet is also variably deficient and there is a large 'sail-like' anterior leaflet that is the hallmark of this condition.

The abnormally located tricuspid orifice results in a part of the right ventricle lying between the atrioventricular ring and the origin of the valve, which is continuous with the right atrial chamber.

This proximal segment is known as the 'atrialized' portion of the right ventricle.

About 50% of the patients have either a patent foramen ovale or a secundum ASD, and 25% have one or more accessory atrioventricular conduction pathways.

The anomaly is said to be associated with maternal lithium ingestion.
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What treatment is available for primary pulmonary hypertension ?

What treatment is available for primary pulmonary hypertension ?

• Diuretics are useful in reducing excessive preload in patients with right heart failure, particularly when hepatic congestion and ascites are present.

• Oral anticoagulants: warfarin is the anticoagulant of choice, in doses adjusted to achieve an INR of
approximately 2.0. Anticoagulants nearly double the 3-year survival rate (Circulation 1984; 70: 580-7).

* Calcium channel blockers: nifedipine, diltiazem. Patients who respond to calcium channel blockers
have a 5-year survival rate of 95% (N Engl J Med 1992; 327: 76-81).

• Intravenous epoprostenol (formerly prostacyclin or prostaglandin I2), which is a potent short-acting
vasodilator and inhibitor of platelet aggregation that is produced by the vascular endothelium (N Engl
J Med 1996; 334: 296-301; N Engl J Med 1998; 338: 273-7).

• Atrial septostomy: the creation of a right-to-left shunt by blade-balloon atrial septostomy has been
reported to improve forward output and alleviate right-sided heart failure by providing blood with a
low-resistance channel, thereby decompressing the right atrium and improving filling of the left side of
the heart (Circulation 1995; 91: 2028-35).

• Lung transplantation and combined heart-lung transplantation: survival rates after the two
procedures are similar. Even markedly depressed right ventricular function improves considerably
with single- or double-lung transplantation.

• Possible future drugs: (a) UT-15, a prostaglandin 12 analogue, has been shown to have sustained
and favourable effects in patients when administered sub-cutaneously (Circulation 2000; 102(18):
11-101); (b) Sitaxsentan, an oral selective endothelin-A receptor blocker, has been shown to produce
sustained improve-ments in pulmonary artery pressure (Circulation 2000; 101(25): 2922-7).
Graham Steell (1851-1942), assistant physician to the Manchester Royal Infirmary, described the murmur in a paper titled The murmur of high pressure in the pulmonary artery (Med Chron (Manchester) 1888; 9: 182-8).
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What is the prognosis in pulmonary hypertension ?

What is the prognosis in pulmonary hypertension ? 

The prognosis is poor: median survival is approximately 3 years from the time of diagnosis, with about one third of patients surviving for 5 years. 

Death usually occurs suddenly, presumably from arrhythmias or right ventricular infarction.
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What are the theories for the cause of primary pulmonary hypertension ?

What are the theories for the cause of primary pulmonary hypertension ? 

• Excess endothelial production of the vasoconstrictor thromboxane relative to dilator prostaglandins such as prostacyclin.

• Excess endothelin-I levels relative to nitric oxide. Inhaled nitric oxide and endothelin-1 antagonists reduce pulmonary hypertension.

• Excessive thrombosis in situ due to increased platelet activation, plasminogen activator inhibitor levels and decreased thrombomodulin.

• Increased serotonin levels.

• Inhibition or downregulation of potassium (Kv) channels in pulmonary artery smooth muscle cells and platelets.

• Activation of elastase and matrix metalloprotease enhances production of mitogens.

• Monoclonal proliferation of endothelial cells.
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What are the pathological features of primary pulmonary hypertension ?

What are the pathological features of primary pulmonary hypertension ? 

They are those of plexogenic pulmonary arteriopathy (which also occurs in post-tricuspid left-to-right atrial shunts such as VSD or PDA, and collagen vascular diseases), characterized by medial hypertrophy and concentric intimal fibrosis of the pulmonary arteries with complex plexiform lesions.

Others have no plexiform lesions or concentric intimal fibrosis, but rather have recanalized thrombotic small pulmonary arteries which are said to be the result of small thrombi or recurrent emboli.

The least common histological pattern is veno-occlusive disease.
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What are the signs of pulmonary hypertension ?

What are the signs of pulmonary hypertension ?
 

• Large 'a' waves in JVP.
. Left parasternal heave.
• Loud or palpable P2.
• Ejection click in the pulmonary area.
• Early diastolic murmur (Graham Steell murmur) due to pulmonary regurgitation.
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What are the functions of pericardium ?

What are the functions of pericardium ?

 • The pericardium protects and lubricates the heart.

 • It contributes to the diastolic coupling of the left and right ventricles - an effect that is important in cardiac tamponade and constrictive pericarditis. 

W. Dressier (1890-1969), US physician educated in Vienna. He worked at the I Manimoides Hospital, Brooklyn, New York.
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What do you know about postcardiotomy syndrome ?

What do you know about postcardiotomy syndrome ? 

It occurs in about 5% of patients who have cardiac surgery, with symptoms of pericarditis from three weeks to six months after surgery. It is initially treated with NSAIDs and systemic steroids in refractory cases. 

Pericardiectomy is rarely required. It is said to result from an autoimmune response and is most likely to be related to surgical trauma and irritation of blood products in the mediastinum and pericardium.
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What is Dressler's syndrome ?

What is Dressler's syndrome ? 

Dressler's syndrome is characterized by persistent pyrexia, pericarditis and pleurisy. 

It was first described in 1956 when Dressier recognized that post-myocardial infarction chest pain is not caused by coronary artery insufficiency.

 It usually occurs 2-3 weeks after myocardial infarction and is considered to be of autoimmune aetiology; it responds to NSAIDs.
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What do you know about the transient constrictive phase of acute pericarditis ?

What do you know about the transient constrictive phase of acute pericarditis ? 

About 10% of the patients with acute pericarditis have a transient constrictive phase which may last 2-3 months before it gradually resolves, either spontaneously or with treatment with anti-inflammatory drugs.

These patients usually have a mod-erate amount of pericardial effusion and, as the effusion resolves, the pericardium remains thickened, inflamed and non-compliant resulting in constrictive haemo-dynamics.

Clinical features include shortness of breath, raised jugular venous pressure, peripheral oedema and ascites.

Constrictive haemodynamics can be documented by Doppler echocardiography and resolution of constrictive physiology can be serially followed by this technique.
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What is the treatment for acute pericarditis ?

What is the treatment for acute pericarditis ? 

• Pain relief (codeine) and anti-inflammatory agents (non-steroidal anti-inflammatory drugs (NSAIDs) such as indometacin).

 • Steroids should be considered only when the pain does not respond to a com-bination of NSAIDs.

 • Treatment of the underlying cause. 

• Colchicine has been used to treat recurrent pain of pericarditis, and rarely peri-cardiectomy may be required for pain even in the setting of no haemodynamic impairment.
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How common is pericardial rub in constrictive pericarditis ?

How common is pericardial rub in constrictive pericarditis ? 

It is not heard in constrictive pericarditis.
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What are the characteristic features of a pericardial friction rub ?

What are the characteristic features of a pericardial friction rub ? 

It typically consists of three components: a presystolic rub (during atrial contrac-tion), a ventricular systolic rub (which is almost always present and usually the loudest component) and a diastolic rub which follows the second heart sound (during rapid ventricular filling).
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Mention some indications for implantable cardiac defibrillators.

Mention some indications for implantable cardiac defibrillators.

 • Cardiac arrest resulting from ventricular tachyarrhythmia not due to a reversible or transient cause (remember: patients who have cardiac arrest unrelated to acute myocardial infarction have approximately a 35% chance of recurrent ventricular arrhythmias within the first year). 

• Spontaneous sustained ventricular tachycardia. 


• Syncope of undetermined origin with inducible sustained ventricular tachycardia on electrophysiological study and when drug therapy is not effective or tolerated. 

• Non-sustained ventricular tachycardia with coronary artery disease and inducible ventricular tachycardia on electrophysiological study that is not suppressible by a class I antiarrhythmic drug.
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What is the pacemaker syndrome ?

What is the pacemaker syndrome ?

 It is seen in individuals with a single-chamber pacemaker who experience symptoms of low cardiac output (dizziness, etc.) when erect; it is attributed to the lack of atrial kick. Pacemaker syndrome is caused by haemodynamic changes as a consequence of inappropriate use of ventricular pacing: it occurs when ventricular pacing is uncoupled from atrial contraction. 

It is most common when the VVI mode is used in patients with sinus rhythm but can occur in any pacing mode when atrioventricular synchrony is lost. Levels of atrial natriuretic factor are high in pacemaker syndrome. 

If pacemaker syndrome occurs in a patient with a VV1 pacemaker the only definitive treatment is to convert to a dual-chamber pacemaker. If the patient has occasional bradycardia then often symptoms may be ameliorated by programming the pacemaker to a lower limit and programming with hysteresis 'on'. 

This allows the patient to stay in normal sinus rhythm for longer periods by minimizing the pacing.
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What are the complications of pacemakers ?

What are the complications of pacemakers ? 

• Erosion through the skin due to mechanical factors. 

• Infection. 

• Lead displacement or lead fracture (the most common site of pacing lead fracture is between the first rib and the clavicle). 

• Pacemaker malfunction. 

• Electromagnetic interference.

 • Pain/ecchymoses at the site of insertion. 

• Pneumothorax.
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Mention some expanded uses of cardiac pacing.

Mention some expanded uses of cardiac pacing. 

• Dual chamber pacing has been used to optimize cardiac output and minimize the outflow tract gradient in patients with hypertrophic obstructive cardiomyopathy. 

• Dual chamber pacing is currently being investigated in dilated cardiomyopathy with heart failure and intraventricular conduction delay to optimize AV delay and improve cardiac output. 

• Dual-site atrial pacing to prevent atrial fibrillation is being evaluated.
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How soon after pacemaker insertion can a patient drive ?

How soon after pacemaker insertion can a patient drive ? 

The patient may not drive until the pacemaker has been shown to be functioning correctly for at least I month after implantation. 

Patients must inform driving licensing authorities and the motor insurers.
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What do you know about permanent pacemakers ?

What do you know about permanent pacemakers ? 

* They are connected to the heart by one or two electrodes and are powered by long-lasting (5-10 years) solid-state lithium batteries. Most pacemakers are designed to pace and sense the ventricles - called the VVI pacemakers because they pace the ventricle (V), sense the ventricle (V) and are inhibited (I) by the ventricular signal. They are inserted under local anaesthesia and fluoroscopic guidance, subcutaneously under the pectoral muscles.

• In symptomatic sinus tachycardia, an atrial pacemaker may sometimes be implanted (AAI).

• In sick sinus syndrome, a dual-chamber pacemaker DDD (because it paces two or dual chambers, senses both (D) and reacts in two (D) ways, i.e. pacing in the same chamber is inhibited by spontaneous atrial and ventricular signals, and ventricular pacing is triggered by spontaneous atrial events) is implanted.

• Rate-responsive pacemakers measure activity, respiration, biochemical and electrical indicators, and change their pacing rate so that it is suitable for that level of exertion.
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What are the indications for a permanent pacemaker ?

What are the indications for a permanent pacemaker ?
 

• Symptomatic bradyarrhythmias (heart rate <40 beats/min or documented periods of asystole >30 seconds when awake). Symptoms include syncope, pre-syncope, confusion, seizures, or congestive heart failure and they must be clearly related to the bradycardia.
 

• Asymptomatic Mobitz type I1 atrioventricular block (N Engl d Med 1998; 338: 1147-8).
 

• Complete heart block.
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