Heart 9

oelomar's version from 2016-05-08 13:22


Question Answer
What is ventricular fibrillation?VF is a medical emergency that requires advanced life support interventions. It is a condition in which there is uncoordinated contraction of the cardiac muscle of the ventricles, making them quiver rather than contract properly. VF is the most commonly identified arrhythmia in cardiac arrest patients. If this arrhythmia continues for more than a few seconds, it will likely degenerate further into asystole.
How is ventricular fibrillation treated?VF rarely reverses spontaneously. The only effective treatment is electrical defibrillation.
What does an ECG show with ventricular fibrillation?Shapeless, rapid oscillations with no hint of organised complexes.
Survivors of ventricular tachycardias such as VF are, in the absence of an identifiable reversible cause, at high risk of sudden death. What is the first-line management in such patients?Implantable cardioverter-defibrillator.


Question Answer
What is the Brugada syndrome?This is an inheritable condition that accounts for part of a group of patients with idiopathic ventricular fibrillation who have no evidence of causative structural cardiac disease. It is the major cause of sudden unexplained death syndrome.
Which group of people is most likely to be affected by the Brugada syndrome?Young male adults in South-East Asia (Thailand, Laos).
How is the Brugada syndrome diagnosed?The diagnosis is made by identifying the classic ECG changes that may be present spontaneously or be provoked by the administration of a class I antiarrhythmic (flecainide): RBBB with coved ST elevation in leads V1–V3.
How is the Brugada syndrome treated?Treatment lies in termination of this lethal arrhythmia before is causes death. This is done via insertion of an implantable cardioverter-defibrillator (ICD), which continuously monitors the heart rhythm and will shock the wearer if ventricular fibrillation is sensed.
Beta-blockers are not helpful in treating the Brugada syndrome and may be harmful. True or false?True.


Question Answer
Quinidine is a class Ia anti-arrhythmic agent and a sodium channel blocker. What are the side-effects of its toxicity?Headache, tinnitus, thrombocytopenia, torsades de pointes (due to the effect of increasing the QT interval)).
What anti-arrhythmic class is best for use post-MI? Give an example of one.Class Ib e.g. lidocaine, mexilitine.
What anti-arrhytmic class is contraindicated for use post-MI? Give an example of one.Class Ic e.g. flecainide, propafenone.
What is long-QT syndrome?A rare inherited or acquired heart condition in which ventricular repolarisation is greatly prolonged leading to a prolonged QT interval on ECG, leading to an increase in the risk of episodes of torsades de pointes.
What are the causes of long-QT syndrome?Many, including Jervell and Lange–Nielsen syndrome, Romano– Ward syndrome, hypokalaemia, hypomagnesaemia, hypocalcaemia, quinidine, sotalol, amiodarone, TCAs, antipsychotics, erythromycin, ciprofloxacin, methadone, bradycardia, mitral valve prolapse, acute MI, diabetes, CNS diseases.
What is Jervell and Lange–Nielsen syndrome?An autosomal recessive congenital long-QT syndrome associated with severe, bilateral sensorineural hearing loss.
What is Romano-Ward syndrome?An autosomal dominant congenital long-QT syndrome.
In acquired long-QT syndrome (i.e. not congenital long-QT syndrome), QT prolongation and torsades de pointes are usually provoked by bradycardia. True or false?True.


Question Answer
LQT1 is one of the phenotypes of long-QT syndrome. How is the arrhythmia provoked in this phenotype?Exercise, particularly swimming.
LQT2 is one of the phenotypes of long-QT syndrome. How is the arrhythmia provoked in this phenotype?Emotion and acoustic stimuli.
LQT3 is one of the phenotypes of long-QT syndrome. How is the arrhythmia provoked in this phenotype?Rest or when asleep.
What are the clinical features of long-QT syndrome?Patients with a long QT develop syncope and palpitations as a result of torsade de pointes. They usually terminate spontaneously but may degenerate to ventricular fibrillation, resulting in sudden death. Between spells of tachycardia or immediately preceding the onset of tachycardia the ECG shows a prolonged QT interval; the corrected QT is usually greater than 0.50s.
How is long-QT syndrome managed acutely?Any electrolyte disturbance is corrected. Causative drugs are stopped. The heart rate is maintained with atrial or ventricular pacing. Mg2+ for acquired long-QT. Intravenous isoprenaline may be effective when QT prolongation is acquired (isoprenaline is contraindicated for congenital long QT syndrome).
How is long-QT syndrome managed in the long-term?Beta-blockade, pacemaker therapy, and occasionally left-cardiac sympathetic denervation. LQT1 patients seem to respond well to beta-blockade. LQT3 patients are better treated with sodium channel blockers. Patients who remain symptomatic despite conventional therapy and those with a strong family history of sudden death usually need ICD (implantable cardioverter-defibrillator) therapy.


Question Answer
What is beta-blocker overdose treated with?Glucagon.
What is cor pulmonale and what causes it?Pulmonary heart disease, also known as cor pulmonale, is the enlargement and failure of the right ventricle of the heart as a response to increased vascular resistance (such as from pulmonic stenosis) or high blood pressure in the lungs.
What are the signs/symptoms of cor pulmonale?Can be non-specific and depend on the stage of the disorder. They include shortness of breath, wheezing, cyanosis, ascites, hepatomegaly, raised JVP, third heart sound.