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the best cardiac clinics in yelahanka new town bangalore Ventricular arrhythmias Ventricular ectopic beats Like SVEBs, VEBs are common and, by themselves, generally harmless. Past attempts to suppress them as harbingers of malignant arrhythmias have caused more harm than good. Nevertheless, recognition of their electrocardiographic morphology and behaviour remain important. VEBs that have a fixed coupling to the preceding beats are thought to represent a localised ventricular re-entry and are said to be extra-systolic (extra-systoles). In the top strip of they each replace a sinus beat, with a sinus P wave buried inside the ectopic QRS; their pauses are exactly (fully) compensatory. In the bottom strip, the pause cannot be quantified but, unlike the aberrant beats of Ashman’s phenomenon in , there is hint of a compensatory pause, even during AF. Also unlike aberrant beats in Figure 3.33, the VEBs do not come after the longest cycles in AF. VEBs with same morphology but variable coupling intervals usually represent a continuous discharge from an ectopic focus, like a fixed-rate electronic pacemaker. They capture the ventricles whenever the latter are not refractory and, when they occur at the right time, produce ventricular fusion beats. Fusion beats occur when impulses from two origins, in the case seen in from the sinus node and the parasystolic focus, occur at almost the same time. The resultant QRS complex has features of both types of beat. These VEBs are called parasystolic
the best cardiac clinics in yelahanka new town bangalore Ventricular arrhythmias Ventricular ectopic beats Like SVEBs, VEBs are common and, by themselves, generally harmless. Past attempts to suppress them as harbingers of malignant arrhythmias have caused more harm than good. Nevertheless, recognition of their electrocardiographic morphology and behaviour remain important. VEBs that have a fixed coupling to the preceding beats are thought to represent a localised ventricular re-entry and are said to be extra-systolic (extra-systoles). In the top strip of they each replace a sinus beat, with a sinus P wave buried inside the ectopic QRS; their pauses are exactly (fully) compensatory. In the bottom strip, the pause cannot be quantified but, unlike the aberrant beats of Ashman’s phenomenon in , there is hint of a compensatory pause, even during AF. Also unlike aberrant beats in Figure 3.33, the VEBs do not come after the longest cycles in AF. VEBs with same morphology but variable coupling intervals usually represent a continuous discharge from an ectopic focus, like a fixed-rate electronic pacemaker. They capture the ventricles whenever the latter are not refractory and, when they occur at the right time, produce ventricular fusion beats. Fusion beats occur when impulses from two origins, in the case seen in from the sinus node and the parasystolic focus, occur at almost the same time. The resultant QRS complex has features of both types of beat. These VEBs are called parasystolic
THE BEST CARDIOLOGIST IN YELAHANKA Mitral regurgitation A regurgitant mitral valve allows part of the left ventricular stroke volume to regurgitate into the left atrium, imposing a volume load on both the left atrium and the left ventricle. Symptoms: Dyspnoea (increased left atrial pressure); fatigue (decreased cardiac output). General signs: Tachypnoea. The pulse: Normal, or sharp upstroke due to rapid left ventricular decompression; atrial fibrillation is relatively common. Palpation: The apex beat may be displaced, diffuse and hyperdynamic if left ventricular enlargement has occurred; a pansystolic thrill may be present at the apex; a parasternal impulse (due to left atrial enlargement behind the right ventricle—the left atrium is often larger in mitral regurgitation than in mitral stenosis and can be enormous). All these signs suggest severe mitral regurgitation. Auscultation Soft or absent S1 (by the end of diastole, atrial and ventricular pressures have equalised and the valve cusps have drifted back together); left ventricular S3, due to rapid left ventricular filling in early diastole; pansystolic murmur maximal at the apex and usually radiating towards the axilla. Causes of chronic mitral regurgitation: (i) Degenerative; (ii) rheumatic; (iii) mitral valve prolapse; (iv) papillary muscle dysfunction, due to left ventricular failure or ischaemia. Mitral valve prolapse (systolic-click murmur syndrome) This syndrome can cause a systolic murmur or click, or both, at the apex. The presence of the murmur indicates that there is some mitral regurgitation present. Auscultation: Systolic click or clicks at a variable time (usually mid-systolic) may be the only abnormality audible, but a click is not always audible; systolic
ECHOCARDIOLOGIST IN GANGAMMA CIRCLE Mitral regurgitation A regurgitant mitral valve allows part of the left ventricular stroke volume to regurgitate into the left atrium, imposing a volume load on both the left atrium and the left ventricle. Symptoms: Dyspnoea (increased left atrial pressure); fatigue (decreased cardiac output). General signs: Tachypnoea. The pulse: Normal, or sharp upstroke due to rapid left ventricular decompression; atrial fibrillation is relatively common. Palpation: The apex beat may be displaced, diffuse and hyperdynamic if left ventricular enlargement has occurred; a pansystolic thrill may be present at the apex; a parasternal impulse (due to left atrial enlargement behind the right ventricle—the left atrium is often larger in mitral regurgitation than in mitral stenosis and can be enormous). All these signs suggest severe mitral regurgitation. Auscultation Soft or absent S1 (by the end of diastole, atrial and ventricular pressures have equalised and the valve cusps have drifted back together); left ventricular S3, due to rapid left ventricular filling in early diastole; pansystolic murmur maximal at the apex and usually radiating towards the axilla. Causes of chronic mitral regurgitation: (i) Degenerative; (ii) rheumatic; (iii) mitral valve prolapse; (iv) papillary muscle dysfunction, due to left ventricular failure or ischaemia.
the best cardiologists in yelahanka new town bangalore Miscellaneous conditions Chamber hypertrophy Left ventricular hypertrophy Although the ECG is reasonably specific, it is not as sensitive as echocardiography in detecting LVH. The LVH voltage alone may be a normal finding in younger subjects, but in adults over 35 years it usually connotes true LVH, especially if corroboratory findings are present ) Unfortunately, LVH with ST/T changes may be impossible to separate from LVH voltage complicated by ST/T changes of different, especially ischaemic, origin . Right ventricular hypertrophy The main criteria for detecting RVH are RAD over +110° and a dominant R wave in V1 (in the absence of its other causes and in the presence of normal-duration QRS) . In congenital heart disease conduction defects often come to obscure the hypertrophy patterns. An atrial (AAI) pacemaker in a patient with anterior myocardial infarction of uncertain age. There is sensing (inhibition) only after some native or paced P waves. The pacemaker captures the atria whenever the latter are not refractory: there is no failure to pace. The middle capture beat is earlier than the other two and has a longer PR interval and aberrant RBBB-type ventricular conduction. This is a pacemaker sensing problem. Reprogramming may enable the pacemaker to sense a smaller atrial amplitude and be inhibited correctly. A DDD pacemaker in trouble: there is no atrial capture and the ventricular complexes are capturing the atria on their own. The retrograde P wave interrupts the T wave and triggers another paced QRS whose retrograde conduction is blocked by the original retrograde P wave. Were it not for this block, an endless loop re-entry (paced) tachycardia would occur. The paced complexes have the typical LBBB/left-axis deviation expected from right ventricular apical pacing. Failure to capture may mean the lead has been displaced or that scarring has developed between the tip of the lead and the myocardium. Sometimes, reprogramming an increase in the output of the pacemaker will fix the problem. a = atrial pacing spike (not followed by a P wave); b = ventricular pacing spike (produced after the atrial spike after a programmed AV delay and followed by a paced ventricular beat); c = retrograde P wave following ventricular paced beat; d = pause caused by blocked retrograde conduction of the previo A DDD or VDD pacemaker with intermittent failure to pace. A 4:3 pacemakerventricular block results in trigeminy even though normal sinus rhythm continues throughout. The normal
PAPULAR CARDIOLOGISTS IN HEBBALA ECG interpretation: points to remember 1 ECG reports should be short and based on clinical information where possible. 2 Check that the patient’s name is on the ECG and that the paper speed and calibration markers are correct. 3 Measure or estimate the heart rate—3 large squares = 100/minute. 4 Establish the rhythm. Look for P waves (best seen in L2). Are the P waves followed by QRS complexes? Look for anomalously conducted or ectopic beats. 5 Measure the intervals: PR, QRS duration and QT interval (for the latter, consult tables, but normal is less than 50% of the RR interval). 6 If the QRS complex is wide (> 3 small squares) consider the possibilities: LBBB, RBBB, WPW or ventricular rhythm or beats. If the pattern is of LBBB, there is no need in most cases to attempt further interpretation. 7 Estimate the QRS axis. In LAD, L1 and aVF diverge and L2 is predominantly negative. In RAD, L1 and aVF converge, while L2 matters little. Indeterminate axis is diagnosed when all six frontal leads are (more or less) equiphasic. 8 Check whether the criteria for LAHB or LAFB have been met. 9 Look for pathological Q waves. In general these are longer than 0.04 seconds and are more than 25% of the size of the following R wave.
POPULAR CARDIOLOGISTS IN H S R LAYOUT Ventricular tachycardia Ventricular tachycardia is defined as three or more ventricular ectopic beats at a rate over 100/minute. It is said to be sustained if it lasts more than 30 seconds. Most broad-complex tachycardias are ventricular (rather than supraventricular with aberrant conduction). The diagnosis of VT is greatly strengthened if there is a history of myocardial infarction or cardiac failure but, oddly enough, the patient’s haemodynamics are of no help. A number of criteria have evolved over the years to help ascertain the diagnosis of VT over aberrancy. These include: evidence of AV dissociation—P waves can be seen unrelated to the QRS complexes (they are usually visible only at relatively slow VT rates) the presence of supraventricular capture or fusion beats visible retrograde conduction with 2:1 block (P waves visible following every second complex) the presence of monophasic R, qR or QR patterns in V1, provided a septal infarction has not modified a RBBB a taller left rabbit ear in RR' or qRR' complexes in V1 n QS complexes in V1 with a slow S descent and sharp upstroke—the opposite of LBBB—or a broad small primary R wave in rS morphology (the Rosenbaum pattern) RAD in the frontal plane with LBBB-like QRS complexes
THE BEST CARDIOLOGISTS IN YELAHANKA Aortic regurgitation The incompetent aortic valve allows regurgitation of blood from the aorta to the left ventricle during diastole for as long as the aortic diastolic pressure exceeds the left ventricular diastolic pressure. Symptoms: Occur in the late stages of disease and include exertional dyspnoea, fatigue, palpitations (hyperdynamic circulation) and exertional angina. General signs: Marfan’s syndrome may be obvious. The pulse and blood pressure: The pulse is characteristically collapsing; there may be a wide pulse pressure. The neck: Prominent carotid pulsations (Corrigan’s sign). Palpation: The apex beat is characteristically displaced and hyperkinetic. A diastolic thrill may be felt at the left sternal edge when the patient sits up and breathes out. Auscultation): A2 (the aortic component of the second heart sound) may be soft; a decrescendo high-pitched diastolic murmur beginning immediately after the second heart sound and extending for a variable time into diastole—it is loudest at the third and fourth left intercostal spaces; a systolic ejection murmur is usually present (due to associated aortic stenosis or to torrential flow across a normal diameter aortic valve). Signs indicating severe chronic aortic regurgitation: Collapsing pulse; wide pulse pressure; long decrescendo diastolic murmur; left ventricular S3 (third heart sound); soft A2; signs of left ventricular failure. Causes of chronic aortic regurgitation: (i) Rheumatic (rarely the only murmur in this case), congenital; (ii) aortic root dilatation—Marfan’s syndrome, dissecting aneurysm. 8• THE PATIENT WITH A MURMUR 305 a b Valve cusps often thickened and calcified Left ventricle may be hypertrophied Ascending aorta may be dilated Systole Diastole S1 A2 P2 S1 Ejection click (Suggests congenital AS) Normal Mild S1 S1 Moderate S1 P2 A2 S1 Severe Reversed S2 Single (S2)
heart specialists in devara besanahalli near silk board bangalore Ventricular tachycardia Ventricular tachycardia is defined as three or more ventricular ectopic beats at a rate over 100/minute. It is said to be sustained if it lasts more than 30 seconds. Most broad-complex tachycardias are ventricular (rather than supraventricular with aberrant conduction). The diagnosis of VT is greatly strengthened if there is a history of myocardial infarction or cardiac failure but, oddly enough, the patient’s haemodynamics are of no help. A number of criteria have evolved over the years to help ascertain the diagnosis of VT over aberrancy. These include: evidence of AV dissociation—P waves can be seen unrelated to the QRS complexes (they are usually visible only at relatively slow VT rates) the presence of supraventricular capture or fusion beats visible retrograde conduction with 2:1 block (P waves visible following every second complex) the presence of monophasic R, qR or QR patterns in V1, provided a septal infarction has not modified a RBBB a taller left rabbit ear in RR' or qRR' complexes in V1 QS complexes in V1 with a slow S descent and sharp upstroke—the opposite of LBBB—or a broad small primary R wave in rS morphology (the Rosenbaum pattern) RAD in the frontal plane with LBBB-like QRS complexes
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