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The use of invasive hemodynamic monitoring is based on the following principal factors: 1. Difficulty in interpreting clinical and radiographic findings of pulmonary congestion even after a thorough review of noninvasive studies such as an echo-cardiogram. 2. Need for identifying noncardiac causes of arterial hypotension, particularly hypovolemia. 3. Possible contribution of reduced ventricular compliance to impaired hemodynamics, requiring judicious adjustment of intravascular volume to optimize left ventricular filling pressure. 4. Difficulty in assessing the severity and sometimes even determining the presence of lesions such as mitral regurgitation and ventricular septal defect when the cardiac output or the systemic pressures are depressed. 5. Establishing a baseline of hemodynamic measurements and guiding therapy in patients with clinically apparent pulmonary edema or cardiogenic shock. 6. Underestimation of systemic arterial pressure by the cuff method in patients with intense vasoconstriction. The prognosis and the clinical status of patients with STEMI relate to both the cardiac output and the pulmonary artery wedge pressure. Patients
PAPULAR CARDIOLOGISTS IN SAHAKARANAGAR Myocardial infarction and ischaemia Recognition of ischaemic changes has gained in importance from the recent increase in percutaneous coronary interventions. It still retains its established importance in other aspects of the management of acute coronary syndromes. Decisions on the immediate treatment of patients with chest pain are made according to findings on the ECG. This is a cheap test that can be performed quickly at the bedside and interpreted without delay
POPULAR CARDIOLOGISTS IN SAHAKARANAGAR 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 fSAor 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.
SAMIKSHA HEART AND DIABETIC CARE IN YELAHANKA Echocardiographic findings in certain cardiac abnormalities It is important to be aware that modern colour flow mapping is so sensitive that small amounts of regurgitation are often detected from quite normal valves. Deciding whether these jets are significant can be difficult and requires experience. Mitral stenosis Thickening and doming of the mitral valve leaflets is visible on M mode and 2D scanning , It may be possible to measure the valve area by planimetry . Secondary changes such as left atrial size and the presence of rheumatic disease of other valves can be seen. Doppler interrogation of the jet of blood entering the left ventricle through the mitral valve will enable estimation of the valve area by a formula called the pressure half-time equation This will usually give accurate and consistent estimates of the valve area and is especially useful for serial measurements over months or years. It will also be possible to detect associated mitral regurgitation with Doppler. Mitral regurgitation and mitral valve prolapse Here the mitral valve may appear normal and abnormal co-aptation of the leaflets is not usually visible . The left atrium will appear enlarged if significant chronic MR is present, and if this is severe left ventricular dilatation will be present. If the MR is due to mitral valve
THE BEST HEART SPECIALIST S IN YELAHANKA ST segment There are two aspects to report: depression and elevation. Depression The ST segment is said to be abnormal if it slopes down 1 mm or more from the J point—the end of the QRS complex (downsloping depression)—or is depressed 1 mm or more horizontally (plane depression). Depression of the J point itself may be normal, especially during exercise, but this upsloping ST depression should return to the isoelectric line within 0.08 seconds. The isoelectric line is defined as the PR or TP segment of the ECG . ST depression may be due to ischaemia, the effect of digoxin, hypertrophy and so on. Elevation ST elevation of up to 3 mm may be normal in V leads (especially the right), and up to 1 mm may be normal in limb leads. This ST elevation is called early repolarisation syndrome or pattern. Otherwise ST elevation may mean an acute myocardial infarction where it is said to represent a current of injury. Pericarditis also causes ST elevation but unlike infarction is usually associated with concave upwards elevation. hypertrophy and conduction defects like LBBB can be associated with ST elevation in leads where the QRS is mostly negative. T waves The T wave is always inverted in lead aVR and often in L3 and V1–V2, and in aVL if the R wave is less than 5 mm tall. Inversion and flattening are common and non-specific findings. Deep (> 5 mm) symmetrical and persistent (days to weeks) inversion is consistent with infarction; broad, ‘giant’ inversion may follow syncope from any cause including cerebrovascular accidents. Like the ST segment, the T wave tends to be directed opposite to the main QRS deflection in conduction defects (e.g. LBBB), VEBs or ventricular hypertrophy (where it is described as secondary ST/T changes or strain pattern). Tall peaked T waves are most often seen as a reciprocal change to inferior or posterior infarcts. They are classically seen in patients with hyperkalaemia. Broader large T waves are seen in early (‘hyperacute’) infarction and sometimes in cerebrovascular accidents. While not diagnostic by themselves (T waves never are), when they are associated with modest ST elevation (especially in V3) and reciprocal depression in the inferior leads, they indicate infarction or ischaemia. When these changes evolve over time they are even more specific for infarction A U wave may be prominent in patients with hypokalaemia, LVH and bradycardia. Isolated
CARDIAC CENTERS IN YELAHANKA NEW TOWN BANGALORE ST segment There are two aspects to report: depression and elevation. Depression The ST segment is said to be abnormal if it slopes down 1 mm or more from the J point—the end of the QRS complex (downsloping depression)—or is depressed 1 mm or more horizontally (plane depression). Depression of the J point itself may be normal, especially during exercise, but this upsloping ST depression should return to the isoelectric line within 0.08 seconds. The isoelectric line is defined as the PR or TP segment of the ECG . ST depression may be due to ischaemia, the effect of digoxin, hypertrophy and so on. Elevation ST elevation of up to 3 mm may be normal in V leads (especially the right), and up to 1 mm may be normal in limb leads. This ST elevation is called early repolarisation syndrome or pattern. Otherwise ST elevation may mean an acute myocardial infarction where it is said to represent a current of injury. Pericarditis also causes ST elevation but unlike infarction is usually associated with concave upwards elevation. hypertrophy and conduction defects like LBBB can be associated with ST elevation in leads where the QRS is mostly negative. T waves The T wave is always inverted in lead aVR and often in L3 and V1–V2, and in aVL if the R wave is less than 5 mm tall. Inversion and flattening are common and non-specific findings. Deep (> 5 mm) symmetrical and persistent (days to weeks) inversion is consistent with infarction; broad, ‘giant’ inversion may follow syncope from any cause including cerebrovascular accidents. Like the ST segment, the T wave tends to be directed opposite to the main QRS deflection in conduction defects (e.g. LBBB), VEBs or ventricular hypertrophy (where it is described as secondary ST/T changes or strain pattern). Tall peaked T waves are most often seen as a reciprocal change to inferior or posterior infarcts. They are classically seen in patients with hyperkalaemia. Broader large T waves are seen in early (‘hyperacute’) infarction and sometimes in cerebrovascular accidents. While not diagnostic by themselves (T waves never are), when they are associated with modest ST elevation (especially in V3) and reciprocal depression in the inferior leads, they indicate infarction or ischaemia. When these changes evolve over time they are even more specific for infarction . A U wave may be prominent in patients with hypokalaemia, LVH and bradycardia. Isolated U inversion is a specific but insensitive sign of coronary disease. 54 PRACTICAL CARDIOLOGY ECG reports Reports should be short and stereotyped, with the description clearly separated from the comment. It is a good general strategy to under-report, especially for a beginner. It is generally wiser to state ‘inferior Q waves noted’ or ‘non-specific ST/T changes’ than to indulge in speculation on possible or probable infarction or ischaemia. ECG labels tend to have serious employment and insurance implications. On the other hand, specific questions on the request form must be addressed, since they constitute the reason for taking the ECG in the first place.
THE BEST CARDIOLOGISTS IN YELAHANKA NEWTOWN BANGALORE ST segment There are two aspects to report: depression and elevation. Depression The ST segment is said to be abnormal if it slopes down 1 mm or more from the J point—the end of the QRS complex (downsloping depression)—or is depressed 1 mm or more horizontally (plane depression). Depression of the J point itself may be normal, especially during exercise, but this upsloping ST depression should return to the isoelectric line within 0.08 seconds. The isoelectric line is defined as the PR or TP segment of the ECG ST depression may be due to ischaemia, the effect of digoxin, hypertrophy and so on. Elevation ST elevation of up to 3 mm may be normal in V leads (especially the right), and up to 1 mm may be normal in limb leads. This ST elevation is called early repolarisation syndrome or pattern. Otherwise ST elevation may mean an acute myocardial infarction where it is said to represent a current of injury. Pericarditis also causes ST elevation but unlike infarction is usually associated with concave upwards elevation . hypertrophy and conduction defects like LBBB can be associated with ST elevation in leads where the QRS is mostly negative. T waves The T wave is always inverted in lead aVR and often in L3 and V1–V2, and in aVL if the R wave is less than 5 mm tall. Inversion and flattening are common and non-specific findings. Deep (> 5 mm) symmetrical and persistent (days to weeks) inversion is consistent with infarction; broad, ‘giant’ inversion may follow syncope from any cause including cerebrovascular accidents. Like the ST segment, the T wave tends to be directed opposite to the main QRS deflection in conduction defects (e.g. LBBB), VEBs ) or ventricular hypertrophy (where it is described as secondary ST/T changes or strain pattern). Tall peaked T waves are most often seen as a reciprocal change to inferior or posterior infarcts. They are classically seen in patients with hyperkalaemia. Broader large T waves are seen in early (‘hyperacute’) infarction and sometimes in cerebrovascular accidents. While not diagnostic by themselves (T waves never are), when they are associated with modest ST elevation (especially in V3) and reciprocal depression in the inferior leads, they indicate infarction or ischaemia. When these changes evolve over time they are even more specific for infarction A U wave may be prominent in patients with hypokalaemia, LVH and bradycardia. Isolated U inversion
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
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
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