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'left ventricular hypertrophy'
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Indications for Hemodynamic Monitoring in Patients with STEMI Management of complicated acute myocardial infarction Hypovolemia versus cardiogenic shock Ventricular septal rupture versus acute mitral regurgitation Severe left ventricular failure Right ventricular failure Refractory ventricular tachycadia Differentiating severe pulmonary disease from left ventricular failure Assessment of cardiac tamponade Assessment of therapy in selected individuals Afterload reduction in patients with severe left ventricular failure Inotropic agent therapy Beta-blocker therapy Temporary pacing (ventricular versus atrioventricular) Intraaortic balloon counterpulsation Mechanical ventilation
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
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.
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
It may also improve arterial oxygenation by reducing pulmonary vascular congestion DIURETICS. Mild heart failure responds well to diuretics such as furosemide, Dose - 10 to 40 mg, repeated at 3- to 4-hour intervals if necessary. It reduces pulmonary capillary pressure reduces dyspnea. Decreased LVDV↓ LV wall tension - ↓ myocardial oxygen requirements and may lead to improvement of contractility and augmentation of the ejection fraction, stroke volume, and cardiac output. The reduction of elevated left ventricular filling pressure may also enhance myocardial oxygen delivery by diminishing the impedance to coronary perfusion attributable to elevated ventricular wall tension. .
Important coronary risk factors 1 Existing vascular disease (coronary, cerebral or peripheral) 2 Age 3 Dyslipidaemia 4 Smoking 5 Family history 6 Hypertension 7 Male sex/hormonal factors 8 Diabetes 9 Renal impairment 10 Obesity 11 Inactivity 12 Thrombogenic factors 13 Other dietary factors 14 Homocystinaemia 15 Psychological factors 16 Elevated hsCRP 17 Abnormal CT calcium score/coronary angiogram 18 Left ventricular hypertrophy (hypertensive patients) 19 Abnormal
THE HYPERDYNAMIC STATE. MI with hyperdynamic state—that is, elevation of sinus rate, arterial pressure, and cardiac index, occurring singly or together in the presence of a normal or low left ventricular filling pressure—and if other causes of tachycardia such as fever, infection, and pericarditis can be excluded, treatment with beta blockers is indicated. Presumably, the increased heart rate and blood pressure are the result of inappropriate activation of the sympathetic nervous system, possibly secondary to augmented release of catecholamines, pain and anxiety, or some combination of these.
Left Ventricular Failure Single most important predictor of mortality following STEMI in patients with STEMI Systolic dysfunction alone or both systolic and diastolic dysfunction can occur. LVDD leads to pulmonary venous hypertension and pulmonary congestion. Systolic dysfunction - ↓ cardiac output and of the ejection fraction. Predictors of LVF infarct size, advanced age and diabetes.[190] Mortality increases in association with the severity of the hemodynamic deficit.
CARDIOLOGIST IN YELAHANKA SECOND DEGREE AV BLICK There are two basic types of second-degree AV block: AV nodal Möbitz type I (Wenckebach) heart block, and the more distal and more sinister Möbitz type II heart block. Möbitz type I heart block is much more common. In Möbitz type I block the PR interval lengthens progressively with each cardiac cycle, until an atrial wave is not conducted. There is recovery of conduction and the next a wave is conducted with a shorter interval and the cycle begins again. The QRS complex is narrow (Fig 3.10) (unless associated with pre-existing BBB). The increment is largest between the first and second conducted P wave, and the PR interval continues to increase by less and less until a P wave is dropped. Möbitz type II heart block is almost always associated with a BBB (Fig 3.11), since its origin is intraventricular (below the AV node), and it tends to lapse suddenly into extreme bradycardia or asystole. It tends to be over-diagnosed, especially in the setting of 2:1 AV block (Fig 3.12). There is no lengthening of the PR interval before an atrial wave is not conducted. At times, atropine or exercise can demonstrate the site of the block, by increasing the block from 2:1 to a higher grade when the underlying mechanism is Möbitz II. Conversely, Wenckebach conduction may improve to 3:2 or better. For a distinction to be made between Möbitz type I and Möbitz type II, at least two consecutively conducted P waves have to be evaluated. This is impossible in 2:1 conduction (block) and can only be reported as 2:1 AV block (Fig 3.12). Yet this is very commonly reported as
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