http://WWW.HEARTDIABETESCARE.COM
SAMIKSHAHEARTCARE 57698d5b9ec66b0b6cfb5b6b False 573 1
OK
background image not found
Found Update results for
'clinical trial data'
9
POPULAR CARDIOLOGISTS IN SILK BOARD Atrial tachycardia with block Atrial tachycardia with block (paroxysmal atrial tachycardia (PAT) with block) is also an autonomous (automatic, ectopic) atrial tachycardia but its P waves are usually smaller (often discernible only in lead V1) and faster. As a result of this high rate, AV block—mostly 2:1, but often variable—is usually present prior to any exposure to drugs or vagal manoeuvres ). inthe past this was one of the classic manifestations of digoxin toxicity. It can be difficult to distinguish from other atrial rhythms such as AF, flutter and even sinus rhythm ..
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
heart doctors in Sahakara Nagar, Bangalore • A clinical approach to hypertension The aims of assessing the hypertensive patient are to: n assess the severity of hypertension n identify any secondary causes n identify aggravating factors n identify target organ damage n assess and manage coexisting CVD risk factors n identify factors affecting the choice of treatment n establish baseline clinical and laboratory data
PAPULAR CARDIOL0GISTS IN BANGALORE A clinical approach to hypertension The aims of assessing the hypertensive patient are to: assess the severity of hypertension identify any secondary causes identify aggravating factors identify target organ damage assess and manage coexisting CVD risk factors identify factors affecting the choice of treatment establish baseline clinical and laboratory data.
THE BEST CARDIOLOGIST IN YELAHANKA A clinical approach to hypertension The aims of assessing the hypertensive patient are to: assess the severity of hypertension identify any secondary causes identify aggravating factors identify target organ damage assess and manage coexisting CVD risk factors identify factors affecting the choice of treatment establish baseline clinical and laboratory data.
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
THE BEST CARDIOLOGISTS IN YELAHANKA nvestigations of possible or probable stable angina Electrocardiography A standard 12-lead ECG should be obtained in all patients. This is likely to be normal in almost half of patients with subsequently proven coronary artery disease. Nevertheless, an abnormal trace lends weight to the symptoms and favours further investigation. Chest X-ray Routine radiology is not essential but may reveal important co-morbidities. It should always be performed in those with clinical evidence of hypertension, pericarditis (p. 174), heart failure or valvular disease, if only as a baseline. It is similarly indicated for patients with suspected or known pulmonary or systemic disease such as rheumatoid arthritis, COPD or alcoholism. Routine blood tests All patients with suspected angina should have the following routine investigations at presentation (NHF grade A recommendation): n fasting lipids, including total cholesterol, LDLs, HDLs and triglycerides—risk factors n fasting blood sugar—risk factor n full blood count—anaemia exacerbates angina n serum creatinine—impaired renal function is a risk factor and can be worsened by some cardiac investigations. If indicated clinically, thyroid function
THE BEST CARDIOLOGISTS IN YELAHANKA A systematic description of ECGs The following eight short steps will enable most ECGs to be described correctly: 1 Check the paper speed and calibration markers. 2 Measure or estimate the heart rate. 3 Estimate the rhythm. 4 Look for P waves. 5 Measure the PR interval. 6 Examine the QRS complex. 7 Check the ST segment. 8 Measure the T wave. ECG interpretation should always be as restrained as practicable, taking into account the clinical context where known and comparison with previous tracings where possible. The possibility of Prinzmetal’s electrocardiographic heart disease must always be borne in mind—that is, do not assume that an abnormal ECG always means heart disease.2.
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.
1
false