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The causes of coronary symptoms The symptoms of coronary artery disease are caused by the reduction of myocardial perfusion that results from narrowing of the lumen of one or more of the coronary arteries. This narrowing is most often the result of atherosclerosis. Other much less common causes include: 1 coronary artery spasm (p. 146) (often in an already diseased segment of artery but sometimes as a result of the use of cocaine) 2 thrombosis (usually on an already diseased, or occasionally aneurismal, segment) 3 embolism (e.g. from an infected aortic valve) 4 congenital coronary abnormality
The causes of coronary symptoms The symptoms of coronary artery disease are caused by the reduction of myocardial perfusion that results from narrowing of the lumen of one or more of the coronary arteries. This narrowing is most often the result of atherosclerosis. Other much less common causes include: 1 coronary artery spasm (p. 146) (often in an already diseased segment of artery but sometimes as a result of the use of cocaine) 2 thrombosis (usually on an already diseased, or occasionally aneurismal, segment) 3 embolism (e.g. from an infected aortic valve) 4 congenital coronary abnormality HEART SPECIALIST IN YELAHANKA
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
CARDIOLOGIST IN SAHAKARANAGAR The causes of coronary symptoms The symptoms of coronary artery disease are caused by the reduction of myocardial perfusion that results from narrowing of the lumen of one or more of the coronary arteries. This narrowing is most often the result of atherosclerosis. Other much less common causes include: 1 coronary artery spasm (p. 146) (often in an already diseased segment of artery but sometimes as a result of the use of cocaine) 2 thrombosis (usually on an already diseased, or occasionally aneurismal, segment) 3 embolism (e.g. from an infected aortic valve) 4 congenital coronary abnormality 5 vasculitis.
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
A risk factor is a demographic characteristic associated with an increased risk of ischaemic heart disease when other variables have been controlled. The presence of a risk factor in an individual increases his or her relative risk of a coronary event (angina, infarction or death). The absolute risk of a coronary event depends on the individual’s total number of risk factors and theirseverity (total risk). Important coronary risk factors are shown in Table 1.1. Risk assessment charts have been developed to estimate a patient’s cardiac risk over a number of years using easily identified risk factors. There are charts for different populations. The charts can be used to predict cardiovascular events or mortality (as in the NHF chart in Fig 1.1 on p. 4) or cardiac risk (systematic coronary risk evaluation system or SCORE charts). These charts can be very helpful in deciding when intervention to reduce risk is warranted; for example, when anti-hypertensive treatment should be commenced for a patient with mild blood pressure elevation. Risk factor reduction involves assessing the presence, severity and importance of risk factors for a
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
This ordinarily consists of monitoring of  is suspected. heart rate and rhythm,  repeated measurement of systemic arterial pressure by cuff,  obtaining chest radiographs to detect heart failure,  repeated auscultation of the lung fields for pulmonary congestion,  measurement of urine flow,  examination of the skin and mucous membranes for evidence of the adequacy of perfusion, and
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
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