Clinical Aspects of Ventricular Repolarization
Create Alert. Share This Paper. Tables from this paper. References Publications referenced by this paper. Maron , William J. Discrete subaortic stenosis: surgical outcomes and follow-up results. Effect of left ventricular outflow tract obstruction on clinical outcome in hypertrophic cardiomyopathy.
Ventricular Relaxation: basic and clinical aspects - Ghent University Library
Martin S. Hypertrophic cardiomyopathy: a systematic review. Barry J. Septal myotomy-myectomy and transcoronary septal alcohol ablation in hypertrophic obstructive cardiomyopathy. A comparison of clinical, haemodynamic and exercise outcomes. A right atrial pressure of more than 10 mm Hg and a ratio of right atrial to pulmonary capillary pressure greater than 0. The low sensitivity of these criteria has been linked to the presence of left ventricular dysfunction and its effect on pulmonary capillary pressure.
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The hemodynamic criteria for ARVI may not be met in patients with left inferior infarction and may only be apparent after rapid administration of a volume load saline. An increase in pressure in the right chambers until it equals that of the left chambers is not specific to ARVI.
leondumoulin.nl/language/series/the-pubic-hair-counter.php The differential diagnosis includes diseases that predominantly affect diastolic function, such as cardiac tamponade, constrictive pericarditis, restrictive cardiomyopathy, or diseases that compromise systolic function, such as thromboembolic pulmonary hypertension. Experimental and human studies have shown that an increase in right atrial contraction improves right ventricular filling flow, ventricular systolic function, and cardiac output. It is important to remember that in the absence of right atrial myocardial ischemia or asynchronous atrioventricular activation, increased right atrial contractility is a compensatory mechanism for ischemic right ventricular dysfunction..
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Prompt diagnosis is important in patients with acute myocardial infarction AMI of the left inferior wall that extends to the right ventricle, especially in the presence of arterial hypotension or cardiogenic shock. Rapid identification of right ventricular infarction allows the use of diuretics or vasodilators to be avoided. The main clinical signs accompanying ARVI are a jugular venous distension; b absence of decreased jugular venous pressure on inspiration Kussmaul's sign ; c arterial hypotension; d bradycardia or atrioventricular block; e tricuspid valve insufficiency; f right ventricular gallop S 3 and S 4 ; g paradoxical pulse reduction of more than 10 mm Hg in blood pressure on inspiration.
The presence and severity of the physical signs of ARVI will depend on the degree of dysfunction and dilatation of the right ventricle; extensive infarction is characterized by the appearance of signs of severe right heart failure, such as hepatomegaly, pulsatile liver, ascites, and peripheral edema.
These signs are not usually observed in the acute phase of infarction and their appearance 2 or 3 weeks later indicates extensive necrosis of the right ventricular myocardium extending to the right atrial myocardium.. Elevation of the ST segment in V 4 R was a very specific sign of right ventricular infarction in 18 cases with postmortem confirmation; survivors with that ECG abnormality had a higher incidence of hypotension and right heart failure than patients with inferior infarction restricted to the left ventricle. Elevation of the ST segment by more than 0.
Elevation of the ST segment in V 3 R and V 4 R can be transient and only registered in the first 24 or 48 hours following onset of infarction. Medrano and de Micheli performed studies in dogs and humans to assess the usefulness of the precordial leads and upper abdominal unipolar leads known as MD right hypochondriac region , ME midepigastric , and MI left hypochondriac region in the presence of right ventricular myocardial infarction Figure 3.
When chemical necrosis phenol was produced in the posterior wall of the right ventricle in dogs, changes were recorded in the epicardial and thoracic leads associated with abolition of electromotive force originating in that region. Figure 3. Electrocardiogram with right precordial and upper abdominal unipolar leads in the right hypochondriac region MD , epigastric region ME , and left hypochondriac region MI , revealing signs of a transmural dead zone in the diaphragmatic surface of the left ventricle: QS complexes in aVF and DIII.
Taken from Arch Inst Cardiol Mex. Medrano and de Micheli 38 also performed experimental studies on infarction of the anterior free wall of the right ventricle and found a reduction in the voltage of the R wave, or QS complexes, in the right epicardial and thoracic leads from V 5 R to V 2 and V 3 , with signs of lesion ST-segment elevation , and epicardial ischemia negative T wave..
The development of disorders of intraventricular conduction such as right bundle branch block, or disorders of the left subdivisions has also been studied with ECG and vectorcardiogram recordings after producing chemical necrosis in the anterior portions of the interventricular septum, and the free wall of the right ventricle. QR complexes with a slurred R wave are recorded in cases with proximal or distal right block Q waves of 35 to 60 ms.
Posterior biventricular infarctions are more common than anterior ones.. Signs of a dead zone in the free wall of the right ventricle are observed more often in posterior biventricular infarctions than in anterior ones. In these cases, the voltage of the ST-segment elevation is higher in the right thoracic leads than in V 2 and V 3 , suggesting invasion of the anterior surface of the right ventricle.. There has been interest in identifying the ECG abnormalities associated with atrial infarction, especially in the P wave and the atrial ST-T segment, for more than 65 years.
The vector for the lesion points forward, elevating the P-R segment in the mentioned leads and in the direct right atrial leads.
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Qp or complex waveforms were recorded in W. In isolated cases with suspicion of right atrial ischemia, intraesophageal recordings have been used to detect ECG changes in the P wave and in the atrial ST segment 48 Figure Figure 4. Recordings with 5 intraesophageal leads, from E 1 the most cranial to E 5 the most caudal , obtained simultaneously to recordings from a precordial V 1 lead in a man aged 43 years.
Note the elevation of the atrial ST segment in the E 1 and E 2 leads, indicating a right atrial lesion. Regarding the presence of ventricular arrhythmias, some studies have reported an increased incidence in patients with biventricular inferior infarction. Echocardiography is useful to reveal the spread of infarction to the myocardium of the right ventricle.
Parasternal images in the short axis and apical 4-chamber views provide the most information. The first shows the right ventricle with a crescent-moon morphology Figure 5 , while in the second, the chamber of the right ventricle tends to be triangular under normal conditions. These images can be used to determine the diameters of the right ventricular cavity as well as the motion of the anterolateral and inferior walls, and of the interventricular septum. Motion of the inferior and lateral walls of the right ventricle can also be assessed in subcostal images.. Figure 5. Parasternal echocardiogram in the short axis.
The right ventricle appears dilated, with a crescent-moon morphology. In patients with extensive right ventricular infarction and hemodynamic deterioration, the images show dilatation of the chamber and defective ventricular wall motion, commonly akinesia of the posteroinferior wall. Defects in the motion of the interventricular septum can be in systole paradoxical motion or in diastole.
Defects in diastole are indicative of increased right ventricular pressure with inversion of the transseptal pressure gradient. Echocardiographic demonstration of wall dyskinesia may be more sensitive than hemodynamic abnormalities for the identification of right ventricular infarction. However, wall motion abnormalities have a low specificity, since segmental dyskinesia caused by ischemia can be present without myocardial infarction.
The use of echocardiography has confirmed that the extent of right ventricular infarction is highly variable, ranging from a small hypokinetic region to marked dilatation of the chamber with a large area of wall dyskinesia.. In theory, the hemodynamic consequences of right ventricular infarction could be recognized by calculation of the ventricular volumes and the ejection fraction.
However, this has not been possible since the complex morphology of the ventricle has limited the use of geometric formulas to calculate its volume. Nevertheless, some echocardiographic parameters have been described that are correlated with the right ventricular ejection fraction obtained by radionuclide ventriculography. These echocardiography parameters include the ratio between the end-diastolic size of the 2 ventricles, descent of the right ventricular base, and inspiratory collapse of the inferior vena cava. Apical and subcostal images can show leftward displacement of the interatrial septum, which is a sign found in very extensive right ventricular infarctions or when ischemia extends to the walls of the right atrium.
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This echocardiographic sign is an indicator of poor prognosis, since it is often associated with arterial hypotension, advanced atrioventricular block, and increased mortality. The right ventricular ejection fraction has been quantified in patients with inferior AMI, with or without extension to the right ventricle. The formula used was based on area-length of a pyramid, taking the ejection fraction equilibrium radionuclide angiography as a reference. Echocardiographic assessment of myocardial reperfusion with contrast agents injected in the peripheral veins or coronary arteries following angioplasty, or thrombolysis has mainly focused on the left ventricle.
A few reports have indicated the usefulness of this technique to assess myocardial perfusion and contractile reserve dobutamine of the right ventricle following postinfarction coronary angioplasty. Significant improvement of overall right ventricular function following dobutamine indicates recovery of a stunned myocardium.
The echocardiographic criteria for right ventricular myocardial viability are as follows: demonstration of systolic thickening of the wall in a previously akinetic segment or recovery of wall thickening in a previously hypokinetic segment. In the presence of right ventricular infarction, the use of Doppler to assess blood flow in the right chambers offers information related to hemodynamic abnormalities.
Spectral analysis of blood flow during right ventricular filling usually reveals 2 peaks: the early diastolic or rapid filling E wave and the end-diastolic following atrial contraction A wave. When the ischemia includes the right atrium, its mechanical activity is diminished or can even disappear extensive atrial necrosis ; this is translated into a reduction or absence of the A wave. It is important to note that there are other conditions in which Doppler analysis of right ventricular filling flow only shows an E wave, as is the case in patients with atrial fibrillation and in some disorders of atrioventricular conduction..
It has been reported that in the presence of very extensive right ventricular infarction, Doppler analysis can reveal that ventricular filling and ejection flows are very slow and last almost the entire cardiac cycle. This flow pattern, similar to that of a vein, indicates that the right ventricle has lost pumping function and behaves as a passive conduit.