Right Ventricular Hypertrophy Changes Research Articles

Cardiovascular Medicine at High Altitude

Altitude physiology began with Paul Bert in 1878. Chronic mountain sickness (CMS) was defined by Carlos Monge in the 1940s in the Peruvian Andes as consisting of excess polycythemia. Hurtado et al performed studies in the Peruvian Andes in the 1950s to 1960s which defined acclimatization in healthy altitude natives, including polycythemia, moderate pulmonary hypertension, and low systemic blood pressure (BP). Electrocardiographic changes of right ventricular hypertrophy (RVH) were noted. Acclimatization of newcomers to altitude involves hyperventilation stimulated by hypoxia and is usually benign. Acute mountain sickness (AMS) in travelers to altitude is characterized by hypoxia-induced anorexia, dyspnea, headache, insomnia, and nausea. The extremes of AMS are high-altitude cerebral edema and high-altitude pulmonary edema. The susceptible high-altitude resident can lose their tolerance to altitude and develop CMS, also referred to as Monge disease. The CMS includes extreme polycythemia, severe RVH, excess pulmonary hypertension, low systemic BP, arterial oxygen desaturation, and hypoventilation.

Right ventricular anomalous muscle bundle. Clinical and laboratory presentation and natural history.

Eighteen patients with right ventricular anomalous muscle bundles associated with ventricular septal defect and one patient with isolated anomalous muscle bundle were studied. The clinical differentiation of these patients from those with isolated ventricular septal defects or tetralogy of Fallot was difficult. Eleven patients were asymptomatic at the time of diagnosis; eight had various degrees of dyspnea on exertion, with three of these having cyanosis. A physiologically split second sound with a pulmonic component of normal intensity and a diffuse thrill and holosystolic murmur maximal at the lower left sternal border suggest the diagnosis. Chest X-rays and electrocardiograms usually show evidence of right ventricular hypertrophy, but may suggest left ventricular hypertrophy in the presence of a large left-to-right shunt. However, the diagnosis is best made by cardiac catheterization with measurement of a pressure gradient in the body of the right ventricle and by selective angiography with the demonstration of a wedge-shaped filling defect in the right ventricle. Progressive obstruction by the muscle bundle occurred in four of seven patients who had repeated catheterization associated with the development of electrocardiographic changes of right ventricular hypertrophy. To date, 11 patients have had surgery; one died before surgery; and surgery is being planned for the remaining patients.

New criteria for the electrocardiographic diagnosis of emphysema and cor pulmonale

1. 1. Pulmonary emphysema produces verticalization of the P axis and a posterior and superior displacement of the mean QRS axis with decreased voltage. Right ventricular overload may also cause verticalization of the P axis, but, on the other hand, produces anterior and rightward displacement of the middle and terminal QRS forces that results in rSr′ patterns or classic changes of right ventricular hypertrophy in precordial leads on the right side, and right axis deviation in limb leads. 2. 2. Electrocardiographic criteria based on these changes are proposed to diagnose pulmonary emphysema with and without right ventricular hypertrophy, and to distinguish such patients from those with right ventricular hypertrophy without emphysema. 3. 3. The proposed criteria clearly separated patients with emphysema from normal subjects and from patients with congenital heart disease with right atrial enlargement, right ventricular hypertrophy, or right bundle branch block. 4. 4. In the series studied, these criteria proved to be as accurate in detecting pulmonary emphysema in the presence of right ventricular hypertrophy or conduction defects on the right side as in their absence. 5. 5. Emphysema with superimposed right ventricular hypertrophy (cor pulmonale) is characterized by rsR′ patterns in precordial leads on the right side, or predominant R waves in these leads in addition to the changes of emphysema described in this report. It is probable that rSr′ patterns or slurred S waves in precordial leads on the right side in these patients may also represent superimposed early right ventricular hypertrophy. 6. 6. Myocardial infarction may mimic or mask the changes produced by emphysema, and emphysema alone may mimic myocardial infarction; hence, the electrocardiographic diagnosis of emphysema is hazardous in the presence of electrocardiographic evidence of myocardial infarction. 7. 7. In the absence of electrocardiographic evidence of myocardial infarction, definite low voltage (0.6 mv. or less in limb leads and Leads V 6) associated with a posteriorly and superiorly oriented QRS vector, and an axis of the P wave greater than +60 degrees in limb leads, is practically pathognomonic of emphysema. 8. 8. This study has again emphasized the importance of distinguishing pulmonary emphysema alone from pulmonary emphysema with superimposed right ventricular hypertrophy. The term “cor pulmonale” should not be applied to emphysema, but rather to right ventricular hypertrophy that results from emphysema or any other pulmonary disease.

Right ventricular hypertrophy. I. Correlation of isolated right ventricular hypertrophy at autopsy with the electrocardiographic findings.

The electrocardiograms of 22 cases showing isolated right ventricular hypertrophy at autopsy were examined for changes suggestive of right ventricular hypertrophy. Only 5 of 22 cases fulfilled at least one of the criteria of Sokolow and Lyon and only three could be diagnosed as having right ventricular hypertrophy by the criteria of Myers, Klein and Stofer. Factors contributing to the development of electrocardiographic changes of right ventricular hypertrophy are discussed.