Diagnosis and Assessment of Pulmonary Arterial Hypertension

According to current guidelines, pulmonary arterial hypertension (PAH) is diagnosed when mean pulmonary arterial pressure (Ppa) exceeds 25 mmHg at rest or 30 mmHg during exercise. Issues that remain unclear are the classification of Ppa values 30 mmHg during exercise is always pathological. We performed a comprehensive literature review and analysed all accessible data obtained by right heart catheter studies from healthy individuals to determine normal Ppa at rest and during exercise. Data on 1,187 individuals from 47 studies in 13 countries were included. Data were stratified for sex, age, geographical origin, body position and exercise level. Ppa at rest was 14.0+/-3.3 mmHg and this value was independent of sex and ethnicity. Resting Ppa was slightly influenced by posture (supine 14.0+/-3.3 mmHg, upright 13.6+/-3.1 mmHg) and age ( or = 50 yrs: 14.7+/-4.0 mmHg). Ppa during exercise was dependent on exercise level and age. During mild exercise, Ppa was 19.4+/-4.8 mmHg in subjects aged or = 50 yrs (p<0.001). In conclusion, while Ppa at rest is virtually independent of age and rarely exceeds 20 mmHg, exercise Ppa is age-related and frequently exceeds 30 mmHg, especially in elderly individuals, which makes it difficult to define normal Ppa values during exercise.

https://erj.ersjournals.com/content/erj/34/4/888.full.pdf

Pulmonary arterial pressure during rest and exercise in healthy subjects: a systematic review

Background This study investigated the effect of the phosphodiesterase 5 inhibitor sildenafil on the pulmonary vascular response to hypoxia in humans and mice. Methods and Results In a randomized, ...

http://cronos.unq.edu.ar/fisgen/respiratorio_viagra.pdf

Sildenafil Inhibits Hypoxia-Induced Pulmonary Hypertension

Pulmonary hypertension has been found to be reversible in certain patients with, cor pulmonale due to chronic bronchitis, bronchiolitis, and/or emphysema. In these individuals, as disturbances in gas exchange are corrected, pulmonary artery pressures fall (1). The high degree of correlation between the level of pulmonary artery pressures and the degree of hypoxemia (2, 3) as well as the pressor response to acutely induced hypoxia (4, 5) has implicated a reduced oxygen tension within the lungs as a major factor in the appearance of pulmonary hypertension (6). Since these patients almost invariably demonstrate hypercapnia, carbon dioxide tension has also been invoked as a cause of pulmonary hypertension (3). Anatomic reduction of the pulmonary vascular bed cannot be assigned a dominant role in the genesis of this hypertension because of its reversibility. Nonetheless, we may assume that the effects of reactivity of the vascular compartment to various stimuli will be more readily discernible in the presence of a restricted bed. Liljestrand has recently come to the conclusion that an increased hydrogen ion concentration in the blood is the chemical stimulus for pulmonary

/pdf/the-influence-of-hydrogen-ion-concentration-and-hypoxia-on-1rlmc2fnd8.pdf

The Influence Of Hydrogen Ion Concentration And Hypoxia On The Pulmonary Circulation

The previous definition of exercise pulmonary hypertension (PH) with a mean pulmonary artery pressure (mPAP) >30 mmHg was abandoned because healthy individuals can exceed this threshold at high cardiac output (CO). We hypothesised that incorporating assessment of the pressure-flow relationship using the mPAP/CO ratio, i.e. total pulmonary resistance (TPR), might enhance the accuracy of diagnosing an abnormal exercise haemodynamic response.Exercise haemodynamics were evaluated in 169 consecutive subjects with normal resting mPAP ≤20 mmHg. Subjects were classified into controls without heart or lung disease (n=68) versus patients with pulmonary vascular disease (PVD) (n=49) and left heart disease (LHD) (n=52).TPR and mPAP at maximal exercise produced diagnostic accuracy with area under the receiver operating curve of 0.99 and 0.95, respectively, for discriminating controls versus patients with PVD and LHD. The old criterion of mPAP >30 mmHg had sensitivity of 0.98 but specificity of 0.77. Combining maximal mPAP >30 mmHg and TPR >3 mmHg·min·L(-1) retained sensitivity at 0.93 but improved specificity to 1.0. The accuracy of the combined criteria was high across different age groups, sex, body mass index and diagnosis (PVD or LHD).Combining mPAP >30 mmHg and TPR >3 mmHg·min·L(-1) is superior to mPAP >30 mmHg alone for defining a pathological haemodynamic response of the pulmonary circulation during exercise.

https://erj.ersjournals.com/content/erj/46/3/728.full.pdf

Criteria for diagnosis of exercise pulmonary hypertension

The effects of acute hypoxia, of graded exercise, or both, on the pulmonary circulation were studied in 17 normal subjects. In 3 of these subjects, and in 3 patients with restricted vascular beds, the effects of these stimuli were compared during successive test periods. In 7 normal subjects, moderate exercise, associated with an increase in cardiac output of approximately 25 per cent, resulted in an average rise in pulmonary arterial mean pressure of 3 mm.Hg. More strenuous exercise in the same subjects, associated with a further increase in cardiac output of approximately 25 per cent, did not elicit further increment in pulmonary arterial mean pressure. In contrast, 10 subjects with normal pulmonary circulations, who responded to acute hypoxia with an average reduction of arterial oxygen saturation of 17 per cent, manifested an average increase in cardiac output of 5 per cent and an average rise in mean pulmonary arterial pressure of 4 mm.Hg. The critical level of arterial blood oxygen saturation for a ...

Effects of Acute Hypoxia and Exercise on the Pulmonary Circulation

The effects of inhaling 5 per cent carbon dioxide in air on the pulmonary arterial blood pressure and flow were studied in 5 subjects with normal pulmonary circulations and in 10 patients with chronic pulmonary emphysema. In the 5 control subjects, with an average increase in arterial P CO CO2 of 6 mm. Hg (37 to 43) and a 3-fold increase in minute ventilation, both pulmonary arterial blood pressure and flow remained unchanged. In the 10 patients with chronic pulmonary emphysema with a similar increase in arterial P CO CO2 (45 to 52) and a 2-fold increase in minute ventilation, there was a 14 per cent increase in cardiac output and a rise in pulmonary arterial mean pressure of 4 mm. Hg. In these patients an increment in pulmonary arterial pressure was invariably associated with an appreciable increment in blood flow. The present study affords no support for the view that the breathing of air enriched with carbon dioxide elicits pulmonary vasoconstriction in either normal subjects or in patients with chronic pulmonary disease.

Effects of Breathing Carbon Dioxide upon the Pulmonary Circulation

Pressure pulses were obtained under direct vision, in the left atrium of subjects without clinical evidence of cardiac disease and in patients with mitral valvular disease, after exposure of their hearts during the course of surgical intervention. It was found that the c wave is produced by valvular closure and the subsequent fall of pressure during early ventricular systole (x wave) is related to atrial relaxation. Evidence is presented that mitral incompetence cannot be determined from direct atrial recordings, unless the Degrees of insufficiency is of great magnitude.

Harry W. Fritts

Papers

Effects of Acute Hypoxia and Exercise on the Pulmonary Circulation

Effects of Breathing Carbon Dioxide upon the Pulmonary Circulation

An Analysis of Normal and Abnormal Left Atrial Pressure Pulse in Man