Chronic Thromboembolic Pulmonary Hypertension And Other Pulmonary Hypertension

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Chronic pulmonary hypertension occurs in about 5% of patients within 2 yr following the first PE. The pulmonary vascular tree is a unique high flow, low pressure system (normal systolic/diastolic pressures 25/10 mmHg; mean 15 mmHg), but a number of pathological states, including PE, can trigger a vicious cycle of structural changes within the pulmonary vasculature, resulting in chronic pulmonary hypertension.

Chronic or recurrent PE can progressively obstruct the pulmonary vasculature, leading to clinical features of chronic pulmonary hypertension accompanied by signs of chronic cor pulmonale. Chronic thromboembolic pulmonary hypertension is present when the systolic and mean pulmonary artery pressures exceed 40 and 25 mmHg, respectively. Pulmonary hypertension of various etiologies (Table 2) can be categorized as mild, moderate, or severe based on PASPs measuring 40-45 mmHg, 46-60 mmHg, or more than 60 mmHg, respectively.

Pulmonary hypertension is most reliably quantified by spectral Doppler measurements of PASP and RAP—both routine measurements on TTE—provided pulmonary stenosis is absent (Fig. 12 and Table 3). These pressures should be interpreted within the context of the clinical presentation and other echocardio-graphic findings. On echocardiography, the hallmark of established pulmonary hypertension and cor pulmonale are signs of chronic right heart pressure overload (Figs. 13 and 14). Possible findings on TTE are summarized in Table 4. TEE provides better visualization of emboli with the pulmonary artery and atria (Fig. 9; please see companion DVD for corresponding video).

The PASP is measured using the simplified Bernoulli equation applied to peak TR velocity by continuous-wave Doppler. To this value, RAP should be added to complete the calculation (Table 3):

TR is present in most normal individuals, but the velocity rarely exceeds 2.5 m/s. Higher TR velocities may indicate pathology. The most common TR velocities

Fig. 14. Images depicting several features of chronic severe pulmonary hypertension and cor pulmonale (Table 4) are shown. Note the massively dilated right ventricle in parasternal views accompanied by tricuspid regurgitation (C) and pulmonary regurgitation (D). Spectral Doppler interrogation across the pulmonic valve confirms marked pulmonary regurgitation exceeding 2 m/s (E). Markedly dilated inferior vena cava (IVC) with complete loss of respirophasic variation was present (F).

Ecocardiografia Immagini

Fig. 14. Images depicting several features of chronic severe pulmonary hypertension and cor pulmonale (Table 4) are shown. Note the massively dilated right ventricle in parasternal views accompanied by tricuspid regurgitation (C) and pulmonary regurgitation (D). Spectral Doppler interrogation across the pulmonic valve confirms marked pulmonary regurgitation exceeding 2 m/s (E). Markedly dilated inferior vena cava (IVC) with complete loss of respirophasic variation was present (F).

Table 4

Echocardiography Findings in Pulmonary Hypertension and Chronic Cor Pulmonale

Two-dimensional echocardiography

• Right ventricular dilatation

• Right ventricular hypertrophy

• Right ventricular dysfunction/hypokinesis

• Signs of right ventricular pressure and volume overload: D-shaped septum (throughout cardiac cycle) Paradoxical septal motion

• Right atrial dilatation

• Dilated inferior vena cava

• Loss of normal inferior vena cava respirophasic movements

Doppler echocardiography

• Reversal of flow: tricuspid valve by color flow Doppler parameters, e.g., increased jet area, proximal isovelocity surface area, vena contracta width

• Reversal of flow: pulmonary valve by pressure half-time and jet length

• Reversal of flow: inferior vena cava and hepatic veins seen in acute PE range between 2.5 and 3.0 m/s, rarely exceeding 3.5 m/s because the previously normal RV cannot generate higher pressures. This contrasts with pressures generated by the hypertrophied RV seen in acute-on-chronic or in recurrent PE and in the setting of chronic pulmonary hypertension, where TR velocities typically exceed 3.5 m/s.

TR velocity is a reflection of the pressure difference between the right atrium and RV, whereas continuous-wave Doppler intensity indicates severity. Therefore a high TR velocity (alone) does not equate to severe TR. TR severity can be assessed using the same Doppler parameters used to assess mitral regurgitant severity (see Chapter 14; e.g., jet areas, vena contracta width, and proximal isovelocity surface area, in conjuction with other echocardiographic parameters in Tables 3 and 4).

The most common pitfall in measuring PASP is failure to obtain the maximum TR velocity. To minimize this, multiple windows (parasternals, apical, and subcostal) and optimal Doppler alignment are necessary. Other Doppler measurements, e.g., acceleration times measured at the pulmonary valve, the TR velocity/velocity time integral ratio, and the pulmonary artery diastolic pressure, may be used.

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Responses

  • Zainab
    Is thromboembolic pulmonary HTN the same as cor pulmonale?
    1 year ago

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