COPD and PHTIntensive Care Training Program

Radboud University Nijmegen Medical Centre

PAO2 ↓

Hypoxic Pulmonary Vasoconstriction

Chronic Obstructive Pulmonary Disease

Pulmonary vascular resistance ↑ / Pulmonary arterial pressure ↑

Cor Pulmonale and RV failure

PHT in COPD

• mPAP > 20 mm Hg (in rest)

• Incidence unknown

• Risk factors: FEV1 < 50% of predicted and PaO2 < 55 mm Hg

Pathology

• Changes in muscular pul- monary arteries and arterioles

• Intima thickening with longitudinal muscle and elastin/collagen deposits

• Increase in smooth muscle cells in media

RV hypertrophy correlates with degree of hypoxemia

PAP = CO

PVR

PCWP

Factors affecting PVR

• Alveolar hypoxia - hypoxic pulmonary vasoconstriction

• Increased PaCO2 and acidosis relatively little effect

• Intrinsic positive end-expiratory pressure

Variability in HPV in COPD patients

23 COPD patients with hypoxic challenge (FiO2 0.13)

Pulmonary hemodynamics in COPD

• mPAP usually between 25 - 30 mm Hg - ≥ 40 mm Hg unusual (FEV1 < 50% and profound hypoxemia)

• mPAP transiently increases during exercise and sleep due to alveolar desaturations

• During exacerbations mPAP may increase with another 20 mm Hg

mPAP during exacerbations

PaO2 mPAP

Consequences

• Untreated mPAP increases approximately 3 mm Hg / year

• Longterm survival lower

Longterm survival

RV function in COPD

• Right ventricle has time to adapt

• mPAP ↑ induces hypertrophy and dilatation resulting in dysfunction

• RV stroke work index increases but RV operates on extension of normal RV function

• CO is usually normal (even with edema) and RVEF is decreased

RV function in COPDStrokevolumeml/m2

RV contractilityContractility appears to be well preservedMeasure SV, EF and RVP

24 patients with COPD

RV failure relatively rare

RV failure in COPD

Characterised by edema formation

Basic principles of pressure measurements

P1

P2

V2V1

Modified Bernoulli’s equationGradient (P2 - P1) = 4V22

Right-sided pressures

• Size, wall thickness, function, septal shift

• Systolic septal flattening → RVsys ↑

• Diastolic septal flattening → RVdias ↑ unless volume overloaded (suggests RV failure)

Qualitative assessment

Determination of RVsys

You need an estimation of RAP

RVsys = PAsys in absence of pulmonary stenosis

CW doppler

TR

RVsys = 4VTR2 + RAP

In > 50% > 10 mm Hg difference with SG

Estimation of PAsys

PAsys = RAP + 4×Vti4

Estimation of PAdias

Can only be estimated if pulmonaryregurgitation is present

PR

PAdias = 4VPR2 + RVDP

Estimation of RAP

If present, use CVP line

IVC size at RA-IVC J/C Respiratory change RAP (mm Hg)

Small (< 1.5 cm) Collapse 0 - 5 mm Hg

Normal (1.5 - 2.3 cm) Decrease > 50% 5 - 10 mm Hg

Normal (1.5 - 2.3 cm) Decrease < 50% 10 - 15 mm Hg

Dilated (> 2.3 cm) Decrease < 50% 15 - 20 mm Hg

Dilated (> 2.3 cm) No change > 20 mm Hg

In spontaneously breathing patients

IVC at RA junction

Right ventricular function

• TAPSE

• Right Ventricular Performance Index

Right ventricular function

Tricuspid Annular Plane Systolic Excursion

Right ventricular function

Right Ventricular Performance Index = Tei

Treatment

• Oxygen

• Vasodilators

• Reduction in hematocrit

• Diuretics