Pulmonary arterial hypertension (PAH) is traditionally defined as an increase in mean pulmonary arterial pressure (PAPm) ≥25 mmHg at rest as assessed by right heart catheterization (RHC) (Galie et al, 2019)
- Recently it has been proposed to include pulmonary vascular resistance (PVR) ≥3 Wood Units (WU) into the definition of pre-capillary pulmonary hypertension (PH) associated with mPAP >20 mmHg, irrespective of aetiology (Galie et al, 2019)
- normal PAPm at rest is 14+3 mmHg with an upper limit of normal of approximately 20 mmHg (97.5th percentile) (Simmonaeu et al, 2019)
Transthoracic echocardiogram (TTE) remains the most important non-invasive screening tool for PH
- Right heart catheterisation remains the gold standard and is considered mandatory for diagnosis of PH (Simmonaeu et al, 2019)
Severity of pulmonary hypertension (mPAP)
- Mild = 20-40mmHg
- Moderate = 41-55mmHg
- Severe = > 55mmHg
MEASUREMENT OF PULMONARY ARTERY PRESSURE
Calculation of PAP from Peak tricuspid regurgitation velocity (ms-1)
- Doppler Echo can approximate pulmonary artery systolic pressure (PASP) using
- tricuspid valve velocity (4v2 = TV pressure gradient)
- estimated CVP (=RA pressure)
- Bernoulli equation
- PASP = RVSP (in the absence of RVOTO or pulmonic stenosis)
- RVSP = 4v2 + CVP
- Mean PAP can be approximated because PAPm = 0.61•sPAP + 2.
- A systolic PAP of 30 mm Hg typically implies a mean PAP more than 20 mm Hg, i.e. pulmonary hypertension
Echocardiographic probability of pulmonary hypertension (PH) in symptomatic patients with a suspicion of PH (from Frost et al, 2019)
|Peak tricuspid regurgitation velocity ms-1||Other “PH echo signs” present||Echo probability of PH|
|<=2.8 or not measurable||No||Low|
|<=2.8 or not measurable|
The mean and end diastolic pressures in the pulmonary artery are directly assessed by measuring peak and end-diastolic velocities of the pulmonary regurgitant (PR) jet
- Diastolic PA pressure (PAPd) = PR end diastolic pressure gradient + RA pressure
- Mean PA pressure (PAPm) = PR peak pressure gradient + RA pressure
Mean pulmonary arterial pressure (PAPm) can also be calculated from the acceleration time of the RVOT VTI.
OTHER ECHOCARGRAPHIC FINDINGS
Echocardiographic signs suggesting pulmonary hypertension (PH) used to assess the probability of PH in addition to tricuspid regurgitation velocity measurement (see above) (from Frost et al, 2019). Echocardiographic signs from at least two different categories (A/B/C) from the list should be present to alter the level of echocardiographic probability of PH.
|A: The ventricles||B: Pulmonary artery||C: Inferior vena cava and right atrium|
|Right ventricle/left ventricle basal diameter ratio >1.0||Right ventricular outflow Doppler acceleration time <105 ms and/or mid-systolic notching||Inferior cava diameter >21 mm with decreased inspiratory collapse (<50% with a sniff or <20% with quiet inspiration)|
|Flattening of the interventricular septum (left ventricular eccentricity index >1.1 in systole and/or diastole)||Early diastolic pulmonary regurgitation velocity >2.2 m·s–1||Right atrial area (end-systole) >18 cm2|
|Pulmonary artery diameter >25 mm|
The underlying cause of PH may also be identified, such as:
- LV failure
- mitral or aortic valve disease
- CCC – Pulmonary hypertension
- Frost A, Badesch D, Gibbs JSR, et al. Diagnosis of pulmonary hypertension. Eur Respir J 2019; 53: 1801904. [PMC free article] [PubMed]
Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health, a Clinical Adjunct Associate Professor at Monash University, and the Chair of the Australian and New Zealand Intensive Care Society (ANZICS) Education Committee. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.
After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.
He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE. He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of LITFL.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.
His one great achievement is being the father of two amazing children.
On Twitter, he is @precordialthump.