Hemodynamics In Pulmonary Hypertension
Pulmonary hypertension occurs when a person has abnormally high blood pressure in the arteries that supply the lungs. Today, invasive catheter-based pressure measurements are required to establish a definitive pulmonary hypertension diagnosis, and guidelines recommend several other screening procedures beforehand to justify more invasive diagnostic methods. Unfortunately, many patients slip through the cracks, living with symptoms and increased risk of complications for multiple years before receiving targeted care for their pulmonary hypertension.
Sensydia has developed the Cardiac Performance System™ (CPS) to help simplify the diagnosis of pulmonary hypertension, and make valuable hemodynamic insights more accessible in routine care. CPS is the only platform designed to provide Pulmonary Artery Pressure (PAP), Pulmonary Artery Occlusion Pressure (PAOP), and Cardiac Output (CO) in a portable, non-invasive, point of care system. With our unique machine learning approach, the CPS is trained to standard measurement methods, allowing CPS to approach the gold standard levels of accuracy that would otherwise require catherization to acquire.
CPS is intended to be used as an objective test to help:
• Diagnose pulmonary hypertension
• Identify patients with abnormally increased pulmonary artery pressures (pre-hypertensive patients)
• Differentiate between pre-capillary and post-capillary pulmonary hypertension
• Detect vasoreactivity and determine the optimal course of treatment
With the disruptive CPS platform, physicians can use hemodynamic measurements as a first line screening and diagnostic tool in the hospital, in the office, and even over telemedicine to confirm pulmonary hypertension status at the first indication of symptoms.
Continue reading to learn more about the critical role of hemodynamic measurement in pulmonary hypertension.
Delayed Diagnosis in Pulmonary Hypertension
Epidemiologists have observed an increasing incidence and prevalence of pulmonary hypertension over the last two decades [1]. Present estimates suggest a pulmonary hypertension prevalence of about 1% of the global population, which increases up to 10% in individuals 65 and older [2].
Patients with pulmonary hypertension can experience shortness of breath, tiredness, lightheadedness, dizziness, chest pain, leg or ankle swelling, or abnormally high heart rate [3]. Beyond the negative quality of life implications of these symptoms, excess pulmonary pressure can cause rapid deterioration of the right heart, leading to right-sided heart failure.
People age 65+ have pulmonary hypertension
Live with symptoms for
2 years before diagnosis
Median survival without specialized treatment
Early diagnosis is absolutely critical to focus treatment and prevent complications. Without specialized treatment, the median survival for individuals with pulmonary hypertension is only 2.8 years [4]. Despite this alarming statistic, non-specific symptoms and a complex diagnostic pathway can delay targeted intervention. As a consequence, patients are often diagnosed late in the course of the disease when pathologic changes are advanced and irreversible. The REVEAL Registry found that one in five patients who were diagnosed with pulmonary hypertension lived with symptoms for over 2 years before their disease was diagnosed [5].
A Complex Diagnostic Pathway
Pulmonary hypertension patients often see multiple specialists and go through several screening procedures before their diagnosis is confirmed (Figure 1).
When a patient presents with a medical history and symptoms that are consistent with pulmonary hypertension, echocardiography is usually the first step towards establishing a diagnosis. While echo on its own is not confirmatory, a trained echo technician can approximate the probability of pulmonary hypertension by measuring tricuspid regurgitation velocity (TRV) and looking for telling signs in the ventricles, pulmonary artery, inferior vena cava, and right atrium. If echo indicates possible pulmonary hypertension, the recommended next step is to determine if an underlying thromboembolic obstruction is present. A ventilation/perfusion (V/Q) lung scan is ordered in this case, and whether or not there’s evidence of obstruction, referral to a catheterization lab for direct pressure measurements follows to confirm pulmonary hypertension diagnosis. If the V/Q scan suggests obstruction, angiographic imaging is also used during the catheterization procedure to look at blood flow in the lungs and identify the source and extent of any blockage [6].
Importantly, diagnosis of pulmonary hypertension today requires direct pressure measurements with right heart catheterization, as alternative methods have not yet met the standard of accuracy set by the catheter-based approach.
Figure 1: Screening procedures recommended in the diagnosis of pulmonary hypertension [6].
As a first line screening tool, CPS can positively augment this pathway and substitute unnecessary screening procedures by allowing primary care physicians and clinical cardiologists to non-invasively acquire accurate diagnostic hemodynamic measures without referral or invasive catheterization. Early confirmation of disease will allow physicians to confidently tailor their treatment efforts towards pulmonary hypertension and proactively coordinate specialty care.
Hemodynamic Measurements in Pulmonary Hypertension
Hemodynamic measurements play an essential role in the management of pulmonary hypertension. Pulmonary artery pressure (PAP), pulmonary artery occlusion pressure (PAOP), cardiac output (CO) readings are used to establish diagnosis, help determine the underlying cause of disease, and help physicians tailor medical therapy.
Establishing Diagnosis
The diagnosis of pulmonary hypertension pivots on pulmonary artery pressure readings. Pulmonary hypertension is defined as mean pulmonary artery pressure (mPAP) greater than 25 mmHg, but a lower threshold of 20 mmHg has recently been proposed by the European Society of Cardiology and members of the World Symposium on Pulmonary Hypertension [7,8].
Differential Diagnosis
High blood pressure in the lungs can be idiopathic with no known cause, or secondary to other conditions that affect the pressure dynamics in the heart, the lungs, or the pulmonary artery itself [7]. Because different underlying causes drastically alter the appropriate course of treatment, clinical groups have been established to differentiate between different sources of pulmonary hypertension (Table 1).
To help classify pulmonary hypertension, hemodynamic measurements can be used to determine if the source of elevated pressure is pre-capillary (in the right heart or lungs), post-capillary (in the left heart), or both (Table 2). Elevated PAOP above 15 mmHg can indicate that pulmonary hypertension is post-capillary, whereas normal PAOP indicates pre-capillary disease. When used to calculate pulmonary vascular resistance (PVR), cardiac output (CO) can provide additional intel that indicates whether or not a patient has combined pre-capillary and post-capillary disease [8].
Pulmonary Vascular Resistance [PVR] = [PAP - PAOP] / [CO]
Optimizing Medications
Table 1: Classifications of pulmonary hypertension [8].
Table 2: Hemodynamic definitions in pulmonary hypertension [8].
In cases of idiopathic pulmonary arterial hypertension, additional hemodynamic testing is done to determine which medications are optimal. Vasoreactive drugs are administered during catheterization to observe how the hypertension responds. If mean pulmonary artery pressure and pulmonary vascular resistance fall by 20%, the patient is labeled as ‘vasoreactive’ and is likely to benefit from oral calcium channel blockers [9].
INVESTIGATIONAL DEVICE DISCLAIMER: The Sensydia Cardiac Performance System (CPS) is an investigational device. It is currently undergoing clinical evaluation under Food and Drug Administration’s Investigational Device Exemption and is not approved for commercial use.
References
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[2] Hoeper, M. M., Humbert, M., Souza, R., Idrees, M., Kawut, S. M., Sliwa-Hahnle, K., …Gibbs, J. S. R. (2016). A global view of pulmonary hypertension. The Lancet Respiratory Medicine, 4(4), 306–322.
[3] Rosenkranz, S., Howard, L. S., Gomberg-Maitland, M., & Hoeper, M. M. (2020). Systemic Consequences of Pulmonary Hypertension and Right-Sided Heart Failure. Circulation, 678–693.
[4] McLaughlin, V. V., Shillington, A., & Rich, S. (2002). Survival in primary pulmonary hypertension: The impact of epoprostenol therapy. Circulation, 106(12), 1477–1482.
[5] Brown, L. M., Chen, H., Halpern, S., Taichman, D., McGoon, M. D., Farber, H. W., … Elliott, C. G. (2011). Delay in recognition of pulmonary arterial hypertension: Factors identified from the REVEAL registry. Chest, 140(1), 19–26.
[6] Hoeper, M. M., Bogaard, H. J., Condliffe, R., Frantz, R., Khanna, D., Kurzyna, M., … Badesch, D. B. (2013). Definitions and diagnosis of pulmonary hypertension. Journal of the American College of Cardiology, 62(25 SUPPL.), D42–D50.
[7] Simonneau, G., Gatzoulis, M. A., Adatia, I., Celermajer, D., Denton, C., Ghofrani, A., … Souza, R. (2013). Updated clinical classification of pulmonary hypertension. Journal of the American College of Cardiology, 62(25 SUPPL.).
[8] Simonneau, G., & Hoeper, M. M. (2019). The revised definition of pulmonary hypertension: Exploring the impact on patient management. European Heart Journal, Supplement, 21, K4–K8.
[9] Rosenkranz, S., & Preston, I. R. (2015). Right heart catheterisation: Best practice and pitfalls in pulmonary hypertension. European Respiratory Review, 24(138), 642–652.