When the lung arteries become a high-pressure system, the heart has to adapt—often in ways that eventually become harmful. Pulmonary hypertension (PH) raises resistance to blood flow through the lungs, so the right ventricle must generate more force to push blood forward. This ongoing workload can reshape the heart, reduce pumping efficiency, and in advanced cases contribute to right-sided heart failure.

This article is for informational purposes only and should not be considered medical advice. Please consult a qualified healthcare professional for personalized guidance and treatment.

Understanding Pulmonary Hypertension

Understanding pulmonary hypertension starts with the basic loop of circulation: the right side of the heart sends oxygen-poor blood to the lungs, and the left side sends oxygen-rich blood to the body. In PH, pressure in the pulmonary arteries is elevated, meaning the right ventricle faces increased “afterload” (the force it must pump against). Initially, the right ventricle may thicken (hypertrophy) to cope, but thickening can reduce flexibility and raise oxygen demand in heart muscle.

As PH progresses, the right ventricle may enlarge (dilate) because it cannot fully overcome the resistance in the pulmonary vessels. This can lead to less effective forward blood flow and higher pressures backing up into the veins. The heart can also be affected indirectly: an enlarged right ventricle may push the wall between the ventricles (the septum) toward the left ventricle, limiting left-sided filling and lowering overall cardiac output—one reason some people feel profound fatigue or lightheadedness.

Causes and Risk Factors

Causes and risk factors for pulmonary hypertension are diverse, and identifying the driver matters because the heart consequences and treatments can differ. Clinicians often group PH by underlying mechanism. Common categories include PH related to left-sided heart disease (such as heart failure with preserved or reduced ejection fraction), PH linked to lung disease or low oxygen levels (for example COPD or interstitial lung disease), chronic blood clots in the lungs (chronic thromboembolic disease), and pulmonary arterial hypertension (PAH), a group where the small pulmonary arteries narrow or remodel.

Risk factors vary by category. Left-heart-related PH is more likely with long-standing high blood pressure, coronary artery disease, valve disease, or cardiomyopathy. Lung-related PH is more likely with chronic lung disease, untreated sleep apnea, or long-term low oxygen. Chronic clot-related PH can follow pulmonary embolism in a subset of patients. PAH may be associated with connective tissue disease, certain congenital heart diseases, portal hypertension, or family history in some cases. Because each pathway creates strain on the right side of the heart through different mechanisms, a careful evaluation helps avoid “one-size-fits-all” assumptions.

Symptoms and Diagnosis

Symptoms and diagnosis often revolve around how the heart and lungs respond to limited blood flow and impaired oxygen delivery during activity. Early symptoms can be subtle: shortness of breath with exertion, reduced exercise tolerance, unusual fatigue, chest pressure, or palpitations. As right-heart strain worsens, fluid may accumulate, causing ankle swelling, abdominal bloating, weight gain from fluid retention, or a feeling of fullness. Some people experience dizziness or fainting, especially with exertion, when the heart cannot increase output to meet demand.

Diagnosis typically starts with a medical history, physical exam, and tests aimed at both confirming PH and clarifying the cause. An echocardiogram estimates pressures and evaluates right-ventricle size and function, as well as valve performance (for example, tricuspid regurgitation that can appear when the right side enlarges). Blood tests, an electrocardiogram, chest imaging, and lung function testing may be used to look for contributing conditions. A ventilation-perfusion (V/Q) scan is commonly used to evaluate chronic clot-related disease. To confirm pulmonary hypertension and measure pressures directly, right-heart catheterization is the standard test; it can also help distinguish PH due to left-heart filling pressures from other forms.

Treatment Options

Treatment options depend on the underlying group of PH and how much the heart has been affected, with goals that often include reducing strain on the right ventricle, improving symptoms, and slowing progression. In PH related to left-sided heart disease, management usually focuses on optimizing heart failure care, controlling blood pressure, addressing valve disease when appropriate, and managing fluid status. In PH related to lung disease, treating the lung condition and correcting low oxygen—sometimes with prescribed oxygen—can reduce stress on the heart.

For pulmonary arterial hypertension, targeted therapies may be considered in appropriate patients under specialist care. These can include medications that influence pulmonary vessel tone and remodeling, such as endothelin receptor antagonists, phosphodiesterase-5 inhibitors, soluble guanylate cyclase stimulators, and prostacyclin pathway therapies. A small subset of patients may respond to calcium channel blockers, but only if specific testing during right-heart catheterization shows vasoreactivity; using these drugs without that confirmation can be unsafe. Supportive strategies may include carefully managed diuretics for fluid overload, selected use of anticoagulation depending on PH type and individual risk, vaccination against respiratory infections, and supervised activity plans.

When PH is caused by chronic organized clots (chronic thromboembolic pulmonary hypertension), surgical pulmonary endarterectomy can be curative in appropriately selected patients, and balloon pulmonary angioplasty may be an option for some who are not surgical candidates. In advanced cases where right-heart function declines despite therapy, referral to specialized centers for consideration of transplant evaluation may be discussed. Throughout treatment, monitoring right-ventricular size and function is central, because the right side of the heart is often the key determinant of symptoms and long-term outcomes in PH.

Pulmonary hypertension affects the heart primarily by forcing the right ventricle to pump against unusually high pressure, which can lead to thickening, enlargement, valve leakage, reduced output, and eventually right-sided heart failure if the condition progresses. Because PH has multiple causes and can look similar across conditions, accurate diagnosis and cause-specific management are essential to protecting both heart function and overall quality of life.