Blood pressure (BP) is the measure of the force of blood against artery walls, expressed as systolic pressure over diastolic pressure. Maintaining balanced BP is integral to cardiovascular health, ensuring adequate blood flow to the body’s organs. The relationship between cancer and blood pressure is complex and bidirectional. Changes in BP can be caused both by the biological effects of the malignancy itself and by the systemic effects of modern cancer treatments.
The Direct Influence of Cancer on Blood Pressure
The physical presence of a tumor can sometimes directly alter blood pressure through paraneoplastic syndromes. These syndromes occur when cancer cells release hormones or hormone-like substances that affect distant organs. For instance, certain tumors, particularly small cell lung cancers, can produce adrenocorticotropic hormone (ACTH). This stimulates the adrenal glands to overproduce cortisol, leading to elevated blood pressure.
Other malignancies, such as renal cell carcinoma, may secrete vasoactive peptides like endothelin-1 or angiotensinogen. Both are powerful vasoconstrictors that narrow blood vessels, increasing systemic vascular resistance and raising blood pressure. Furthermore, cancer can trigger chronic systemic inflammation, releasing cytokines that modify vascular tone and contribute to BP dysregulation. This inflammation is a general mechanism creating an environment prone to hypertension, independent of medical intervention.
Cancer Treatment-Related High Blood Pressure
Modern cancer therapies, particularly targeted drugs, are the most common cause of newly developed or worsened high blood pressure. A major class of drugs implicated is vascular endothelial growth factor (VEGF) signaling pathway inhibitors. These agents, including tyrosine kinase inhibitors and monoclonal antibodies, are designed to block the signals tumors need to grow new blood vessels.
The VEGF pathway is also necessary for maintaining the health of normal blood vessel linings (endothelium). Inhibiting this pathway causes endothelial dysfunction, significantly reducing the production of nitric oxide (NO), a natural vasodilator. This lack of NO, combined with increased endothelin-1, narrows blood vessels, increasing resistance and elevating blood pressure. Hypertension is an expected toxicity of these drugs, occurring in 30% to 80% of patients, and its onset may suggest the drug is effectively hitting its target.
Other treatment classes also risk causing hypertension through different mechanisms. Immunotherapies and proteasome inhibitors can induce inflammatory responses or damage the kidneys, impacting fluid balance. Supportive medications like corticosteroids, often used to manage side effects, cause sodium and water retention, increasing blood volume and subsequent hypertension. Poorly controlled high BP is a serious concern, increasing the risk of heart failure, stroke, and kidney damage, sometimes necessitating temporary interruption of the anti-cancer therapy.
Factors Leading to Low Blood Pressure in Cancer Patients
A drop in blood pressure, known as hypotension, often signals an acute systemic issue or disease complication. Severe dehydration is a frequent cause, often stemming from treatment side effects like uncontrolled nausea, vomiting, or diarrhea, resulting in significant fluid loss. When the body lacks sufficient fluid volume, the force of blood flow naturally decreases, leading to lower blood pressure readings.
Uncontrolled infection is another dangerous cause, potentially escalating to sepsis or septic shock. In septic shock, the overwhelming inflammatory response causes widespread vasodilation and fluid leakage out of the vessels, leading to a dramatic drop in blood pressure. Certain chemotherapy agents, such as bleomycin, can also directly contribute to hypotension through fluid shifts or cardiac effects.
Advanced disease states also predispose patients to low BP, notably through cancer cachexia, which involves severe wasting and fluid depletion. This physical decline, combined with poor nutritional intake, reduces the volume of circulating blood. Acute blood loss from gastrointestinal bleeding or other sites, often a complication of the cancer or its treatment, immediately lowers blood pressure due to rapid volume depletion.
Monitoring and Managing Blood Pressure Changes During Cancer Care
Monitoring of blood pressure is a fundamental part of cancer care, especially when patients receive high-risk therapies like VEGF inhibitors. Patients are advised to monitor their BP at home daily during the first cycle and then at least every two to three weeks for the duration of therapy. The goal is to identify and treat new or worsening hypertension quickly to prevent serious cardiovascular events and avoid treatment delays.
The target blood pressure is generally below 130/80 mmHg, though this is adjusted based on individual risk factors. If BP rises above 140/90 mmHg, or lower in patients with existing heart or kidney conditions, the oncology team usually initiates antihypertensive medication. Common medications used include angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), or dihydropyridine calcium channel blockers.
Patients must contact their care team immediately if they experience a sudden drop in BP accompanied by dizziness or fainting, or if readings are consistently high (above 160/100 mmHg). Readings exceeding 180/110 mmHg often necessitate a temporary hold on cancer therapy until BP can be safely controlled. Effective management requires close collaboration between the oncologist and a cardio-oncology specialist to balance cancer treatment needs with cardiovascular protection.