Coastal hypoxia—harmfully low levels of oxygen—is a mounting problem that jeopardizes coastal ecosystems and economies. The northern Indian Ocean is particularly susceptible due to human‐induced impacts, vast naturally occurring oxygen minimum zones, and strong variability associated with the seasonal monsoons and interannual Indian Ocean Dipole (IOD). We assess how natural factors influence the risk of coastal hypoxia by combining a large set of oxygen measurements with satellite observations to examine how the IOD amplifies or suppresses seasonal hypoxia tied to the Asian Monsoon. We show that on both seasonal and interannual timescales hypoxia is controlled by wind‐ and coastal Kelvin wave‐driven upwelling of oxygen‐poor waters onto the continental shelf and reinforcing biological feedbacks (increased subsurface oxygen demand). Seasonally, the risk of hypoxia is highest in the western Arabian Sea in summer/fall (71% probability of hypoxia). Major year‐to‐year impacts attributed to the IOD occur during positive phases along the eastern Bay of Bengal (EBoB), where the risk of coastal hypoxia increases from moderate to high in summer/fall (21%–46%) and winter/spring (31%–42%), and along the eastern Arabian Sea (i.e., India, Pakistan) where the risk drops from high to moderate in summer/fall (53%–34%). Strong effects are also seen in the EBoB during negative IOD phases, when the risk reduces from moderate to low year‐round (∼25% to ∼5%). This basin‐scale mapping of hypoxic risk is key to aid national and international efforts that monitor, forecast, and mitigate the impacts of hypoxia on coastal ecosystems and ecosystem services.

PDO modulates tropical Pacific oxygen content and OMZ volume on decadal time scales.• The PDO-induced variations are of the same order of magnitude as the anthropogenic deoxygenation signal.• Currently available data are too sparse to resolve and isolate the PDO-induced and anthropogenic signals.

PDO modulates tropical Pacific oxygen content and OMZ volume on decadal time scales.• The PDO-induced variations are of the same order of magnitude as the anthropogenic deoxygenation signal.• Currently available data are too sparse to resolve and isolate the PDO-induced and anthropogenic signals.