ERA16FA001 · Piper PA32R 301

Nearing the conclusion of a cross-country, instrument flight rules flight in instrument meteorological conditions, the private pilot was entering a procedure turn in advance of conducting an instrument approach to the destination airport. The pilot reported to air traffic control that he was outbound on the procedure turn but did not subsequently report when the airplane was inbound. Shortly thereafter, a military flight on the frequency reported hearing a "mayday" call and that the airplane was "going down." No further communications were received from the accident airplane. Radar and GPS data showed the airplane in a right, rapidly descending spiral. Witness statements and the distribution of the wreckage indicated that the airplane experienced an in-flight breakup. A postaccident examination of the airframe and engine revealed no evidence of mechanical malfunctions or failures that would have precluded normal operation. Fractures to the right wing and stabilator were consistent with overstress and likely occurred during an attempted recovery from the descending spiral.

The pilot's autopsy revealed severe atherosclerosis in the vasculature of the brain and heart. There was near-total occlusion of the right frontal and middle cerebral arteries. In the heart, the left anterior descending coronary had 80% occlusion, while both the right and circumflex coronary arteries showed 40% atheromatous occlusion. In addition, the myocardium displayed indications that the pilot had experienced a previous heart attack. The pilot's wife was unaware of a previous heart attack or heart condition, and the pilot had not reported any heart issues to the Federal Aviation Administration.

The pilot had very low levels of pseudoephedrine in his system at the time of the accident. Although his use of this powerful vasoconstrictor may have further increased his risk of an acute cardio- or cerebro-vascular event, given the low levels, it is unlikely that any direct psychoactive effect of the drug contributed to the accident. Finally, the pilot had 0.06 ug/ml of chlorpheniramine, a sedating antihistamine, in his postmortem blood. Although the pilot lost control of the airplane, there was no evidence of impaired behavior or decision-making before the loss of control. Therefore, it is unlikely that the sedating effects of the chlorpheniramine contributed to this accident.

Given the circumstances of the accident and pilot's cardiac conditions, it is possible that he became acutely incapacitated by a sudden cardio- or cerebro-vascular event and that could have resulted in the loss of airplane control. Because the pilot suffered fatal blunt force injuries within a few minutes after symptoms began, no findings indicating the acute event would be expected to be visible on autopsy, and none were found; thus, it could not be determined whether the loss of control was the result of incapacitation or if there was another reason that the airplane departed controlled flight and the pilot was unable to regain control.

Verbatim NTSB analysis and probable cause from the NTSB dataset