By Joseph W. Bergeron
How did Jesus die? In the ancient world, execution by crucifixion involved a slow, agonizing death without obvious injury to vital organs. Jesus’s cause of death was crucifixion. However, the physiological process resulting in cessation of life, medically termed the mechanism of death, is unclear. Consequently, there has not been a clear consensus among physicians as to what physiological mechanism ultimately caused him to die. Some proposed mechanisms of Jesus’s death have included: cardiac rupture, suffocation, and shock. Some say Jesus didn’t die at all, an idea referred to as the “swoon theory.” Which of these propositions, if any, provides the most plausible explanation for the mechanism of Jesus’s death?
The Swoon Theory
Crucifixion was Rome’s most brutal form of execution, the summum supplicium (Latin for “the supreme penalty”). Romans considered crucifixion obscene and reserved it for capital criminals, political insurgents, and runaway slaves. Crucifixion of Roman citizens was very rare. Archaeological finds of crucifixion victims are rare since bodies were left on the cross to be eaten by scavenging animals. One could request the body for burial but authorities required verification of death before the remains were released. Allowing a capital criminal to survive crucifixion would mean death for the soldiers in charge. Thus, it is not possible that Jesus escaped alive.
Cardiac Rupture from Emotional Agony
From a medical perspective, extreme emotional stress simply does not suggest cardiac rupture. Physicians may see cardiac rupture after a heart attack but typically two to three days later, not immediately. In rare cases, a heart attack can cause a hematoma in the cardiac muscle and rupture of the heart more rapidly. However, a massive heart attack cannot be solely attributed to emotional stress. Moreover, a fatal heart attack in a healthy young man like Jesus is implausible. Thus, the proposition that Jesus’s heart ruptured from emotional agony has largely fallen out of favor.
Fatal Stab Wound
Did Jesus die when the spear ruptured his heart? Some have concluded that blood flowing from Jesus’s side (John 19:34) meant that he was still alive at that moment, the premise being that dead bodies don’t bleed. However, this does not follow. A large clot in the heart shortly after death could be unstable and reliquefy. It is noteworthy that a team of soldiers pronounced Jesus dead before plunging a spear into his side (John 19:33). Soldiers on a Roman crucifixion team had credible expertise in pronouncing death. Their own lives depended on making sure the job was finished. With reasonable certainty, Jesus was dead before the spear entered his chest.
A Czech surgeon, R. W. Hynek, and a French surgeon, A. Le Bec, knew of torture where victims suspended with their arms directly overhead and feet unsupported appeared to suffocate. This observation led them to propose in the early twentieth century that Jesus similarly suffocated. The French surgeon Pierre Barbet also believed Jesus suffocated and popularized the theory in his book, A Doctor at Calvary (1953).1 Barbet believed blood flow bifurcation on the arms in the image of the Shroud of Turin supported his supposition that Jesus had to pull himself up in order to breathe. He also believed that crurifragium, the practice of breaking legs (John 19:31), supported suffocation as the mechanism of death, believing victims had to push up with their legs to breathe. However, Dr. Barbet’s assumptions about blood flow patterns on the Shroud of Turin and crurifragium seem to be a priori conclusions.
There is little empirical evidence that Jesus suffocated. Suspension torture as described by Hynek, Le Bec, and Barbet is unlike crucifixion in many ways. Suspension torture could cause rapid death, by some reports within three hours. Crucifixion could last for days. Crucifixion reenactment studies have failed to demonstrate difficulty breathing, or impaired blood gas exchange. Study participants were also unable to pull up with their arms or push up with their legs.2 Also, we know from Scripture that Jesus had conversations with Mary, John, and the felons crucified with him while on the cross (Luke 23:39–43; John 19:25–27). The ability to converse while being crucified makes suffocation implausible.
Shock and Trauma-Induced Coagulopathy
Traumatic hemorrhagic shock seems to be the best explanation for Jesus’s mechanism of death. Shock is the generalized effect of decreased blood perfusion and resultant tissue damage from oxygen deprivation. In trauma, shock is caused by injury and blood loss. Symptoms include weakness, confusion, sweating, feeling clammy, rapid heart rate, and palpitations. Physiological effects include systemic inflammation, tissue ischemia, and an acidic shift in blood pH (acidemia). Unchecked, the effects of shock can be progressive and unrecoverable even with the best of treatment.
Jesus’s beatings were extraordinary. He was first beaten at the home of Caiaphas the high priest. Roman soldiers applied a second beating, which would have been particularly harsh due to Roman antisemitism and finding Jesus guilty as a political insurgent; namely, King of the Jews. Soldiers used a whip (flagellum) having leather strips with dumbbell-shaped pieces of lead tied in the ends to act as cutting implements. Scourging caused blunt trauma and lacerations from head to toe. Such beatings likely rendered Jesus unable to carry the horizontal section (patibulum or crossbar) of the cross, estimated to weigh about 60 pounds, to the execution site. Jesus seems to have been progressing into shock before he reached the crucifixion site.
Trauma-induced coagulopathy is a potential complication of shock where the blood loses its ability to clot. This can have a progressive, snowball effect. Precipitating factors include tissue injury with blood loss, decreased core body temperature (hypothermia), and decreased blood pH (acidemia). The severity of his beatings and cool ambient temperatures (John 18:18) set the stage for coagulopathy to develop.
Pathophysiological processes were occurring in Jesus’s body that surpassed what was happening to the others crucified that day. The others were still alive after Jesus was pronounced dead by Roman soldiers. Pilate himself was surprised at how quickly Jesus died (Mark 15:44)—six hours, unusually rapid for a method of execution that could last for days. Coagulopathy may explain why Jesus succumbed to shock so rapidly. Coagulopathy may also explain why blood poured from his chest wound after he had already died.
The Greater Meaning
Jesus spoke of his death at the Last Supper, a Passover Seder. There he lifted the ceremonial Cup of Blessing (also called the Cup of Redemption) and stated “This cup is the new covenant in my blood” (Luke 22:20). Jesus was pointing to Jeremiah’s prophecy of a new covenant when God would change the hearts of his people and forgive their sins (Jeremiah 31:31–34). This pivotal event in human history—a new covenant between God and mankind—was inaugurated at Jesus’s crucifixion. God’s relationship with humanity was redefined. Forgiveness and spiritual transformation were available to all who would believe.
Why does the mechanism of Jesus’s death matter? Jesus appeared to make a medical statement at the Last Supper. Holding the cup, he said “This is my blood of the covenant, which is poured out for many for the forgiveness of sins” (Matthew 26:28). Jesus seems to have been intimating that the mechanism of his death would be exsanguination (blood loss), namely by traumatic hemorrhagic shock. From a medical standpoint, the Gospel descriptions of Jesus’s torture and death seem credible. This analysis offers intrinsic evidence of the authenticity of the Gospel accounts of Jesus’s death.
- Joseph W. Bergeron, The Crucifixion of Jesus: A Medical Doctor Examines the Death and Resurrection of Christ (Rapid City, SD: Crosslink Publishers, 2019).
- Joseph W. Bergeron, “The Crucifixion of Jesus: Review of Hypothesized Mechanisms of Death and Implications of Shock and Trauma-Induced Coagulopathy,” Journal of Forensic and Legal Medicine 19 (2012): 113–16, doi:10.1016/j.jflm.2011.06.001.