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NARRATOR: Two minutes into the game,
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John's heartbeat has almost doubled to one hundred 20 beats per minute.
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Even though he's the slowest player on the field,
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his heart is beating faster than anyone else's.
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John's oxygen intake also adapts to his needs.
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He breathes faster and more deeply to supply his hungry muscles.
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He's taking in nearly twenty times more air than normal.
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His heart keeps up its frenetic beat to pump this extra fuel to his legs.
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Simply to keep him in the game,
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John's heart and lungs are working at their limit.
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But by doing so, they're placing him in mortal danger.
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Blood is being forced faster and faster through his diseased coronary arteries.
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Flowing at five times the normal speed, blood cells etty and swirl around his plaques.
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Bombarded by red blood cells, one fragile plaque is under unbearable strain.
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Its thin membrane is ripped open.
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Within moments, blood cells start to clot around the rupture.
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Anywhere else in John's body this clotting response might save his life,
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but here in his narrow artery, the effect is quite the opposite.
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The clot in John's artery traps more and more passing blood cells.
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It grows bigger, and the flow of blood to John's heart slows down.
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Downstream, the heart muscle cells are in peril.
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Their oxygen supply is dwindling, just when they need it most.
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His starving cells send pain signals to his brain.
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But John has never experienced pain from his heart before.
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To him it feels just like indigestion.
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He has no idea that this is the start of a heart attack.
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The growing clot is now blocking two thirds of his artery.
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John's indigestion is getting worse.
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He feels a vice-like pain in his left arm.
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His brain is confused, overloaded with the escalating pain signals coming from his heart.
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For the first time in his life, the regular beat of John's heart
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is under threat.
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A patch of 4 million muscle cells is running low on oxygen.
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>>John! What's up? What's the matter?
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NARRATOR: Five minutes after his heart attack began, John's body is struggling to deal with the crisis.
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His brain has triggered a surge of the hormone adrenaline into his blood stream.
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This is one of the most primitive and powerful reactions in the human body.
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Adrenaline arrives in his heart, and soaks into its inner walls.
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The pacemaker begins to accelerate.
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John's heart is racing at 140 beats per minute,
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even faster than when he was running around.
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But now all its efforts are focused on its own starving muscle.
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>>Call an ambulance.
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NARRATOR: But adrenaline can do nothing about the growing clot, which fills 90% of his artery.
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The supply of oxygen to his heart cells is down to a trickle.
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They are forced to shutdown the function which absorbs most of their energy.
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They stop beating.
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Leaving the rest of his heart to take up the slack.
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John's weakened heart cannot sustain its beat much longer.
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[ambulance sirens]
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>>We were just playing a game of football.
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>>How's the pain now John?
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NARRATOR: It's now fifteen minutes since his heart attack began.
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And the flow of blood through John's artery is almost totally blocked.
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The heart muscle cells no longer have the energy to hold themselves in one piece.
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Their thin membranes are starting to leak.
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>>You're going to be okay John. Just hang on in there.
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NARRATOR: John's injured heart is wearing itself out.
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Its beat is getting weaker.
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The effects are beginning to tell on the rest of his body.
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John is struggling to breathe because his lungs are filling with fluid.
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As his heart weakens, blood backs up in the vessels coming from his lungs.
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The extra pressure forces liquid out of his blood,
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into the airsacs of his lungs.
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If the process doesn't stop, he could drown in his own body fluid.
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>>You must keep this on.
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Nice steady breaths now.
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[radio] >>bringing in a 45 year old male, possible MI, ETA three minutes, over.
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>>Just hold on John, we're nearly there.
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They'll sort you out.
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NARRATOR: The lack of oxygen in John's body is beginning to affects his brain.
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He's dizzy and disoriented.
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Time is running out for John.
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His starved heart muscle cells are beginning to burst and die.
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If he's not treated within the next twenty minutes,
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his heart will be so badly damaged it will never beat normally again.
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>>What's the story?
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>>John Palmer, 45 year old.
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Collapsed with chest pains playing football,
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no past history of being hypertensive. BP 90 over 50, technocardio 120.
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>>When did you pain start John?
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>>I don't know.
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>>They said about half an hour ago.
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>>Don't worry John, we'll tune up and sort it out.
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>>Are you his friend?
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>>Yeah.
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>>Do you know if he's got a heart problem, can you give us details to reception?
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>>One, two, three!
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NARRATOR: John is losing 500 heart cells each second.
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And unlike most cells in his body, they can never be replaced.
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By measuring the pattern of electricity in John's heart, the ECG locates the dying patch of muscle.
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Now his only hope is that his blocked artery can be cleared by a clot busting drug.
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Tissue plasmitogen activator or TPA.
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The TPA must reach the clot before so many heart cells die that his heart stops, and he dies too.
