Car­diac sud­den death of­ten re­sults from a rhythm dis­or­der

The Weekend Australian - Travel - - Health - SI­MON COWAP

FROM time to time in any med­i­cal prac­tice, you hear about pa­tients who un­ex­pect­edly ‘‘ drop dead’’. While the great like­li­hood is they had a car­diac cause of their sud­den death, the com­monly as­cribed cause of a ‘‘ mas­sive heart at­tack’’ re­veals some con­fu­sion about what this fre­quently used term ac­tu­ally means.

Out­side the con­text of sud­den death, peo­ple of­ten use the words heart at­tack to re­fer to an episode of se­vere chest pain, per­haps ra­di­at­ing to the jaw or arm, of­ten ac­com­pa­nied by sweat­ing, breath­less­ness, faint­ness and gen­er­ally feel­ing aw­ful. This ba­si­cally cor­re­lates with the med­i­cal term my­ocar­dial in­farc­tion — my­ocar­dial mean­ing heart mus­cle, and in­farc­tion mean­ing tis­sue that has died as a re­sult of lost blood sup­ply.

It is the most se­ri­ous man­i­fes­ta­tion of is­chaemic heart dis­ease, is­chaemia mean­ing un­der­per­fu­sion with blood. The un­der­per­fu­sion comes about from ath­er­o­scle­ro­sis — choles­terol-rich athero­ma­tous plaques build­ing up on the lin­ing of the coro­nary ar­ter­ies and clog­ging them up.

My­ocar­dial in­farc­tion typ­i­cally oc­curs when th­ese plaques rup­ture, ex­pos­ing the un­der­ly­ing ma­te­rial to the blood and trig­ger­ing the for­ma­tion of a clot that com­pletely blocks off the artery. The re­sult­ing pro­longed de­pri­va­tion of oxy­gen and other nu­tri­ents to the sur­round­ing heart mus­cle causes death of the af­fected fi­bres, which are even­tu­ally re­placed by scar tis­sue that (un­like mus­cle) can­not con­tract.

De­pend­ing on how much mus­cle tis­sue is dam­aged, the pump­ing abil­ity of the heart may be af­fected. If re­duced se­ri­ously enough, this will re­sult in heart fail­ure, a con­di­tion where the heart is un­able to pump enough blood to ad­e­quately meet the needs of the rest of the body.

Lesser de­grees of is­chaemia oc­cur dur­ing an at­tack of angina. Angina oc­curs when there is a re­versible mis­match be­tween the heart mus­cle’s de­mand for blood and the artery’s ca­pac­ity to sup­ply it. Typ­i­cally this hap­pens when the heart works harder dur­ing ex­er­cise, but the nar­rowed artery is un­able to carry any more blood. The af­fected mus­cle ex­pe­ri­ences a rel­a­tive lack of oxy­gen, re­sult­ing in sim­i­lar pain, but does not die and re­cov­ers with rest.

In real life, of course, things are more com­pli­cated. Not all my­ocar­dial in­farcts are painful, and it is not al­ways pos­si­ble to tell if some­one is hav­ing bad angina or an in­farct — we of­ten need blood tests and an ECG (elec­tro­car­dio­gram, a read­out of the heart’s elec­tri­cal ac­tiv­ity over a pe­riod of time).

But while in­farcts can cause heart fail­ure, and sud­den death is very much as­so­ci­ated with is­chaemic heart dis­ease, death is not usu­ally the di­rect re­sult of wide­spread is­chaemic mus­cle dam­age. Rather it re­sults from a prob­lem of car­diac rhythm.

The heart is unique among mus­cles in that it gen­er­ates its own rhyth­mic con­trac­tions. While heart rate is in­flu­enced by nerve ac­tiv­ity and hor­mones like adren­a­line, the heart can beat by it­self. It has its own pace­maker, the sino-atrial node, and a net­work of spe­cialised fi­bres for spread­ing im­pulses through­out the heart in a way that re­sults in the syn­chro­nised con­trac­tion needed for ef­fec­tive pump­ing.

A heart beat­ing in this nor­mal way is said to be in si­nus rhy­hthm, usu­ally at a rate be­tween 60 and 100 beats per minute at rest.

There are nu­mer­ous disor­ders of car­diac rhythm, the most se­ri­ous of which is called ven­tric­u­lar fib­ril­la­tion. In this state the mus­cle of the main pump­ing cham­bers of the heart twitches rapidly and lacks co-or­di­na­tion, and ef­fec­tive cir­cu­la­tion ceases abruptly. The pa­tient col­lapses, loses con­scious­ness, and with­out in­ter­ven­tion brain death en­sues shortly af­ter. Of­ten, but not in­vari­ably as­so­ci­ated with is­chaemic heart dis­ease, this is the mech­a­nism of most car­diac sud­den death.

There are many other, less lethal, rhythm dis­tur­bances where the heart beats too fast, too slowly, or with less co-or­di­na­tion. They may cause black­outs, weak­ness or pal­pi­ta­tions. Some­times you may not have symp­toms and the most sig­nif­i­cant prob­lem is not car­diac dys­func­tion, but the as­so­ci­ated risk of stroke. So along with your blood pres­sure, it’s al­ways worth get­ting your pulse checked for rate and rhythm, and hav­ing an an­nual elec­tro­car­dio­graph. Si­mon Cowap is a GP prac­tis­ing in New­town, Syd­ney

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