Lyrics · 完整歌詞
An early electrocardiogram helps direct the assessment of acute chest pain,
while symptoms,
serial findings and the wider clinical context determine the next steps.
ST elevation signals complete coronary occlusion by a fibrin-rich thrombus
and demands immediate reperfusion:
primary percutaneous coronary intervention with a door-to-balloon time below 90 minutes
where a catheter laboratory exists,
or fibrinolysis within 30 minutes where it does not.
The laboratory is activated when the ECG is read,
never after troponin returns,
because every hour of delay converts salvageable myocardium into scar.
Without ST elevation,
a raised troponin defines non-ST-elevation infarction and a normal troponin unstable angina,
and invasive timing then follows risk: within 2 hours for haemodynamic instability,
within 24 hours for a GRACE score above 140,
and within 72 hours for intermediate risk.
Beneath the ECG lies a ruptured plaque.
Exposed collagen and tissue factor summon platelets,
which adhere through von Willebrand factor and glycoprotein Ib,
activate by releasing adenosine diphosphate and thromboxane A2,
and aggregate when the glycoprotein IIb/IIIa receptor changes shape;
because that receptor cannot bind its neighbour directly,
fibrinogen must bridge each pair of platelets.
Each antiplatelet class severs one link: aspirin irreversibly inhibits cyclo-oxygenase-1,
clopidogrel and ticagrelor block the P2Y12 receptor, abciximab,
eptifibatide and tirofiban occupy glycoprotein IIb/IIIa,
and vorapaxar antagonises the thrombin receptor PAR-1.
An early electrocardiogram helps direct the assessment of acute chest pain,
while symptoms,
serial findings and the wider clinical context determine the next steps.
The right ventricle rewrites the rulebook.
Because the right coronary artery supplies both the inferior wall
and the right ventricle,
an inferior infarction may disable a thin-walled chamber
whose contractile force is roughly one sixth of the left ventricle's a
passive conduit steeply dependent on preload.
The triad of hypotension, distended neck veins and clear lung fields,
confirmed by ST elevation of 1 mm or more in V4R,
therefore inverts the treatment of left heart failure: nitrates, morphine and diuretics,
which all reduce preload, are contraindicated,
whereas 1 to 2 litres of intravenous saline restores right ventricular filling,
dobutamine follows if fluid fails,
and reperfusion of the right coronary artery remains the definitive cure.
Valve disease answers two questions:
does the murmur fall in systole or diastole,
and does blood fail to pass a valve that should open
or leak through one that should close?
Mitral stenosis produces a low-pitched mid-diastolic rumble with an opening snap,
loudest at the apex with the bell in the left lateral position,
and it depends on diastolic time for filling.
Pregnancy attacks both vulnerabilities at once,
raising plasma volume by roughly 50 per cent
and accelerating the heart rate,
so the transvalvular gradient and left atrial pressure climb
until pulmonary oedema follows;
hence mitral stenosis carries the highest maternal cardiac mortality of any valve lesion.
Management slows the heart with a beta-blocker, restricts salt,
and turns to percutaneous balloon valvuloplasty when symptoms persist,
while ACE inhibitors and angiotensin receptor blockers are contraindicated in pregnancy.
An early electrocardiogram helps direct the assessment of acute chest pain,
while symptoms,
serial findings and the wider clinical context determine the next steps.