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#心肌梗塞的心電圖診斷

急性心肌梗塞在心電圖上最早出現的是鄰近兩個導程的超急性對稱型T波幅度升高(hyperacute T change)，緊接著是ST波段上升。

J點 (J Point): QRS波的終點與ST波段起始點的交界點，即為J點，是用來決定ST波段改變的大小的基準點。

依據2018 MI 定義，心肌缺氧的心電圖都需要出現在同組群(contiguous)兩個導程上，才能符合診斷。例如對大於40歲男性而言，V2之ST上升 >0.2 mV，V1>0.1 mV，則符合心肌梗塞的診斷。但如果是男性其ST上升只出現在V2,V3，且 >0.1 mV，及<0.2 mV，結果是正常的。如果是女性， V2, V3 的ST上升<0.15 mV，亦是正常。

#病理性Q波(Pathological Q wave)

無LVH 及LBBB之前提之下，先前的心肌梗塞的Q波(亦即病理性Q波)，其特點如下：

1. V2–V3的Q波 ≥ 0.02 秒，或V2及V3出現QS波
2. 在I, II, aVL, aVF 之Q波 ≥ 0.03秒，深度 ≥ 1mm
3. Q波出現在V4-V6之同組群任何兩個導程(I, aVL；V1–V6；II, III, aVF)
3. V1-V2的R波 ≥ 0.04秒及R/S >1，及同向的T波變化(無傳導阻滯情況下)

Q波的意義：

1.Q波可以是心肌纖維化而產生，而沒有冠狀動脈疾病。
2.心肌受損後，數分鐘至小時後出現的Q波意味著心肌壞死。
3.急性心肌缺氧早期，或急性心肌梗塞立即實施血管再通暢治療，都可能出現短暫的Q波。

#LBBB患者的心肌梗塞心電圖

在所有因急性冠心症就診的病人中， 心電圖呈現LBB者約佔2%。這些人通常較多為年老、女性、有心臟病史、高血壓與心衰竭。長期追蹤來看，心電圖呈現LBBB且疑似AMI的患者，統計起來有較高的major adverse cardiac events (MACE) 比率。

LBBB患者的心肌梗塞心電圖
Sgarbossa Criteria (1996)

(1)任意導程出現同向 (concordant) 的ST elevation ≥1mm (最重要)，
(2) V1, V2或V3出現ST depression ≥1mm，
(3)任意導程出現反向 (discordant) 的 ST elevation ≥ 15mm，
Sgarbossa Criteria第3條件比較爭議，敏感度與專一度不足信賴。Dr Smith SW在2012提出改版。原來的第三要件：任意導程出現反向 (discordant) 的 ST elevation ≥ 5 mm，改為ST上升/S波深度≥ 25%

Smith-Modified Sgarbossa Criteria (2012)
(1)任意導程出現同向 (concordant) 的ST elevation ≥1mm，
(2) V1, V2或V3出現ST depression ≥1mm，
(3)任意導程出現反向 (discordant) 的 ST上升/S波深度≥ 25%

2018 ESC/ACC/AHA提出的更簡化：
任意導程出現同向 (concordant) 的ST elevation ≥1mm，即可診斷LBBB患者的心肌梗塞

#AMI
#ECG
#LBBB
#Pathological_Q_wave

繼續閱讀詳細內容↓↓↓#

Circ ECG Challenge Response! Regarding the 74 year old woman with SSS and a PM:

Diagnosis: normal sinus rhythm, premature atrial complexes in a bigeminal pattern, A sensed V paced, pseudofusion

The rhythm is irregular, with longer and shorter intervals which are equivalent to each other. Therefore the rhythm is regularly irregular. The average rate is 72 bpm. Each of the QRS complexes is preceded by a pacing stimulus. Therefore this is ventricular pacing. Before each QRS complex there is a P wave (+, *) with a stable PR interval. The mode of the pacemaker is A sense V paced or P wave synchronous ventricular pacing. The irregularly results from every other QRS complex which is slightly early or premature (v). The early QRS complex is preceded by a P wave (*) that has a morphology that is different from the P wave (+) of the other QRS complex. Therefore every other QRS complex is a premature atrial complex. The P wave of the QRS complex that is not premature (+) is positive in leads I, II, aVF, and V4-V6; therefore this is a normal sinus rhythm with premature atrial complexes in a bigeminal pattern. The sinus QRS complex has a normal duration (0.10 sec) with a terminal S wave in leads I and V5-V6 (←) and an R’ in V1 (→), resembling a right bundle branch block. However, it is not wide enough to be considered a full right bundle and is an intraventricular conduction delay to the right ventricle (although sometimes referred to as an incomplete right bundle branch bloc). The axis is physiologic left between 0° and -30° (positive in leads I and II and negative in lead aVF). The QT/QTc intervals are normal (400/440 msec). As this is not the morphology seen with a right ventricular pacemaker (in which there would be a left bundle branch block morphology) or a biventricular pacemaker (in which there would be a QS morphology or deep Q wave in lead I), the QRS complex is not the result of the pacing stimulus and is therefore the baseline QRS complex. There is a pacemaker stimulus which therefore does not capture. Therefore, this is termed pseudofusion and occurs because the intrinsic PR interval is the same as the AV delay of the pacemaker. The premature atrial complex is also preceded by a pacemaker stimulus. The QRS complex is slightly wider (0.12 sec) and has less of a right bundle branch block morphology with less of a terminal S wave in leads I and V5-V6. It does not have a morphology of either a right or biventricular paced complex. Therefore, there is still pseudofusion present but because the premature atrial complex is associated with a slightly longer time of AV nodal conduction (due to decrimental conduction) more of ventricular activation results from the pacemaker stimulus.