肺結核を疑われて紹介された患者の入院後の検査で, 肺放線菌症と思われた1例を経験したので報告した. 症例は26才男子で, 鼻汁, 発熱を主訴とし, 胸部X線で肺結核を疑われ当院を紹介され入院した. しかし入院後の喀痰検査で結核菌が証明されず, 細胞診を行つたところ放線菌が証明された. 肺放線菌症と診断し, ペニシリン投与により全治した.

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症例は55歳女性。喀血を主訴に近医で入退院を反復していたが, 完治しないため当院へ入院した。胸部単純X線写真では, 中葉の無気肺像を, 気管支鏡検査では, 右B^5a入口部にポリープ状の腫瘤を認めた。直視下生検の結果, 放線菌塊が検出された。ペニシリン投与で喀血は止まったが, 気管支動脈造影で, 気管支動脈の増生像および肺動脈へのシャントを認めたため, 再喀血を予防する目的で, 中葉切除を行なった。

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症例は25歳, 男性. 発熱および左胸部痛にて当院を受診し, 胸部X線写真で左肺門部に腫瘤影を認めた. 諸検査にても確定診断に至らず, 画像上前縦隔腫瘍が疑われ, 開胸手術を行った. 開胸時, 舌区は無気肺になっており, 腫瘤は前縦隔ではなく左S⁴に存在し, 同部を楔状切除した. 切除肺の病理組織標本で硫黄顆粒を認め, 肺放線菌症と診断した. 本邦における肺放線菌症報告例は, 1963～1995年の間に80例あり, 特に1980年以降は漸増傾向にある. 我々が集計した80例を臨床的に検討すると, 本症は40～50歳台の男性に好発し, 口腔内病変との合併が多く, 胸部X線写真では腫瘤影を呈する例が多い, などの特徴が認められた. また, 開胸手術による病理学的検索にて, 初めて確定診断に至る例が多かった. 診断に難渋する胸部X線写真上の腫瘤影では, 本症の可能性に留意すべきと考える.

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One hundred and twenty-six asthmatic cases were studied by using electro- and vector-cardiograms during asthmatic attack and attack-free interval, and results obtained were as follows:
1. Electrocardiographic changes during the attack were sinus tachycardia, taller and peaked P waves and ST depression in leads II, III, and aV_F, the shifting of P and QRS axis towards the right, deviation of transitional zone to the left, and decreased T amplitude in all leads.
2. The vectorcardiographic changes during the attack were deviation of maximum P vector to right anterior and inferior, increased maximum P vector, narrow P-loop in frontal plane, deviation of maximum QRS vector to right superior and posterior, deviation of terminal QRS vector to right posterior, deviation of maximum T vector to left posterior in horizontal plane, and increased QRS-T angle.
3. Some cases of asthmatic patients showed left-sided heart changes on electro- and vector-cardiograms; ST-depression in leads-V₅ and V₆, deviation of maximum T vector to right anterior in horizontal plane, and deviation of ST-vector to the right in Frank lead scaler electrocardiogram.
4. Most of these changes in electro- and vectorcardiograms during asthmatic attack disappeared after the attack in the same individuals.
5. Transient right heart strains in electro- and vectorcardiograms were predominent in most cases during the attack, but the others showed left-sided heart changes. These cahnges suggested the effect of asthmatic attack on heart functions.

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Electric potentials from the heart as recorded in the clinical vectorcardiogram may be modified by disease primarily involving the lungs. This report was designed to evaluate vectorcardiographic changes and gas analysis in 10 adults (7 cases with choronic pulmonary obstruction and 3 cases without chronic pulmonary obstruction) during bronchospastic attack and in attackfree state. Vectorcardiographic changes consisted of:
1) Max QRS vector in 8 cases during the episode of bronchospastic attack showed a tendency to shift toward the right posterior and inferior direction. There were 2 exceptions in which direction of max QRS vector in the frontal plane was in the right superior quadrant and max QRS vector in the horizontal plane deviated to the right posterior quadrant. These findings are indicative of respiratory failure and right side overloading due to hyperin flatedlung, hypoxia and hypercapnia.
2) An increase of rightward terminal QRS forces was noted in severe obstructive pulmonary patients. These patients showed the evidence of RV overloading on VCG during bronchospastic attack.
3) A decrement of max QRS vector magnitude in horizontal plane, a decrement of left maximum spatial vector manitude and an increment of rightward terminal QRS forces were closely related to a decrement of PO₂ and an increment of PCO₂. Alternation of max QRS vector magnitude and RV overloading may well reflect hyperinflated lung due to ventilat o ry impairment and respiratory failure due to hypoxia.
4) Deviation of max T vector to left posterior in horizontal plane correlated with an increment of rightward QRS forces and a decrement of PO₂ due to bronchospastic attack. These findings are also regulated in RV overloading due to bronchospastic attack.
5) A decrement of max T vector magnitude was related to a decrement of PO₂ and an increment of PCO₂ due to bronchospastic attack. This primary T change can be explained also on the basis of respiratory insufficiency.
6) Max P vector magnitude was increased significantly during bronchospastic attack. These changes of the QRS loop were reversible and returned to the origin al pattern after relief of bronchospastic attack in all of subjects. Right heart overload was induced temporarily during bronchospastic attack and well reflected VCG changes. These changes of electrical and anatomical condition, induced by bronchospastic attack, around the heart would have a partial influence on these VCG changes.

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高血圧症患者の歯科治療は危険性が高い。それは, 高血圧症は血圧が高いと言うことだけでなく, 高いことによって継発した脳と心臓の病態変化が歯科治療によるストレスによって生理的状態から逸脱し, 生命に危険な状態を生じることがあるからである。罹患率が高く, 無症状で推移する例もあり, 初診時に歯科で血圧をルーチンに測定しない現状から, 問診で高血圧症であることが分らない場合には思わぬ事故に遭遇することがある。
したがって, まず患者が高血圧症であることを知ることが大切であり, 臨床はそこから始まる。本稿ではすでに高血圧症であると診断されている患者の歯科治療にたいして, 歯科麻酔科ではどのような対応をしているのか, すなわちどのような循環管理をしているのか, その基本となる考え方と方法を述べた。

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