網路內科繼續教育
有效期間:民國 90年02月01日 90年02月15日

    Case Discussion

A 55 year-old man suffered from chest tightness, dyspnea, and palpitation in recent days.

Brief History

     This patient had been well until this June, when he suffered from general malaise, chest discomfort, and shortness of breath for one month. Body weight loss with ten kgs in one month was also noted. He had a health check-up at a clinic where iron deficiency anemia was told (Hb: 2.9 g/d, MCV: 67.1 fL, Ferritin: 4.38 ng/mL). He then visited a university OPD for help on August 14. Besides, a S3 gallop and lower leg edema were found, which were later proved due to high output heart failure by cardiac echo. His symptoms improved after component therapy and iron supplementation. However, orthopnea, exertional dyspnea, chest tightness, and persistent palpitation developed since late October. He visited ER on November 3.

     On reviewing his past history, he denied any systemic diseases. He has no history of allergy. He underwent cholecystectomy in 1990 and partial gastroectomy due to upper gastrointestinal bleeding in 1966.

     On examination, the blood pressure was 140/80 mmHg and irregular pulse rate with 140 beats per minute. The body temperature was 37.9℃ and respiratory rate 26 per minute. The conjunctiva was mild pale and the sclera was anicteric. There were no neck lymphadenopathy or goiter palpable. The jugular vein was engorged. Chest auscultation showed fine crackles over bilateral lung fields. The heart sound was grade II/VI systolic murmur noted at left lower sternal border. The abdomen was soft and bowel sound was hypoactive. Bilateral lower limb edema was found. The work-up at ER included: ECG (Figure 1) showed atrial fibrillation (Af) with rapid ventricular rate and inverted T on leadV5~V6, II, III, and aVF and CXR (Figure 2) disclosed cardiomegaly with bilateral pleural effusion with atelectasis of RML and RLL.

Laboratory Data

1. CBC/DC

 

WBC
(K/μL)

RBC
(M/μL)

HB
(g/dL)

MCV
(fL)

PLT
(K/μL)

Seg
(%)

Lym
(%)

Eos
(%)

11/3

8.42

3.55

8.6

76.9

298

75.2

3.5

 0.1

11/7

16.41

4.22

10.6

76.5

297

89.4

4.7

1.6

 2. ABG

 

pH

PaCO2
(mmHg)

PaO2
(mmHg)

HCO3-
(mEq/L)

B.E
(mEq/L)

FiO2

Ventilator
Mode

11/3

7.42

31.5

77.0

19.8

-3.7

0.3

nasal cannula 3 L/min

3. BCS

 

BUN
(mg/dL)

Cre
(mg/dL)

CK
(U/L)

CK-MB
(U/L)

Troponin I
(ng/mL)

Na
(mmole/L)

K
(mmole/L)

11/3

27

0.7

336

39

0.428

136

3.8

11/4

 

3.1

133

17

 

 

 


 

T/D Bil
(mg/dL)

AST
(U/L)

ALT
(U/L)

rGT
(U/L)

ALP
(U/L)

11/3

3.4/2.3

245

198

 

 

11/4

5.5/3.1

636

575

33

240

4. Iron profile

 

Iron (μg/dL)
Range: 50 ~ 150

TIBC (μg/dL)
Range: 250 ~ 370

Ferritin (μg/L)
Range for woman:
10 ~ 200

11/5

11

303

280

 5. Thyroid function

 

hsTSH (μIU/mL)
Range: 0.400 ~ 4.000

Free T4 (ng/dL)
Range: 0.80 ~ 1.90

11/4

0.003

3.49

6. Viral markers

 

Anti-hepatitis C

HBsAg (EIA)

IgM-Anti-HAV

11/6

negative

negative

Negative

 

Clincial course & treatment

     Under the impression of Af with rapid ventricular response, decompensated congestive heart failure (CHF) and suspceted non-Q myocardial infarcction, he was admitted to MICU. Orthopnea improved after prescribed with diuretics, captopril and intravenous digoxin. Pleural effusion was drained with the characters of transudate. Echocardiography showed preserved LV contractility with enlarged LA and LV and no significant valvular abnormality was found. The tachycardia persisted despite the usage of intravenous digoxin, and daily dosage of 50 mg of carvedilol. Amiodarone (900mg per day) was prescribed and heart rate decreased to 80 beats per minute gradually after 1 days' treatment. Due to no obvious CAD risk factors and unknown etiology of atrial fibrillation, thyroid function was checked  with the results compatible with hyperthyroidism. Amiodarone was substituted by sotalol (160mg twice daily) and carbimazole (10 mg three times a day) was also given. By the way, abnormal liver function was noted without the evidence of viral origins, which was attributed to liver congestion. Unfortunately, Torsade de pointes occurred with loss of consciousness on November 5. The condition was improved after cardioversion and supply with magnesium . Sotalol was replaced by continuous intravenous infusion of esmolol. An episode of spiking fever (39°C) happened on November 7. Thyroid storm was highly suspected; the medications were shifted to diluted Lugol's solution (10 mL t.i.d), Rinderon (4mg qd), propranolol (40mg q.i.d), and propylthiouracil (100 mg q8h). Not only did the fever and tachycardia ameliorate half a day later but the patient's consciousness recovered also. Extubation was done smoothly and he was transferred to general ward on November 9. He was discharged with stable conditions on November 18. The follow-up CXR also disclosed resolution of heart size.

案例分析

本案例的病程必須分成三個部份來看;

        第一部份:缺鐵性貧血所造成的高心搏量型心衰竭。如本案例所述,病人仍然會有心臟衰竭的表徵(容易疲倦、胸口不適、及運動耐受性不足),甚至x光片也有心臟擴大,肋膜積水。這些表現與一般的心收縮力不足之心臟衰竭很難區分;很重要的一點在理學檢查上可觀察到病人有非常嚴重的貧血( 通常Hb< 5.0 /dL). 此時對於病人的處置,就必須加上輸血治療,並且找出貧血的原因,才能根治。

        第二部份:病人於住院前開始有心臟衰竭的徵狀,這時候要作一些鑑別診斷。由心臟衰竭的原因開始著手,可分成幾點(1)心搏出量減少者(low output),包含有(a.)收縮性(systolic dysfunction)如 late hypertension, diabetic, toxic, valvular,(b.)舒張性(diastolic dysfunction)如 ischemic, early hypertension, aortic stenosis, hypertrophic obstructive cardiacmyopathy (2)心搏出量增加者(high output),如sepsis, anemia, thyrotoxicosis, arteriovenous fistula。 本案例病人由臨床症狀來看並不是很容易區分原因,但是由住院後之檢查來看,心臟衰竭的症狀在治療之後有改善,但是Atrial fibrillation with rapid ventricular response,雖經使用Digoxin仍無法緩解,其原因無法用瓣膜性或用肺部問題解釋,因此對於不明原因新近發生的 Atrial fibrillation,我們應予測量甲狀腺功能,病人最後證實是甲狀腺功能亢進,經給予治療而使心跳得以控制。本案例病人臨床上的表現,並沒有典型甲狀腺功能亢進者所該有的,這在中老年人有部分病人可能會如此,也有人會以心臟衰竭或atrial fibrillation 表現,甚至有些老人會表現倦怠,食慾不振等,這是必須注意的。

        第三部份:病人證實是Hyperthyroidism之後,我們一方面使用Antithyroid drug,一方面為了避免干擾甲狀腺功能而停用Amiodarone,以sotalol取代,而病人住院後三天,即Amiodraone 使用一天之後,產生thyrotoxicosis 之症狀,經給予steroid, s-blocker及propylthiouracil 之後,獲得緩解。此病人發生thyrotoxicosis 之原因是否與Amiodarone 有關較難確定。文獻上報告通常必須要累積到相當劑量之後才有可能發生。甲狀腺功能異常,統計約2.1%-12.1%的人會發生甲狀腺功能亢進。若病人已知有甲狀腺功能異常,則應該要儘量避免使用Amiodarone以免干擾甲狀腺功能,惡化已存在的症狀。

繼續教育考題
1.
(B)
病案中,病人初次至門診求診,被診斷為貧血引起之心臟衰竭,是屬於何種型態?
A低心搏出量
B高心搏出量
C右心室型態
D侷限型式
2.
(C)
對於貧血引起的心臟衰竭,其治療下列何者為非?
A給予利尿劑
B給予氧氣
C給予強心劑
D給予輸血治療
3.
(B)
病案中,病人住院時所表現的心臟衰竭,依據病史,理學檢查及X光片,其原因較不可能是?
A瓣膜性
B右心室型態
C低心搏出量
D心律不整
4.
(D)
病案中,病人住院後其心律為atrial fibrillation with rapid ventricular rate,其原因最後確認為?
ATheophylline 中毒
B肺心症(cor pulmonale)
C風溼性心臟病
D甲狀腺功能亢進
5.
(A)
對於心臟衰竭病人,用於控制心室節律(Ventricular rate)的藥物較常使用者為?
(1)Digitalis (2)Diltiazem (3)Diazoxide (4)Amiodarone
A(1),(2),(4)
B(1),(2),(3)
C(2),(3),(4)
D(1),(3),(4)
6.
(D)
有關甲狀腺機能亢進,下列何者為非?
A甲狀腺機能亢進,病人可以表現有不整脈(arrhythmia)
B甲狀腺機能亢進的病人,使用Amiodarone必須小心,甚至停用
C甲狀腺機能亢進發生於年輕女性,其原因大部分是因為自體免疫疾病(Graves' disease)
D甲狀腺功能亢進,病人一定表現有心悸、腹瀉、體重減輕、緊張及腹瀉
7.
(B)
甲狀腺機能亢進危象(Thyroid storm)可以用何種藥物治療?
(1)Corticosteroid  (2)Diluted Lugol's solution  (3)Propranolol (4)Propylthiouracil  (5)Phenoxybenzamine
A(1),(2),(3),(5)
B(1),(2),(3),(4)
C(2),(3),(4),(5)
D(1),(2),(4),(5)
8.
(A)
有關Amiodarone之敘述,何者為非?
A為Class II Antiarrhythmic drug
B使用結果是使QT interval 延長
C有很長的半衰期(>50 days),有很高的組織分佈性
DAmiodarone可用於心臟衰竭病人
9.
(D)
Amiodarone之藥物副作用,下列何者正確?
A使用Amiodarone不會有角膜沈積(corneal microdeposits)
B使用Amiodarone不會引起肝功能變化
C使用Amiodarone不會引起肺功能變化
D以上皆非
10.
(C)
Amiodarone 可能影響下列器官系統,何者正確?
(1)角膜 (2)皮膚 (3)腎臟 (4)神經
A(1),(2),(3)
B(1),(3),(4)
C(1),(2),(4)
D(2),(3),(4)

答案解說

答案解說:

1 貧血引起的心臟衰竭為高心搏出量型,不過因血液攜帶氧量不足,因此一旦病人活動時仍然會有運動耐受性不良現象。

2 貧血引起的心臟衰竭必須給予輸血治療, 一般來說心臟收縮功能仍然維持平衡不需給予強心劑治療

3 右心室型態之心臟衰竭,聽診時肺野應該是清澈的,X光片不會有肋膜積水

4

5 Diazoxide 為α -blocker是vasodilator,用於控制血壓

6 (1)Amiodarone 會干擾甲狀腺功能,引起功能亢進或低下
   (2)老年人甲狀腺功能亢進,不一定有典型症狀表現,甚至有時會倦怠,食慾不振

7 甲狀腺危象必須使用(1)類固醇, (2)ß-blocker, (3)抑制甲狀腺之藥物如propylthiouracil, 而phenoxybenzamine為治療pheochromocytoma之藥物

8 Amiopdarone為class III antiarrhythmic drug 使refractory period 延長,造成QT interval延長

9 Amiodarone 會引起甲狀腺功能異常,約5-10%病人會pulmonary fibrosis,肝功能異常,photosensitivity 及peripheral neuropathy,幾乎所有病人都會有Corneal microdeposits 對視力不會有很大的影響

10、同第9題


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