2012年2月15日 星期三

congestive heart failure





83歲女性
       主訴:嚴重呼吸困難、無法平躺(端坐呼吸)、下肢水種,約2-3
       近來一個月有漸進性呼吸困難心悸、食慾不佳,藥物服用不規則情形
       過去病史:高血壓及心律不整病史數十年
       血壓 150/100 mmHg
       呼吸快速 (每分鐘24)
       頸靜脈鼓張
       心跳快速不規則 (每分鐘約150)
       第二級收縮期及舒張期心雜音
       雙側肺底囉音
       下肢水腫
  CHF introduction:盛行率: 0.4%-2% (全球約有2千萬人)
       主要是老年人的疾病:
       大於 65歲的老年人中6-10% 心衰竭
       較常發生在男性,但因女性較長壽,人數仍占一半
       心衰竭住院的病人中有80%是大於 65歲的老年人
       流行病學研究顯示,心衰竭的病患中,約有一半人仍有正常或是相對
足夠的左心室射血分率(normal or preserved EF (EF4050%)
       因此目前大致可以將心衰竭病患分為兩類
       (1) HF with a depressed EF (commonly referred to as systolic failure) or
       (2) HF with a preserved EF (commonly referred to as diastolic failure).
       心衰竭定義
心衰竭(Heart failure)是一個臨床的症候群 (syndrome),它可能是因為病患有先天性或後天性的心臟結構或功能的異常,使得他發生了臨床的綜合症狀 (symptoms: 呼吸困難和疲倦) 和徵候 (Signs: 水腫和肺部溼囉音),導致病患需要常常住院治療,生活品質不佳,而且可能縮短壽命
Considerable overlap between the etiologies of HF with depressed and preserved EF.
       In industrialized countries, coronary artery disease (CAD) has become the predominant cause in men and women and is responsible for 60–75% of cases of HF. Hypertension contributes to the development of HF in 75% of patients, including most patients with CAD.
       Both CAD and hypertension interact to augment the risk of HF, as does diabetes mellitus.
       In 20–30% of the cases of HF with a depressed EF, the exact etiologic basis is not known. These patients are referred to as having nonischemic, dilated, or idiopathic cardiomyopathy if the cause is unknown.
       Prior viral infection or toxin exposure (e.g., alcoholic or chemotherapeutic) may also lead to a dilated cardiomyopathy.
       A large number of the cases of DCM are secondary to specific genetic defects, most notably those in the cytoskeleton.
       Most of the forms of familial DCM are inherited in an autosomal dominant fashion.
       Mutations of genes encoding cytoskeletal proteins (desmin, cardiac myosin, vinculin) and nuclear membrane proteins (lamin) have been identified thus far.
       DCM is also associated with Duchenne's, Becker's, and limb girdle muscular dystrophies. (neuromuscular disease)
       Conditions that lead to a high cardiac output (e.g., arteriovenous fistula, anemia) are seldom responsible for the development of HF in a normal heart.
       However, in the presence of underlying structural heart disease, these conditions can lead to overt HF.
       Mechanical stretch of the myocyte,
       Circulating neurohormones (e.g., Norepinephrine, angiotensin II),
       Inflammatory cytokines [e.g., Tumor necrosis factor (TNF)],
       Other peptides and growth factors (e.g., Endothelin),
       Reactive oxygen species (e.g., Superoxide, NO).

高心輸出量心衰竭:
 Conditions that lead to a high cardiac output (e.g., arteriovenous fistula, anemia) are seldom responsible for the development of HF in a normal heart.
       However, in the presence of underlying structural heart disease, these conditions can 
lead to overt HF.
會有微損傷

暫時的改變道長久的不可逆變化 破壞終末棄官





心肌受傷 CO下降 啓動一連串神經荷爾蒙機制 造成短期適應 但長久卻是反效果


壓力過載:收縮壓上升 肌纖維平行增加 造成肥大 肥大會抑制擴大
體積過載:舒張壓上升 肌節連續增加 造成擴大 擴大抑制舒張壓力的增加 




Systolic dysfunction: 
      Sustained neurohormonal activation results in transcriptional and posttranscriptional changes in the genes and proteins that regulate excitation-contraction coupling and cross-bridge interaction. Collectively, these changes impair the ability of the myocyte to contract and, therefore, contribute to the depressed LV systolic function observed in patients with HF.
       Diastolic dysfunction:
      Myocardial relaxation is an ATP-dependent process. reductions in ATP concentration, as occurs in ischemia, lead to slowed myocardial relaxation. Alternatively, if LV 
filling is delayed because LV compliance is reduced (e.g., from hypertrophy or fibrosis), LV filling pressures will similarly remain elevated at end diastole.
       LV remodeling:
      changes in LV mass, volume, shape, and composition of the heart that occur following cardiac injury and/or abnormal hemodynamic loading conditions.
      Prolate ellipsoid à more spherical shapeà increased wall stressà LV dilationà worsening LV function+ increased oxidative stress+  sustained expression of stretch-activated genes
      Functional mitral regurgitation





2012年2月14日 星期二

Cardiogenic shock


Systemic hypoperfusion:
      cardiac index [<2.2 (L/min)/m2]
      sustained systolic arterial hypotension (<90 mmHg),
      elevated filling pressure [pulmonary capillary wedge pressure (PCWP) > 18 mmHg].
    


It is associated with in-hospital mortality rates >50%
       Major causes 
      Acute myocardial infarction (MI): most common
       Most often due to massive MI (5-10%)
      dead myocardium does not contract
      40% loss of muscle mass or greater
      Cardiomyopathy or myocarditis or cardiac tamponade: less frequent


昨天看到的病人是hereditary and preipartum-

associated DCM 造成的heart 


failure 兩側下肢水腫 端坐呼吸 今天作心導管和心臟切片 準備換心


       Leading cause of death of patients hospitalized with MI.
       Early reperfusion therapy for acute MI decreases the incidence of CS.
       The rate of CS complicating acute MI fell from 20% in the 1960s but has plateaued at ~8% for >20 years.
       Shock is typically associated with ST elevation MI (STEMI) and is less common with non-ST elevation MI
       LV failure accounts for ~80% of the cases of CS complicating acute MI.
       Acute severe mitral regurgitation (MR), ventricular septal rupture (VSR), predominant right ventricular (RV) failure, and free wall rupture or tamponade account for the remainder.
       Shock is present on admission in only ¼ of patients who develop CS complicating MI; ¼ develop it rapidly thereafter, within 6 h of MI onset. Another ¼ develop shock later on the first day.
       Subsequent onset of CS may be due to reinfarction, marked infarct expansion, or a mechanical complication.
       Initial damage/event
       Cascade of inflammatory and other mediators- histamine, LTs, PAF, lactic acid, myocardial depressant factor
       Increased oxygen demand, worsened coronary perfusion
       Damage begets more damage
        
        
        
Presentation•       Acute MI typical presentation
Tachycardia, cool clammy skin, hypotension, poor peripheral pulses, decreased urine output, MS changes
       Jugular vein distension, pulmonary congestion
       Rule out surgically corrected causes-
      valves, papillary rupture, tamponade
       Lab studies specific for underlying cause
      cardiac enzyme, Complete blood count (CBC), electrolytes, coagulation factors, arterial blood gas, etc..
      X-ray, echocardiography, Electrocardiography, etc
       ABCs: airway, breathing,circulation
      Oxygen
      Ventilation
      Vasopressors (volume expansion?)
       Central line placement
       Address cause
      revascularization, PCI (percutaneous coronary intervention), stent, thrombolytics
       Nitrates, morphine
      reduce pain
      hypotension dangerous
       Dopamine, dobutamine
       Amrinone, milrinone
       Beta blockers when able
      BP, HR limitations
       Misc: diuretics, antiplatelet, LMWHs (low molecular weight heparin), etc
Outcome

       Very very poor
      70% with medical management
      perhaps 30-50% with surgical/cath lab intervention
       Prevention
       Early identification

2012年2月9日 星期四

急性心肌梗塞常規醫囑


1. Ac myocardiac infarction. 
2. Condition: critical. 
3. Activity: On bed rest.
 4. Nasal O2 3-4L/min for 3-12 hrs 
5. NPO until chest pain free, then, on low residue soft diet 
6. Take B.P. and PR q4h (if unstable, q1/2 hr until stable), notify if HR<60 or
>110; BP<90 or >150; RR<8 or >22. 
7. Record daily intake and output 
8. On ECG mnitor 
9. N/S 500 ml i.v. to keep iv line open 
10.Check cardiac serum marker 
11.Nasal cannula inhalation with rate of 3-4 L/min. (goal: keep O2 saturation
92%) 
12.Aspirin 325 mg chewing, st, then 160mg-325 mg qd.
*13.rt-PA 15 mg iv bolus, 0.75 mg/kg i.v. drip for 30 min (總量<50 mg) then 0.5 mg/kg i.v. drip for 1hr, 總量<35 mg (total dose<100 mg); Streptokinase 150 million i.v.for 1hr。在 T1MI 
14 之研究報告,與病人接受足量之 t-PA(100mg)相比,病患接受 abciximab(一種 GP Iib/IIIa 抑制劑)及半量之 t-PA(50mg)可達到較高之 T1MI grade 3 血流(冠狀動脈攝影相當於正常血 流,不過目前健保局尚未同意這種治療。
14.病人使用 rt-PA(alteplase)reteplase 時給予 Heparin 60 u/kg bolus (最大 不超過 4000u),之後靜注 heparin 800-1000u/hr 48 小時;如病人使用 streptokinase anistreplase(APSAC),則只對引起全身血栓之高危險病 人,譬如年齡>70 歲,大片心前壁心肌梗塞,過去已有心肌梗塞,心臟衰 竭或休克,估計須臥床 6 天以上,或過去有深部靜脈栓塞病史者則可繼續 給予口服 warfarin,直到能下床走為止。
15.給予乙型阻斷劑以維持心跳<70/分。 16.第一天用 NTG i.v. drip ,之後如有持續胸痛,可口服 Isosorbide dinitrate
95-10mg tid 17.如胸痛厲害可給予靜注 Morphin 25mg.q 5-30 min, prn(注意低血壓及呼吸
抑制之副作用) 18.當病人有哮喘病史又合併心跳過快(SVT)時,可用 Diltizem30-60 mg or
Verapamil 40-80 mg tid 
*19.ACE 抑制劑:通常在 6 小時之後才使用,若病患使用血栓溶解劑,而症狀及血行動力學已穩定時,可口服小劑量而在 48 小時內逐漸增加到適量。 
*20.有症狀之心跳慢可用 Atropin:0.5mg i.v.,必要時 5 分鐘後可再給予 0.5mg,
直到 2mg 為止 *:星號代表需要時才使用

胸痛分類





急性冠心症hyperacute T 波,ST 段下降 >1mm,ST 段上升,或出現異 常Q波
症狀:壓迫感,窒息感,悶痛或大片前胸部 或胸骨下疼痛有好幾分鐘,甚至>15 分鐘(不穩定型心絞痛)。疼痛可能放 射到上臂,頸部,或下頷。
急性心包膜炎ST 段上升出現在所有胸前導 程或全部 12 個導程
症狀:聽診可聽到摩擦聲(friction rub)胸痛 位置在前胸部,很少會往其他地方放 射出去,在身體前傾時會減輕
主動脈剝離胸部 X 光可見中膈腔變寬,有 時有心包腔積液,電腦斷層可 見典型之主動脈剝離
症狀疼痛之程度與冠心症相似,常可造成 心肌梗塞,心包填塞症,休克或因急 性主動脈閉鎖不全而有心臟衰竭。如 剝離位置在降主動脈或腸系膜動脈可 引起上背部(inter scapular)疼痛,或 腹部疼痛,身體檢查可能會有 pulse deficits 及神經檢查異常
急性心肌炎第一或第二度房室傳導阻滯,期外收縮(APC or VPCs)
症狀曾有類似上呼吸道發炎病史,如影響心臟功能可能會有胸痛及運動時呼吸困難,甚至心臟衰竭症狀
自發性氣胸有時有竇性心跳過快,X 光可 見氣胸
症狀:突然產生之胸痛,過去可能有氣胸或 慢性肺病病史,如氣胸太大會引起呼 吸困難,聽診會有單側呼吸音下降
肺栓塞或有類似心肌缺氧般之心電圖 變化,出現S1Q3T3,竇性心跳 過速等。
症狀:胸部中央疼痛,早期為悶痛,後來變 得相當尖銳,刺痛,吸氣時會加重。 臨床上有急性肺心症,心搏出減少, 血壓降低,心跳快,缺氧,或許有長 期臥床病史。
Tietze's syndrome(病毒性肋軟骨炎):心電圖無變化
症狀:前胸部尖銳疼痛,不會向外放射,呼 吸或轉身運動時變劇,局部有壓痛感
食道炎會痙攣:心電圖無變化
症狀:燒灼或壓迫感,位於胸部或許會放射 到喉嚨。過去曾有胸部疼痛病史,在 進食或喝飲料時會減輕或加重。

2012年2月8日 星期三

pulmonary embolism


Name: XX   F/53 
Present illness:Left chest pain 5 days\No other systemic disease
Risk factorOvarian cyst s/p  operation one year
Chest CT scan:
Filling defects in Lt pulmonary
trunk, Lt inferior pulmonary
artery & branches 
Hampton sign(+)
Diagnosis:  
      Pulmonary embolism with Lt
       pleuris and pleural effusion



定義:
1. Pulmonary embolism refers to obstruction of the pulmonary artery or one of its branches by material (eg, thrombus, tumor, air, or fat) that originated elsewhere in the body.
2. Acute vs chronic
3. Massive vs submassive
4. It should be suspected anytime there is hypotension +elevated central venous pressure (or neck vein distension), which is not otherwise explained by acute myocardial infarction, tension pneumothorax, pericardial tamponade, or a new arrhythmia.
特別注意:低血壓合併CVP升高(排除掉acute MI, tension PT, pericardiac tamponade時)
機轉:

ØPulmonary arterial obstruction --> platelets release vasoactive agents as serotonin -->­ vascular resistance上升
Ø­alveolar dead space 上升--> V/Q mismatch --> gas exchange下降
ØStimulate irritant receptor -->alveolar hyperventilation(過度換氣!)

ØReflex bronchoconstriction -->airway resistance(氣道阻力又上升)
ØLung edema -->pulmonary compliance下降
Ø ­ RV afterload 上升--> RV dilatation, dysfunction, ischemia
ØIf ASD presence --> prardoxical embolism ® Rt to Lt shunt ® severe arterial hypoxemia
大部份死因:進行性又心衰竭-->cardiac output 下降
血流下降因素:梗塞 休克 懷孕 骨盆腔腫瘤 手術前後靜脈阻塞
易形成血栓:凝血因素 sickle cell diz, protein C, S 缺乏 癌症(adenocarcinoma) 口服避孕藥 , nephrotic syndrome, IBD, antithrombin III deficiency
預測PE的可能性:
包含的項目:DVT的有無、其他可能診斷、心跳、不動、之前有過DVT or PE、癌症

另外一個發表於內科學期刊的Geneva score
這一分數表多加了年齡、開刀、症狀來預測:症狀有:單側下肢痛、單側下肢靜脈觸痛單側水腫 此外心跳大於74下就越來越差了
診斷:
Clinical symptoms and signsDyspnea, pleuritic pain, tachypnea (R.R.³ 20/min),cough, hemoptysis, tachycardia, rales, phlebitis, increased P2
呼吸困難、肋膜痛、呼吸急促、咳、吐血、心跳快、溼羅音、靜脈炎、P2聲音增強
Laboratory data

D-dimer
Electrocardiogram:Right ventricular strain with an S1Q3T3
Nonspecific ST-T wave change

***影像診斷:

Normal radiographic appearances
Regional oligemia: Westermark sign
Increase in size of a proximal pulmonary artery: knuckle sign
Elevated hemidiaphragm
  Associated linear atelectasis
Focal consolidation (infarcts)
  Usually basal, rarely cavitate
Pleural effusion
白箭頭間:westermark sign(focal vasoconstriction)