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日
•
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次)
•
頸靜脈鼓張
•
心跳快速不規則 (每分鐘約150下)
•
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%有 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 (EF≧40–50%) 。
•
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.
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
沒有留言:
張貼留言