20.2
心不全 II: 病態生理
収縮性心不全と代償機構
収縮性心不全（HFrEF、収縮機能低下を伴う心不全とも呼ばれる）は、最も一般的な心不全のタイプです。この状態では、心室から拍出される血液量が減少します。大動脈弓と頸動脈洞には圧受容器があり、血圧の低下を検出して交感神経系（SNS）を活性化し、アドレナリンおよびノルアドレナリン…
収縮期心不全の病態生理学は、左心室が血液量を減少させることから始まります。
大動脈弓と頸動脈洞の圧受容器がこの減少を検出し、交感神経系がエピネフリンとノルエピネフリンを放出するきっかけとなり、心拍数と収縮性を高めます。
交感神経刺激は、皮膚、胃腸管、腎臓の血管収縮も引き起こします。
低心拍出量による腎灌流の減少と交感神経の活性化は、レニン放出をトリガーします。.
レニンはアンジオテンシノーゲンをアンジオテンシンIに変換し、アンジオテンシンIは肺のアンジオテンシン変換酵素によってアンジオテンシンIIに変換されます。
アンジオテンシンIIは、血圧と後負荷を増加させ、アルドステロン放出を刺激し、ナトリウムと体液貯留を引き起こします。
さらに、膨満した心室から放出されるナトリウム利尿ペプチドは、血管拡張と利尿を促進しますが、多くの場合不十分です。
最終的に、心臓への負荷の増加は心筋の収縮性を低下させ、心室拡張、肥大、リモデリング、および早期心筋細胞死を引き起こし、拡張期心不全を引き起こします。
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Q1: What triggers the sympathetic nervous system response in systolic heart failure?
Baroreceptors in the aortic arch and carotid sinuses detect reduced blood pressure from decreased cardiac output. This triggers the sympathetic nervous system to release epinephrine and norepinephrine, which increase heart rate and contractility to support the weakened myocardium and restore blood pressure.
Q2: How does reduced renal perfusion activate the renin-angiotensin-aldosterone system?
Low cardiac output and sympathetic activation cause vasoconstriction in the kidneys, reducing renal perfusion. This triggers renin release, which converts angiotensinogen to angiotensin I. Angiotensin-converting enzyme in the lungs then converts angiotensin I to angiotensin II, a potent vasoconstrictor that raises blood pressure and afterload.
Q3: What role does aldosterone play in fluid overload during heart failure?
Angiotensin II stimulates the adrenal cortex to release aldosterone, which causes renal tubules to retain sodium and fluid. This increases blood volume and preload, contributing to the fluid overload characteristic of heart failure and further burdening the weakened heart muscle.
Q4: Why are natriuretic peptides insufficient to counteract heart failure progression?
Natriuretic peptides like BNP and ANP are released from distended cardiac chambers to promote vasodilation and diuresis. However, their effects are typically insufficient to counteract the adverse effects of prolonged sympathetic activation, renin-angiotensin-aldosterone system activation, and other neurohormonal mechanisms driving heart failure.
Q5: How does increased cardiac workload lead to ventricular dilation and hypertrophy?
As myocardial contractility decreases, end-diastolic blood volume increases, stretching myocardial fibers and causing ventricular dilation. The heart responds to increased workload by thickening its muscle, a process called ventricular hypertrophy. These structural changes constitute ventricular remodeling, which further impairs cardiac function.
Q6: What is the vicious cycle of heart failure and how does it progress?
Low cardiac output triggers compensatory mechanisms that increase the heart's workload, worsening the condition. Neurohormones like angiotensin II promote myocardial hypertrophy and fibrosis, causing cell death and loss of contractility. This cycle eventually leads to diastolic heart failure, where a stiff ventricle resists filling and decreases cardiac output.
Q7: What adverse effects result from prolonged sympathetic nervous system activation?
Prolonged sympathetic activation causes vasoconstriction in the skin, gastrointestinal tract, and kidneys, reducing perfusion to vital organs. This triggers renin release and activates the renin-angiotensin-aldosterone system, leading to increased blood pressure, fluid retention, and elevated preload and afterload that further stress the failing heart.