A few theories have been proposed but catecholamine surge is still debated yet widely cited- explained here:
A)⬆️ICP👉Excessive catecholamine surge
B)Differential effect of catecholamine on myocardium
Let’s understand each concept & at the end it’ll all make sense
A)⬆️ICP👉Excessive catecholamine surge
B)Differential effect of catecholamine on myocardium
Let’s understand each concept & at the end it’ll all make sense
A)
Any catastrophic neurological🤕can cause sudden⬆️in circulatory catecholamines due to activation of Hypothalamus-pituitary-adrenal (HPA) axis. But the key factor is SUDDEN- like in aSAH.
Any catastrophic neurological🤕can cause sudden⬆️in circulatory catecholamines due to activation of Hypothalamus-pituitary-adrenal (HPA) axis. But the key factor is SUDDEN- like in aSAH.
Measurement of circulating epinephrine levels, were 1000x baseline in group 1 and 200x in group 2.
Group 1👉 1000x baseline⬆️of epinephrine
Group 2👉 200x baseline⬆️of epinephrine
**SUDDEN EXPLOSIVE⬆️IN ICP (aSAH) HAS MORE HEMODYNAMIC IMPACTS THAN SLOW SUSTAINED⬆️ICP**
Group 1👉 1000x baseline⬆️of epinephrine
Group 2👉 200x baseline⬆️of epinephrine
**SUDDEN EXPLOSIVE⬆️IN ICP (aSAH) HAS MORE HEMODYNAMIC IMPACTS THAN SLOW SUSTAINED⬆️ICP**
B)
🧠has immense control over🫀through autonomic nerves. But🗝️here is to understand the DISTRIBUTION.
Sympathetic innervation of ventricle is heterogeneous.
Sympathetic nerves concentration👉base>>apex👉gradient of ventricular tissue catecholamines from base>>apex. (482037)
🧠has immense control over🫀through autonomic nerves. But🗝️here is to understand the DISTRIBUTION.
Sympathetic innervation of ventricle is heterogeneous.
Sympathetic nerves concentration👉base>>apex👉gradient of ventricular tissue catecholamines from base>>apex. (482037)
Kawano et al (12644879) studied autonomic nerve distribution in healthy autopsied hearts by histochemical analysis for AChE (parasympathetic) & Tyrosine Hydroxylase-TH (sympathetic) in the nerve endings.
Based on rat models:
At⬆️⬆️concentration, Epinephrine causes B2AR signal change from Gs (+ve inotropic)👉Gi (-ve inotropic)
LV apex being more responsive to Epi than base👉hypokinetic
LV base being less responsive to same Epi concentration remians ++inotropic
**Takotsubo**
At⬆️⬆️concentration, Epinephrine causes B2AR signal change from Gs (+ve inotropic)👉Gi (-ve inotropic)
LV apex being more responsive to Epi than base👉hypokinetic
LV base being less responsive to same Epi concentration remians ++inotropic
**Takotsubo**
Bottomline:
✅Aneurysmal rupture & sudden⬆️ICP👉surge in catecholamines
✅Hypersensitivity of apical myocardium👉B2AR signaling form Gs to Gi
✅Apical myocardium more responsive than base at same epinephrine concentration
❤️🔥❤️🔥End result is Takotsubo❤️🔥❤️🔥
✅Aneurysmal rupture & sudden⬆️ICP👉surge in catecholamines
✅Hypersensitivity of apical myocardium👉B2AR signaling form Gs to Gi
✅Apical myocardium more responsive than base at same epinephrine concentration
❤️🔥❤️🔥End result is Takotsubo❤️🔥❤️🔥
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