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Phys2 Int CV Control

QuestionAnswer
What vascular structures are controlled by the sacral parasympathetics? The arteries of the external genitalia.
What is the ratio of Epi:NE released by the chromaffin cells in the adrenal medulla? 9:1
How does NE and sympathetics influence the kidneys? Causes increased Na+ resorption OR decreased Na+ excretion. This also causes water retention which will raise BV and Inc CO
What are the 3 components of the medullary CV center? 1.Vasomotor (excitatory, tonically active). 2.Cardioacceleratory (symp). 3.Cardioinhibitory (parasymp). **1&2 are excitatory **Regulates using a negative feedback system
What are the 2 main High pressure baroreceptors? **STRETCH RECEPTORS** 1.carotid sinus: Activate b/w 40-180mmHg, responds to MAP, Pulse pressure, and rate of change. CN IX. 2.Aortic Arch: range of activation is 110mmHg and up.
What is the only influence parasympathetics have on inortopy? Excentuated antagonism, it occurs only with a massive outflow of adrenergic response to dappen the NE effects.
Where is the Cardioinhibitory section of the medullary CV center originate from? 1.Nucleus ambiguous. 2.DMV (dorsal motor nucleus of Vagas)
What is the difference between high pressure receptors and low pressure receptors? Where they are located!! High pressure receptors are located on the high pressure side of the heart. Low pressure receptors are on the low pressure side of the heart.
What are the locations of low pressure receptors (cardiopulmonary receptors) 1.Pulmonary artery. 2.Junction b/w atria and their corresponding veins. 3.Atria. 4.ventricles
What happens to onset the baroreflex when someone goes from sitting to standing? 1.Dec Venous Return (BL pools in legs). 2.Dec SV (dec EDV). 3.Dec CO. 4.Ded MAP (MAP=COxTRP).
What is the REFLEX response to the decreased MAP expeirenced immediately after standing up? 1.Dec stretch in high pressure baroreceptors. 2.Dec firing rate to medullary CV center. 3.Dec PNS activation of SA/AV node M rec. 4.Inc SNS activation: A)Inc B1 activation (Inc HR & CO), B)Inc A1 in veins (Inc VR, SV, CO), C)Inc TPR, D)Adrenal EPI
How will prolonged standing affect the baroreceptor firing rate? It will decrease firing rate due to dec: VR, EDV, SV, CO, MAP. Therefore the medullary CV center will inc symp by activating B1 and A1 receptors. Also activates the RAAS system.
What is the RAAS system and what does it contribute to? Long term adjustments to aterial pressure. 1.Renin (released from jusxtaglomerular cells when NE binds to B1). 2.Angiotensinogen-> AngI-> AngiotensinII. 3.Aldosterone is released from Adrenal cortex in response to AngII. **Works to raise BV and BP
What are the 3 locations targeted by Angiotensin II? 1.Adrenal Cortex: Aldosterone is released (dec Na+ excretion). 2.Renal Proximal tubule (dec Na+ exctretion). 3.Peripheral Arterioles (Inc SVR or TPR). **this will raise BV and BP
How will Increased arterial pressure affect the firing rate to the medullary CV center? There will be increased stretch thus increased firing. The PNS will be activated and the SNS inactivated.
What can happen to the baroreceptor firing rate with sustained HTN? They adapt, and fire rate is reduced. **Lose their ability to initiate a dec in CO and SVR
How can you terminate a supraventricular arrhythmia without medication? Have patient stand on head or press on carotid sinus to load the baroreceptors. **this increases vagal outflow.
What is the main function of low pressure receptors? stretch receptors that Detect fullness, and exert tonic inhibition on SNS.
What is the atrial receptors (low pressure receptors) response to Increased stretch? 1.Inc HR. 2.Renal vasodilation (increased the urine output to decrease BV). 3.Dec hypothalamus' release of ADH. 4.Myocytes release ANP (causes Inc Na+ and water excretion).
What are low pressure receptors response to decreased stretch? 1.Inc SNS to kidney. 2.Inc release of ADH from hypothalamus. 3.Inc release of AVP
In general, stretch of high pressure receptors causes? stretch of low pressure receptors? 1.reflex response works to decrease BP. 2.reflex response works to decrease BV by activating kidneys
Does SNS Epi affect MAP? not too much, stays relatively the same
Effects of atrial natriuretic peptide (ANP) 1.Kidneys excrete Na+ and water (dec BV and MAP). 2.Inhibits renin, angII, aldosterone, and ADH/AVP (Prevents water retention and vasoconstriction).
Where is ANP released from? low pressure Atrial myocytes in response to stretch
Where does AVP (ADH) come from? Synthesized in the hypothalamus, released from the pituitary.
When is AVP or ADH released? What does it do? 1.Inc plasma osmolality. 2.Dec Vol. 3.Circulating AngII. **causes vasoconstriction (Inc TPR) and Na+ and Water retention in kidney (Inc BV and thus BP)
High pressure baroreceptors respond only to? low pressure barorreceptors? High: Arterial pressure change. Low: Atrial volume change.
What is vaso-vagal syncope? Fainting
What is the mechanism behind fainting (vaso-vagal syncope)? A dec symp (vasodilation & dec venous return) outflow and inc parasymp (bradycardia & dec CO) outflow from the medullary CV center due to certain stimuli: 1.Emotional stress. 2.Acute pain. 3.sight of BL. 4.Phlebotomy.
What do chemoreceptors regulate? when do they regulate arterial pressure? Peripheral sense: dec pO2, Inc pCO2 & H+. Central sense: Inc H+. Important AP regulation during hypoxia
Responses to Inc chemoreceptor firing if there is NO respiratory movement. 1.Vasoconstriction. 2.Bradycardia.
Response to Inc chemoreceptor firing normally 1.Vasoconstriction. 2.Tachycardia (want to continuously replenish the pO2 to the cell-BL interface.
Patients in pain (most common)? (Deep pain)? Common: Inc Symp, Dec para. Deep:Dec symp Inc para
Created by: WeeG