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Phys2 Int CV Control
Question | Answer |
---|---|
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 |