Regulation Of Arterial Blood Pressure Flashcards
Ultimate goal of cardiovascular reflexes
. Defend cerebral oxygen and glucose delivery via cerebral blood flow
Most direct way is to maintain arterial BP and cerebral perfusion pressure
General reflex control mechanism
. Is there is change in regulated or sensed variable away from setpoint, afferent pathways send info to brainstem and/or hypothalamus that integrate this into and activate the appropriate efferent pathways to make adjustments in physiologic parameters to bring variable back to setpoint
Different pathways arterial pressure can be regulated
. W/in seconds via neural reflex changes in CO and TPR
. Changes in blood volume in minutes to hours due to capillary fluid shifts
. Neurohumoral reflex alterations in control of slat and water excretion by kidneys
Arterial baroreflex
. Fast-acting reflex used to monitor and adjust arterial BP on beat to beat basis
. Particularly powerful in responding to acute hypotension
. Main function is short-term regulation
.
Arterial baroreflex sensors
. Sensors at arch of aorta and carotid sinus
. Free sensory n. Endings that respond to mechanical stretch of arterial walls
. Considered high pressure receptors to distinguish from receptors for low pressures on venous side
. Mean pressure in aorta is major determinant of amount of stretch of baroreceptors
. Sensitive to pulse pressure too, greater the pulse pressure, the greater the afferent activity at any mean pressure (important for times w/ change in PP but not MAP like w/ mild hypovolemia or standing upright)
. Sensitivity can be altered by change in a. Compliance or direct damage to receptor
Arterial baroreflex afferent pathways
. Afferent input from aortic baroreceptor travels to brainstem via vagus and from carotid sinus baroreceptors via CN IX
Arterial baroreflex integrating centers
. Afferent info enters brainstem via nucleus tractus solitarius (NTS)
. From NTS the info is sent to cardioinhibitory area (controls vagal efferent output to heart) and drives medullary vasomotor areas
. Rostral ventrolateral medulla (RVLM) drives preganglionic sympathetic fibers in intermediolat. (IML) cell column in spine
. This controls postganglionic sympathetic activity to vasculature and heart
. Entire area call medulla cardiovascular center
. Setpoint is property of integrating centers
Arterial baroreflex efferent pathways
. To the heart: vagus and cardiac sympathetic nn.
. To vascular beds: sympathetic adrenergic nn.
. Sympathetic preganglionic fibers innervates adrenal medulla releasing E and NE when stimulated
Arterial baroreflex response if bp is acute elevated
. Inc. stretch/loading on receptor
. Inc. afferent n. Activity to NTS causing response from integrating centers
. Inc. PNS to SA node to rapidly dec. HR
. Dec. SNS to SA node
. Dec. SNS to cardiac m. And peripheral resistance vessels
. Result in dec. HR, TPR, SV, and CO ultimately dec. MAP back towards normal
Arterial baroreflex response if bp is acutely decreased
. Dec. stretch/inloading on receptor
. Dec. afferent n. Activity to NTS causing response from integrated centers
. Dec. PNS to SA node to inc. HR
. Inc. SNS to SA node
. Inc. SNS to cardiac m. And peripheral resistance vessels
. This inc. HR, SV, CO, TPR, and ultimately inc. MAP to normal
. Inc. SNS to splanchnic capacitance vessels will shift venous blood into central circulation as well
Arterial baroreflex during dynamic exercise
. Normal cardiovascula response inc. MAP and PP due to rapid inc. in HR and SV
. This can be sustained due to baroreceptors are reset to high pressure setpoint w/o change in sensitivity of the reflex
. Function of control of integrating centers
. Resetting the baroflex at start of exercise allow the rise of HR and SV needed to support inc. O2 demand and delivery to mm.
Arterial baroreflex during hypertension
. Reflex is less sensitive in people w/ chronic hypertension
. Due to inc. stiffness of carotid sinus that dec. baroreceptor sensitivity to stretch
. Dec. baroreflex sensitivty implies that acute fluctuations in bp are less effectively buffered
. Strong suspicion that chronic baroreceptor dysfunction contributes to elevated resting sympathetic tone in some people w/ chronic hypertension
Arterial baroreflex w/ aging
. Sensitivity dec. w/ age
. Acute fluctuations are less effectively buffered
Valsalva maneuver
. Forced expiration against closed glottis OR expiration at high resistance
. Expiration against closed glottis inc. intrathoracic pressure
Valsalva maneuver phases
. 1: bride inc. in BP from mechanical transmission of inc. thoracic pressure to arterial circulation
. Progressive dec. in venous return lowers CO
. 2: fall in CP russets in bp dec. initiating reflex tachycardia and inc. SNS to peripheral vasculature
. Release of force expiration occurs
. 3: brief drop in bp due to sudden dec. in intrathoracic pressure
. 4: surge in venous return pumped into constricted arterial tree causes rapid inc. in bp that overshoots basal levers
. Bp surge initiates reflex bradycardia
Valsalva maneuver function in clinical setting
. Assesses status of arterial baroreflex
. HR and BP are measured
. Continous fall in BP during phase 2 and lack of BP overshoot accompanied by little difference in HR btw phases 3 and 4 indicated dysfunction in neural reflex arc for bp control
Peripheral arterial chemoreflex
. Chemoreceptors in carotid bodies (receive highest blood flow per unit tissue in body)
. Activated by dec. PO2 (hypoxia), inc. PCO2, and acidosis
. Afferent input to brainstem via CN IX
. Afferent info enters brainstem via NTS and is integrated in respiratory center of brainstem
. Efferent output is via vagus and sympathetic nn.
Peripheral arterial chemoreflex response when patient is spontaneously breathing
. Inhibition of vagal activity and inc. SNS to heart and resistance vessels
. Results in inc. HR by a lot, inc. TPR and BP
. Degree that BP inc. depends on level of arterial baroreceptor stimulations and end-organ hypoxic vasodilation
Peripheral arterial chemoreflex response when patient is holding breath or has fixed ventilation
. Setting of hypoxemia results in inc. SNS to resistance vessels and icon. Vagal activity to SA node that causes inc. TPR and dec. HR
. When ventilation is allowed to inc., the inc. lung afferent input to medullary control centers inhibits vagal output and you see mild tachycardia response to stimulation of peripheral chemoreceptors
. Extent of HR response depends on severity of hypoxemia
Cardiopulmonary baroreceptors
. Low pressure baroreceptors
. Atrial receptors and left ventricular receptors are sensory of blood volume
Atrial stretch receptors
. In atria at the junction of veins w/ the atria
. Directly sense atrial filling via stretch
. High the atrial volume, the greater the frequency of firing of receptors
Ventricular mechanoreceptors w/ unmyelinated vagal afferents
. Response w/ inc. in firing to elevations in LV EDP
Unloaded/ dec. firing when LV EDP dec.
Ventricular chemically-sensitive receptors w/ unmyelinated vagal afferent
. Response to ischemia
. Reflex response is bradycardia and sympathetic withdrawal (Bezold-Jarisch reflex)
. Reflex depressor response observed in some patients during coronary angio due to stimulation of cardiac ventricular receptors by contrast material
Atrial stretch reflex sensor, afferent pathway, and integrating center
. Atrial B-type stretch receptors
. Vagus n. Is afferent path
. Integrating center via NTS, afferent project to medullary CV centers
Atrial stretch reflex response is blood volume is inc.
. Inc. HR to inc. central BV (bainbridge reflex), if BP and CVP simultaneously inc. the net HR effect is based on cardio accelerator effect of atrial receptors, bainbridge predominates during acute volume loading
. Selective inhibition of SNS to kidney to inc. renal blood flow and dec. Na reabsorption to dec. BV
. Inhibition of vasopressin release from pituitary (via CN X to hypothalamus) to trigger H2O loss
. Inc. release of ANP from atrial cells to inc. loss of H2O through kidneys, inhibit renin and aldosterone release
. Overall dec. BV via loss of Na and water through kidneys
Atrial stretch reflex if blood volume or central venous pressure is low (Hemorrhage)
. Inc. SNS to kidney
. Inc. vasopressin preloaded
. Dec. ANP release
. Little effect on HR
. Overall conservation of H2O and Na via kidneys
. Replacement of lost volume requires intake
Receptors w/ sympathetic afferents response to ___
Ischemic pain
Chemical receptors w/ unmyelinated vagal afferents response to ____
Ischemia
Mechanical receptors w/ unmyelinated vagal afferents response to ___
Changes in LV EDP
LV mechanoreflex sensor, afferent pathway, and integrating center
. LV mechanoreceptors w/ unmyelinated vagal (c-fibers) afferents primarily located in the inferopost. Wall
. Integrating center via NTS, project to medullary CV centers
LV mechanoreceptor response to acute rise in LVEDP
. Reflex bradycardia from inc. Vagal activity
. Dec. BP secondary to abrupt SNS withdrawal to skeletal mm. And viscera
. May be responsible for syncope in patients w/ severe LV outflow obstruction
. May be responsible for abrupt bradycardia in severe hemorrhage
. Similar to effect of stimulating chemically sensitive LV receptors w/ non-myelinated vagal afferent (Bezold-Jarisch)
LV mechanoreceptor response to unloading
. Reflex SNS activation to kidneys, splanchnic circulation, and skeletal m. To support BP
. Effect works in concert w/ reflex vagal withdrawal and SNS activation assoc. w/ unloading of arterial baroreceptors if arterial BP is also affected w/ dec. BV
Capillary fluid shift for intermediate bp control
. Alterations in MAP change capillary hydrostatic pressure
. If BP dec., Pc inc. and fluid moves into interstitial space (opposite for BP inc.)
. Compensatory responses to dec. BP amplify this effect by causing arteriolar vasoconstriction (dec. Pc favoring absorption to restore arterial pressure) known as autotransfusion
What occurs over time if exogenous toxin or out of control immune response causes massive vasodilation in skeletal m. And visceral circulation
. Immediately TPR dec. which would dec. systemic BP
. Arteriolar vasodilation causes net inc. Pc favoring filtration
. Shifts fluid into interstitial space dec. intravascular volume and dec. arterial pressure
RAAS control of blood pressure
. Renin release stimulated by dec. bp/BV/ inc. SNS to kidney
. Renin cleaves AI from angiotensinogen (made in liver)
. AI converted to AII by ACE in lungs (some in endothelial tissue)
. AII is potent vasoconstrictor (inc. TPR) and stimulates aldosterone release from adrenal cortex
. AT1R mediates vasoconstrictor effects of AII and triggers aldosterone
. AII also has direct effect on Na reabsorption in kidney
. Aldosterone enhances Na absorption in kidney to expand extracellular fluid compartment
. ACE breaks down vasodilator bradykinin
Vasopressin control of blood pressure
. Released when bp dec. significantly to have vasoconstrictor effects (inc. TPR)
. Has indirect effect via BV regulation
. Dec. in BV unloads atria stretch receptors -> inc. vasopressin release from pituitary -> inc. H2O reabsorption in kidney collecting duct
. Conservation of H2O attempts ti restore BV and bp
. Opposite if BV is elevated
ANP control of blood pressure
. Defends against excessive BV expansion
. Modulates ECF Na content
. Promotes dec. absorption of Na to dec. H2O in ECF
. Vasodilator effect that in kidneys enhances filtration leading to loss of H2O and Na in urine
. Suppresses RAAS by inhibiting renin release and synthesis and release of aldosterone in adrenal cortex
. Levels low at normal plasma volume
. Exerts effects through natriuretic peptide receptor (NPR-A)
. Neutral endopeptidase (NEP) degrades natriuretic peptides
Brain natriuretic peptide (BNP)
. Found in CNS
. Also released by cardiac ventricular cells
. Related to ANP
. Release inc. w/ inc. stretch on ventricular walls
. Clinical marker for inc. LV filling pressures and LV dysfunction assoc. w/ CHF
. Inc. levels of plasma BNP support diagnosis of acute CHF in dyspneic patient
Kidneys control over blood pressure
. Major regulator of Na and H2O loss from plasma
. Alters reabsorption in direct response to arterial pressure
. If arterial pressure inc., renal output of Na and H2O inc. above intake until pressure normalizes
. If arterial pressure dec., renal output of Na and H2O dec.
. If intake of H2O and Na continues then eventually arterial pressure will return to normal
Diuretics
. popular antihypertensive drug
. Target kidney’s ability to conserve Na and H2O
