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Physio > Regulation Of Arterial Blood Pressure > Flashcards

Regulation Of Arterial Blood Pressure Flashcards

1
Q

Ultimate goal of cardiovascular reflexes

A

. Defend cerebral oxygen and glucose delivery via cerebral blood flow
Most direct way is to maintain arterial BP and cerebral perfusion pressure

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2
Q

General reflex control mechanism

A

. 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

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3
Q

Different pathways arterial pressure can be regulated

A

. 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

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4
Q

Arterial baroreflex

A

. 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
.

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5
Q

Arterial baroreflex sensors

A

. 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

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6
Q

Arterial baroreflex afferent pathways

A

. Afferent input from aortic baroreceptor travels to brainstem via vagus and from carotid sinus baroreceptors via CN IX

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7
Q

Arterial baroreflex integrating centers

A

. 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

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8
Q

Arterial baroreflex efferent pathways

A

. 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

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9
Q

Arterial baroreflex response if bp is acute elevated

A

. 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

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10
Q

Arterial baroreflex response if bp is acutely decreased

A

. 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

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11
Q

Arterial baroreflex during dynamic exercise

A

. 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.

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12
Q

Arterial baroreflex during hypertension

A

. 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

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13
Q

Arterial baroreflex w/ aging

A

. Sensitivity dec. w/ age

. Acute fluctuations are less effectively buffered

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14
Q

Valsalva maneuver

A

. Forced expiration against closed glottis OR expiration at high resistance
. Expiration against closed glottis inc. intrathoracic pressure

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15
Q

Valsalva maneuver phases

A

. 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

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16
Q

Valsalva maneuver function in clinical setting

A

. 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

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17
Q

Peripheral arterial chemoreflex

A

. 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.

18
Q

Peripheral arterial chemoreflex response when patient is spontaneously breathing

A

. 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

19
Q

Peripheral arterial chemoreflex response when patient is holding breath or has fixed ventilation

A

. 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

20
Q

Cardiopulmonary baroreceptors

A

. Low pressure baroreceptors

. Atrial receptors and left ventricular receptors are sensory of blood volume

21
Q

Atrial stretch receptors

A

. 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

22
Q

Ventricular mechanoreceptors w/ unmyelinated vagal afferents

A

. Response w/ inc. in firing to elevations in LV EDP

Unloaded/ dec. firing when LV EDP dec.

23
Q

Ventricular chemically-sensitive receptors w/ unmyelinated vagal afferent

A

. 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

24
Q

Atrial stretch reflex sensor, afferent pathway, and integrating center

A

. Atrial B-type stretch receptors
. Vagus n. Is afferent path
. Integrating center via NTS, afferent project to medullary CV centers

25
Q

Atrial stretch reflex response is blood volume is inc.

A

. 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

26
Q

Atrial stretch reflex if blood volume or central venous pressure is low (Hemorrhage)

A

. 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

27
Q

Receptors w/ sympathetic afferents response to ___

A

Ischemic pain

28
Q

Chemical receptors w/ unmyelinated vagal afferents response to ____

A

Ischemia

29
Q

Mechanical receptors w/ unmyelinated vagal afferents response to ___

A

Changes in LV EDP

30
Q

LV mechanoreflex sensor, afferent pathway, and integrating center

A

. LV mechanoreceptors w/ unmyelinated vagal (c-fibers) afferents primarily located in the inferopost. Wall
. Integrating center via NTS, project to medullary CV centers

31
Q

LV mechanoreceptor response to acute rise in LVEDP

A

. 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)

32
Q

LV mechanoreceptor response to unloading

A

. 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

33
Q

Capillary fluid shift for intermediate bp control

A

. 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

34
Q

What occurs over time if exogenous toxin or out of control immune response causes massive vasodilation in skeletal m. And visceral circulation

A

. 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

35
Q

RAAS control of blood pressure

A

. 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

36
Q

Vasopressin control of blood pressure

A

. 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

37
Q

ANP control of blood pressure

A

. 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

38
Q

Brain natriuretic peptide (BNP)

A

. 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

39
Q

Kidneys control over blood pressure

A

. 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

40
Q

Diuretics

A

. popular antihypertensive drug

. Target kidney’s ability to conserve Na and H2O

Physio (62 decks)

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