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Physio Test 2 > Blood Pressure Reg > Flashcards

Blood Pressure Reg Flashcards

1
Q

Mean arteriole pressure - Major factors and

A

=CARDIAC OUTPUT AND TOTAL PERIPH RESISTANCE

  • CO = SV X HR
  • SV= Preload X Inotropy
  • Preload = Blood volume X Venous compliance
  • Blood volume dependent on Kidneys
  • Neurohumoral factors effect all levels
  • Vessicular anatomy, vessicular and tissue factors effect TPR
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2
Q

Aortic pressure pulse is seen:

A

Dicrotic notch: aortic valve is still closing, some of blood is moving into coronary circulation

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3
Q

Calculate mean pressure?

A

1/3SBP+2/3DBP

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4
Q

actual pressure is closer to systolic or diastolic blood pressure?

A

Diastolic - thats why the calculation for mean pressure is weighted toward DBP (cyclic mean is about 93 and diastolic BP is about 80 normally)

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5
Q

pulse pressure generated at large arteries why? from what?

A
  • When the heart beats the fast moving blood has its own pulse as it moves toward the capillaries. (pressure wave reflection)
  • when it hits the capillaries part of that wave bounces backward
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6
Q

As we move away from the heart MAP inc/dec?

A

Decreases from aorta to periph branches

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7
Q

capacitance=

A

ability of the vessels to accommodate the flow

-the tone on these vessels allows the vessels to handle the rise and drop in pressure

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8
Q

CO=

A

HR x (EDV-ESV)

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9
Q

Systolic ejection regulated by

A

force generated, contractility

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10
Q

Diastolic filling regulation by

A

changes in diastolic interval (duration of filling) and venous return (rate of filling)

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11
Q

During excercise what happens to SV?

A

SV relatively unchanged due to decreased ESV and EDV and CO increases due to increased HR

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12
Q

Diastolic interval- what happens at higher HR?

A

decreased at high HR, unless accompanied by increased contractility (decreases ESV)

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13
Q

Venous capacitance is what and what controls it?

A
  • related to how much volume is stored in veins
  • SNA (sympathetic nervous system) activation contracts sm. muscle of veins and causes a decrease in capacity, increasing venous return
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14
Q

Modulation of Diastolic Filling factors:

A
  • diastolic interval (shortens with inc HR)
  • Venous capacitance (Symp nervous sys activation decreases in capacitance and inc venous return
  • gravity
  • Right atrial pressure (increase right atrial pressure = reduce venous return due to decrease in atrial capacitance or reduction in r ventricular output
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15
Q

Regulation of TPR

A
  • MAP=CO x TPR
  • Resistance: blood viscosity and vascular hindrance
  • viscosity -slow changes (inversely related to temp; concentration of RBC; and inc with inc plasma proteins)
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16
Q

Modulation of Vascular Hindrance: 3 main factors:

A
  • –Physical factors:
  • temperature causes large changes in diameter of vessels of cutaneous circ. esp.
  • mechanical forces due to pressure changes or compression/stretching (reactivity to physical changes varies by vascular bed: autoregulation, also compression i.e., foot falling asleep)—i.e., increase BP causes vasoconstriction of smooth muscles
  • –Chemical factors:
  • Vasodilation: histamine, BK, PG (PGE2), K+, EDRF (NO) [pa]racrine mechanism
  • Vasocostriction: Ang II, ADH/AVP, PG (TXA2), catecholamines
  • –Neural regulation:
  • DR vasodilator fibers- local, not much effect on TPR
  • PNS- vasodilation, but little innervation of vessels so not much effect on TPR
  • SNS/cholinergic (skel. muscle)- vasodilation
  • SNS/adrenergic- major regulator, causes vasoconstriction except in cerebral and coronary circ.
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17
Q

Part of the brain that controls BP stuff?

A

medulla

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18
Q

Neural Circuitry- Medulla:

A

—Nucleus of the solitary tract (NTS)
-Main visceral sensory nucleus in the brainstem
-Inputs: glossopharyngeal and vagal afferents
-Outputs: (caudal) parasympathetic preganglionic neurons, premotor autonomic centers, others (basically send info on control to symp and parasymp)
—Dorsal motor nucleus (DMN) of the vagus
-Inputs: cell bodies in Nucleus Ambiguous (upper brain)
-Outputs: parasympathetic preganglionic neurons
—Nucleus ambiguous (NA)
-Inputs: upper
-Outputs: vagal, parasympathetic output to heart (and other organs)
—Rostral ventrolateral medulla (RVLM)
-Regulates arterial tone and cardiac output
-Inputs: peripheral baroreceptors and chemoreceptors, higher brain regions (i.e., NTS, hypothalamus)
-Ouputs: sympathetic preganglionic neurons (IML) –> GOES TO ALL ORGANS
—Area postrema (AP)
“-Privileged” area - IT SENSES WHAT IS CIRCULATING
-Inputs: circulating factors, visceral afferents
-Outputs: NTS, other preautonomic sites in brainstem

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19
Q

Neural Circuitry- hypothalamus

A
  • –Paraventricular nucleus (PVN) of the hypothalamus
  • Inputs: adjacent AV3V region (structures along the 3rd ventricles), NTS and brainstem, others
  • Outputs: posterior pituitary (magnocellular neurons- oxytocin and vasopressin release), median eminence (neuroendocrine chemicals), pre-autonomic projections (brainstem and spinal cord)
  • Esp. vasopressinergic neurons (temperature and blood pressure regulation) and corticotropin-releasing hormone (stress response)
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20
Q

Neural Circuitry- Functional Divisions

A
  • –Vasoconstrictor center- activated in response to lower BP “SNA outflow”
  • detect changes in pH, blood pressure and dissolved gas concentrations via baroreceptors and chemoreceptors
  • Some chemoreceptors in medulla to monitor CSF
  • –Cardioexcitatory center- activated in response to lower BP “SNA outflow”
  • –Cardioihibitory center- activated in response to higher BP “PNA outflow”
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21
Q

loacl metabolic control of the functional divisions:

A

(functional divisions= vasoconstrictor center, cardioexcitatory ceneter, and cardioinh center)
-Chemical modulation of blood flow will influence neuronal activity, i.e., ↓O2, ↓pH, ↑CO2 —> signals there is a lot of metabolic processes going on!!==> CHANGES BLOOD FLOW

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22
Q

Parasympathetic effects:

A
  • Eye: pupillary constriction
  • Salivary glands: stimulate watery salivation
  • Heart: decrease HR
  • Lungs: bronchiole constriction
  • Digestive tract: stimulate motility
  • Liver
  • Bladder: contraction
  • Rectum: relaxation of internal sphincter
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23
Q

Sympathetic effects:

A
  • Eye: pupillary dilation
  • Sweat glands (cholinergic): stimulation
  • Salivary glands: stimulate viscous salivation
  • Heart: increase HR, contractility
  • Lungs: bronchiole dilation
  • Digestive tract: reduced motility
  • Liver: glygenolysis
  • Bladder: inhibition of contraction
  • Rectum: inhibit relaxation of internal sphincter
  • Vasculature: vasoconstriction (skeletal muscle, sweat gland, adrenal medulla- ACh)
  • Pilomotor muscles: contraction
  • Spleen: contraction
  • Adipose tissue: FFA release
  • adrenal gland: release of NE which reinforces response
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24
Q

cholinergic receptors - location and subtypes

A
  • ganglia, neuroeffector junctions (also has some symp nervous system)
  • types= 1) nicotinic (ganglia) - ION CHANNELS
    2) Muscarinic (neuroeffector junction) - gprotein coupled)
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25
Q

adrenoreceptors

A
  • alpha1- g-protein coupled- IP3/DAG pathway, sm. muscle cont., gland secretion - longer effect (ag.- Phenylephrine, antag.- Prazosine &
    affinity: E≥NE≫Iso)
  • alpha2 - AC inhibition, inhibit NE release (ag.- clonidine, antag.- yohimbine; & affinity:E≥NE≫Iso)
  • β1: stimulate AC, cardiac excitation
    (ag. -dobutamine, antag.- metoprolol
    aff. : Iso>E=NE)
  • β2: stimulate AC, sm. muscle relaxtion
    ag. - terbutaline
    aff. : Iso>E>NE
26
Q

Autonomic Modulation of BP

A
  • –Vascular tone
  • Increase tone (a.k.a. vasoconstriction)
  • Decrease tone (a.k.a. vasodilation)
  • –Chronotropy (HR)
  • Negative chronotropic effects
  • Positive chronotropic effects
  • –Inotropy (how hard is the force)
  • Negative inotropic effects
  • Positive inotropic effects
27
Q

Norepinephrine:

A

α agonist, some β1 and β2 effects

28
Q

Phenylephrine:

A

(NE) α agonist, increase vasoconstriction, no β AR activation

29
Q

Epi→

A

β agonist, some α effects at high concentrations

30
Q

isoproterenol:

A

(epi) β agonist, increased HR and vasodilation

31
Q

Nitroglycerine:

A

vasodilator, does not work through AR

32
Q

Short-term BP Regulation

A

Reflex activation (or inhibition) of the SNA

33
Q

Inhibitory Reflexes

A
  • Activation causes a decrease in sympathetic nerve discharge
  • (MAIN) Baroreceptor reflex: High (and low) pressure sensors
34
Q

Excitatory Reflexes

A
  • Activation causes an increase in sympathetic nerve discharge
  • Chemoreflex
  • Cardiac sympathetic afferent reflex
  • Exercise pressor reflex
  • CNS ischemic response
35
Q

Baroreceptor-

A
  • High Pressure Receptors
    -Stimulated by stretch
    -Location: Carotid sinus, aortic arch
    -Innervation: Hering’s nerve (carotid sinus), Vagal afferents (aorta and heart)
    -Effect on- SNA, PNA (paras), Heart, Peripheral Vasc., Adrenal medulla
    I-nhibitory reflex
    -ACUTE BP regulation
36
Q

baroreceptor reflex

A

1) high BP
2) inc in baroreceptor affarents (inc firing)
3) NTS (central integration of sensory inputs) sneses this inc firing
4) modification of sympathetic outflow (RVLM)
5) lowers BP

37
Q

Baroreceptor adaptation to hypertension and what issues with antihypertensives?

A
  • after a while of High BP yor baroreceptors adapt and call that new pressure the normal pressure
  • Works to keep the new blood pressure constant
  • issues: reflex tachycardia and orthostatic hypotension
38
Q

baroreceptor is only good for what kind of bp regulation?

A

SHORT TERM ONLY - Itll reset itself/adapt to new consistent pressures

39
Q

Low Pressure Receptors location and function:

A
  • Location: atria and pulmonary circulation

- Function: volume receptors: Low pressure system contains most of blood volume- good place to sense blood volume

40
Q

Low Pressure Receptors reflex: name and what happens:

A
  • Henry-Gauer Reflex
  • Increased CVP (central venous pressure)→↑nerve activity (vagal afferents) →↓ CNS activity →↓ADH →diuresis (lose water)→ ↓CVP→↓ stretch
  • ↑ADH→ vasoconstriction→ ↑CVP
  • Stretch of atria also elicits atrial natriuretic factor release to increase sodium excretion in kidneys
41
Q

inhibitor systems:

A

baroreceptors (stretch) and low pressure (volume) recepotros

42
Q

excitatory reflexes:

A

Chemoreflex
CSA Reflex
Exercise Pressor Reflex
CNS Ischemic Response

43
Q

Chemoreflex location, stimulus and response;

A
  • Excitatory relfex - raise pressure if low
  • Location of receptors: aortic arch, carotid body, CNS
  • Stimulus: (change in) Low O2 , High CO2, Low pH
  • Decreased BP → decreased blood flow to receptors → Low O2 → increased afferent activity → increased SNA→ increased BP and HR→ increased flow→ increased O2 delivery to receptors
44
Q

Cardiac Sympathetic Afferent Reflex: location stimulus and response:

A
  • excitatory
  • Location: heart wall, ventricular receptors
  • Stimulus: (ischemia) metabolites, i.e., BK (bradykinin), Pg (Prostaglandin), K+, ROS, Substance P, adenosine
  • Afferent impulse sent to brain stem to cause an increase in SNA (outflow) to increase BP.
  • Can be exaggerated in disease states
45
Q

Exercise Pressor Reflex location, stimulus and response:

A
  • Location: skeletal muscle (to CNS)
  • Stimulus: increased stretch and metabolites produced (ischemia) during exercise
  • Results in increased SNA and therefore BP (also increased HR and CO, hyperventilation, decreased gastric motility and urine production through a central mechanism)
  • Can be exaggerated in CVD
46
Q

CNS ischemic response-

A
  • exitatory - SHORT TERM RESPONSE
  • CNS ischemia (decreased perfusion of CNS) causes increased SNA→ vasoconstriction, increased HR, increased contractility, increased adrenal medulla activity→→increased blood pressure→ reduced CNS ischemia (increased CNS perfusion)
  • last effort to maintain cerebral perfusion
  • works best at low pressure - once blood flow gets to low they die so you die.
47
Q

Local Control of Vascular Tone

A
  • —Autoregulation of flow:
  • Myogenic mechanism: Inc. MAP → arteriolar distention → smooth muscle contraction → inc. resistance → tissue perfusion maintained
  • Metabolic mechanism: i.e., reactive hyperemia (occluded vessel there is a build up of metabolites and when it is clreaed all released and get vasodialation (reacting to ischemic response)
48
Q

Long-term Control of BP

A
  • –Hormones controlling vascular tone
  • Epinephrine (Epi)
  • Norepinephrine (NE)
  • –Hormones controlling salt and water reabsorption from the kidney
  • Renin
  • Angiotensin II (Ang II)
  • Aldosterone (ALDO)
  • Vasopressin (AVP/ADH)
  • Atrial natriuretic factor/peptide (ANP)
49
Q

Adrenal medulla control of BP:

A
  • humoral (hormonal)
  • Adrenal medulla releases Epi (and little NE)
  • Direct vasoconstriction (alpha1) of blood vessels
  • Increase proximal Na+ reabsorption (early area of tubule) - sodium coming back into flow = water coming back into flow
50
Q

Renin-Angiotensin-Aldosterone-AVP system

A

-Controlled by renal perfusion and renal sympathetic nerves
-Response: increased renin release facilitates increased conversion of angiotensinogen (made in liver) to AI (angiotensin 1) →AI converted to AII (angiotensin 2) via ACE1 (ENZYME LOCATED IN LUNGS)→AII (angiotensin 2 acts on 3 things—>
1) Increased BP directly via action on VSM of arterioles
2) Increased aldosterone production from adrenal cortex
-Aldo increases sodium (and water) reabsorption in kidneys which increases blood volume to increase blood pressure
3) Increased release of AVP/ADH from hypothalamus to cause both vasoconstriction (V1) and increased water reabsorption in distal tubule (V2) to increase blood volume, both of which will increase blood pressure
(RATE LIMITNG STEP IS RENIN)

51
Q

Control of Renin Secretion - inreasing renin

A
  • Renal sympathetic innervation of juxtaglomerular cells =JGA - jave renin packaged and let it go with stim of sympathetics
  • Intrarenal Baroreceptors: Decrease Renal BP → Decrease Stretch → Increase Renin
  • Low sodium: Macula Densa (senses Na concentration); Decrease Na+ delivery to distal tubule → increases renin
52
Q

ADH (=AVP)

A
  • Anti-diuretic hormone, arginine vasopressin
  • Synthesized in supraoptic and paraventricular neurons of the hypothalamus
  • Released in response to stimulus (increase in extracellular osmolarity)
  • Hypothalamic osmosensors: highly sensitive
  • Volume sensors (stretch receptors)- powerful but not sensitive: Only sensitive to (A LOT OF) volume loss, not gain
53
Q

low plasma volume - path to inc plasma volume with ADH?

A

-dec plasma colume –> dec arterial pressure —> decrease of baroreceptor firing –> INCREASE ADH —> inc in was reabsorption –> decrease water excretion —> inc plasma volume

54
Q

too much water ingested .. pathway to get rid of it with ADH?

A

-excess water ingested –> dec fluid osmolarity —> decrease firing of hypothalmic osmoreceptors –> DECREASE ADH —> decrease water reabsorption –> inc water excrestion

55
Q

Atrial natriuretic peptide pathway

A
  • inc blood volume = inc in atrial stretch
  • atrial myocytes release ANP = 3 effects
    1) hypothalamus –> stimulates decrease in vasopressin = inc solium and water excretion
    2) inc in plasma ANP = kidney has direct effect on inc sodium and water excretion, kidney inc glomular filtration rate and decreases renin secretion to increase sodium and water excretion
    3) adrenal cortex —> decrease aldosterone =increase sodium and water excretion
56
Q

Pressure-natriuresis relationship always impaired in

A

hypertension. -impaired response to Na load

57
Q

Response to Standing

A
  • Cardiac filling pressure reduced; SV decreased
  • Baroreceptors sense reduced BP and inform brain of the situation
  • Brain reduces PNS outflow to the heart and increases SNS outflow to the heart and vasculature
  • Increased HR and contractility increase CO
  • Peripheral vasoconstriction increases BP
58
Q

Carotid Sinus Massage on supraventricular tachycardia

A
  • activates vagus

- can distinguish supraventricular from ventricular originating tachycardia

59
Q

Carotid Sinus stimulation for HTN treatment

A
  • HTN - hypertension (some)- loss of baroreflex sensitivity results in aberrant SNA increases
  • implantable device in carotid artificially activates BR by sending generating voltage
60
Q

Renal Denervation for HTN treatment

A
  • Drug resistant HTN (surgical intervention)
  • Catheter-based radiofrequency ablation of renal nerves
  • –Interrupts efferent and afferent signals
  • Current research suggests BP-lowering (SNA-lowering) effect due to afferent nerve interruption
  • Efferent interruption also contributes by removing stimulus of SNA on renal water and sodium reabsorption
61
Q

low blood pressure on renin which receptor related?

A

INCREASE RENIN SECRETION –> Beta one receptors tell kidney to inc renin (beta blockers decrease how mcuh renin is secreted)

Physio Test 2 (10 decks)

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