Study guide

What are the two types of control utilized by the body?

-Acute
-Long terms

What dictates where the blood goes during acute control?

Metabolites

What occurs throughout long term control?

Body increases the number of capillaries and blood vessel growth occurs

Function of the circulatory system:

To meet the metabolic needs of each tissue by controlling blood flow

4 major needs of tissue via blood?

-Nutrient delivery (O2)
-Waste removal (CO2)
-Maintain proper ion concentrations
-Transport hormones and other specific substances

How does metabolism affect blood flow?

Greater metabolism = greater blood flow

What happens to blood flow during exercise?

-Metabolism increases by 60 fold
-So blood flow increases by 20 fold

What organ in the body has the highest metabolic activity?

Adrenal glands

how is acute control achieved?

Rapid changes in blood flow via vasoconstriction and vasodilation

When does local blood flow increases?

-Tissue metabolism increases
-Oxygen availability decreases

What factors instigate long term control?

Increase or decrease in use of tissues

What are 4 examples of factors that influence oxygen supply and demand?

-High altitude
-Pneumonia
-Carbon monoxide poisoning
-Cyanide poisoning

When does the blood flow rate increase due to these factors?

When arterial oxygen saturation approaches 25%

What happens during cyanide poisoning?

Decrease of oxygen usage by local tissues, increases local blood flow

What are the 2 theories for the regulation of local blood flow?

-Vasodilator theory
-Lack of oxygen/nutrient theory

What occurs according to the vasodilator theory?

-Increased tissue metabolism rate which causes formation of metabolites
-Increase vasodilator formation rate

Where do vasodilators act?

-Precapillary sphincters
-Arterioles
-Metarterioles

What substances act as vasodilators?

-Adenosine
-Carbon Dioxide
-Lactic acid
-Adenosine phosphate compounds
-Histamine
-K
-H

What role does oxygen play in vasodilator theory?

Deficiency of oxygen increases adenosine and lactic acid formation which both play a role in coronary blood flow

What is the basis for the oxygen/nutrient deficiency theory?

Oxygen is required to maintain smooth mm contraction

What are the two states which precapillary sphincters, arterioles, and metarterioles exist in?

-Open (relaxed)
-Closed

What is the transition between the 2 states?

Vasomotion

What occurs when tissue oxygen levels fall according to this theory?

-Metabolism increases
-Oxygen level fall in smooth mm
-Loss of contractility

What role does glucose play in local blood flow?

Deficiency could cause local tissue vasodilation

What other nutrient deficiencies could cause vasodilation?

-aa
-fa
-Vit B

What occurs when these nutrients are deficient?

The peripheral blood flow in the body increases 2-3 fold

What is reactive hyperemia?

Blood flow is occluded for several minutes creating a massive lack of oxygen, then when occlusion passes due to increase in blood flow the oxygen debt is repayed

What is active hyperemia?

When a tissue increases its function and needs more nutrients, a massive depletion of nutrients in the tissue occurs; therefore vasodilator substances are released
-Occurs during intense exercise

What is autoregulation?

Acute increase in arterial pressure causes an immediate rise in blood flow, after several minutes the blood flow returns to normal but the pressure is kept high

what are the 2 tissues that have specialized mechanisms of acute blood flow? how?

-Kidneys --> tubuloglomerular feedback
-Brain --> concentration of Co2 and H

What is endothelial-derived relaxing factor?

Idea that blood flow causes stress on vessels and those vessels release vasoconstrictors or vasodilators in response

Origin of sympathetic nervous system? Parasympathetic?

Thoracolumbar spinal cord; cranial sacral spinal cord

What ANS branch acts on vessels?

Sympathetic only

How does the nervous system control arterial pressure short term?

Just redistributes blood flow to different areas of the body by increasing the pumping activity of the heart and providing rapid control of arterial pressure

What effect does sympathetic system have on heart rate and force of contraction?

Increases it

How does the parasympathetic system effect heart rate?

Decreases it

Where does the SNS innervate?

Vasculature of internal viscera and the heart and peripheral vasculature

What is the major sympathetic ganglia that innervates the heart and peripheral circulation?

Caudal cervical, stellate, and celiac ganglia

What vessels are innervated by the SNS?

-All
-Except capillaries, precapillary sphincters, and most of the metarterioles

What does the innervation of small arteries and arterioles allow the SNS to do?

Increase the resistance to blood flow, thereby decreasing the rate of blood flow to tissues

What does the SNS do to large vessels?

-Decrease the volume of vessel
-Vasoconstrict (arterioles)
-Translocate the blood to the heart which increases the blood to the heart and increases cardiac output (veins)

What type of fibers does the SNS carry?

Large number of vasocontrictors

What does the VMC transmit?

-Parasym impulses through the vagus nerve to heart
-Symp impulses through spinal cord and periphearl sympathetic nerves to almost all blood vessels

Where does the sensory area receive inputs?

Through the vagus and glossopharyngeal nerves

What does outputs from the sensory area control

The activities of the vasoconstrictor and vasodilator areas of the vasomotor center, thus providing reflex control of circulatory function

When does the vasoconstrictor area of the VMC transmit impulse? What is this called

Continuously to the sympathetic vasoconstrictor nerve fibers of the entire body; sympathetic vasoconstrictor tone

What does spinal anesthesia do?

Blocks all sympathetic transmission from the spinal cord to the periphery

What happens to AP from spinal anesthesia?

Falls to 50 mmHg due to loss of vasoconstrictor tone

What happens when there is an injection of NE?

Blood vessel constricts and the AP rises until decreases again

What does the VMC control besides vasoconstrictor activity?

Activity of the herat

What does the lateral part of the VMC do?

Transmits excitatory impulses through sympathetic nerve fibers to the heart to increase HR and contractility

What does the medial portion of the VMC do?

Transmit parasym impulses to the heart to decrease HR

What does the VMC do to nerve?

Norepi released at the nerves ending acts on alpha receptors of vascular smooth mm to cause contractions

What does VMC do to adrenal glands?

Norepi and epi released into blood and constrict vessels

What does epi do?

Vasodilation through beta receptor in certain tissues

What is the role of the nervous system in control of AP?

Causes rapid increase in AP

What occurs for rapid increase of AP to occur by nervous system?

-Arterioles are constricted
-Veins are constricted
-Heart is stimulated to enhance pumping

What does constricted arterioles do?

Increase peripheral resistance which increases AP

What does constricted veins do?

Displaces blood out of larger peripheral blood vessels towards to heart which increases the volume of blood to heart chambers

What does enhanced heart pumping do?

Increased HR and force of contraction which increases AP

IN general, what are the steps to increases BP?

Increase TPR --> increased AP --> increased venous return --> increased CO --> increased BP

What happens to muscles during exercise

Increased blood flow due to increased metabolism in tissues; results in vasodilation

What does an additional increase of blood flow during exercise result from?

Simultaneous increase in AP caused by sympathetic stimulation during exercise

What causes AP to be elevated above normal during heavy exercise?

Activation of reticular activating system in the brain stem which increases the sym outflow from vasoconstrictor and cardioacceleratory areas of VMC

What is AP control regulated by?

Baroreceptor reflex

Baroreceptor reflex is initiated by?

Stretch of receptors

What are stretch receptors?

Spray type nerve endings in the arterial wall at the carotid bifurcation and aortic arch

What type of system is the baroreceptor reflex?

Negative feedback
(increase firing = negative feedback to lower BP)

When is the greatest gain for baroreceptor?

Normal pressure of 100 mmHG when receptors most sensitive

What is the speed of baroreceptor response?

-Extremely rapid
-Rate of impulse firing increases in the fraction of a second during each systole and a decrease again during diastole

When do baroreceptors respond much more rapidly?

To changing pressure than to stationary pressure

What happens where there is increased emotion?

-Increased PNS and decreases SNS which causes vasodilation
-This decreases HR and CO which decreases BP and leads to fainting
(Called vasovagal syncope)

Where does increased AP send baroreceptor signals?

From carotid and aortic body to the nucleus tractus solitartium (NTS) of medulla

Baroreceptor signal activation causes:

-Inhibition of VMC of medulla of vagal parasym center
-Causes dilation which decreases HR and contraction
-AP decreases due to TPR resistance and CO decreasing

What does low pressure do to a baroreceptor reflex?

Pressure rise back to normal

What happens when carotids are occluded?

-Reduces sinus pressure which results in baroreceptors become inactive and lose inhibitory effect on VMC
-VMC activates and causes aortic AP to reise

What does release of occlusion result in?

Pressure in carotid sinus rises and causes the aortic pressure to fall immediately

Primary purpose of arterial baroreceptor system?

Reduce minute to minute variation in AP

When are baroreceptors useful?

For the short term; this is because they rest every 1-2 days if AP returns to higher pressure so they dont work in long term

Say pressure goes from 100 to 160, baroreceptor kicks in to decrease pressure. What happens if it is unable to do this?

The number of impulses gradually decreases over the hours and further less in a day until rate of firing will be normal
this is baroreceptor resetting

What plays the main role in prolonged regulation of mean arterial pressure?

Renal body fluid pressure control system

How do chemoreceptors control AP?

Sensitive to changes in oxygen, CO2, or H+ loss

Where are chemoreceptors located?

On carotid bodies and the aortic arches

How do chemoreceptors act?

They excite nerve fibers that pass through Herrings' nerves and the vagus nerves to VMC of brain

What happens when AP falls below critical level?

-Diminished O2 or excess CO2 so chemoreceptors activated
-Signal from chemoreceptor into VMC excites these centers and elevates AP back to normal

When do chemoreceptors become activated?

Only when AP falls below 80 (aka only effective at low pressure)

Where else are stretch receptors located?

Atrial and pulmonary arteries have low pressure stretch receptors in their wall

Atrial and pulmonary stretch receptors play an important role in minimizing AP changes in response to

Blood volume changes

Where else are signals from aorta also transmitted?

To hypothalamus to decrease secretion of ADH

What does the decreased afferent arteriolar resistance in the kidneys cause?

Glomerular capillary pressure to rise with increase in the filtration of fluid into the kidney tubules

What does lack of ADH cause?

Decreases reabsorption of water from tubules

What does increases in atrial pressure cause?

-Increases HR
-Stretching of sinus node on atria = 15% increase in HR

What can further increase of HR be brought about by?

Bainbridge reflex (nervous reflex)

What is the most of the reflex control of AP achieved by?

-Baroreflex
-Chemoreflex
-Low pressure receptors
all in PNS

What happens when the blood flow in the VMC in the brain stem decreases severly?

Causes cerebral ischemia which activates CNS ischemia response

Where does the CNS ischemia response originate?

In the VMC due to an oxygen deficiency

Result of CNS ischemic response

-Maximum sympathetic outflow which causes vasoconstriction
-Entire circulatory system is tightened and heart enhanced in an effort to restore oxygenated blood to brain

CNS ischemia response is referred to as:

Last ditch stand

When does the CNS ischemic response get activated?

Only when the blood pressure falls below 60 mmHG

What is cushing rxn?

Special type of ischemic response where increase in CSF around brain compresses it and cuts off blood supply

What does cushing rxn initiate?

CNS ischemia that increases AP to rise above the CSF pressure so blood will flow to vessels to relieve it

What is the abdominal compression reflex?

When baroreceptor reflex increases, sympathetic outflow also go to abdominal vessels to cause constriction to force blood from those mm back into circulation

What is skeletal mm contraction?

Veins compressed by mm contraction displace blood back to the heart which increases venous return

What happens when the body contains too much ECF?

Blood volume and AP rise which tells kidneys to excrete excess ECF and return AP to normal

What are the two methods the kidney uses to get ride of extra ECF?

-Pressure diuresis (water)
-Pressure natiuresis (salt)

What is the renal output curve for pressure diuresis?

Urinary flow is zero at 60 mmHg but increases 8 times normal at 200 mmHg

What is the renal output curve for pressure natriuresis?

Sodium output also increases in response to an increase in pressure

What happens in kidneys with a lack of nervous control in terms of CO?

Loss of fluid brings CO and AP back to normal; kidneys excrete the excess fluid from the body

How can arterial pressure be increases long term?

-Shift urinary output curve to the RIGHT
-Increase fluid/electrolyte intake

What is equation for AP?

AP= CO x TPR

Why does salt increase ECF?

It is not easily excreted so it accumulates and indirectly causes ECF vol increase (bc water follows it)

What does an increase in osmolarity of the ECF stimulate?

-Hypothalamic neurons increase ADH release
-This causes kidneys to reabsorb large quantities of water from renal tubular fluid
-This causes ECF to increase

What is hypertension?

When mean arterial pressure is above 110
(Sys over 135, dia over 90)

Salt increase does what to BP

Increases it

Primary aldosternoism:

-Volume overload hypertension
-Caused by excess aldosterone levels

Aldosterone effect:

-Increases rate of absorption of salt and water
-Increases ECF

What is circulatory effects of angiotensin II

-Increase AP
-Increases TPR
-Causes renal retention of salt and water which increases BP and CO over time

How does AngII act directly on kidneys to cause salt and water retention?

-Constricts renal arterioles = decreased blood flow
-Slow blood flow = decrease in pressure = rapid osmotic reabsorption of fluid from tubules
-Increases tubular reabsorption of salt and water

What happens to renal fx curve with Ang II?

Shifts it to high pressure

Neurogenic hypertension

-Due to strong stimulation of sympathetic nervous system
-Vasoconstriction everywhere

Effects of mean arterial pressure, renal blood flow, and CO during hypertension?

-MAP increases
-Renal blood flow decreases
-CO normal

What happens to pressure control during hemorrhage?

-Constriction of veins to send blood to heart
-Increases HR and contractility
-Constricts peripheral arterioles to impede blood flow out

What shifts fluid through tissue capillary wall to readjust the blood volume?

Pressure in capillary falls, fluid absorbed by capillary osmosis from tissue into circulation to build up blood volume and increase pressure

Cardiac index formula

Cardiac output/square meter of body surface

Increased stretch of myocardial mm fibers =

Increase in CO

What is bainbridge reflex?

-Control of CO by increase HR
-Acts on VMC by stimulating sym and vagi
-Increases amount of blood in cambers which stretches myocardial walls

Normal CO

5

Dinitrophenol has what use in nervous system control of CO

Causes intense dilation of peripheral blood vessels by increasing metabolism of all tissues of the body by 4 fold

Beriberi causes?

-Diminished ability of tissues to use cellular nutrients
-So local tissues cause dilation

Beriberi results in

-Fall in TPR
-Increases VR and CO

What does hyperthyroidism result in

-Decrease in TPR
-Leads to increased VR and CO

What is anemia?

-Decreased viscosity of blood and decreased oxygen delivery to tissues
-Leads to dilation

What does anemia cause?

-Decreases TPR
-Leads to increases VR and CO

An AV shunt causes?

-Decreased TPR
-Increased VR and CO

Factors that decrease venous return?

-Decreases blood volume
-Acute venous dilation
-Obstruction of large veins

How does external pressure effect CO?

If intrapleural pressure is increased; CO is decreased

2 determinants of mean circulatory filling pressure

-Degree of sym stimulation on peripheral aa and vv
-Amount of blood in circulatino

How does SNS affect psf?

increases it
(bc it constricts)

How does blood volume affect psf?

Greater volume = greater psf

Relationship of VR and psf?

Factors that increase or decrease do the same to VR
(greater the system is filled = easier it is for blood to flow into heart)

Pressure gradient for VR?

Between RA pressure and psf

VR formula

(psf-RAP)/resistance to VR

What happens when the resistance in the vein increases?

-Damming of blood in systemic circulation
-Venous pressure rises very little because veins are highly distensible so VR decreases

What happens with arteriole and artery resistance increases?

-Blood accumulates and since they arent very distensible, pressure increases
-Pressure overcomes resistance and increases the VR back to normal

Resistance to VR formula

2/3 VR + 1/3 arteriolar resistance

What does transfusion cause?

An increase in psf and decrease in resistance to VR
(increase in vol distends vessels so theres less resistance)

Effect of sympathetic stimulation on CO?

-Makes heart a stronger pump
-Increases the psf by contraction of peripheral vessels and increases resistance to VR

Relationship between AV shunt and CO

-Increase in CO due to sudden opening, decreases peripheral resistance so AP falls
-Sympathetic reflex restores AP, which increases psf and shifts VR curve to right; this increases CO
-Blood volume increases due to slight reduction in AP and decreases sym

NE receptors

Alpha to cause contriction

Epi receptors

Beta to cause dilation

Effects of mass sympathetic discharge during exercise?

-Heart stimulation (increase in HR and contraction)
-Arterioles constricted (active are dilated)
-psf increased due to mm walls of veins being contracted; this increases VR; which increases CO

What does an increase in AP during exercise do?

-Constriction of arterioles (except in active)
-Increased pumping of heart
-Increase in psf

What is VR dependent on during exercise?

psf

Direction for a heart contraction?

Outside to inside

Lowest pressure on heart

Epicardium

Highest pressure on heart

On endocardium; has pressure of both the epicardium and myocardium pressing on it

Sympathetic nervous system has what effect on RA pressure

increases it

After moderate heart failure, what is responsible for bringing the cardiac output from 2 to 4? Responsible for bringing CO back up to 5?

Sympathetic; kidney

Major cause of decompensated heart failure?

Inability of the heart to pump enough blood to allow the kidneys to excrete fluid and electrolytes

What occurs during decompensated heart failure?

-Progressive retention of fluid
-Elevation of rsf, RAP
-Edema in lungs
-Dyspnea
-Death

What is occuring in coronary system during decompensated heart failure?

With each beat, less oxygen is given to coronary system, becomes a viscous cycle

Purpose of negative fluid balance in decompensated heart failure?

Increases VR/CO by increasing blood volume and psf

2 ways to treat decompensated heart failure?

-Cardiotonic drugs
-Diuretics

What happens during left heart failure?

-PULMONARY edema
-Increased pulmonary filling pressure (rises over colloidal osmotic)
-Pulmonary congestion

What occurs during low output cardiac failure by the body to try and regain control

Positive feedback

2 types of high output failure

-Beriberi
-AV shunt

3 causes of reduced renal output during cardiac failure:

-Decreased filtration
-Activation of renin-angiotensin system
-Increased aldosterone

2 types of rheumatic valvular lesions

-Stenosis
-Regurgitation

2 systolic murmurs

-AV valvular regurgitation
-Aortic/pulmonic valvular stenosis

2 diastolic murmurs:

-AV valvular stenosis
-Aortic/pulmonic regurgitation

When is aortic stenosis murmur heard?

At any time; across a room

When is an aortic regurgitation murmur heard?

Diastole

When is a mitral stenosis heard?

At end of diastole

What 4 things occur with an aortic stenosis or regurgitation?

-Hypertrophy of LV
-INcrease in blood volume
-LV failure
-Pulmonary edema

What 3 things occur during a mitral stenosis or regurgitation?

-Pulmonary edema
-Enlarged LA
-Atrial fibrillation

What factors could impede VR

-Diminished blood vol
-Decreased vascular tone
-Obstruction

What 2 reasons for circulatory shock w/o a decrease in CO

-Excessive metabolism
-Abnormal tissue perfusion (septic shock, etc)

Hemorrhagic shock is the common cause of shock, what occurs?

Hypovolemia decreases filling pressure, which decreases VR and CO

When shock occurs what is the first line of response

Baroreceptor

The sympathetic system works to maintain what

Arterial pressure more than the CO

Coronary and cerebral blood flow is protected during shock how

Autoregulation

Difference between progressive and non-progressive shock

-Length of time in shock
-Degree of hemorrhage

What is responsible for the correction during non-progressive shock

Negative feedback system

6 steps for correcting shock:

-Baroreceptors
-Chemoreceptors
-CNS ischemic response
-Reverse stress relaxation of circulatory system
-FOrmation of angiotensin and vasopressin
-Compensatory mechanism returns blood vol to normal

When do you know progressive shock has set in?

-Circulatory system structures start to deteriorate
-Positive feedback sets in
-CO decreases

What 2 things can happen to tissue in progressive shock

-Necrosis
-Acidosis

How much blood should be transfused in anaphylactic shock?

None; wont help