Chapter 20: Vessels & Circulation Flashcards
Bulk flow
Movement of large volumes of H2O & Solutes by osmosis but also by physical force on blood vessels
2 types: filtration & diffusion
Capillaries:
Exchange of gas, nutrients, wastes, & hormones through diffusion. Usually pinocytosis.
Filtration:
Bulk flow out of a blood vessel at origin or start of a capillary (near arteries)
Reabsorption:
Bulk flow into a blood vessel towards end of capillary
Bulk flow is determined by:
1) Hydrostatic Pressure
2) Interstitial Pressure
3) Colloid Osmotic Pressure
Hydrostatic Pressure:
Physical pressure of fluid on its structure
Interstitial Pressure:
Hydrostatic pressure of the interstitial fluid on the exterior of the blood vessel
Colloid Osmotic Pressure:
Pressure due to the movement of water. Which is determined by the amount of dissolved substances in the fluid (especially protein concentration)
Types of colloid pressure:
1) blood colloid osmotic pressure
2) interstitial colloid osmotic pressure
Blood colloid osmotic pressure:
- lots of dissolved substances (esp. Proteins)
* opposite direction to the blood pressure
Interstitial colloid blood pressure:
Few proteins, very low
Net filtration pressure:
Difference in hydrostatic pressure & colloid osmotic pressure.
Determines filtration direction & quantity
NFP= (HPb + HPif) - (COPb-COPif)
Difference in hydrostatic pressure =
BP-IP
Ip is always very low=0
Difference in colloid osmotic pressure =
Bloop Cop - Interstitial Cop
If Net filtration pressure is +
= Filtration
Fluid moving out of blood vessels
If net filtration pressure is -
=reabsorption
Fluid moving into blood vessels
Difference in hydrostatic pressure of Arterial end of capillary:
*BP = 35 mm of Hg (mercury)
-
*IP = 0 mm of Hg (mercury)
Difference in hydrostatic pressure (HP) =35
Arterial end of capillary is:
Hypothetical because these values change depending on age & distance from Heart Rest vs. Active
Difference in colloid osmotic pressure at Arterial end of capillary:
*Blood colloid osmotic pressure = 26mm Hg
-
*Interstitial colloid osmotic pressure= 5 mm Hg
Difference in colloid osmotic pressure (cop) = 21 mm Hg
At Venous End of Capillary:
Blood moves from one end of the capillary to the other end
Net filtration at venous end of capillary:
*Difference in HP
BP=16 mm Hg
IP= 0mm Hg
16-0=16
*Difference in colloid osmotic pressure
BP=26 mm Hg
IP= 5 mm Hg
26-5=21
16-21=-5 mm Hg
How many miles of blood vessels?
600,000 miles of BV
We don’t have enough blood to fill all BV so body controls blood flow to areas that need it the most.
Local blood flow
Blood that is delivered to a specific region
Measured by perfusion
Goal of CV system:
Adequate perfusion for all tissues
Degree of vascularization
Amount of blood vessels in a given tissue
Angiogenesis
Process in which the body grows new blood vessels
Regression
Process by which the body disassembles unneeded blood vessels
Local regulator factors that alter blood flow:
Vasoactive chemicals
1) vasodilators
2) vasoconstrictors
Vasodilators:
Dilate arterioles and relax precapillary sphincters
1) nitric oxide
2) elevated levels of carbon dioxide, H+/acidity of blood, K+
Vasoconstrictors:
Constrict arterioles and close precapillary sphincters
1) prostaglandins & thromboxanes
- we’ve seen in action during hemostasis
Blood pressure:
Force per unit area of blood on wall of BV
Blood pressure gradient:
Difference in BP from 1 end of BV to the other
Total blood flow resting:
= 5.25 L/min
Arterial blood pressure:
Blood flow is pulsing in arteries due to ventricular contractions
Average in healthy individual = 120/80 mm Hg
Highest at ventricular systole, arteries are stretched = systolic pressure
Lowest at ventricular diastole, arteries recoil = diastolic pressure
Systolic pressure
Arteries are stretched
Diastolic pressure
Arteries recoil
Pulse pressure:
The additional pressure on arteries when the heart is resting vs contracting
Measures elasticity and recoil of arteries
SP-DP =120-80 = 40 mm Hg
Highest closest to the heart
High pulse pressure:
Means arteries are not elastic, not stretching due to atherosclerosis (clogging of arteries)
Mean arterial pressure (MAP)
DP + PP/3
Describes how well the body is perfused. Need MAP of 70-110 mm Hg
Highest closest to the heart
If Mean arterial pressure (MAP) is too high/low:
Too much perfusion= edema & kidney damage
Too low perfusion= inadequate perfusion
Capillary blood pressure:
By the time blood reaches the capillaries–not pulsatile, no fluctuations between systole & diastole
Capillary Blood pressure at arterial & venous ends:
Arterial end: 40 mm Hg
Venous end: 20 mm Hg
Venous blood pressure:
- not pulsatile
- 20 mm Hg in venules & 0 mm Hg in veins
(BP is insufficient to move blood when standing–need valves in veins)
- has two pumps that move blood in veins:
1) skeletal muscle pumps in limbs
2) respiratory pump in thoracic cavity
Skeletal muscle pump
- in the limbs
* as muscles contract, they squeeze the blood up the veins while valves prevent back flow
Respiratory pump:
- in thoracic cavity
* diaphragm contracts and relaxes increasing and decreasing pressure in both major ventral cavities
Resistance:
The amount of friction the blood most overcome as it travels through the blood vessels
- opposes blood flow
- peripheral resistance–in BV not heart
Factors affecting resistance:
1) blood viscosity
2) blood vessel length
3) vessel radius
Blood viscosity:
Thickness of blood due to formed elements and plasma proteins.
- Thicker= more friction
- caused by Anemia, dehydration
Blood vessel Length
*obesity creates need for longer vessels
Vessel Radius
*narrower vessels have more friction
*in terms of friction:
arteries < arterioles < capillaries
–vasoconstriction/vasodilation can change that
5 ways of neural regulation of blood pressure:
CV center of Medulla Oblongota
1) cardiac center
2) Vasomotor center
3) Baroreceptors
4) Chemoreceptors
5) High Brain Centers
Cardiac Center:
speeds up/slows down HR and strength of contraction
* cardioaccelatory center
* cardioinhibatory center
Cardioaccelatory Center:
Sympathetic pathways to SA node and myocardium
Cardioinhibitory Center:
Parasympathetic pathways to SA node and AV node
Vasomotor Center
Sympathetic pathways release E & NE
Which causes vasodilation in skeletal muscle & coronary vessels
Which caused vasoconstriction in most of the body ESPECIALLY in veins
Which causes:
1)increased peripheral resistance raises BP
2)larger circulating blood (shunted away by
most of the body)
Baroreceptors:
Dendrites in tunica Externa that detects stretch in BV.
The firing rate increases when stretch increases (and vice versa)
1)in aorta to detect systematic BP
*send info back to CV center through vagus
nerve
2)in carotid to detect BP in head and neck
*send info back to CV through glossy
pharyngeal nerve
Low BP: more sympathetic signals increases
hearts contraction rate & strength
High BP: fewer parasympathetic signals
decrease info to more sympathetic
signals to increase vasoconstriction/
peripheral resistance
Chemoreceptors
Detect high C02, low PH, and very low 02;both activate vasoconstriction
1) Aortic bodies in Aorta
2) Carotid body in Carotid Arteries
Higher Brain Centers
Hypothalamus increased BT, exercise
Hormonal regulation of blood pressure:
1) Renin-Angiotensin system
2) Atrial Natriuretic Peptide
Renin-angiotensin system:
Low BP sensed by kidney or sympathetic stimulation
Kidneys release renin enzyme into blood
Renin converts angiotensinogen in blood to angiogenesin I.
Angiotensin I travels to the lung via blood
Angiotensin converting enzyme (ACE) mostly in lungs converts angiotensin I to angiotensin II.
Angiotensin II’s effects/jobs:
1) powerful vasoconstrictor
2) stimulates thirst center
3) decreases urine output
4) signals release of aldosterone from adrenal cortex or anti diuretic hormone from posterior pituitary
Aldosterone:
Increase absorption of Na & water in the kidney reducing fluid losses to maintain pressure
Antidiuretic Hormone:
Hypothalamus detects, signals pituitary to release
increases water absorption in the kidney
Also stimulates thirst center
Can also cause vasoconstriction in large doses
Atrial Natriuretic Peptide:
Released from the heart if too much stretch in walls of heart
Stimulates vasodilation
Increases urine output
Baroceptor in Aorta:
detects systematic BP
*send info back to CV center through vagus nerve
Baroreceptor in carotid:
Detects BP in head and neck
- sends info back to CV through
glossopharyngeal nerve
Low BP baroreceptor
More sympathetic signals increases hearts contraction rate & strength
High BP baroreceptor
Fewer parasympathetic signals decrease info to more sympathetic signals to increase vasoconstriction/ peripheral resistance
Blood hydrostatic pressure (BP)
hydrostatic pressure of the blood on the
interior wall of the blood vessel
