Physiology Test 2 Flashcards
Humoral Control of Circulation
(Vasodilators)
Bradykinin
Histamine
Atrial naturetic peptide
Serotonin
Prostaglandins
Humoral Control of Circulation
(Vasoconstrictors)
NE (and Epi)
Angiotensin II
ADH
Control by Ions & Other Factors (Vasodilators)
K+
Mg++
H+
Acetate & citrate (mild)
CO2 (esp. in brain)
Control by Ions & Other Factors (Vasoconstrictors)
Ca++
Long term regulation
is more effective than short term
Long term changes
are due to changes in vascularization
Angiogenesis
formation of new vessels. In response to O2 demand (maximal, not average)
Requires vascular growth factors
vascular growth factors
VEGF – vascular endothelial growth factor
FGF – fibroblast grown factor
PDGF – platelet-derived growth factor
Angiogenin
VEGF
vascular endothelial growth factor
FGF
fibroblast grown factor
PDGF
platelet-derived growth factor
Inhibition of vascularization
Angiostatin
Endostatin
Vasoconstrictors (Endothelin)
Released in response to vessel injury
Prevents blood loss
Vasodilators
NO
Released from endothelial cells in response to shear stress (important in larger vessels)
Half life of ~6 sec
Activates guanylate cyclase, which converts GTP to cGMP, which activates PKG, causing relaxation
Kidneys
Tubuloglomerular Feedback (in Urinary)
Brain
Also regulated by CO2/H+
Skin
Tied to body temperature regulation
Myogenic Theory
Sudden stretch of small vessels leads to contraction
Theory: Stretch of smooth muscles opens mechanically-gated Ca++ channels
Increase in Ca++ in vascular smooth muscle leads to increased contraction
Reactive Hyperemia
Increase in flow in response to blocked flow
Active Hyperemia
Increase in flow in response to increased metabolism
O2 Demand Theory
O2 decrease in tissues leads to relaxation of smooth muscle
Because O2 is needed for contraction
Relaxation reduces resistance
Flow increases
Vasodilator Theory
Metabolism produces vasodilator substances
Adenosine
Adenosine phosphate compounds
Histamine
CO2
K+
H+
Substances reduce resistance
Flow increases
Physics of Flow
Flow through a vessel is determined by
pressure difference between ends of vessel
Delta P or P1 - P2
Resistance of vessel
Flow (Q) = Delta P/R
Increases in metabolism
increase flow
Decreases in O2
increase flow
Long-term Control
(days, weeks, months)
Increase/decrease in size/number of blood vessels
Acute Control (seconds)
Vasodilation/vasoconstriction
Arterioles, metarterioles, precapillary sphincters
Local Control of Blood Flow
Each tissue controls its own blood flow
Based on tissue needs
Delivery of O2
Delivery of other nutrients: glucose, amino acids, fatty acids
Removal of CO2 and H+
Maintenance of ion concentrations
Transport of hormones and other substances
Flow proportional to metabolic needs
Lymph Flow
Aided by skeletal muscle pump
Smooth muscle in lymphatic vessel walls
Lymphatic System
Returns fluid and proteins to the blood
(2-3L/day)
Fluid in lymphatic vessels is called lymph
Prevents edema
Absorbs lipids from GI tract
Role in immune system
Net Filtration Pressure
NFP = outward pressures – inward pressures
NFP = (Pc + πif) – (πp + Pif)
Interstitial Fluid Osmotic Pressure (πif)
Tends to pull water out of capillaries by osmosis
Due to proteins in interstitium (very low)
Capillary/Plasma Osmotic Pressure (πp)
Tends to pull water into capillaries by osmosis
Due to presence of proteins (albumin/globulins) in plasma
Interstitial Fluid Hydrostatic Pressure (Pif)
Would tend to pull fluid into capillaries, BUT pulls fluid out of capillaries due to lymphatic drainage
Capillary Hydrostatic Pressure (Pc)
Tends to push fluid out of capillaries
Hydrostatic Pressure
pressure fluid puts on walls
Colloid Osmotic Pressure
pressure solutes put on water, drawing water toward solutes
Vasomotion
Intermittent flow of blood through capillaries due to regulation via precapillary sphincters and metarterioles or small arterioles
Due to O2 levels of tissue
Capillary Differences
Brain
Tight junctions – continuous capillaries
Liver
Large clefts - sinusoids
GI tract
Clefts smaller than liver, but still large
Kidney glomeruli
Small oval windows – fenestrated capillaries
Capillary Walls
One cell thick endothelium
Basement membrane
~0.5 μm total thickness
Contains pores
Intercellular cleft
Caveolae
Microcirculation
Over 10 billion capillaries with surface area of ~500-700 m2
Transport of nutrients to the tissues
Removal of cell waste
Very thin walls
Controlled by arterioles in each tissue along with precapillary sphincters
Peripheral Venous Pressure
Elevated RAP can lead to
backing up of blood in the veins
elevated peripheral venous pressure
Increased abdominal pressures cause pressure in veins of legs to increase even more
Gravitational/ hydrostatic pressure causes pressure in feet (of standing person) to be high
Opposed by venous valves & pumps
Faulty valves lead to varicose veins
Similar in arteries
Venous Resistance
Veins have very little resistance (when distended)
When compressed, they do have resistance
Central Venous Pressure
Pressure in the right atrium (RAP)
Normally 0 mmHg
Regulated by
Ability of heart to pump blood out
Tendency of blood to flow into right atrium
Increase in venous return leads to increased RAP
Increased blood volume
Increased large vessel tone/peripheral venous pressures
Dilation of arterioles (decreases resistance & allows rapid flow to veins)
Decreased cardiac function
Decrease in RAP
Rapid heart rate
hemorrhage
Venous Return
Amount of blood returning to the heart through veins
Veins as a Blood Reservoir
~65% of blood is in veins
Blood can be transferred to arterial system when needed (to maintain BP)
Other reservoirs in body:
Liver, spleen, large abdominal veins, venous plexus
Vein Functions
Move blood toward heart
Blood reservoir
Control of cardiac output
Vein Structure
Compared to arteries:
Both have endothelium and fibrous tissue
Thinner wall
Less muscle
Valves that ensure one-way flow of blood
Pulse Pressure
Depends on stroke volume and compliance
Increased stroke volume increase pulse pressure
Increased compliance decrease pulse pressure
Mean Arterial Pressure (MAP)
MAP = Diastolic Pressure + 1/3(Pulse Pressure)
Dependent on cardiac output and total peripheral resistance
MAP = CO X TPR
Blood Pressure Measurement
BP is measured by auscultation
Blood supply to artery is cut off by inflating the cuff to above-systolic pressure
Pressure is released in cuff while listening for Korotkoff sounds (sound of blood being forced through constricted artery)
First sound is when pressure in cuff is equal to systolic pressure
Last sound is when pressure in cuff is equal to diastolic pressure
Pressures
Systolic – height of pressure pulse
Diastolic – lowest point of pressure pulse
Pulse Pressure = Systolic Pressure – Diastolic Pressure
Volume Pressure Relationships
Any given change in volume within the arterial tree results in larger increases in pressure than in veins
When veins are constricted, large quantities of blood are transferred to the heart, thereby increasing cardiac output
Vascular Compliance
Total quantity of blood that can be stored in a given portion of the circulation for each mmHg.
Compliance = Distensibility X Volume
Or
Increase in volume/ Increase in pressure
Vascular Distensibility
Fractional increase in volume for each mmHg rise in pressure
Vascular distensibility =
increase in volume/Increase in pressure X original volume
Autoregulation of Flow
Increase in pressure leads to increase in resistance
Decreases in pressure lead to decreased resistance
Determinants of Resistance
l – length
η – viscosity
r − radius
R = 8lη/πr4
Resistance
Opposition to flow
Can be calculated
R = ΔP/F
Blood Pressure
Force exerted by blood against vessel walls
Units: mm Hg or mm H2O (for very low pressures)
Laminar vs. Turbulent Flow
Laminar flow is silent
Turbulent flow causes murmurs
High velocities
Sharp turns
Uneven vessel surfaces
Narrowing of vessels
Murmurs are useful for diagnosis
Physics of Flow
Flow through a vessel is determined by
pressure difference between ends of vessel
ΔP or P1 - P2
Resistance of vessel
Flow (Q) = ΔP/R
Flow
Quantity of blood that passes a given point in a given amount of time
Generally described in ml/min
Overall flow is 5L/min (cardiac output)
Circulation Principles
Blood flow to tissues (local) is controlled by what specific tissues need.
Cardiac output is controlled by sum of all local tissue flows.
Blood pressure is controlled independently of flow.
Velocity of Blood Flow
Velocity is speed of flow Units?
Velocity = Blood Flow/Cross sectional Area
Venules/Veins
Return blood to heart under low pressure
Serve as a blood reservoir
Systemic capillaries
Site of exchange between plasma and tissues or lungs
Water
Solutes
Gases
Pulmonary capillaries
Site of O2 and CO2 exchange with alveoli
Arterioles
Control blood flow
Major site of resistance
Aorta/Arteries
Carry blood under high pressure
Different types
Elastic/conducting
Muscular/distributing
ANS Effects on HR (Parasympathetic)
Vagal nerve releases Ach at SA node
Ach binds to M2 muscarinic receptor
GPCR (Gi)
Causes hyperpolarization
Increased K+ permeability
Decreased transmission of impulses (conduction)
Decreases HR
And therefore CO
Not much effect on contractility
ANS Effects on HR (Sympathetic)
Releases NE at SA node and throughout heart
β1 receptors at SA node
GPCR (Gs)
Causes depolarization
Increases rate of conduction of impulse
β1 receptors throughout
Increases force of contraction
HR up to 180-200bpm
Increases SV
Through increased contractility
CO up to 15-20L/min
Frank-Starling Law
Increased EDV causes increased SV (all other factors remaining unchanged)
Increased EDV
Venous return
Sympathetic innervation of veins
Respiratory pump
Skeletal muscle pump
Heart will pump all blood that comes into it
Extra blood into it creates extra stretch
Extra stretch results in more force
Preload
Degree of myocardial stretch before contraction
Due to venous return
Frank-Starling Law
Afterload
Due to arterial pressure
Contractility
Due to Ca++-troponin binding (allowing crossbridges)
Ca++ levels
In SR
Entering from ECF
L-type Ca++ channel phosphorylation state
Phospholambin phosphorylation state
Increases Ca++-ATPase on SR
Sympathetic system
β1 receptors lead to increased cAMP, PKA, and phosphorylation of phospholambin
Cardiac Force
Muscle tension
Stroke Volume (SV)
amount of blood expelled from one ventricle during one cardiac cycle
SV = EDV-ESV
Cardiac Output (CO)
Amount of blood pumped by one ventricle in a given time period
CO = SV X HR
Cardiac cycle involves changes in
Electrical activity (ECG)
Volume
Pressure
Purkinje Fibers
Carry signal throughout ventricle walls
Rapid conduction, due to prevalence of gap junctions
AV Bundle/Bundle of His
Transfers signal from atria to ventricles
Branches into left and right branches that carry signal down septum to apex
AV Node
Transfers electrical signal from atria to ventricles
Delays impulse
This allows atria to fully contract before ventricles contract
AV Node delay: 0.09 sec
AV Bundle delay: 0.04 sec
Internodal Pathways
Carry signal from SA node to AV node
SA Node
Located in right atrium
Acts as pacemaker
Leaky Na+ channels
Membrane potential goes down to ~ -55mv
When membrane potential reaches -40 mV, slow Ca++ channels open, causing action potential
After 100-150 ms, Ca++ channels close and K+ channels open more, thus returning membrane potential to -55mV
Electrical Pathway through
the Heart
SA (sino-atrial node)
Internodal pathways
AV (atrio-ventricular node)
Bundle of His
L & R bundle branches
Purkinje fibers
Functions of the
Cardiovascular System
Transport
Needed things to the tissues
Nutrients
Oxygen
Enzymes
Waste products away from the tissues
Hormones for signaling
