cardiovascular physiology Flashcards
circulation
- pressure-driven bulk flow of blood through system of tubular vessels and other passages that brings the fluid to all parts of the body
- rapidly transports O2, CO2, nutrients, organic wastes, hormones, agents of immune system, heat, other commodities through body
circulatory system
- system of vessels/ other blood passages, and blood itself
cardiac muscle
- striated w intercalated disks so they contract at once
- regions of cell membrane which interdigitate
- all cells are excited in unison and so contract as a unit-> pumping action
- when one cell contracts, it pulls 2 along which spread mechanical events
- inherent rhythmicity (normally set by pacemaker)
- cardiac muscles are electrically refractory during the entire electrical event and for several msec after (prevents summation of contraction)
- heart muscles can’t go into tetni (allows ventricle to fill with blood between APs)
- much of Ca++ comes from exterior of cell rather than from SR
intercalated disks
join adjacent muscle cells (muscle fibers)
gap junction
- two cells that meet at intercalated disks are also joined to each other there by gap junctions (the cytoplasm of each cell is continuous with that of the other cell)
- at gap junction, AP in one cell is transmitted electrically to other cell (when one cardiac muscle cell generates AP and contracts, adjacent cells quickly generate APs and contract almost synchronously)
function of vascular system
1) supplies O2 and energy in form of glucose and fatty acids
2) picks up CO2 and metabolized things and takes them to liver
3) CVS carries hormones
4) CVS in renal filtration: based on BP
5) immune system
6) thermoregulatory
(in insects CVS doesn’t carry O2)
types of CVS
1) nones (ex: protosoans)
- cytoplasmic streaming provides same function that CVS does
- good diffusion with such a large surface/vol ratio
2) circulatory medium is SW or FW
3) gastrovascular cavity (combo of digestive and vascular system)
4) true vascular system: 2 types (open and closed)
open system
in most inverts
- heart-> arteries-> sinus cavities (open)
- returns to veins
- in this system, you can’t develop high BP
- common to have well-developed central heart
- blood leaves discrete vessels and bathes at least some nonvascular tissue directly
- often BP affected by body movement
closed system
- blood is always inside closed vessel
- birds, mammals, verts
- there is always at least a thin vessel wall separating the blood from other tissues
- heart-> arteries-> capillary beds-> veins-> heart
decapod crustacean heart
- each muscle cell is innervated and contracts when stimulated by nerve impulses
- cardiac ganglion is attached to inside of dorsal wall of heart
- a posterior neuron= pacemaker-> excited other posterior neurons-> activate anterior neurons-> muscle cells of heart contract in unison
invert heart
most inverts have a single chamber heart except mollusk with 2 chambers
insect heart
heart is a long tube in the dorsal portion of body (dorsal heart)
- blood goes forward in the dorsal side by a series of contractions
- when heart muscles relax, ligaments hold ostia open and blood goes in
- insects also have axillary (accessory) hearts in the base of wings, legs, antenni
** circulatory system is not very important-> low HR, low pressure**
pericardial membrane
ventral to the heart
ostia
hole in the side of heart where hemolymph enters when heart is relaxed
alary muscles
muscles or ligaments attached to dorsal surface and a membrane
crustacean heart
- compact, saclike, single-chambered structure
- open circulatory system
- fillinf through ostia and some through large veins
- beat initiated neurogenically
- all vessels that connect to heart are arteries
- arteries are valved at origin and leave heart in several direction
mollusc heart
- open systems with 2 chambered heart
cephalopods
- closed system-> greater BP but their systemic and brachial hearts are single chamber
- maintain rapid rates of blood flow through systemic circuit of relatively high resistance by maintaining high pressure in systemic arteries
advantages of two chambered heart
- heart must collect blood and pump out under a large pressure, so heart must be strong-> non-elastic-> have trouble filling
atrium
filling chamber with thin walls
- under some pressure atrium contracts and fills ventricle which can forcefully contract and emit blood
function of pericardial membrane
- in open system: collecting area for blood to go into heart
- in closed system: its a rigid structure-> when the heart contracts the pressure decreases in the pericardial space and this pulls blood in and into the heart during the relaxation of atrium
teleost heart
2 chamber heart, but functionally its really a 4 chamber connected in series
sinus venosus
thin wall, own contractile motions
- great veins empty into this
pacemaker (teleost)
in the floor on ventral portion of atrium
bulbous arteriosus
like an aorta
- doesn’t contract on its own, but is elastic
- consists of vascular smooth muscle and elastic tissue and does not contract in sequence with other heart chambers-> serves as elastic chamber that smoothes pressure oscillations and pressure reservoir between contractions
elasmobranch heart
3 chambers
- no sinus venous, has conus arteriosus instead of bulbous
- atrium and ventricles are same as teleost
conus arteriosus
includes cardiac muscle and contracts in sequence with ventricle, helping pump blood
compared to mammals of similar body size…
fish have smaller hearts and lower C.O.-> lower O2 demands, lower MR
lampreys
closed system comparable to teleost
hagfish
- open system (only vert with this)
- branchial heart: pumps blood out into cavity
- greater # of cardinal hearts int he head region
- also hepatic liver hears
- greater # of caudal hearts
circulation in fish
- blood pumped to gills to get oxygenated
- ventral aorta: very compliant (maintains smooth blood flow in the gills despite oscillations of heart contraction)
- input pressures for respiratory circulation are higher than those for systemic circulation because loses a lot of energy going through the capillary beds of gills
inactive vs active fish hearts
- species of fish that are relatively inactive/sluggish tend to have relatively small hearts, little development of myocardium and low C.O.
- athletic species have large hearts, great development of myocardium, high C.O
lungfish circulation
- circulatory system maintains separation between blood oxygenated and deoxygenated blood
- have lung structures (some with gills somewhat degenerated
- 3 chamber heart similar to amphibians (functionally a 4 chamber heart, partial septum in ventricle)
circulation in reptiles
- 3 chamber heart (except for crocodiles with 4 chambers)
- partially divided ventricle(partial septa-> pulmonary arteries receive deoxygenated blood; tissue that divides chambers are pressed so tightly against opposing structures during contraction as to create complete barriers to blood flow from one chamber to another-> temporally separate in systole)
- two completely separate atrial chambers present-> oxygenated blood enters left atrium, systemic venous blood enters right atrium from sinus venosus
crocodiles
complete septum
- vasoconstriction of pulmonary artery during diving
- ventricle is completely divided into 2 chambers by septum
- have 2 systemic aortas (from left and right ventricles)
- aortas re connects shortly after their exit from ventricles
- achieves selective distribution of oxygenated (to systemic circuit) blood and deoxygenated (to lungs) blood
bird and mammal circulation
- regular 4 chamber heart in parallel
- structurally theres a separate pulmonary and systemic vessels
- can have separate BP (but same volume)
- pulmonary pressure is lower than systemic
- cardiac output is the same on both sides
fetal circulation
- problem: a fetus cannot get rid of CO2 across the lungs
- in mammals: fetus obtains O2 from the circulation of the mother (via the placenta)
A) fetal circulation shows a bypass of pulmonary participation
B) Ductus Arteriosus (hole from pulmonary artery to aorta, shunting blood to systemic system)
C) Also a hole in septum between right and left atrium - foramen ovale: shunting blood from right to left heart and out to systemic circulation
these structural adaptations are normally eliminated shortly after birth
bird fetal circulation
- O2 taken up across egg shell
- O2 comes from chorioallantois-> mixes with systemic blood (deoxy)-> enters right atrium, shunts to left atrium, then to left ventricle, then to aorta
- skips pulmonary circulation via holes in interatrial septum
pacemaker
controls the pumping of heat (ie: controls and provides regular rhythmicity to cardiac muscle contractions)
- consists of cells which are capable of spontaneous activity
- these are modified muscle tissues in mammals which exert spontaneous electrical activity
- controlled by cardiovascular center in brain
Sine-Atrial Node (SA Node)
- in mammals is one specific pacemaker of the heart
- primary pacemaker because it had fastest rhythmicity
- stimulates whole heart to contract
- located at junction of the superior vena cava with the right atrium
- SA node fires an electrical impulse which is spread through the RA muscle to AV node
Atrium-Ventricular node (AV node)
- electrically connects the atrium with ventricle
- electrical impulse is spread into the endocardium via “bundle of His” and Purkenje System (spreads through muscle)
SA and AV node, bundle of His, and Purkenje system allow for…
spread of electrical current and causes the heart to contract as a whole
- depolarization of right atrial muscle enters AV node and traverses node slowly-> depolarization spreads down atrioventricular bundle, bundle branches, Purkinje fibers more rapidly
Purkinje fibers
large distinctive muscle cells that branch into ventricular myocardium on each side
spread of depolarization
SA node initiates heartbeat by spontaneously depolarizing-> spread rapidly through both atria-> atrial contraction-> spread into ventricular system is slower because it requires activation of conducting system-> spread through AV node is slow-> once activated, depolarization goes rapidly through conducting system into ventricles-> wholesale ventricular depolarization and contraction
electrical conduction
slow conduction through the AV node allows the atrium to contract before ventricles
conduction
process by which depolarization spreads through myogenic/vertebrate heart
systole
period of contraction
diastole
period of relaxation
sinus venous
- has the pacemaker in amphibians, reptiles, and elasmobranchs
pacemaker in teleost
pacemaker in floor of ventral surface of atrium
myogenic heart
- comtains pacemakers made of modified muscle tissues (ex: mammals)
- electrical impulse to contract originates in muscle cells or modified muscle cells
neurogenic heart
- pacemaker is modified neural tissue
- impulse to contract originates in neurons
- rhythmic depolarization responsible for initiating heartbeats originates in nervous tissue
pacemaker electrical events
- spontaneous activity of the pacemaker stems from an unstable resting potential (ie: slow depolarization that has nothing to do with outside influences)
pacemaker potentials
slow depolarization to a threshold level, then fires
- membrane potential of spontaneously active cell undergoes continuous upslope of depolarization between action potentials until it reaches threshold for AP
- repolarizing phase of AP restores membrane to hyperpolarized level that depolarization begins from
-Ca++ channels gradually become inactivated during plateau depol
- perm of K+ gradually inc (dec in K+ permeability-> buildup of positive charge inside)
- at threshold, cell fires with events similar to neurons (ie: inc Na+ permeability)
ramp depolarizations
pacemaker potentials determine rate of impulse generation by cell
heart muscle electrical events
- repolarization is very slow because the inc Na+ permeability is prolonged , also there’s a delay in the change in K+ perm, in Ca++ entry
- most electrical events are over by the time the heart becomes relative refractory
important things to remember about heart
- NO tetnizing event, little summation
- cardiac muscle is absolutely refractory during most of AP
EKG (electrocardiogram)
surface recording of AP myocardial fibers
P wave
depol (by SA node) of atrium
QRS wave
ventricle depol (by AV node)
S-T wave
ventricle repolarization
mechanical events of cardiac cycle
- atrial systole starts after P wave
- ventricular systole starts near the end of the R wave
- Ventricular systole ends just after the T wave
- contractions produce sequential changes in pressures and flows in the hear chambers and blood vessels
- in diastole: valves between atrium and ventricles are open, and aorta and pulmonary valves closed (blood flows into heart)
- contraction of atrium (systole) propels additional blood into ventricles
- Ventricular systole: Nisometric until aortic and pulmonary valves open-> inc pressure
- ejection: valves are open
ventricual ejection
when ventricular pressure rises high enough to exceed aortic pressure-> aortic valve opens-> blood gushes into aorta
- end of this phase= aortic pressure exceed ventricular pressure-> aortic valve shuts-> isovolumetric relaxation
when ventricular pressure drops below atrial pressure->
atrioventricular valve opens inward-> ventricular filling
pressure in right vs left ventricle
- left = 120 mmHg
- right= 25 mmHg
perfusion
the forced flow of blood through blood vessels
blood pressure
principle factor that drives blood to flow through vascular system
systolic pressure
highest pressure during contraction
diastolic pressure
lowest pressure reached during relaxation
control of circulation
1) in heart
2) in vascular system
cardiac output
volume of blood ejected (from ventricle) per unit time
CO= HR x SV
stroke volume
how much blood is pumped with each contraction
sympathetic vs parasympathetic
HR
- sympathetic= raise HR (inc depol), enhance force/speed of contraction
- parasympathetic = opposite
cardiac output for homeotherms
smaller animals have higher CO ( have higher HR and MR)
control of CO
- with control of HR or SV by pacemaker with innervation
- mammals in general will increase HR when CO needs to be inc
- almost all other verts will inc SV
cardiac output per until of body weight…
trend
tends to inc as body size dec-> small mammals meet their relatively high weight-specific demands for O2 transport by maintaining high weight specific rates of blood flow (high HR)
during exercise
- rate of O2 delivery can be inc by inc rate of blood flow or by extracting more O2 from each unit of volume of blood that circulates
- dec in total resistance of systemic vasculature during exercise
- vasodilation in vascular beds of active muscles is response for much of dec in resistance
how do they control HR or SV
- pacemaker system controls HR
- this system is innervated by parasympathetic and sympathetic fibers
pacemaker control
- innervation is major means of controlling circulation
- by vagus nerve- CIC-CVC complex
CVC
= cardiovascular center in medulla of brain
- one region of CVC is cardioinhibitory center (CIC)
CIC (Cardioinhibitory center)
- depressor of blood pressure
- site of dorsal motor nucleus of vagal nerves which run from medulla to heart
- depressor region, parasympathetic cholinergic, Ach
vagus nerve
- rt vagus innervates SA node
- Left vagus innervates AV node and heart muscle
- acts to dec heart rate
- fires tonically
- part of parasympathetic system
- cholinergic fibers of parasympathetic innervate SA and AV nodes (release Ach)
Ach
- acts to inhibit the pacemaker by inc K+ permeability (ie: making it more negative inside)
- this hyperpolarizes the membrane which reduces the rate of depolarization of the pacemaker potential
- may also dec Ca++ conductance
- freq of firing with Ach in vagal nerve dec
- more elongated pacemaker potential because of inc in K+ permeability
- with Ach (via muscarinic acceptors, cGMP) the pacemaker potentials are more graded (slows HR)
- reduces velocity of conductance from atrium to ventricle
- vagus also dec spread of conductance process to AV node (slower HR)
VAGUS IS PRIMARY CONTROL OF HEART
atropine
- blocks muscarinic receptors
- inc Hr from 70 to 150 beats/min
vasomotor center (VMC)
- another region of cardiovascular center
- a pressor area (sympathetic adrenergic, NE)
- part of sympathetic adrenergic fibers-> releasing Norepi
- innervates SA node, AV node, and other regions of heart
- NOT TONIC (ie: only happens during exercise, to inc HR and force contraction)
- also contains depressor region (sympathetic cholinergic, Ach)
- adrenergic fibers innervating smooth muscles are tonically active, if they’re cut, system will dilate
Norepi
- inc depol quickly to inc HR
- via beta adrenergic receptors and cAMP
- inc rate of decline in K+ perm
0 inc conductance in Ca++ channel making AP bigger and inc strength of each entraction
0 inc NA+ perm - mediated by cAMP
- makes pacemaker potentials more steep
- also affects heart muscle to make it relax
- relaxing-> inc distensibility
- affects starlings law: the more sarcomeres are pulled apart (ie: relaxed) they will contract with more force when they do contract
- NE inc conductane velocity through AV node
- inc conduction velocity to AV node so heart contracts more as a unit
- speed and force of contraction inc
- inc force of contraction also inc SV-> inc BP
- also reacts with adrenergic receptors in vascular smooth muscle and causes vasoconstriction to inc BP
caffeine
inhibits breakdown of cAMP, inc HR and force of contraction
beta blockers
dec HR
Epi and NE
inc rate and force of contraction and distensibility of ventricle
- released by adrenal medulla (sympathetic adrenergic fibers)
- inc HR and SV (also vasoconstriction)
what causes cardiovascular system changes
- sensory systems (baroreceptors, chemoreceptors, other regions of brain)
- hormonal control
- thoracoabdominal pump
- changes elicited via parasympathetic and sympathetic control of heart pacemaker
baroreceptors
- tonic pressure receptors
- monitor BP all thoughout vascular system
- feeds info back to CVC
inc BP(triggers responses to)->
dec CO-> dec resistance, dec HR, and force of contraction
- via inc vagal activity
- (will also dec ADH to dec BP)
chemoreceptors
what do they monitor
- monitor pH, pCO2, and pO2 of blood
- these are affected by respiration and heart rate
inc in pCO2->
dec O2-> dec pH-> inc HR-> inc ventilation
hormonal control
- generally of lesser importance
thyroid hormone
increases HR
thoracoabdominal pump
- during respiration-> inc HR and CO
- with a breath, you dec pressure in thoracic cavity
- this inc blood flow into heart and inc amount of blood coming to your heart from veins
stucture of CVS
- heart
- arteries, arterioles, metarterioles
- capillary beds
- venules, veins
microcirculatory bed
- networks of microscopically tiny blood vessels, small systemic organs, and tissues
- arteries, capillaries, venules
precapillary sphincter
- smooth muscle where the metarterioles join the cap beds
- they can close down and shut off blood to cap beds
- innervated by sympathetic adrenergic and cholinergic fibers (mostly innervating arterioles)
- participate in controlling blood flow to capillary beds
Arterio-Venous Anastomosis
- bypass
- arteries to veins directly
thorough fare channels
- bypass
- around the cap beds (metarterioles connected with venule via a capillary)
- cap bed exchanges gases and nutrients; if tissues have enough, they can be bypassed
- during heat conservation responses
vascular system control of circulation
- Hemodynamics: fluid flow in tube, mstly based on unreal situation
- flow of blood is mostly laminar (streamline) as opposed to turbulent (w/ eddies)
- with laminar flow: velocity is greatest in center, and zero at the wall
- parabolic velocity profile
Laminar flow
Outermost of concentric layers of liquid (the layer immediately next to wall) does not move at all and layers closer to center move faster and faster
Viscosity
- a lack of intrinsic slipperiness between layers of liquid moving at different linear velocities
- plasma is more viscous than water, while blood is a lot more than water
- viscosity of blood depends on diameter it flows through
- greater diameter, greater viscosity
- in capillaries, viscosity of whole blood is like viscosity of plasma
Primary control of vascular system
Through smooth muscle innervation
- contraction of SM-> Dec diameter of vessel, inc resistance
Elasticity
High elasticity allows the vessels to snap back and leads to even blood flow
atrial system
- elastic
- less compliant and acts as pressure reservoir
- this maintains even blood flow despite pulses generated by heart contractions
- generally arteries have thick walls and more smooth muscles (except pulmonary artery is very distensible)
- smaller arteries and arterioles are resistance vessels, principle site of peripheral resistance
arterioles
- walls of smooth muscle and connective tissue-> responsible for vasomotor control of blood distribution
- dec radius of lumen= vasoconstriction
- inc= vasodilation
- controlled by sympathetic autonomic nervous system
arteries
- have thick walls that are heavily invested with smooth muscle and with elastic and collagenous connective tissue
- can convey blood under considerable pressure from heart to peripheral parts of circulatory system
venous system
- very compliant
- small changes in pressure can produce great changes in volume
- less elastic: acts as blood reservoir
- great change in volume has little effect on pressure
- low pressure system
- overall muscular contraction is important
local controls
ensures that the most active tissues have the most dilated vessels, greatest blood flow
dilators
cause SM to relax and dilate blood vessels, not via innervation
- inc CO2 in muscle, dec O2, dec pH, inc heat
- also K+, lactic acid
- histamine: released by injured tissues
- kinins: vasodilating peptides
- nitric oxide
local vasoconstrictors
- serotonin: released from platelets in injured area
- dec temp
- endothelins: vasoconstricting peptides released from endothelium
widespread circulating vasoconstrictors
- hormones
- norepi: general vasoconstriction
- Epi: mostly vasoconstriction, but vasodilates vessels in skeletal muscles
- Angiotensin II: very potent vasoconstrictor
- Arginine vasotocin
- in general, circulatory vasoconstrictors aren’t the major control, neural innervation more important
Sympathetic adrenergic system
causes vasoconstriction
sympathetic cholinergic system
causes dilation
innervation
- on arterial side, inc vasoconstriction-> inc BP
- on venous side, inc constriction-> inc flow to heart and inc arterial blood flow
adrenergic fibers
- cardiovascular center (CVC) controls adrenergic fibers
2 sets of fibers come down from VMC
1) Pressor region: NE, Tonic to SM
2) Depressor region: Ach, not tonic
Pressor region
inc firing of adrenergic fibers-> vasoconstriction
- innervates vessels in all parts of body, metarterioles, precap sphincters
depressor region
primarily inhibits the firing of adrenergic fibers
- sympathetic cholinergic fibers releasing Ach
- not tonic
- dec rate of tonic discharge of vasoconstricting nerves
sympathetic vasodilator system
- originates in cerebral cortex
- cholinergic which travels with sympathetic nerves
- innervates resistant vessels in skeletal muscles
- causes dilation, brough into play during exercise
- no tonic
- has input into endpt-> vasodilation
- may also synapse on end of adrenergic fiber to dec freq of firing-> dilation
giraffes cardiovascular adaptations
- BP in aorta must be very high to supply the carotids
- 4 chamber heart: can have 2 diff BP
- right ventricle: supplies normal BP to heart
- left ventricle: supplies aorta with great BP
- left ventricle is hypertrophies
hypertrophied
more muscular
- hytrophied ventricle is secondary, yet needed to pump more blood (heart pumping against high pressure)
what produces high BP
1) Cardiac output
2) vascular system
3) both
- CO in giraffes is normal on weight specific basis
- vascular system controls high BP here
- high amount of constriction throughout body in capillary beds (ie: close down more capillary beds to inc pressure)
why doesn’t giraffe blow brains out
- quick change to dec cardiac output; and dec vascular resistance
- pronounced vasodilation of vessels in lower body when head is lowered
- pronounced vasoconstriction of vessels in lower body when head is raised (also prevents pooling of blood in lower body)
diving animals
- adaptations to conserve O2 and make the most efficient use of limited amount of O2
- ex: seals
- while diving-> dec HR (bradycardia)
- with dec HR, you might expect a dec BP; but aortic BP is almost normal
- musst be great amount of vasoconstriction; great vascular resistance-> great peripheral vasoconstriction
- all shut down, except to vital organs (only circulation to heart-lungs-heart-brain is maintained)
- tissues go anaerobic
diving reflex
- common to all mammals, birds, and reptiles
- dec HR, inc vascular constriction, dec CP
- vagal reflex
- true reflex response controlled by sensory receptors on face (just needs to be wet)
- humans HR dec from 70-40 beats/min
lung inflation
- tends to supress cardioinhibition and peripheral vasoconstriction caused by chemoreceptors
- nondiving-> inc CO2-> inc HR and vasodilation
- but when diving-> vasoconstriction and dec HR4
