Definitions: Cardiovascular System Flashcards
Right heart
volume pump
delivers high volumes of blood at low pressures
Pulmonary vessels
function in blood - gas exchange an serve as volume reservoirs
left heart
pressure pump
the energy source for the circulatory system
Elastic arteries
their elastic behavior allows them to serve as a “surge pump”.
energy is stored in the elastic fibers during the contraction phase (systole) and is released during the relaxation phase (diastole)
Muscular arteries
function as low resistance conduits that rapidly deliver blood to the tissues
Arterioles
collectively termed “resistance vessels”
serve as variable resistors that regulate the flow of blood into capillary beds
range in diameter from 5-100um
give rise to capillaries directly or metarterioles
Capillaries
one cell layer separates blood from tissue space
site of nutrient and waste exchange
contain no connective tissue or smooth muscle
Venous vessels
serve as a volume reservoir
these vessels function in both the storage and mobilization of blood
Pulmonary circulation
blood flow through the lungs
Systemic circulation
blood flow through all organs of the body except the lungs
Cardiovascular circuit
pumps in series, resistance circuits in parallel
the CO of the right heart must equal the CO of the left heart
Phase 0
rapid upstroke, depolarization (QRS)
rapid depolarization due to increased gNa (fast Na channels open)
K+ conductance declines
Phase 1
initial rapid repolarization (QRS)
repolarization due to the “h” gates closing the fast Na channels
Phase 2
plateau (ST segment)
caused by slow Na+-Ca++ influx channel
K+ conductance continues to decrease
Phase 3
repolarization (T wave)
decline ini Na+-Ca++ slow channel and a restoration of the normal K+ efflux
Phase 4
resting membrane potential (RMP) isoelectric
NaO > Nai
CaO > Cai
KO > Ki
gNa+ and gCa++ are low - gK+ is high
refractory periods
periods of reduced excitability
Absolute refractory period (ARP)
interval from beginning of the AP to a point in phase 3 when the membrane potential reaches approximately -50 mV
no stimulus can elicit an AP
extends through the maximum tension development of the muscle
Tetanus
repetitive stimuli at increasing frequency
Relative Refractory Period (RRP)
AP can be elicited but would require a greater than normal stimulus
resultant AP would have lower than normal amplitude and a reduced rate of ride due to the fast Na+ channels not having been completely reset
Supernormal Period (SNP)
a stimulus of less than normal magnitude can bring the membrane to threshold and initiate AP
APs generated during this time propagate slowly
Sinoatrial (SA) node
ordinarily displays the highest order of rhythmicity
consists of a bundle of specialized neuromuscular tissue
cells here have unstable RMP (responsible for Pacemaker activity)
region with the most rapid rate of decay of K+ conductance
unstable resting membrane potential in SA nodal cells
prepotential
pacemaker potential
diastolic depolarization
Sympathetic
increases conduction velocity
Parasympathetic
decreases conduction velocity in AV node
Reentry
occurs when an excitation wave reexcites some region through which it has recently passed
reentry circuits can be either random or ordered
Must have: unidirectional block and the effective refractory period of the reentered region must be shorter than the propagation time around the loop
Ca++ induced Ca++ release
depolarization of the sarcolemma (SL) causes influx of Ca++ through voltage sensitive Ca++ channels → Ca++ entering the cell binds to the Ca++ release channel located in the membrane of the SR, thereby activating channel opening
Charge movement coupled Ca++ release
activation of the Ca++ channel by membrane depolarization is associated with concomitant activation of charge movement → this activation is transmitted via a spanning protein to the Ca++ release channel, thereby, initiating Ca++ release (the spanning protein could be a subunit of the Ca++ channel or an extrinsic protein)
Inositol triphosphate (IP3) induced Ca++ release
depolarization activates voltage sensitive phospholipase C (PLC) resulting in the conversion of PIP2 to IP3 → IP3 binds to the Ca++ release channel and activates channel opening
Preload
tension or stretch in the wall of the LV just before the onset of contraction
determined by EDV
Afterload
tension nor stretch in the wall of the LV just before the aortic valve opens
related to aortic pressure
Frank-Starling Relationship
relates changes in initial myocardial fiber length (i.e. preload) to force or pressure development by the ventricle
describes length dependent changes (i.e. preload) in cardiac performance
Contractility
the performance of the heart at a given preload and afterload
a length independent change in cardiac performance
Atrial Systole
first phase of the cardiac cycle
LV pressure begins to increase
Mitral valve closes at the end of phase
4th heart sound would be heard
P-Q
Isovolumic contraction
phase 2 of the cardiac cycle
Aortic valve opens at the end of phase
Aortic pressure begins to rise
1st heart sound is heard here
R-S
Rapid ejection
3rd phase of cardiac cycle
Aortic pressure and LV pressure begin to peak
LA pressure starts to rise gradually
Aortic blood flow rises and peaks
Ventricular volume decreases
Reduced ejection
4th phase of the cardiac cycle
Aortic valve closes at end
LV pressure and Aortic pressure decrease
LA pressure is increasing
aortic blood flow decreasing
T wave
Isovolumic relaxation
5th phase of the cardiac cycle
Aortic valve closes at beginning
Aortic pressure somewhat plateaus
LV pressure significantly decreases
Mitral valve opens at end
LA pressure peaks
heart sound 2 is heard
Rapid Ventricular Filling
Aortic presure decreases
LA and LV pressure begin to plateau
Aortic blood flow plateaus
ventricular volume increases
third heart sound heard
Reduced ventricular filling - diastasis
Ventricular volume peaks
Aortic, LV, and LA pressure bottom out
aortic blood flow is 0
P wave starts at end
Cardiac Cycle Loop
start at lower left hand corner
read to the right and around
Cardiac Cycle: Mitral valve opens
dot at lower left hand corner
occurs when LV pressure drops below that of the left atrium
Cardiac Cycle: rapid filling
dip between first and second point
blood rushes into the LV as it continues to relax → volume increases, however, the pressure decreases during this phase since the ventricle is actively relaxing
Cardiac Cycle:third heart sound
recorded near the end of the rapid filling phase when the ventricle reaches its elastic limit
Cardiac Cycle: slow (reduced) filling phase
ventricle continues to fill due to continuous venous return - the slow filling phase contributes ¼ to ⅓ of LVEDV → ventricular pressure rises slightly during this phase
Cardiac Cycle: atrial contraction
final contribution of blood to LVEDV prior to isovolumic contraction
Cardiac Cycle: mitral valve closes
as ventricular pressure begins to increase the mitral valve snaps closes, recording the first heart sound
lower right hand point
Cardiac Cycle: isovolumic contraction
right vertical bar
steep rise in ventricular pressure → ventricular volume remains constant until ventricular pressure exceeds aortic pressure, forcing the aortic valve open → the opening of the aortic valve ends isovolumic contraction
Cardiac Cycle: systolic ejection (rapid and reduced ejection)
top curve
during this phase ventricular and aortic pressures rise and fall together because the aortic valve provides an open communication between the two chambers
Cardiac Cycle: aortic valve closes
near the end of systolic ejection both ventricular volume and pressure are decreasing → when ventricular pressure drops below aortic pressure the aortic valve closes creating the 2nd heart sound →The closure of the aortic valve marks the end of systole (end systolic pressure point)
Cardiac Cycle: isovolumic relaxation
left vertical line
during this phase there is a steep drop in ventricular pressure with no change in ventricular volume
Pressure
force in a fluid system
expressed as force/unit are → dynes/cm2 → mmHg in US
one of the principle determinants of the rate of flow
Hydrostatic pressure
the pressure produced by the height of a column of a liquid
important when considering the effect of postural changes on the cardiovascular system
Transmural pressure
pressure across the wall of a blood vessel
essentially equal in head, heart, and foot when lying down
when standing: decreases above heart, increases below heart
Compliance
The pressure change which occurs in the organ with a given volume change is indicative of organ compliance
compliance of an organ or vessel can be altered by changing the mechanical properties of the walls (ΔV/ΔP)
reduced by aging and atherosclerosis
Poiseuille’s Law
Flow is non-pulsatile
Flow is laminar
Fluid is a Newtonian Fluid
Length
flow is inversely proportional to the length of the tube
Radius
flow varies directly proportional to the fourth power of the radius
doubling the radius of a tube results in a 16-fold increases in flow (24)
Viscosity
the ratio of sheer stress to shear rate of the fluid
the internal friction of a fluid which opposes the separation of its laminae → a force must be applied to overcome viscosity in order to move one layer of fluid past another (laminar flow)
Laminar flow
as blood flows through the vasculature the fluid appears to flow in discrete cylindrical lamina
Total peripheral resistance (TPR)
the resistance of the entire systemic circulatory circuit
Autoregulation
intrinsic tendency of an organ to maintain a constant blood flow despite changes in arterial perfusion pressure
exists over limited range of pressures beyond which flow changes with perfusion pressure
Active hyperemia
blood flow increases within seconds of the beginning of muscular exercise and returns to control values following completion of exercise
Reactive Hyperemia
increased blood flow which occurs following the interruption of blood flow to a tissue
Endothelium Relaxing Factor (EDRF)
NO
produced in endothelial cells
relaxes muscle cells
Endothelial Sheer Stress (ESS)
flow induced modulation of blood vessel diameter
vessel diameter increases as flow is progressively increased in a vascular segment with intact endothelium
Vasodilators
dilate vessels
arachidonic acid metabolites → PGI2, PGE2, PGD2
Atrial Natriuretic Factor (ANF)
Adenosine
Nitric Oxide (NO) → EDHF
Histamine
Vasoconstrictors
constrict vessels
arachidonic acid metabolites → TxA2, PGF2a, LTC4, LTD4, LTE4
angiotensin II
arginine vasopressin
endothelin
adrenomedullary hormones (epinephrine, norepinephrine)
Arachidonic acid (eicosanoids)
released from membrane phospholipids → metabolized by cyclooxygenase or lipoxygenase → form prostaglandins or leukotrienes → produces vasoconstrictors (TXA2, PGF2ac) and dilators (PGD2, PGE2, PGI2)
Angiotensin II
Renin cleaves angiotensinogen → forms angiotensin I → Kininase II converts angiotensin I to angiotensin II (vasoconstrictor)→ binds cells in adrenal cortex and regulates release of aldosterone (promotes sodium reabsorption)
Bradykinin
vasodilation and increased capillary permeability
involved in vascular responses to tissue injury and immune reactions
produced near sweat glands
Atrial Natriuretic Factor (ANF)
aka atrial natriuretic peptide (ANP)
released when atria or ventricles are significantly stressed
promotes sodium excretion
vasodilator
Adensosine
reduced oxygen tension causes hydrolysis of ATP to ADP and AMP → enzyme 5’- nucleotidase (is phosphorylated) catalyzes hydrolysis of AMP to adenosine → adenosine diffuses into the interstitial space → dilates arterioles → increases blood flow and oxygen delivery → adenosine reenters cell → rephosphorylated to AMP by adenosine kinase
Vasopressin
released from posterior pituitary in responce to increased plasma osmolarity or decreasing blood volume/pressure
promotes water reabsorption
vasoconstrictor
infusions increas TPR
Histamine
release is associated with antigen-antibody reaction in allergic and immune response
activated mast cells and circulating basophils release histamine → causes local vasodilation and increased vascular permeability
Baroreceptor Reflex
keeps BP at a constant level
regulates pressure from a certain set point
only good at preventing abrupt changes in BP
Metarterioles
branch from arterioles and give rise to capillaries
can serve as bypass channels to the venules
Nutrient Flow
blood flows through the capillaries which provides for exchange of nutrients and metabolites
Non-nutrient flow (shunt)
the blood flow bypasses the capillaries and passes directly from arterioles to venules
Precapillary sphincters
regulate blood flow through the capillary
smooth muscle that constricts and dilates based on metabolic activity
Flow limited diffusion
some substances aren’t allowed to leave the capillary, others are
concentration gradient in capillary limits how much of a certain substance can get to a cell
Diffusion limited diffusion (transport)
diffusion is limited by the size of a molecule or the diffusion distance between the capillary and the parenchymal cell
Ultrafiltration
fluid movement
Hydrostatic Pressure
arteriolar blood pressure
principle force favoring filtering across the capillary wall
Filtration
occurs wen the algebraic sum is positive
from capillary to interstitial space
Reabsorption
occurs when the value is negative
movement of fluid from interstitial space to capillary
Edema
abnormal increase in the volume of interstitial fluid in a tissue or organ
swelling
