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139 Cards in this Set

  • Front
  • Back
As heart rate increases, what happens to contractilty and why
contractility increases, b/c inc HR means more AP's, which means more Ca influx, and more contractions.
Why must total systemic blood flow = cardiac output
b/c once blood leaves ventricle (CO), the organ systems are in paralell
Which blood vessels are under the highest pressure
arteries (b/c they receive blood directly from the heart)
Volume of Blood which moves through a vessel per unit of time
Blood flow V/time
Force per unit area of blood
Blood pressure
continuity equation
Flow = velocity * area
As you move distally away from the heart, what happens to cross sectional area of vessels and blodd velocity
Since CA increases, velocity decreases (V=F/A)
Why is blood flow in vessels the same
because they are in series
Where does Vmax occur
at the center of the blood vessel
Where is velocity O
near the wall of the blood vessel
What predicts whether flow will be laminar or turbulant
Reynolds Number
Laminar flow
Turbulant flow
NR> 3000
Reynolds Number
R = ρ * v * D/η
n = viscosity
D = diameter
v = velocity of blood
what does Pouseuille's eqn describe? what is it?
Blood Flow
F = ∏ *r^4*∆P/8Lη
(pies r 4 p's)
what is the pressure difference in the poseuille eqn attributed to
pressure diff produced by the contraction of the heart
According to Poseuille eqn, if delta P is zero, what is flow
simplified Poseuille eqn
F = delta P/R
Mean Blood Pressure
Right atrial pressure is close to 0, so we can use pressure in the proximal aorta. MBP = CO * TPR
Organs are in paralell to each other...
Pressure is the same
Flow & Resistance are not =
Distensibility of a vessel, formula
Compliance = Vol/P
Higher the compliance, the more volume it can hold
If compliance decreases (stiffer), what happens if volume increases
an increase in volume will produce a larger increase in pressure than it did before
How much higher is outside [Ca] than inside
10,000 higher outside
Steps of Cardiac Muscle Contraction
1) triggered by electrical signals
2)volted L type channels open
3)Ca that entered with L channels, bind to RYR receptors in the SR
4) Ca released from both bind to troponin
5)Crossbridge cycle
6) relaxation (channels close and Ca is pumped back out)
Is relaxation of cardiac myocytes active or passive
active, uses ATP
How is Ca pumped back out of cell after contraction is done
SERCA uses ATP to pump Ca back into SR
What normally inhibits SERCA from pumping Ca out of cell and back into SR
protein phospholamban
what are 2 ways Ca can leave the cell after contraction
Active transport with SERCA and the Na-Ca exchanger(NCX)that uses
What are 2 ways to regulate force
1) increase length
2) vary intracellular Ca via sympathetic NS
Starlings Law
Length Tension relationship (increase length, increase force)
Calcium concentration is a major determinant of the force of cardiac contraction
Force increases to maximum as [Ca] increases until 100% of max force is reached
How is intracellular [Ca] regulated
by sympathetic NS and the NT norepinephrine
where does cardiac depolarization initiate
SA node
what is the order of depolarization through the heart
SA node
AV node
Which part of the heart has the longest refractory period (conducts AP slowest)
AV node
Pacemaker of the heart
SA node
Parasympathetic (ACh) effects on phase 4 of the AP
Phase 4 is depolarization
ACh increases the duration of phase 4 depolarization and reduces heart rate.
Sympathetic (norepinephrine) effects on phase 4 of the AP
decreases the duration of phase 4 depolarization and increases heart rate
Helps to ensure that the electrical activation of all portions of the ventricles are synchonrous
His Purkinje (fastest conduction velocity in the heart)
Occurs during the P wave
Atrial depolarization
(right atrium at front of P wave and left atrium at hte end of P wave)
Occurs during the PR interval
Depolarization of Atrial, AV node, Bundle of His, and purkinje
PR Interval
time it takes for the AP to spread from the artia to the AV node
QRS Complex
depolarization of ventricles
flat line after T line
all cells of hte heart are resting
Abnormalaity shown by a shakey area before QRS - no P wave
Atrial fibrillation (complete loss of synchronous of excitation adn resting phases)
Abnormality shown by a EKG that looks like a scribbled line
ventricular fibrilation (ventricle quivers and heart needs shocked to reset to threshold)
cycle length formula
Cycle Length = 60/HR
Cycle length lasts from one AP to the next
contraction and ejection of blood
resting and filling of blood
shorter part of the cardiac cycle
Why is blood flow through left and ride side equal
they are in series with each other
Side of the heart where pressure is higher
left side is 4-5 time higher; so if there is a hole blood flows left to right
Arrangement of systemic organs
paralell: organs receive blood of identical composition
The flow through systemic organs can be controlled independently of other organs because...
all organs are in paralell
Organs that have blood flow in excess of what they need for basic metabolism needs
blood conditioning organs (skin, kidneys, lungs)
they get blood solely for their metabolic needs (not excess)
brain, heart and muscle (these dont tolerate blood fluctuations as well as blood conditioning organs)
Cardiac output for adequate blood supply
Flow equation
F = Change in P/Resistance
Only ways to change blood flow through an organ
Pressure difference and vascular resistance(most common)
F = ΔP/R
Why does blood flow through organs
b/c the pressure difference exists between the arteries supplying it and the veins draining it
Since change in pressure is the same in organs , how is cardiac output distributed amoung organs
based on their resistances to flow
is blood flow through organs passive or active
passive (occurs only because venous pressure is kept lower then arterial pressure)
Ventricle pressure drops below aorta pressure, why and what happens then?
Ventricle contracts, inc pressue. Blood will be forced from high P to low P, out of ventricle through aorta.
Ventricle pressure falls below atrium pressure, why and what happens then?
ventricle relaxes, pressure falls. The Av valve can open and the ventricle can fill with blood from atrium.
What is the purpose of gap junctions in the heart
AP can conduct from one cell to the next via gap junctions that conecct all heart cells as one unit
initites the AP and contains slow conducting cells
SA node - pacemaker cell
Assures all cells contract at the same time
purkinje fibers
what happens if cardiac filling increases
volume ejected also increases (Starlings law: inc EDV inc SV)
sympathetic nerve fibers effects (norepinephrine)
inc HR
inc AP conduction rate
inc force of contraction
inc rate of contraction/relax
parasympathetic nerve fibers effects (acetylcholine)
interacts with muscarinic receptors to:
dec HR
dec AP conduction velocity
dec contraction of atrial cells
what is an increase in parasymp activity usually coupled with
sympathetic activity
Main ions in cardiac cell membrane potential
Ca, Na (high outside)
K (high inside)
When mitral and aortic valves are closed
Since volume is not changing, Isovolumic (IVC), pressure is rising though due to contraction
SV equation
volume that fills the ventricle
Volume that is left after ejection
Blood pressure eqn
Ejection fraction
final closing of valves is due to what
small retrograde of blood flow
S1 - what does it mark
start of systole due to the closing of AV valve, which causes vibrations of cardiac structures
S2 - what does it mark
closure of aortic valve, end of systole
ventricular preload
(resting) end diastolic volume, because it is the resting length of hte cardiac muslce fibers
Most important regulators of SA node
para and sympa b/c they have immediate effects
Tension - Muscle Length relationship
As muslce length is increased, force created is increased
Influences on Stroke Volume (5)
1) HR
2) Preload - EDV
3) Afterload - total arterial pressure
4) Contractility
5) Diastolic ventricular compliance
low compliance = stiff heart
Force or pressure that the ventricle must overcome to eject the stroke volume
Relationship between HR and tme for ventricular filling
If HR is increased(arrythimia), the ventricular filling can be reduced so much that SV, CO and blood pressure decrease
which are more distensible, veins or arteries
where is most blood of the body
veins of hte systemic organs
does gravity affect venous return
yes, b/c CV system is composed of distensible vessels not rigid tubes
Distention of veins due to gravity can cause:
pooling of blood in the lebs, decrease n venous return to the heart
What assist in venous return and overcome gravity
closing of venous valves decreases weight of fluid column, contraction of muscle funcations as a pump
Why does average venous return equal cardiac output
b/c the CV system is a closed circuit
what is the realtionship between CVP (central venous pressure) and CO (cardiac output)
CO increases, CVP decreases
(as we increase CO, we are taking blood out of the veins)
CVP increases, CO increases
what arises when a Starling curve and a vascualar fxn curve are plotted together?
intersection point is an equillibrium point, the CVP
what flows are equal at the intersection point of a cardiac adn vascular function curve
total arterial flow, total venous flow, total system capillary flow
List the arterial system in order of decreasing pressure
heart pump, arteries, arterioles, capillaries, venules, veins
Pulse pressure
PP = Ps-Pd
Mean Arterial(Blood) Pressure
Formula and definition
pressure in the large arteries over a cardiac cycle
MBP = Pd + 1/3 (PP)
How is BP controlled
Baroreceptor reflex
Effects of the baroreceptor reflex
the increases in arterial pressure lead to an immediate decrease in sympathetic nerve activity and a simultaneous increase in parasympathetic nerve activity (vice versa)
What initiates the baroreceptor reflex
pressure sensing by stretch sensitive baroreceptor nerve endings in the walls of arteries
After initiating pressure sensitive receptors what happesn
neural centers in the brain adjust autonomic nerve activty in response to info received from baroreceptors
Components of the baroreceptor reflex
1) sensory receptors (arterial baroreceptor)
2) Afferent pathways (to CNS)
3) CNS - sends signals to para or sympa
Where are the afferent pathways of hte baroreceptor reflex found
walls of the aortic arch (aortic receptors)
carotid sinus (either side of the neck)
what does increased stretch cause
increased AP generation by arterial baroreceptors (sent to parasympathetic in this case; GABA inhibits the sending of AP to the sympathetic)
What can pass through microvessels, what cant
can: small molecules and water (K, Na, Cl); lipids
cant: proteins
Why are microvessels efficient exchange sites
thin walls and large surface area
Name 4 mechanisms of blood flow
neural, humoral, metabollic, myogenic
Neural mechanism of blood flow
sympathetic vasoconstrictor nerves release norepinephrine, which increases tone
Humoral mechanism of blood flow
histamine and bradykinin cause dilation of arterioles and constriction of venules
Metabolic (local) blood flow control
oxygen delivery to a tissue can be matched to oxygen consumption by altering the resistance of the arterioles, which in turn alters blood flow
Myogenic mechanism of blood flow control
when vascular smooth muscle is stretched, it contracts. So when arterial pressure is increased, the walls are stretched and then contract to maintain constant flow in teh face of increased pressure.
Fluid Movement ini microvessels eqn
FM = k[(Pc + ∏i)-(Pi + ∏p)]
If Fluid movement in microvessel is 0
no net flow
Fluid movement is positive
favors filtration
Fluid movement is negative
Favors absorption
What is diffusion across microvessels calcualted by
Ficks law
J = -P*A*(Cin-Cout)
P is the permeability
What happens if large particles get into interstitial space
filtration forces will exceed reabsorption (edema results)
Function of plasma proteins (albumin)
osmotic pressure rises b/c plasma has a higher protein concentration than does interstitial fluid
why does the left coronary artery have higher flow
left ventricle has more tissue mass
Why is capillary density higher in the heart than skeletal muscle
b/c cardiac cells are smaller in diameter (more room for capillaries)
Why are myocardial capillaries more effective than skeletal muscle cells
the distance hte molecules must diffuse is smaller
Coronary Blood flow
What determines coronary blood flow
Blood pressure, CVR and mainly myocardial compression, metabolic control, mass
metabolic control of coronary blood flow
exercise and adenosine (product of metabolism that results in vasodilation and inc blood flow)
Myocardial ischemia
oxygen supply does not meet demand
What does hypoxia increase the production of
adenosine (vasodilator)
what change does ischemia cause in the EKG
change in ST segment
Signs of ischemia
change in ST segement and angina
Treatment of ischemia
to increase blood flow (thrombolytic agents, baloon angioplasty) or by decreasing myocardial energy consumption(dec HR, Dec work or inc efficiency)
most imp vasodilator that controls cerebral vascular resistance
CO2, adn inc in CO2 causes vasodilation of cerebral arteries, which results in inc blood flow to remove excess CO2
Why dont many circulating vasoactive substances affect cerebral circulation
b/c their large molecule size cant cross the blood brain barrier
Cushing response
-intercranial pressure inc
-compression of arteries
- CO2 inc b/s it is not adeequately removed
- medulla chemoreceptors respond and cause intense vasoconstriction (inc BP, dec HR)
2 types of exercise
dynamic (aerobic)
static (anerobic)
why is it important to warm up
to give CV and respiratory system to catch up to Oxygen demand (O2 debt)
what is payback
O2 consumption stays high until your body temp goes back down
normal O2 consumption
3.5 mL O2/min/kg