Cardiovascular Physiology Flashcards
Site of highest resistance in the cardiovascular system
arterioles
regulation of arterioles
ANS
Largest total cross-sectional and surface area
Capillaries
Contain the highest proportion of the blood
Veins
Velocity of blood flow equation
v = Q/A
Equation for Cardiac Output
Cardiac Output = (MAP-RAP)/(TPR)
MAP is mean arterial pressure
RAP is right atrial pressure
TPR is total peripheral resistance
CO = SV*HR
Poiseuille’s Equation
factors that change resistance of blood vessels
R = (8nl)/(pi*r^4)
n is viscosity of blood
l is length of blood vessel
Parallel resistance
1/R + 1/R + 1/R
when an artery is added in parallel, the total resistance decreases
Series Resistance
R = R+R+R
arrangement of BVs in an organ, total resistance is the sum of resistances
pressure decreases as it flows though a series of BV
Reynolds Number
predicts whether blood flow will be laminar or turbulent
Turbulent blood
high reynolds number, can cause bruits
decreased blood viscosity like anemia, increased blood velocity (narrowing of BV)
Capacitance
compliance, the distensibility of blood vessel
inversely related to elastance
C = (vol)/(pressure)
Mean Pressures in Systemic Circulation
Aorta - 100mmHg
Arterioles - 50mmHg
Capillaries - 20mmHg
Vena Cava - 4mmHg
Arterial Pressure
Systolic pressure is highest pressure
Diastolic pressure is lowest pressure
Most important determinant of pulse pressure
Stroke Volume
Eqtn for mean arterial pressure
DBP + 1/3 of pulse pressure
DBP + 1/3 (SBP-DBP)
Pulmonary Wedge Pressure
Estimates left atrial pressure
P wave
arterial depolarization
Decreased PR interval
increased conduction velocity through AV node (can be from sympathetic NS)
Increased PR interval
decreased conduction velocity through AV node (parasympathetic NS or heart block)
QRS complex
depolarization of the ventricles
QT interval
Beginning of Q wave to end of T wave
entire period of depolarization and repolarization of ventricles
PR interval
Initial depolarization of ventricle
beginning of P wave to beginning of Q wave
ST segment
isoelectric, period when ventricles are depolarized
from end of S wave to beginning of T wave
T wave
ventricular repolarization
Cardiac AP (Vent, Atria, Purkinje) - Phase 0
upstroke, from transient increase in Na conductance
Cardiac AP (Vent, Atria, Purkinje) - Phase 1
initial repolarization from outward current because of movement of K ions
Cardiac AP (Vent, Atria, Purkinje) - Phase 2
plateau of the AP
caused by transient increase in calcium conductance
inward calcium current by an increase in K conductance
Cardiac AP (Vent, Atria, Purkinje) - Phase 3
repolarization, K conductance predominates - large outward K current Ik
Cardiac AP (Vent, Atria, Purkinje) - Phase 4
RMP, period during which inward and outward currents Ik1 are equal
SA Node - Phase 0
upstroke AP, caused by increase in Calcium conductance
- increase causes an inward calcium current
SA Node - Phase 3
repolarization caused by an increase in K conductance - outward K current
SA Node - Phase 4
slow depolarization - inward Na current called If
Upstroke of AV node
Inward calcium current (like the SA Node)
Time required for excitation to spread throughout the cardiac tissue
Conduction Velocity
fastest conduction velocity in the heart
Purkinje system, slowest is AV node (PR interval)
Ability of cardiac cells to initiate APs in response to inward, depolarizing current
excitability
Effective refractory period
conducted AP cannot be elicited (cardiac)
decreases HR by decreasing the firing rate of SA node
Negative Chronotropic Effect
increases HR by increasing the firing rate of SA node
Positive Chronotropic Effect sympathetic effect (NE on B1)
decreases conduction velocity through the AV node, slowing the conduction of APs from atria to the ventricles
Negative dromotropic effect - increases PR interval
increases conduction velocity through the AV node, speeding the conduction of APs from atria to ventricles
Positive dromotropic effect - decreases PR interval
sympatehtic effect
decreases HR by decreasing phase 4 depolarization
Negative chronotropic effect - parasympathetic on heart, decrease If
decreases conduction velocity through AV node by decreasing inward calcium current and increase outward K current
Negative dromotrophic effect - parasympathetic on heart, increases PR interval
Intercalated Disks
Cardiac Muscle that caontain gap junctions
form dyads with SR
Cardiac T-tubules
Inotropism
ability of heart to contract, related to intracellular calcium
Positive staircase of Bowditch staircase
increased HR increases force of contraction in stepwise fashion as intracellular calcium increases
Postextrasystolic potentiation
beat the occurs after an extrasystolic beat
2 Mechanisms that increase force of contraction
- increases calcium current during plateau
2. increase calcium pump of SR by phosphorylated phospholamban thus increase calcium for release in subsequent beats
Digitalis, cardiac glycosides
increase force of contraction by inhibiting Na/K-ATPase
which increases Calcium intracellularly
Preload
end-diastolic volume which is related to Rt atrial pressure
Afterload
for left ventricle - aortic pressure
for right ventricle - pulmonary artery pressure
Maximal Velocity of contraction
when afterload is zero
Frank-Starling
Increase in VR or EDV will cause an increase in SV and CO
Increase Contractility will ____ cardiac output
increase
for any level of RAP or EDV
Width of pressure-volume loop
Stroke Volume
Increased preload on pressure-volume loop
causes an increase in stroke volume (width of graph gets bigger)
it is from increase EDV from increase VR
Increased afterload on pressure-volume loop
causes a decrease in stroke volume (smaller width)
increases height of loop (thus skinnier and taller than normal)
due to increased aortic pressure
Increased contractility on pressure-volume loop
causes an increase in SV (width gets bigger)
decrease in end-systolic volume
wider and taller pressure volume loop
Stroke Volume
volume ejectied from the ventricle with each beat
SV = EDV-ESV
Ejection Fraction
fraction of EDV ejected in each SV, related to contractility
normal is 55%
EF = SV/EDV
Stroke Work
work the heart performs on each beat
aortic pressure)*(SV
primary energy source for stroke work
Fatty Acids
Cardiac Output by Fick Principle
CO = (O2 consumption)/(O2 in pulm v - O2 in pulm a)
a wave on venous pulse curve
atrial systole
4th heart sound
filling of ventricle by atrial systole (not audible in normal adults)
begins after onset of QRS wave
isovolumetric ventricule contraction
First heart sound
AV valve closes
Split of 1st heart sound
because mitral valve closes before tricuspid valve
2nd heart sound
Aortic Valve Closes
3rd heart sound
rapid flow of blood from atria into ventricles
normal in children, not in adults
Dicrotic notch or incisura
blip in aortic pressure tracing, occurs after closure of aortic valve
Baroreceptor Reflex
stretch receptors in the carotid sinus near the bifurcation of common carotid arteries
decrease stretch leads to decrease firing rate of carotid sinus nerve (Hering, CN IX)
will decrease Parasymp and increase Sympathetics
4 effects of AngII
1) stimulates the synthesis and secretion of aldosterone
2) increases Na/H-exchange to increase Na reabsorption
3) increase thirst
4) vasoconstriction of arterioles to increase TPR and arterial pressure
Effects of Aldosterone
increase Na reabsorption in renal distal tubule to increase ECF and BV
slow process because needs to be synthesized first
Cause for AngII release
decreased arterial pressure which causes decreased renal perfusion
Cerebral Ischemia
pCO2 increases in brain
Chemoreceptors cause an increase in sympathetics to heart and BV
Cushing reaction
response to cerebral ischemia
vasomotor center increases sympathetics outflow to heart and BV causing a profound increase in arterial pressure
Chemoreceptors in carotid bodies and aortic arch
decrease in pO2 activate vasomotor centers producing vasoconstriction, increase in TPR and increase in arterial pressure
ADH/Vasopressin
V1-receptors: on arterioles, a vasoconstrictor that increases TPR
V2-receptors: on distal tubules and collecting ducts, water reabsorption
ANP
from atria in response to increased blood volume and atrial pressure
relaxes vascular smooth muscle, dilate arterioles
excretion of Na and water
inhibtis renin secretion
How O2 and CO2 cross cell membranes
simple diffusion
Starling equation
Fluid flow = Kf[(Pc-Pi)-(osmc - osmi)] fluid flow + it is net fluid out of capillary (filtration) fluid flow (-) the net absorption P means hydrostatic pressure
factors that increase filtration
increase capillary hydrostatic pressure
decrease interstitial hydrostatic pressure
decrease protein concentration in capillaries
increase protein concentration in capillaries
Organs that exhibit autoregulation
Heart, Brain, Kidney
blood flow remains constant over a wide range of perfusion pressures
Active Hyperemia
blood flow to an organ is proportional to its metabolic activity
Ex is blood flow to skeletal muscle during exercise
Reactive hyperemia
increase of blood flow to an organ that occurs after a period of occlusion of flow
Myogenic Hypothesis
explains autoregulation of blood flow
vascular smooth muscle contracts when it is stretched
Metabolic Hypothesis
tissue supply of oxygen is matched to the tissue demand for oxygen
vasodilators are produced:: CO2, H, K, lactate, and adenosine
Histamine on Blood Vessels
arteriolar dilation and venous constriction
increase Pc to increase filtration
bradykinin on blood vessels
arteriolar dilation and venous constriction
increase Pc to increase filtration
Serotonin on blood vessels
Arteriolar constriction to prevent blood loss
implicated in vascular spasms of migraine headaches
Prostaglandin E
vasodilator
Prostaglandin F
vasoconstrictor
Thromboxane A2
vasoconstrictor
local metabolic factors in the coronary circulation
hypoxia and adenosine
most important vasodilator for cerebral circulation
CO2
Primary regulator of blood flow to skeletal muscle at rest
Sympathetic
- alpha-1: vasoconstriction
- Beta-2: vasodilation
Local metabolites for skeletal muscle
lactate, adenosine, potassium
Cardiovascular Changes when person is Standing
blood pools in veins, blood vol and VR decrease thus decreases SV and CO
Arterial pressure decreases
Compensatory mechanism: carotid sinus baroreceptors will increase sympathetics
Cardiovascular Changes when person is Exercising
Sympathetics to heart and BV will increase
arteriolar resistance in the skin, splanchnic regions, kidneys and inactive muscles is increased
decrease TPR
Cardiovascular Changes with hemorrhage
increase HR, contractility, TPR, cenoconstriction, renin, AngII, aldosterone, circulation NE and Epi, ADH
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