Systemic Circulation and Hemodynamics - Dr. Rogers Flashcards
Arteries with P
stress volume : high flow and pressure = BP
Arterioles
moderate P, SM walls
change resistance of blood
Capillaries
LARGE CROSS SECTION area, exchange site
Veins
Low P, large V, contract to move blood to arterial side = increase BP
greatest cross section area
capillaries
greatest blood V
Veins
blood flow =
Q= Pressure gradient (delta P)/Resistance (R)
Poiseullies law
resistance through tube calculation
R =
(8nl)/ (pi r^4)
n = viscosity
r= radius
l = length
if P stays the same how does R decrease
increase r of tube
+ increase flow rate to keep P the same
How to find viscosity
Hematocrit = (RBC: plasma) ratio increased hematocrit (high RBC) ----> lower BF
R of 8 tubes in series
you add the R for each = TOTAL R
*increases total R
R of 8 tubes in parallel
this lowers the TOTAL R
* capillaries are like this
another thing Q = to
over all heart function
Q= CO = (A P - V P) / TPR
greatest control of BF
TPR in arterioles
what increases and decreases TPR
Increase : increase sympathetic N to arterioles = vasoconstriction
Decrease : decrease sympatetic N to arterioles = vasodilation
how to calculate V of blood in BVs
V = Q/CSA
CSA: cross sectional area of vessle
highest and lowest V is found
highest : As
lowest : capillaries
3 things that make BF more likely to be turbulent
- high V
- large CSA
- low Viscosity
what is Reynolds Number
N= pdv/n
p - density
d- diameter
*if N > 2000 = laminar –> TURBULENT transition
what does turbulence cause
bruits sounds + lesions = arteriosclerosis
compliance
delta V/ delta P
* shows vascular capacitance
highest compliance
lowest complience
highest : veins
lowest : arteries
what condition can cause decrease in compliance
arterosclerosis, causes artery to be unable to distend (systole) and recoil (diastole) as much
reason Veins have compliance and what can this lead to is not functioning right
they have SM flexible walls
if the SM constrict (decrease v, same P) = lowers compliance = more blood pushes to arteries
= INCREASE BP
where is the biggest pressure drop in the circulation
arterioles
before the largest P drop in the circulation, what keeps the P high
Aorta, Large As, Small As all have high P due to Aorta having so much pulsatile action
Lowest BP
Highest BP
DIASTOLE : 80mmHg
SYSTOLE : 120mmHg
Pulse Pressure
SBP-DBP = 40mmHg
proportional to SV
How to calculate the Mean Arterial Pressure (MAP)
1/3 (SBP) + 2/3(DBP)
(DBP) + 1/3(pulse Pressure)
80-40/3 = 93.3mmHg
Dichroctic Notch
when aortic valve closes
compliance in the practical setting
SV/ Pulse Pressure
compliance and Pulse Pressure relationship
as compliance increases the pulse pressure decreases
increases R on compliance
decrease in R, lowers P, which increases Compliance
what happens in Arteriosclerosis
increase SPB, PP, and MAP
STAYS SAME : DBP
What happens in Aortic Stenosis
decrease SBP, PP, MAP
STAYS SAME : DBP
what does increasing TPR do
Increase in DBP, SBP, MAP
STAYS SAME : PP
3 things about Venous Pressure
- Low P
- Large V
- High Compliance
Venocontriction of veins causes
compliance
radius
decrease compliance
small change in r (no large R change)
= increased flow back to heart
Venous Pressure waves (3 of them)
A wave
C wave
V wave
* part of jugular pressure
A wave
mid P wave to R wave )when A contracts
C wave
Ventricular Contraction: (has the bulding of the AV valve up into A
V wave
after Ventricles contracted and the AV valves are closed = blood flows into Atrium and stays there
when the valves open the V wave is gone
3 parts of microcirculation
- Arterioles : extensive SM
- Metarterioles : less SM connecting Arterioles and Venules
- Capillaries: Branches from the Metarterioles, have precapillary sphincters
where are capillaries the largest in exchange and the smallest in exchange
LARGEST : Liver and GI
SMALLEST : Brain
vesicular transport across capillaries when needed are called
caveolae
Vasomotion
the metareterioles and precapilllary sphincters constrict in an oscillating way (every few sec) = oscillating BF
* REGULATED BY O2 LEVELS
vasomotion and O2 levels
high and low
high O2 : constriction more often
low O2 : the sphincters remain open more
Starling Equation shows what
- H2O moving into capillaries (- direction) = ABSORPTION
2. H2O moving out of capillaries (+ direction) = FILTRATION
4 forces in capillary exchange
- C = intravascular P
- i = Extravascular (interstitial) P = Pif
- P = Hydrostatic P
- (pi) = Osmotic (oncotic) P
what causes absorption into capillaries
which Ps
- Interstitial Fluid P *
- Plasma Colloid P*
- osmotic (oncotic) P*
what causes filtration into capillaries
which Ps
- Interstitial fluid colloid osmotic P*
- Capillary P *
- Intravascular P (hydrostatic intravascular P)*
location of absorption and reabsorption
ABSORPTION : arteriolar end
REABSORPTION : venous end
Capillary Hydrostatic Pressure
Pc
capillary forces fluid OUT
highest at arteriolar end
Capillary Osmotic Pressure
(pi)p or (pi)c = colloid osmotic P
Plasma proteins, NA, K in capillaries force fluid INTO capillaries
Interstitial Hydrostatic Fluid Pressure
Pif =
- : force fluid OUT from capillaries
+ : force fluid INTO capillaries
Interstitial Osmotic Pressure
(pi)if = force fluid OUT from capillaries
equation for net capillary exchange
Kf = [(Pc-Pi) - (pic - pii)]
* if + that means net FILTRATION
capillaries cant reabsorb what
proteins
what do lymph carry and what moves substances for them
fluid, proteins, chylomicrons (lipids)
Muscle contractions
what alters Pc
elevated Venous Pressure (heart failure) = increase
what alters Pi
restricted lymph flow = increased
what alters pic
reduced albumin (starvation, liver failure) = decrease
what alters pii
restricted lymph flow or inflammation = i think decrease
Acute Control of BF happens how
fast changes in local vasodilation and vasoconstriction
when does O2 availability decrease to tissues
high altitudes
pneumonia
CO poisoning
Cyanide poisoning
Autoregulation of BF happens when and how
during changes in arterial pressure (metabolically or myogenically)
* fast increase in Arterial P = immediate increased BF
= returns back to normal within minutes
Metabolic theory for autoregulation
increased Arterial P = too much O2 and nutrients delivered to tissues = hyperemia
Myogenic theory for autoregulation
increased Arterial P = SM stretch in vessel= causes it to constrict = reduce BF back to normal
*no H or N needed
Vasodilator theory
low O2 increases vasodilators
vasodilators
adenosine, CO2, adenosine phosphate, histamine (from mast cells), K+, H+
Bradykinin (also increase permeability) made from Kallikrein
O2 demand theory
not enough O2 = vasodilation of precapillary sphincter in SM
Metabolic Control
- reactive hyperemia : tissue supply blocked for 2min
2. Active hyperemia : tissue metabolic rate increased high for 2min
vasoconstrictors (4)
- N + H = NE and E
* mostly NE - Angiotensin 2 : increase TPR, decrease NA+ and H2O excretion = increase BP (+ vasoconstrictor)
- Vasopressin (ADH)
- Serotonin : from tissue damage or hemostasis
ions control BF how for Ca+2
ICM CA+ = vasocontriction
ions control BF how for K+
vasodilation
ions control BF how for Mg+ —-I SM contractions =
Mg+ —-I SM contractions = vasodilator
ions control BF how for H+
vasodilation
ions control BF how for acetate and citrate
vasodilation
ions control BF how for CO2
some vasodilation (MOST IN BRAIN)
SYMPATHETIC EFFECT ON:
- small a and arterioles
- Large vessels
- Heart
- increase TPR = decrease BF
- decrease the Blood volume to push blood forward to the heart
- increase HR and Contractility
Coronary BF happens when
during repolarization of the ventricle—-> diastole*
controlled by adenosine + hypoxia, metabolic
Cerebral Blood Flow happens when
autoregulated
injury
BP below 50mmHg
under metabolic, PCO2, H+
as BP increases, it vasocontricts (HOWEVER FLOW STAYS THE SAME* when autoregulated
vasodilation + edema
vasoconstriction
pulmonary circulation
higher RV and pulmonary A
MAP 15mmHg
* keep arterial P low
At rest: blood flow is Skeletal muscle does what and is controlled by
controlled by central receptors + baroreceptors (NE and a-adrenergic)
During Exercise: blood flow is Skeletal muscle does what and is controlled by
CO increases, TPR decreases = dilation of BVs
Muscle BV dilation also done by : ATP, adenosine, NO, K+, lactate and Epi–> B-adrenergic R
*hyperemia can happen after
rise is body temperature does what to BV flow
a-1-adrenergic R induced causing constriction which is inhibited by SYMPATHETIC ACTIVATION
= vasodilation and movement of vessels closer to skin
trauma to skin releases what causing what triple response
HISTAMINE
- red line
- red flare
- red wheal (edema)