Test 1, Deck 3 Flashcards
what is the equation for ejection fraction?
EF= EDV-ESV/EDV * 100 (normally 60%)
what is the ejection fraction a clinical index of?
left ventricular contractility
systolic heart failure
decreased contractility (depends on activity) - shifts contractility line down
diastolic heart failure
decreased compliance, reduced preload (can’t fill normally because volume creates more pressure)
- shift diastolic pressure-volume curve up
factors that determine preload
- pressure gradient from atria-ventricle
- time for ventricular filling (hr)
- ventricular compliance
- atrial function (kick)
factors that determine contractility
- sympathetic nerve activity
- drugs (digitalis)
- disease (infarct)
factors that determine afterload
- aortic pressure (hypertension)
- ventricular outflow tract resistance (valvular or subaortic stenosis)
- ventricular size- dilated hearts= larger afterload
venous return
rate at which blood returns to the thorax (central venous pool) from the periphery
central venous pool
the volume of blood enclosed by the right atrium and great veins (IVC, SVC)
cardiac output and what it equals
rate at which blood leaves CVP and is pumped out of the heart; equals venous return
relationship between cardiac output and central venous pressure? which variable is independent? what is this called?
as you lower cardiac output (& venous return), the blood backs up in the central venous pool & you get a higher central venous pressure
up CO/VR, down CVP (inverse relationship)
CO is the independent variable
vascular function curve
what is Pmc? what is it a relationship between? what is it normally?
- mean systemic circulatory pressure- the pressure in the venous system that occurs when the heart stops;
- relationship between volume of blood and the capacity of the system (venous tone)
- 7 mmHg
what happens when CVP= Pmc?
blood flow ceases- have no gradient for return
if you increase cardiac output, what happens?
decrease CVP, increase venous return (via pressure gradient)
what happens at negative CVP?
large veins collapse
which curve does transfusion shift?
vascular function curve
- higher CO for lower pressure
which curve does sympathetic stimulation shift?
cardiac function curve
- increases venous tone which increases venous return
- higher CO for lower pressure (shifts up and left)
increase venous return by increasing peripheral venous pressure (PVP)
- increased sympathetic venoconstriction
- increased skeletal leg pump
- increased blood volume
- cardiac contraction
increase venous return by decreasing central venous pressure (CVP)
- respiratory pump activity (decreased intrathoracic pressure)
- cardiac suction (heart going from circular to oblong)
how do valves change venous return?
maintain pressure gradient between peripheral and central venous pools
where do you measure CVP (central venous pressure) graphically?
intersection of vascular function curve and cardiac function curve
which curve does heart failure shift?
- cardiac function curve
- shifts down progressively
- hypervolemia also shifts vascular function curve out
2 main things that shift venous function curve
blood volume
venous tone
what happens with hemmorage?
- shifts the venous function curve down;\
- sympathetics boost it back up AND boost the cardiac function curve to give you same CO at reduced CVP
what is Poiseuille’s law?
flow= (change in pressure)/(resistance)
OR
flow=(change in pressure * pi * r^4)/ (8Lviscosity)
what is the main way in which flow is regulated?
by changing vessel radius (r^4)
what is viscosity; what is the equation; how does it relate to velocity, hematocrit, and radius
- lack of slipperiness
- viscosity= sheer stress/sheer force (p/v)
- inverse relationship w/ velocity
- direct relationship with hematocrit
- direct relationship with radius due to axial streaming
what is the definition of a non-newtonian fluid?
a fluid whose viscosity changes based on sheer stress (pressure) and force (velocity)
as a vessel diameter gets smaller, hematocrit _________ because of ________
decreases; plasma skimming
laminar vs turbulent blood flow
laminar- parallel concentric layers
turbulent- disorderly patterns (murmurs, endothelial damage, thrombi); leads to Krotokoff sounds
what is the reynold’s # and its equation?
- propensity for turbulent blood flow
- R#= (densitydiametervelocity)/(viscosity)
what is Bernouilli’s principle and its equation?
in CONSTANT FLOW system (aka there are no escape routes), total energy remains constant
total energy = potential energy + (1/2)*(density *velocity^2)
aka if blood is going faster, will have decreased lateral pressure on the walls
what is the laplace relationship and its equation?
- the force ripping the balloon apart
- wall tension= (pressure * radius)/wall thickness
what happens with an aneurysm?
decreased velocity
increased pressure
increased radius
decreased wall thickness
ALL increase wall tension
example of low wall tension
capillaries in feet- have small radius, can resist a lot of force
what allows arterioles and precapillary sphincters to control vessel diameter and blood flow?
- a high wall thickness/radius ratio; this provides low wall tension (laplace)
- also have low volume-high pressure- low compliance- high resistance
cross sectional area and the velocity of blood flow
total cross sectional area is inversely related to the velocity of blood flow
what holds 60% of blood volume
veins (larger cross sectional area than arteries)
series vs parallel resistance
- series- add them up (think vessles- aorta to large arteries to capillaries to arterioles, etc.)
- parallel- less than an individual- (think organs- open more up, have less resistance)); inverse- 1/r1 + 1/r2 etc
what is pulse pressure and where does pulse pressure become greater?
- systolic-diastolic pressure
- further you go away from the heart- greatest in ankle
- large in arteries
what is mean arterial pressure?
what is MAP determined by?
what happens to it throughout the circulatory system?
- avg pressure in the aorta and proximal arterial system during one cardiac cycle
- diastolic pressure + 1/3 PP
- declines- driving force- greatest in aorta?
3 layers (‘tunica’) of arterial wall
- intima: connective tissue, endothelials, IEL
- media: smooth muscle & EEL
- adventitia- connective tissue w/ vasa vasorum, innervation
relationship between compliance and pressure
higher compliance (e.g. elastin), lower pressure
wall thickness/diameter ratio tells you what
greater ratio, better control of the system- greatest in arterioles, provides lots of resistance
where are continuous capillaries found?
muscle, connective tisues
where are fenestrated capillaries found?
kidney, intestines
where are discontinuous/sinusoidal capillaries found?
liver, bone marrow, spleen
what is the ‘windkessel’/hydraulic filtering?
when the aortic valve closes, the recoil of the aorta wall recoiling (was pushed out by systolic pressure) sends a second wave of pressure throughout the system, maintaining diastolic pressure
relationship between compliance and pulse pressure
low compliance- high pulse pressure- high afterload- high O2 consumption
what is pressure pulse?
the wave of energy that passes through the aorta at 5 m/sec and increases to 10-15 m/sec in arteries- velocity increases as compliance decreases
what are some specific determinants of mean arterial pressure?
- cardiac output (hr * sv)
- peripheral resistance
(& baroreceptor, exercise, disease) - blood volume
- arterial compliance
primary determinants of systolic & diastolic pressure?
systolic- cardiac output
diastolic- peripheral resistance
if you decrease compliance, what happens to pulse pressure?
decrease compliance, increase pulse pressure
increase resistance, what happens to pulse pressure?
increase diastolic pressure (and some systolic)
what regulates peripheral arterial resistance?
changes in the arteriolar radius (viscosity would, but doesn’t change)
two types of ways to change arteriolar radius?
local- myogenic, endotheial, metabolites
global (extrinsic)- baroreceptor, hormonal, sympathetics (aka not specific)
which is the main player of the autonomic nervous system in regulating mean arterial pressure?
sympathetics- acts on heart, veins, arterioles
(increases HR, contractility, veno/vasoconstiction)
- increasing CO increases BP
changes that occur during exercise
- cardiac output rises (increase in contractility and hence stroke volume) BUT when HR reaches max, SV decreases
- systolic pressure rises (increase in SV)
- peripheral resistance decreases (skeletal capillaries open up)
- enhanced O2 extraction
- increases venous return (muscle and respiratory pump, venoconstriction)
- pulse pressure widens
- MAP increases- more time in systole
structures of microcirculation
precapillary resistors (arterioles, metarterioles, sphincters), exchange vessels, and venules
characteristics of capillary blood flow
- slow
- intermittent, not uniform/1 direction
- follows pressure gradients
what is a Rouleaux formation?
- stacks of RBCs
- blood cells squeezing through capillaries at an angle, touching allows for good gas exchange
pressure gradients in capillaries
hydrostatic- 32 to 15
osmotic- 25
what is the main force that holds things in? what is the most clinically relevant protein and what does it attract?
- plasma osmotic (oncotic) pressure
- albumin- attracts sodium (and water back into blood); produced by liver
what determines capillary hydrostatic pressure?
pre and post capillary resistance to arterial and venous flow
what happens when you decrease the pre/post capillary resistance ratio?
- decrease pre resistance- more water flowing in OR
- increase post resistance- less water able to flow out
- OVERALL increase capillary hydrostatic pressure
when hydrostatic pressure is greater than osmotic pressure, you get
filtration
examples of vasodilators
prostacyclins, EDRF, NO, adenosine, H+, CO2, K+
examples of vasoconstrictors
endothelin (ET)
important structural features of lymphatic system
- unidirectional flow of plasma & protein
- valved, thin walls
- non-fenestrated, no smooth muscles
- return to subclavian veins
factors governing lymph flow
- amount of filtration
- skeletal muscle activity
- valves
specific causes of edema
- reduction in plasma protein (albumin- liver failure), renal disease
- increase cap. hydrostatic pressure (congestive heart failure)
- increased permeability of membrane (burns)
- lymphatic obstruction (surgery)
what is edema?
excess fluid accumulation in interstitial space
which has a greater influence on hydrostatic pressure- arterial or venous pressure?
- venous; excessive arterial pressure is normally dissipated by resistance
what is resting sympathetic tone and what is it due to
- vascular constriction under resting conditions (basal tone) plus a small level sympathetic nerve activity due to being awake
- due to tonically released norepinephrine
active vs passive mechanisms
- can be sympathetic or parasympathetic
- active- change in resistance away from basal arterial tone
- passive- change in resistance towards basal tone
two types of inputs
sympathetic adrenergic- increases resistance
sympathetic cholinergic- decreases resistance
which type of sympathetic fibers cause active vasodilation?
sympathetic cholinergics (release Ach as opposed to Ne)
what are alpha-1 receptors?
- adrenergic receptors
- on vascular smooth muscles
- cause vasoconstriction
- not on coronary/cerebral vessels (never want to constrict flow to the brain or the heart)
what are beta-2 receptors?
- adrenergic receptors
- on heart, are secondary receptors that stimulate heart rate and contractility
- on smooth muscles, cause vasodilation
baroreceptors- anatomy
located on carotid sinus (MOST BLOOD FLOW IN BODY) & aortic arch (structures with LESS vascular smooth muscle)
baroreceptors- mechanism
- are mechanoreceptors (respond to stretch)
- fire more frequently by an increase in arterial pressure (vice-verse for decrease)
- join 9&10 to medulla
- decrease in stretch/firing= increases sympathetics and inhibits parasympathetics
ways sympathetics/PS change via baroreceptor
1) peripheral vasoconstriction (sympathetics)
2) increase in heart rate (s and ps)
3) increase in contractility (s)
baroreceptors respond to changes/absolute pressure and are more responsive to phasic/constant pressure
changes & phasic
what are chemoreceptors activated by?
low arterial PO2**, high arterial PCO2 (shifts curve up), and high H+
at a low CO2 concentration, receptors are ___ sensitive to a drop in O2
less
what do chemoreceptors stimulate?
vasoconstriction (sympathetics)
bradycardia (parasympathetics) BUT this is overruled by respiratory system which promotes tachycardia (stretch receptors in the lungs inhibit vagal nerve activity)
what is the hormonal control of the circulator system? over what time frame and circumstances does it take place?
- renin-angiotensin-aldosterone
- dehydration or heart failure over weeks
RAA pathway
- increase in fluid volume
- low arterial pressure (baroreceptors)
- renin is released from JGA kidney cells in afferent arterioles
- renin converts angiotensinogen to angitensin 1
- ACE enzymes in lungs & kidneys convert 1 to 2
- result in vasoconstriction of renal vessels
- stimulates aldosterone release which pulls Na back into blood from kidneys
- acts on hypothalamus to stimulate thirst and ADH
local mechanisms responsible for vascular resistance
autoregulation (myogeneic, metabolic)
endothelial
mechanical
what is autoregulation? what are the two primary mechanisms?
- when an abrupt increase in flow caused by an increase in arterial pressure is counteracted by an increase in resistance to maintain constant flow
- myogenic (smooth muscle contracts in response to stretch)
- metabolic (production of adenosine, H+, Co2= VASODILATORS)
auto-regulation among different organs
strong- heart, brain, kidney, skeletal muscle
weak- splanchnic
little- skin, lungs
what is it called when you see a decreases in diameter in response to an increase in pressure with or without the endothelium
autoregulation
what is it called when you see an increase in diameter in response to an increase in pressure gradient, but only with endothelium; what it is due to
endothelial-mediated mechanism (exercise);
due to increase in sheer stress of blood, result of increase in EDRF
what is active hyperemia?
increased blood flow caused by increased tissue activity (skeletal and cardiac muscle)
what is reactive hyperemia?
overshoot of blood flow in response to a metabolic debt created by a temporary occlusion
how does mechanical activity regulate blood flow?
increase in tissue pressure (think during a bicep curl) compresses small vessels and alters blood flow
where does mechanical activity regulate blood flow
muscle contraction, alveolar pressure, tumors, aortic stenosis
what is shock a primary reaction to?
cardiovascular system is unable to supply enough blood to the body; LOW BLOOD PRESSURE
