Clinical measurement of blood flow Flashcards
purpose of circulation
to deliver oxygen
DO2
how is DO2 measured?
mlO2/min
depends on blood flow (L/min) and oxygen concentration (mlO2/L)
how much O2 does a healthy adult consume at rest?
200-250mL/min O2
OER
oxygen extraction ratio
each organ has their own value
when does OER change
if DO2 falls OER increases to compensate
when OER is maximised delivery of oxygen becomes supply-dependant
what is shock?
inadequate organ perfusion, due to acute failure of circulation to meet metabolic demands of tissues, often characterised by hypotension
what is preload?
filling
end diastolic volume
how much blood is delivered to the heart before it contracts
starlings law
force of contraction is proportional to initial myocardial fibre length
end diastolic stretch of myocardial fibres
compliance
determines the relationship between left ventricular end diastolic volume and left ventricular end diastolic pressure
isn’t constant
measuring compliance
use paired measurements to see where on ventricular compliance curve the preload is
JVP and CVP
can be used to measure preload but not accurate because pressure doesn’t equal volume because of compliance
what is contractility?
how well the heart contracts
intrinsic myocardial function
inotropic state
difficult to measure
calculate contractility
dP/dt
what is afterload?
load against which the heart must eject blood
what affects afterload?
LV diameter ventricular wall thickness ventricular wall stiffness aortic elastance aortic diastolic BP aortic valve pathology
What is systemic vascular resistance?
resistance of arterial circulation
what determines systemic vascular resistance?
arteriolar tone - vasoconstriction and vasodilation
what affects systemic vascular resistance?
autonomic nervous system
drugs
what drugs affect systemic vascular resistance?
nitrates
adrenaline
afterload
preload
SVR
they are all interrelated
decrease in afterload may decrease preload
cardiogenic shock pathology
muscle
conduction system
valves
what is the problem in cardiogenic shock?
contractility
heart rate
stroke volume
what happens to preload in cardiogenic shock ?
high
what happens to SVR in cardiogenic shock?
high
what happens to cardiac output in cardiogenic shock?
low
treatment of cardiogenic shock
PCI thrombolysis DVVC pacing drugs surgery
pathology of hypovolaemic shock
haemorrhage
dehydration
burns
what is the problem in hypovolaemic shock?
preload
what happens to preload in hypovolaemic shock?
low
what happens to SVR in hypovolaemic shock?
high
what happens to cardiac output in hypovolaemic shock?
low
treatment for hypovolaemic shock
control
PRCs
fluids
burns centre
pathology in obstructive shock?
PE
tamponade
tension pneumothorax
what is the problem in obstructive shock?
afterload and preload
what happens to preload in obstructive shock?
high
what happens to SVR in obstructive shock?
high
what happens to cardiac output in obstructive shock?
low
pathology of distributive shock
septic
anaphylactic
problem in distributive shock
SVR
what happens to preload in distributive shock?
normal/low
what happens to SVR in distributive shock?
low
what happens to cardiac output in distributive shock
high
treatment of obstructive shock
thrombolysis
surgery
pericardiocentesis
decompression
treatment of distributive shock
sepsis 6 and source control and noradrenaline
adrenaline and source control
why measure blood flow?
to identify complex or combination pathology
cause of shock is unclear
titrate therapies
cardiac surgery
monitor transplanted organs - renal artery doppler
assess organs for transplant
what affects stroke volume?
preload
contractility
afterload
what drugs affect systemic vascular resistance?
vasopressors
what intervention affect heart rate?
electricity
drugs
what interventions affect preload?
fluid
offload
what drugs affect contractility
inotropes
what drugs affect afterload?
vasodilators
how to measure cardiac output?
methods vary in how invasive they are
echocardiography
oesophageal doppler
dilutional techniques
echocardiography
measure aorta diameter and heart rate and stroke volume to calculate cardiac output
oesophageal doppler
uses doppler effect to measure speed of blood in descending aorta
estimation of cross-sectional area of aorta
Stroke volume = area x stroke distance
dilutional techniques
based on steward hamilton principle
inject dye upstream
rate of change on concentration downstream is related to rate of flow
normal aortic pressure
100-140/60-90
normal left atrial pressure
2-12
normal left ventricular pressure
100-140/2-12
normal right ventricular pressure
25/2-6
normal right atrial pressure
2-6
normal pulmonary artery pressure
25/8-12
normal pulmonary artery wedge pressure
8-12
signs of inadequate cardiac output
examine kidney, brain and skin
urine output will decrease
consciousness will reduce, altered mental status and agitation
capillary refill with lengthen
how to monitor urine output?
insert catheter - if worried about organ perfusion
how does the body defend BP?
baroreceptors in carotid body and aortic arch
what does BP tell us about cardiac output and tissue perfusion?
nothing
normal BP doesn’t mean normal cardiac output
gives some information about contractility
height of dicrotic notch can give information on volume status
what does hypotension suggest?
patient cannot maintain normal BP while cardiac output is falling so patient has run out of physiological reserve
what is the dicrotic notch?
small and brief increase in arterial BP that appears when the aortic valve closes
JVP/CVP
reflects pressure in right atrium
doesn’t tell much about preload
CVP is poor measure of volume status
change in CVP more useful - paired values to determine location on compliance curve
assessing sympathetic tone
presence of sweating, tachycardia or core-peripheral temperature difference
sympathetic overdrive = how hard they need to work to maintain BP
Mottling
don’t ignore
can indicate prognosis is about to worsen!
warm big toes
temperature of big toe correlates with cardiac output
can suggest prognosis
cold big toe
peripheral vasoconstriction and rising lactate
Lab tests in assessing cardiac output and blood flow
lactate
central venous saturation
lactate
over 4mmol/L = 40% mortality
raised lactate
needs intervention
when is lactate raised?
conditions of low oxygen delivery
produced in anaerobic metabolism
central venous saturation
saturation of blood returning to heart
surrogate marker for OER and adequacy of oxygen delivery
central venous saturation and cardiac output
falling central venous saturation could indicate poor cardiac output
what does low central venous saturation suggest?
demand is greater than supply
what does high central venous saturation suggest?
not necessarily reassuring
may imply failure of oxygen delivery to metabolically active capillary beds so oxygen is not removed from the blood
what happens in a septic patient?
vasodilation due to inflammatory mediators causing reduced SVR and so BP falls reflexes initiated Heart rate increases, contractility increases (tachycardia and hypercontractility) cardiac output rises high CO and vasodilation capillary stasis no oxygen delivery to tissues capillary density falls
what can restore flow to tissues in sepsis?
nitrate as it dilates capillaries
exact cardiac output
more important to assess adequacy of blood flow than knowing the exact cardiac output
cardiac output tells us a little about tissue blood flow and less about oxygen use
