hemodynamic monitors and equipment Flashcards
during oscillometric method of BP measurement, MAP is measured when
amplitude of oscillations are greatest (most accurate data obtained form oscillometric method)
ideal bladder length and width of BP cuff
length: 80% of extremity circumference
ideal width: 40% of extremity circumference
is the pressure utilized to occlude artery different when cuff is too small or large?
yes, pressure utilized to occlude artery is less when cuff is too large and
more when cuff is too small
as the pulse moves from the aortic root to the periphery, what happens to SBP DBP and PP
SBP increases
DBP decreases
PP widens
describe SBP DBP and PP at aortic root
SBP is lowest
DBP is highest
PP is narrowest
describe SBP DBP and PP at radial artery
SBP is higher
DBP is lower
PP is wider
describe SBP DBP and PP at dorsalis pedis
SBP is highest
DBP is lowest
PP is widest
what happens to the dichrotic notch as you move further away from the heart
it moves further from the systolic peak
for every 10cm change, the BP changes
7.4mmHg
for every inch change, the BP changes
2mmHg
arterial wave form analysis:
SBP
DBP
PP
contractility
SV
dichrotic north
SBP: peak of wave form
DBP: trough of wave form
PP: peak value minus trough value
contractility: up stroke
SV: area under curve
dichrotic notch: closure of aortic valve
a line transducer should be at the level of the
right atrium
if you want to monitor CPP, where do you put aline transducer
external auditory meatus (corresponds to circle of willis)
what happens when a line is under damped
baseline re established after several oscillations
SBP over estimated, DBP under estimated, MAP is accurate
causes include stiff tubing (catheter) and whip (artifact)
what happens when a line is over damped and causes (5)
baseline is established with no oscillations
SBP under estimated, DBP over estimated, MAP accurate
causes: air bubble in pressure tubing, clot in catheter, low flush bag pressure, kinks, loose connection
tip of CVP catheter should rest (and normal value)
just above junction of vena cava and RA
1-10mmHg
how far is pulmonic artery (where PA cath is placed) in relation to vena cava junction?
25-35cm
how far to insert CVC to vena cava/right atrial junction?
subclavian (either side)
RIJ, LIJ
R/L median basillic
femoral
how much further to insert catheter from vena cava/right atrial junction to get to
right atrium
right ventricle
PAOP position
pulmonary artery
if you encounter resistance when pulling PA cath back, what is probably happening
knotted in chordae tendinae (get CXR)
complication of CVC’s while obtaining venous access include
arterial puncture
pneumothorax
air embolism
neuropathy
catheter knot
catheter resistance while inserting CVC complications include
bacterial colonization on catheter
bacterial colonization of heart or pulmonary artery
myocardial or valvular injury
sepsis
thrombus formation
thrombophlebitis
misinterpretation of data
complications that can occur when floating PA catheter include (4)
pulmonary artery rupture
R bundle branch block
complete heart block (if pre existing LBBB)
dysthrythmias
obtaining access via left IJ has added risk of
puncturing thoracic duct. can cause chylothorax
do you float a PAC in a patient with LBBB
LOL, no. you can cause a RBBB when you get in the right atrium then
ded
classic presentation of pulmonary artery rupture
hemoptysis
ID the parts of this right atrial wave form and the correlating mechanical events of the heart
ID how the CVP wave form correlates with electrical events of the heart
A wave mechanical event and electrical event
right atrial contraction
just after P wave (atrial depol)
C wave mechanical event and electrical event
right ventricular contraction (bulging of tricuspid into RA)
just after QRS complex (ventricular depol)
V wave mechanical event and electrical event
passive filling of RA
just after T wave begins (ventricular repol)
X descent mechanical event and electrical event
RA relaxation
ST segment
Y descent mechanical event and electrical event
RA empties through open tricuspid valve
after T wave ends
how does PEEP affect CVP
PEEP increases CVP because it increases PVR
where (and when) CVP should be measured
at phlebostatic axis. (4th ICS at mid anteroposterior level)
measured at end expiration (not affected by intrathoracic pressure, reading in relation to solely atmospheric pressure)
normal CVP value
1-10mmHg
CVP is a function of (3)
intravascular volume
venous tone
RV compliance
factors that increase CVP
transducer below phlebostatic axis
hypervolemia
RV failure
tricuspid stenosis or regurg
pulmonic stenosis
PEEP
VSD
constrictive pericarditis
pericardial tamponade
factors that decrease CVP
transducer above phlebostatic axis
hypovolemia
explain why this would occur
loss of a wave: afib, v pacing if underlying rhythm is asystole
explain why this would occur
atrium contracting and emptying against high resistance –> large a wave
tricuspid stenosis
diastolic dysfunction
MI
chronic lung disease leading to RV hypertrophy
AV dissociation
junctional rhythm
asynchronous v pacing
PVC’s
explain why this would occur
increased volume and pressure in RA manifests as increased V waves ( c and v waves may blend into each other)
tricuspid regurg
acute increase in intravascular volume
RV papillary muscle ischemia
which findings are observed when tip of PAC enters this area?
dichrotic notch, increased DBP
PA waveform: RAP
same as CVP (so nothing new to add)
PA waveform: RVP
systolic pressure increases
DBP = CVP
PA waveform: PAP
SBP remains same
DBP rises
dichrotic notch formed during pulmonic valve closure during diastole
PA waveform: PAOP
waveform is akin to CVP of left heart
a wave caused by left atrial systole
c wave is caused by mitral valve elevation into LA during LV systole (is-volumetric contraction)
v wave is caused by passive left atrial filling
which lung zone should the tip of the PAC be placed?
west zone 3 (provides most accurate estimation of LVEDP)
west zone review (1-3)
how can you tell the tip of the PAC is in west zone 3
PAOP > pulmonary artery end diastolic pressure
nonphaseic PAOP tracing
inability to aspirate blood from distal port when balloon is in wedged position
when does PAOP over estimate LVEDV/P?
under estimate?
over estimate: PEEP and diastolic dysfunction, impaired LV compliance (ishchemia), MV disease (stenosis or regurg), left to right cardiac shunt, tachycardia, PPV, COPD, pHTN, non west zone placement of PAC
under estimate: aortic insufficiency
which situation under estimates CO obtained by thermodilution method
high injectate volume
explain thermodilution method
injection of 5% dextrose or .9% NaCl of known quantity and temp is bolused through proximal port on PAC
each injection should occur during the same phase of the respiratory cycle and be completed in <4 seconds
usually average 3 separate injections
area under curve (AUC) is inversely proportional to CO
if CO is high, injectate rapidly goes towards AUC and waveform is smaller. takes more time for low CO to travel past tip so AUC is larger
ways thermodilution method under estimates CO
injectate volume too high
injectate solution too cold
ways thermodilution method over estimates CO
injectate volume too low
injectate solution too hot
partially wedged PAC
thrombus on tip of PAC
ways thermodilution method is unable to estimate CO (2)
intracardiac shunt
tricuspid regurg
drawback to continuous CO (CCO)
its an average of the CO for 3-6m so is not helpful in unstable patient
mixed venous O2 sat is a function of 4 variables (and equation/normal value)
- Q= CO (L/min)
- VO2 = O2 consumption (mL O2/min)
- Hgb = (g/dL)
- SaO2 = loading of HGB in arterial blood (%)
normal = 65-75%
when can mixed venous O2 become an indirect monitor of CO
when Hgb, SaO2, VO2 are all held constant
factors that decrease SvO2
increased O2 consumption (stress, pain, thyroid storm, shivering, fever)
decreased O2 delivery (decreased PaO2, decreased HGB, decreased CO)
factors that increase SvO2
decreased O2 consumption (hypothermia, cyanide toxicity), increased O2 delivery (increased PaO2, HGB, CO)
sepsis and SvO2
causes high output CO state. even though it causes end organ hypoxia, O2 essentially bypasses organs and causes increase in SvO2
SvO2 and cyanide poisoning/Na NTP
impairs O2 uptake by tissues, increases SvO2
SvO2 and left to right shunt
oxygenated blood travels from left to right heart and is added to p.venous blood
explain pulse contour analysis
provides measure of preload responsiveness as a function of how stroke volume changes during the respiratory cycle (assuming PPV)
(aka changes in intrathoracic pressure during PPV can affect SV)
preload responsiveness can be assumed when 200-250mL bolus increases SV by
10%
limitations to pulse contour analysis include (6)
spontaneous ventilation
small Vt
PEEP
open chest
RV dysfunction
dysrhythmias
tip of TEE probe should be positioned at
~35cm from incisors (T5/T6) or at third intercostal junction
define peak velocity r/t TEE
index of contractility
define flow time r/t TEE
timing of flow from LV during systole
define flow time corrected (FTC) r/t TEE
flow time indexed to a HR of 60BPM
define mean acceleration r/t TEE
average speed of up stroke of wave form (cm/sec)
define cycle time r/t TEE
time of one cardiac cycle
define stroke distance r/t TEE
how far SV is pumped along aorta per beat
TEE waveform decreased versus increased preload
TEE waveform decreased versus increrased afterload
TEE waveform deceased versus increased inotropy
limitations r/t esophageal doppler
aortic stenosis
aortic insufficiency
disease of thoracic aorta
aortic cross clamping
after CPB
pregnancy
normal PAOP value
5-15mmhg
SvO2= (equation)
normal 65-75%
change via a vasodilator (ex clevidipine)
