Apex- Monitors and Equiptment > Hemodynamics Flashcards
A blood pressure cuff that is too large:
A- falsely increases BP measurement
B- requires less pressure to occlude the artery
C- increases risk of radial neuropathy
D- has a bladder width of less than 40% of the circumference of the extremitiy
B. requires less pressure to occlude the artery
The ideal bladder length and width of a BP cuff should be what % of the extremity circumference
80% length
40% width
Where is SBP/DBP the lowest vs highest
& Where is the PP most narrow vs widest
At the aortic root → SBP lowest, DBP highest, PP narrowest
At the dorsalis pedis artery → SBP is highest, DBP is lowest, and PP is the widest
Arm positioning:
For every 10cm change, the BP changes by ________ mmHg.
For every 1” change, the BP changes by ________ mmHg
10cm = 7.4mmHg change
1” = 2mmHg change
If the BP cuff location is above the heart, the BP reading wil lbe falsey (increased/decreased) - why
what if it’s below the heart?
above the heart- falsely decreased → less hydrostatic pressure
below the heart - falsey increased → more hydrostatic pressure
If the BP cuff is 10” below the level of the heart. What is the true BP at the level of the heart?
10” x 2mmHg = 20mmHg
20mmHg less than what’s displayed on the monitor
Why should BP cuff measurement probably be avoided in someone with a previous axillary lymph node dissection?
It is thought it could impair lymphatic drainage and cause limb edema but is controversial
3 most common causes of an over-dampened arterial-line waveform:
2 other things to check for
- air bubbles in the tubing
- clot at the catheter tip
- low flush bag pressure
kinks or a loose connection
Arterial line associations:
Initial upstroke →
Peak of the waveform →
Dicrotic notch →
Trough of the waveform →
Area under the curve →
Peak minus trough value →
Initial upstroke → contractility
Peak of the waveform → systolic BP
Dicrotic notch → Aortic valve closure
Trough of the waveform → Diastolic BP
Area under the curve → Stroke volume
Peak minus trough value → Dicrotic notch
Where should your a-line transducer be leveled at?
What if your concernred about cerebral perfusion?
Right atrium
External auditory meatus (corresponds with the circle of Willis)
Characteristics of your BP components with an underdampened a-line system
2 things that could cause it
2 signs in your waveform that may indicate it’s underdampened
SBP will be overestimated
DBP will be underestimated
MAP = accurate
stiff/noncompliant tubing & catheter whip (artifact)
multiple artifacts present in the waveform + after flushing the system, theres severeal oscillations that occur prior to re-establishing baseline
Why should you probably always be looking at MAP when evaluating arterial lines
bc if your system is overdampened or underdampned, your MAP will always be accurate
What are the specific BP characterstics of an over-dampened arterial line system?
2 things you’ll notice in your waveform
5 things that can cause it
SBP is underestimated
DBP is overestimated
MAP is accurate
loss of dicrotic notch & no oscillations following a flush
air bubble in tubing, clot in catheter, low flush bag pressure, kinked tubing, loose connection
Where should the tip of the CVP catheter rest?
just above the junction of the vena cava and the right atrium (not inside the right atrium)
When inserting a central line in the right IJ, how far should the catheter be advanced to achieve the correct placement?
15cm
Where should the tip of the PA catheter reside?
how far from the VC junction?
in the pulmonary artery, distal to the pulmonic valve
25-35cm from the VC junction (so ~45cm from skin)
While floating a swan, what is the classic presentation of a pulmonary artery rupture?
hemoptysis
Other than close proximity, why do we access the right IJ over the left IJ?
Left IJ carriers the highest risk of injuring the thoracic duct (risk of chylothorax)
What is the most common complication while obtaining central access?
dysrhythmias
The incidence of catheter- related infection increases after how many days?
3 days
Why don’t we place the CVP tip in the right atrium?
can cause dysthryhmias, thrombus formation, and cardiac perforation
fill out chart
label distances
If you advance a PA catheter 10cm beyond the calculated distance and still dont see the expected waveform, what should you assume and do?
assume the catheter coiled
→ deflate the balloon, withdraw the catheter to the junction of the VC and RA and try again.
if you encounter resistance while pulling back, the catheter is possibly knotted or entangled with the chordae tendineae → get CXR to rule out
What kind of complications can occur while obtaining central venous access (5)
Arterial puncture
PTX
Air embolism
Neuropathy
Catheter knot
What kind of complications can occur while floating a PA catheter? (4)
- PA rupture (hemoptysis)
- RBBB
- CHB if pre-existing LBBB
- Dysrhythmias
A- Wave
atrial systole , occurs just after the P wave (atrial depol)
RA contraction
What is the CVP waveform a reflection of?
The pressure in the RA
3 peaks (a,c,v), 2 troughs (x,y)
Each represents pressure changes in the RA as blood moves in and out
Describe what is happening with the atria vs ventricles in each segment
CVP is
A. Falsely increased by placing the transducer abover the zero point
B. increased by PEEP
C. decreased by pericardial tamponade
D. Unchanged by a ventricle septal defect
B. Increased by PEEP
PEEP increases PVR creating an additional resistance agaisnt RV ejection which an increase RVEDP and CVP
Normal CVP in the adult
1-10mmHg
Where should CVP be zeroed at
4th ICS, mid anteroposterior level (phlebostatic axis)
Factors that increase CVP (4)
- Hypervolemia
- Tricuspid stenosis or regurg
- Pulmonary HTN
- Cardiac tamponade
T/F- a low CVP is almost always caused by hypovolemia
True
unelss the transducer is moved above the zero point
What is this CVP wave form showing
When would this occur and what are 2 causes?
Loss of a wave
Afib and V-pacing if underlying asystole
What’s depicted?
Conditions that cause it?
Large A- wave
Tricuspid stensosis, diastolic dysfunction, myocardia ischemia, chronic lung disease (RV hypertrophy), AV disassociation, Junctional rhythm, asynchronous V-pacing, PVCs
What’s going on here
What causes it (3)
Large V-Wave
TR allows a portion of the RV volume to pass through the closed by incompetent valve during RV contraction → this increases the volume and pressure in the RA and manifests as large V waves
What PA waveform is this
what is it the same as and what is the normal value
Right Atrial pressure
= CVP
Normal = 1-10mmHg
What PA waveform is this?
2 key things as to how the wavefrom changes from the previous site
Right Ventricular Pressure
15-30/0-10mmHg
Systolic pressure increases and diastolic pressure = CVP
What PA waveform is this?
How do the pressure change from previous location & what is the dicrotic notch formed by?
PAP
15-30/5-15
systolic pressure remains the same, distolic pressure rises
dicrotic notch is formed by the pulmonic valve closure during diastole
PA waveform
what is this waveform equivelent to?
PAOP
5-15mmHg
equivilent to the CVP of the left heart
a wave = left atrial contraction (systole)
c wave = mitral valve elevation into the LA during systole (isovolumetric contraction)
v wave = passive LA filling
Which findings are observed when the tip of the pulmonary artery catheter enters the region shown in the image (select 2):
Dicrotic notch and increased DBP
What are 3 things that could signify the tip of the PAC is NOT in zone 3
- PAOP > PA end diastolic pressure
- nonphaseic PAOP tracing
- Inability to aspirate blood from the distal port when in the wedged position
When does PAOP overestimate LVEDV? (select 2):
-PA catheter tip in West zone 3
- PEEP
- Diastolic dysfunction
- AI
PEEP & Diastolic dysfunction
Anything that impairs the normal pressure gradient between the PAC tip and the LV can impact your interpretation of PAOP (LAP) - makes sense
PAOP overestimates LVEDV with PEEP and diastolic dysfunction
PAOP underestimates LVEDV with AI
ehhhh
2 conditions where PAOP overestimates LVEDV
what condition underestimates it?
PEEP and diastolic dysfunction
underestimates → Aortic insuffiency
Which situation underestimates cardiac output obtained by the thermodiluation method?
A. Over-warmed injectate
B. Right-to-left intracardiac shunt
C. High injectate volume
D. Partially wedged PAC
C. High injectate volume
Which port of the PAC is used for the thermodilution method of assessing cardiac output?
2 key things with each injection
proximal port
- each injection should occur during the same phase of the respiratory cycle
- injection should be completed in < 4 seconds
Using the thermodilution method of assessing CO, the area under the curve is (directly/inversely) proportional to cardiac output
AUC is INVERSELY related to CO
→if CO is high, the injectate rapidly travels towards the distal tip of the PAC and the AUC is smaller
→ if CO is low, it takes longer for the injectate to travel past the distal tip of the PAC and the AUC is larger
What 4 conditions can overestimate CO when using the thermodilution method of assessing CO?
What 2 conditions can underestimate CO
What 2 conditions have an unpredictable effect on CO
overstimate → injectate volume too low/hot
partially wedged PAC
thrombus on tip of PAC
underestimate → injectate volume too high/too cold
unable to predict → intracardiac shunt, tricuspid regug
Factors that increase mixed venous o2 saturation (select 2):
-thyroid storm
-sodium nitroprusside toxicity
-anemia
-sepsis
SNP toxicity & sepsis
Cyanide toxicity → impaired o2 utilization
Sepsis → high cardiac output state + arterial admixture
anemia reduces o2 delivery and decreases SvO2
Thyroid storm increases o2 demand and decreases SvO2
Mixed venous o2 sat is dependent on what 4 variables
- CO
- O2 consumption
- Hemoglobin
- Hemoglobin saturation%
What is SvO2 and what is the normal value
Mixed venous o2 saturation
65-75%
What factors REDUCE SvO2
mixed venous o2 saturation
increased o2 consumpution → pain, stress, thyroid storm, shivering, fever
decreased o2 delivery → decreased PaO2, hgb, CO
What factors increase SvO2
mixed venous o2 sat
decreased o2 consumpution → hypothermia, cyanide toxicity
increased o2 delivery → increased PaO2, Hgb, CO
How does sepsis affect SvO2 and why?
it increases it
→ sepsis creates a high CO state with an arterial admixture (sepsis causes end-organ hypoxia, but oxygen essentially bypasses the tissues [arterial admixture] and SvO2 remains elevated).
Why is a PAC required to measure SvO2?
mixed venous o2 saturation
bc different organs exract different amounts of o2 - so a venous sample must contain blood returning from the SVC, IVC, and coronary sinus > a mixing of these 3 souorces occurs in the PA
Preload responsiveness is expected to be present if a 250mL fluid bolus increases the stroke volume in excess of what %?
10%
general rule
Why is there variation in pulse contour when a patient is “dry” and on PPV
A positive pressure breath compresses the pulmonary vasculature and augments LV filling > increased stroke volume
At the same time, it impedes RV filling
So you have an initial increase in SV, followed by a decrease SV due to that previous decrease in RV filling
What are 6 situations where pulse contour analysis won’t provide reliable data?
- spontaneous ventilation
- use of peep
- small tidal volumes
- open chest
- dysrhythmias
- RV dysfunction
Which conditions limit the reliability of the esophageal Doppler monitor? (select 2):
- hypovolemia
- aortic stenosis
- aortic cross-clamp placement
- esophageal disease
Aortic stenosis (or insuffiency) and aortic cross clamp
position of TEE probe
~ 35cm from the incisors (T5-6)
Relative contraindication to TEE
esophagel disease (varices)
risk of traumatic injury
Relative contraindication to TEE
esophagel disease (varices)
risk of traumatic injury
When preparing to transition off CPB, the SvO2 decreases from 64% to 56%. What are the MOST likely etiologies of this finding (select 2):
-light anesthesia
-initiation of dobutamine infusion
-anemia
-hypothermia
Anemia & light anesthesia
SvO2 is reduced by things that increase o2 consumption (light ansethesia) or decrease o2 delivery (anemia)
Hypothermia reduces O2 consumpution and would increase SvO2
Dobutamine infusion would increase O2 delivery and increase SvO2
When preparing to transition off CPB, the SvO2 decreases from 64% to 56%. What are the MOST likely etiologies of this finding (select 2):
-light anesthesia
-initiation of dobutamine infusion
-anemia
-hypothermia
Anemia & light anesthesia
SvO2 is reduced by things that increase o2 consumption (light ansethesia) or decrease o2 delivery (anemia)
Hypothermia reduces O2 consumpution and would increase SvO2
Dobutamine infusion would increase O2 delivery and increase SvO2
Which components of the CVP waveform correlate with ventricular systole (select 2):
-c wave
-y descent
-a wave
-x descent
c wave and x descent
(a wave and y descent correlate with ventricular diastole)
(peak of the v wave correlates with the shift from ventricular systole to diastole)
Match each component of the CVP waveform to its corresponding mechanical event:
-c wave, v wave, a wave, x descent
-RA passive filling, RV cx, RA cx, RA relaxation
a wave → RA contraction (active filling)
c wave → RV contraction
x descent → Right atrial relaxation
v wave → passive filling of the right atrium
y descent → right atrium empties through an open tricuspid valve
What conditions increase the amplitude of the v wave on the CVP waveform? (select 2):
-complete heart block
-RV hypertrophy
-papillary muscle ischemia
-TR
TR & papillary muscle ischmia
V wave = passive filling of the right atrium
→ during TR, a portion of the RV volume flows back retrograte across the incompetent tricuspid valve.
→papillary muscle ischemia can cause TR.
