Module 4: Hemodynamic Ax Flashcards
(148 cards)
1
Q
what does hemodynamic monitoring involve?
A
advanced methods of assessing a patient’s CO, and allows us to gather and trend data on all its components
2
Q
what does the process of hemodynamic monitoring require?
A
the use of specialized equipment and techniques which serve as the basis for decision-making aimed at optimizing the cardiovascular systems’ role in delivering oxygen to tissues and organs
3
Q
when selecting a modality for hemodynamic monitoring, what must you consider?
A
the care needs of the patient as well as their underlying disease process, comorbidities, and goals of care
4
Q
where is the insertion site of the cannula for invasive pressure monitoring?
A
varies depending on the type of assessment required; ie. to measure preload pressure of R ventricle, catheter enters venously and terminates just above right atrium. to measure afterload, catheter needs to be placed in an artery
5
Q
what does invasive pressure monitoring measure?
A
pressures in both the arterial and venous systems
6
Q
what are the components of the hemodynamic monitoring system?
A
1) invasive catheter and high pressure tubing connecting pt to transducer
2) transducer (receives physiological signal from the catheter and tubing and converts it into electrical energy)
3) flush system (maintains patency of the fluid-filled system and catheter, prevents blood from backing up, providing source for flushing and assessing line accuracy)
4) bedside monitor (contains the amplifier with recorder, which increases the volume of the electrical signal and displays it on an oscilloscope and on a digital scale in mm Hg)
7
Q
what is the basic setup for the hemodynamic system?
A
1) bag of NS used as flush system. some hospitals add heparin as an anticoagulant
2) system = IV tubing, 3 way stopcock, in-line flow device attached for continuous fluid infusion and manual flush
3) pressure transducer
8
Q
what is the pressure infusion cuff set to?
A
inflated to 300mm Hg creating a continuous infusion rate of ~3cc/hr
9
Q
why must high-pressure tubing be used to connect the invasive catheter to the transducer?
A
to prevent dampening (flattening) of the waveform
10
Q
why do some units avoid the use of heparin in the NS flush setup?
A
there is a concern for development of heparin-induced antibodies that can trigger HIT
11
Q
if heparin is added to flush solution, what patient monitoring is required?
A
platelet count
12
Q
when are flush solutions, lines, stopcocks, and disposable transducers changed?
A
q96hrs
13
Q
can you use dextrose solutions as your flush solution?
A
no
14
Q
what baseline measurements are necessary to ensure accuracy of hemodynamic pressure readings?
A
1) calibration of the system to atmospheric pressure, aka zeroing transducer
2) determining midaxillary axis for transducer height placement, to level the transducer accurately
15
Q
how do you calibrate the equip to atmospheric pressure?
A
three way stopcock nearest to transducer is turned simultaneously to open the transducer to air and to close it to the pt and the flush system
16
Q
what is atmospheric pressure?
A
760 mm Hg at sea level
17
Q
what is the midaxillary line known as and what is it used for?
A
phlebostatic axis; physical reference point on the side of the chest that is used as a baseline for consistent transducer height placement
18
Q
where is the phlebostatic axis?
A
4th sternal ICS where it joins the sternum and side of the chest that is one half of
the depth of the lateral chest wall; approximates the line of the atria
19
Q
which transducers is the phlebostatic axis used for?
A
central venous pressure (CVP)
and pulmonary artery (PA) catheter transducers
20
Q
what does the level of the transducer “air reference stopcock” approximate the position of?
A
the tip of an invasive hemodynamic monitoring
catheter within the chest
21
Q
what does leveling the transducer mean?
A
we are aligning the transducer with the level of the left atrium
22
Q
what is the purpose of leveling the transducer?
A
to line up the air–fluid interface with the left atrium to correct for changes in hydrostatic pressure in blood vessels above and below the level of the heart
23
Q
can you eyeball the position of the transducer?
A
no it can lead to inaccurate placement
24
Q
what happens if the transducer is placed below the midaxillary line/too low?
A
there is increased hydrostatic pressure in the tubing and pressure reading is falsely high
25
For every inch the
transducer is below the tip of the catheter, the fluid pressure in the system _______
increases the measurement by 1.87mm Hg
26
what happens if the transducer is placed above the atrial level/too high?
gravity and low fluid pressure give a very low pressure reading
27
For every inch the transducer is positioned above the catheter tip, the measurement _______
is decreased by 1.87mmHg
28
CVP, pulmonary artery pressure (PAP), and
pulmonary artery occlusion pressure (PAOP) can be reliably measured at?
HOB backrest positions from 0 (flat) to 60 degrees if the patient is lying supine
29
If a pt is so hemodynamically unstable or hypovolemic that raising the HOB negatively affects intravascular volume
distribution, the first priority is to?
correct the hemodynamic instability and leave the patient in a lower backrest position
30
if pt is in lateral position, where do you measure for leveling?
in the 30-degree and 90-degree lateral positions with the head of the bed flat
30 degree = one-half of the distance from the surface of the bed to the left sternal border
90 degree right lateral position = 4th ICS at the mid-sternum
90 degree left lateral position = e left parasternal border
(beside the sternum)
31
can measurements from transducer be recorded in non-supine positions?
yes
32
when is levelling done?
- after insertion
- at the beginning of every shift
- any time the patient's position changes in relation to the transducer
33
what does a 10cm height difference between the transducer and the phlebostatic axis do to BP?
changes BP by ~7.5mm Hg
34
what happens if you do not level the transducer?
you will get inaccurate pressure readings and it may lead to inappropriate treatment decisions
35
when is zeroing done?
- after insertion
- at the beginning of every shift
- any time there is a disconnection between the transducer and the monitor
36
does the transducer need to be zeroed every time a pt is moved?
no
37
what happens if you don't zero the transducer to atmospheric pressure?
can result in inaccurate pressure readings and may lead to inappropriate treatment decisions
38
order of flow of signal from patient to monitor
fluid filled compartment -> cannula -> high pressure tubing -> transducer -> cable -> monitor
39
what is arterial pressure monitoring?
minimally invasive method of hemodynamic monitoring that enables continuous access to arterial blood and provides a real-time display of arterial BP
40
what is the most common site for arterial pressure monitoring?
the radial artery due to its accessibility and collateral circulation to the hand via the ulnar artery
41
what are alternative sites for arterial pressure monitoring?
femoral, brachial, and dorsalis pedis arteries
42
what are indications for continuous arterial access and pressure monitoring?
- in critical situations where BP is/could become labile
- when NIBP monitoring is not obtainable or reliable
- when there is need for frequent arterial/venous blood sampling
43
what info does arterial pressure monitoring provide?
- waveform tracings of pressure for visual or calculated analysis to assess fluid responsiveness
- visual correlation between ECG waveform and CO
44
what are potential complications of arterial pressure monitoring?
- pain & swelling @ the insertion site
- accidental dislodgement
- thrombosis/embolization/ hematoma
- hemorrhage
- limb ischemia
- catheter-related infection including bacteremia
- iatrogenic blood loss from frequent sampling
- pseudoaneurysm
- HIT
- vasospasm
45
what are symptoms of vasospasm?
pain, decreased BP, severe damping of waveform, loss of arterial pulse
46
what is the system and safety checks for arterial pressure monitoring system?
- Inspect insertion site for redness, bleeding, drainage, and infection.
- Monitor temperature and skin colour to distal limb (circulation).
- Assess connection sites.
- Ensure pressure bag is inflated to 300 mmHg.
- Check that the flush solution bag contains the correct solution and that enough fluid is in the bag.
- Line date: The entire system (external to the patient) is changed q4 days. The catheter itself remains in place if site is not showing signs of complications.
- Level, zero, and assess square wave
- Check alarm parameters.
47
T or F: Alarms must be set to reflect blood pressure parameters ordered by the physician
true
48
can you turn off the arterial BP alarms while an arterial line is in situ?
no - dislodged arterial line can result in rapid exsanguination; low pressure alarm may be your first alert to this complication
49
interventions for a dislodged arterial line
- Apply pressure to the site for five minutes or until bleeding stops; follow with pressure dressing
- Assess ABCs
- Call for help if patient unstable (you may also need pressure dressing supplies brought to you while you maintain pressure on the site).
- Apply NIBP cuff and set cycle frequency based on patient condition
50
what can turning off alarms or incorrectly setting alarms lead to?
critical errors caused by unobserved changes in BP readings
51
what does the arterial line waveform represent?
pressure changes that occur in an artery during each cardiac cycle
52
what are the basic components seen on a bedside monitor?
- ECG waveform and HR
- arterial waveform, ABP, and calculated MAP
- SpO2 waveform and oxygen saturation
53
what does a rapid upstroke between the DBP and the SBP represent?
left ventricular contraction and begins when aortic valve opens
54
dicrotic notch
reflects a slight rebound of pressure created by the closure of the aortic valve and marks the end of systole
55
where is the SBP read on the waveform? what about DBP?
highest point; lowest point
56
what does the steep decrease in the waveform following the dicrotic notch represent?
decreasing pressure in the arterial system during diastole
57
potential problem: no pressure tracing or absent waveform on monitor.
what are causes? interventions?
Causes: Catheter or tubing may be kinked, stopcocks may be turned off, catheter is dislodged or against the vessel wall. Also consider loss of cardiac output, PEA/asystole.
Interventions: ax ABCs, check site and system from pt to monitor, ensure correct scale is programmed in monitor
58
what does a square waveform test do?
aka dynamic frequency response test, verify accuracy of BP readings
59
how do you conduct the square waveform test?
pull the manual fast flush valve on the transducer to release a small bolus of fluid past the sensor - will show how system responds to rapid increase in pressure
60
normal square waveform
shows a sharp increase in pressure (when flush valve is opened), a sharp decrease in pressure when valve is released/closed (making a “square” top), then one or two oscillations before the waveform returns to normal
61
overdamped square waveform
- shows minimal to no oscillating response following release of fast flush valve
- appears flattened, or damped, with a slower upstroke, rounded peak and dicrotic notch, and slower downstroke
62
overdamped effects on accuracy: falsely decreased SBP and/or elevated DBP and narrowed pulse pressure while the MAP often remains normal
causes and interventions?
Causes: pressure bag not inflated to 300 mmHg, flush bag fluid low, air bubbles in the circuit, blood clots, loose or open connections, kinking or obstruction in the circuit
Interventions:
- Check site, line setup and connection to monitor
- Ensure correct scale is programmed in monitor
- Ensure pressure bag is inflated to 300 mmHg
- Ensure fluid bag has enough fluid for pressure bag to squeeze
- Ensure line is free of bubbles
- Tighten all connections
- Assess position of cannula in the vessel
- Correlate reading with NIBP
- Consider if line needs to be removed/location changed
63
underdamped square waveform
- shows additional oscillations following release of the fast flush valve
- can be described as “overshot” or having “fling.”
- correlating arterial waveform has sharp peaks.
64
underdamped effects on accuracy: Falsely elevated SBP and/or decreased DBP, widened pulse pressure, while the MAP often remains normal
causes? interventions?
Causes: excessively stiff tubing, a defective transducer
Interventions:
- check site, line setup and connection to monitor
- ensure correct scale is programmed in monitor
- correlate reading with NIBP
- consider if line needs to be removed/location changed
65
what three actions need to occur to ensure interventions are based on accurate monitoring?
- level to phlebostatic axis
- zero the system
- perform a square waveform test
66
when it is critical to assess accuracy of the arterial line?
- immediately after initiation and connection to monitor
- when arterial waveform appears abnormal
- when ABP changes unexpectedly or does not correlate with physical assessment
- when system becomes disconnected for any reason
67
is levelling required with every position change?
yes
68
what is considered the gold standard for blood pressure measurement?
intra-arterial pressure monitoring
69
why is it important to correlate pressure monitoring findings with NIBP findings?
- If there are any discrepancies between the two measurements, it cues us to explore whether they are due to equipment malfunction or to the patient’s overall physical condition. A discrepancy of 5 mmHg–10 mmHg is usually considered acceptable.
- If the arterial line malfunctions or becomes accidentally dislodged, knowing about any discrepancies between the two measurements ahead of time will ensure continuity of treatment and prevent drastic changes to interventions based on different readings.
70
when is correlation of the readings done?
at the beginning of each shift and any time the accuracy of the monitored value is in question
71
what happens if the NIBP cuff is on the same arm as the radial art-line?
will see a temporary flattening of the waveform and your low-pressure alarm will be triggered
72
what variances occur in ABP reading when the insertion site is farther away from the heart?
- higher SBP
- steeper systolic upstroke
- lower DBP (less pronounced than SBP increase)
- wider pulse pressure
73
why do the variances in ABP reading occur when insertion site is farther away?
there is increased hydrostatic pressure, decreased vessel diameter and vessel elasticity, and wave reflections off branching vessels and walls
74
what correlation with the ECG are we looking for?
whether each heartbeat captured on the ECG reading produces CO
75
what factors influence preload?
venous return (circulating blood volume and its ability to return to the heart)
cardiac rhythm (impacting atrial kick and filling time)
ventricular ability (compliance and contractility)
76
influencing factor: venous return - what are assessment cues?
- fluid responsiveness (PPV/SVV, passive leg raising, fluid challenge)
- POCUS (IVC ax)
- CVP
- fluid balance (I&O, daily wts, mucus membranes, skin turgor)
- heart sounds
- vasodilatory states
77
influencing factor: cardiac rhythm - what are assessment cues?
- HR
- ECG rhythm
78
influencing factor: ventricular ability - what are assessment cues?
- BW (lytes, cardiac enzymes)
- cardiogenic pulm edema
- cardiac imaging
- cardiac history
- heart sounds
79
what does assessing preload using fluid responsiveness involve?
monitoring the effects of small increases in fluid volume on CO
80
pulse pressure variation and stroke volume variation
measures of arterial waveform changes that reflect the effects of intrathoracic pressure changes caused by positive pressure ventilation on blood return to the heart
81
what does positive pressure ventilation do to preload and contractility?
- positive pressure ventilation artificially ventilates the lungs
- increased intrathoracic pressure compresses vena cava, decreasing blood return to heart = decreased preload = decreased contractility = decreased CO
82
what might an SVV or PPV greater than 10-15% indicate?
hypovolemia and positive response to a fluid challenge
83
when are PPV and SVV less reliable indicators of fluid volume responsiveness?
in patients who are spontaneously breathing, have cardiac arrhythmias, have low tidal volumes, or poor lung compliance
84
what is the purpose of passive leg raising?
utilizes the body's venous reserves to evaluate the response of CO by shifting blood from the lower extremities into the central circulation, mimicking the effects of a small fluid bolus
85
how do you perform passive leg raising?
1. begin in a supine, semi-recumbent position with HOB at 30–45 degrees
2. Obtain baseline measurements: MAP, calculated CO, SVV, or PPV
3. In a quick-like motion, drop the HOB to 0 degrees and lift both legs to 45 degrees, holding them up for 1 min
4. Observe any changes in CO and obtain subsequent measurements
86
the amount of fluid returning to the heart from the lower torso is typically how much?
300mL but depends on individual physiology; can range from 150-500mL
87
what do you do to ensure accurate assessment of fluid return?
continuously monitor the effect of a passive leg raise on CO
88
what is commonly used for monitoring effects of passive leg raise on CO?
arterial pressure measurement; visualization using methods such as esophageal doppler and echocardiography can also be effective
89
what value would indicate potential fluid responsiveness when using arterial pressure measurements?
an increase in stroke volume indicated by an 10% or more increase in MAP from baseline
90
what patient population can PLR be performed on?
patients who are spontaneously breathing, have cardiac arrhythmias, and low tidal volumes or impaired lung compliance
91
how does the mini fluid challenge work?
same way as PLR to assess the impact of increased preload on contractility
92
what is the risk of administering fluids to assess fluid responsiveness?
- potential for fluid overload and hemodilution
- important to be cautious with fluid admin in pts experiencing HF or acute lung injury
93
POCUS
provides info about preload by visualizing the IVC and its movement during the respiratory cycle
94
what happens if a pt is hypovolemic and you're doing a POCUS?
the IVC walls will “collapse” with the fluctuation of the respiratory cycle
95
what happens if a pt is normovolemic or hypervolemic and you're doing a POCUS?
there will be less fluctuation of the IVC walls with respiration
96
CVP
measurement of pressure through a central venous catheter (CVC) that ideally terminates in the superior vena cava, just above the right atrium
97
what does CVP measure?
preload in the right ventricle; when the cardiac cycle reaches the end of diastole and the tricuspid valve is open, there is direct communication of pressure between the right ventricle and the tip of the catheter above the right atrium
98
where is the tubing for CVP connected to?
distal port of the central line
99
what are the most frequent sites for CVC insertion?
subclavian or IJ
100
when is CVP monitored?
its an intermittent assessment
101
what is a normal CVP?
2-6mmHg for a pt with normal cardiac function
102
what is important for properly interpreting CVP readings?
considering the patient's underlying physiology and other assessment findings
103
when are CVP readings most accurate?
at the end of expiration because ventilation can affect preload
104
afterload
force that the heart must generate to pump blood out into the circulatory system; the resistance that the left ventricle encounters as it ejects blood into the aorta and the rest of the body
105
three primary factors affecting afterload
vessel diameter, aortic valve structure, blood viscosity
106
what is commonly used to continuously monitor and make decisions related to afterload?
invasive arterial pressure monitoring
107
does identification of aortic valve impedance and hematocrit results provide continuous insight into a pt's condition or response to interventions?
no
108
influencing factor: vessel diameter
assessment cues?
- NIBP/ABP (SBP/DBP, MAP, pulse pressure)
- signs of peripheral vasoconstriction or vasodilation (skin temp, cap refill, pulse strength)
109
influencing factor: aortic impedance
ax cues?
- ECG
- cardiac imaging
110
influencing factor: blood viscosity
BW (Hct)
111
what other afterload assessments should be included?
- baseline/normal BP and MAP before coming to hospital
- previous BP and MAP—look at the trends
- current interventions and meds
- underlying patho
- conclusions about the other components of CO
112
T or F: any condition that impedes blood flow from the left side of the heart can lead to a decrease in CO
True
113
right sided-afterload
resistance that the right ventricle must overcome to pump blood through the pulmonary circulation for oxygenation
114
what pulmonary circulation pathologies affect afterload and how?
pulmonary hypertension and PE; increases the resistance that the right ventricle must pump against
115
contractility
strength and efficiency of the heart muscle’s contraction during systole
116
influencing factor: ventricular ability
assessment cues?
- EF, ventricular function (commonly obtained by echo)
- cardiogenic pulmonary edema
- current preload and afterload status
- abnormal ECG rhythm/rate
- cardiac history
- BW (lytes involved in muscle contraction, cardiac enzymes)
- meds
117
influencing factor: end organ indicators
end organ perfusion conclusions including global markers (lactate, SCVO2)
118
For an average healthy heart, preload remains stable up to?
120bpm; after this, contractility can begin to decrease d/t decreased VFT but is offset by increase in HR keeping CO stable
119
when does the increase in heart rate no longer balance the decrease in stroke volume, and CO diminishes?
beyond 160bpm
120
echo
allows for a visual evaluation of heart structures and their functioning, including the valves, septal deformities, and abnormalities in cardiac wall movement; can also identify problems like inflammation, infection, and the presence of clots in the ventricles
121
EF
a measurement, expressed as a percentage, of the amount of blood (preload) that is pumped out of the ventricles during each contraction, relative to the amount of blood that was in the ventricles before the contraction
122
normal EF
average is about 70%, with >50% considered normal
123
what is another way to assess contractility?
being able to visualize ventricular wall movement
124
what does an increased preload cause?
decreased contractility and CO
125
what does a decreased preload cause?
decreased contractility and CO
126
what does decreased contractility cause?
decreased CO and decreased preload (if there is sufficient circulating volume to create a backup of pressure)
127
what does increased afterload cause?
decreased contractility
128
what are the key hemodynamic compensatory mechanisms?
- neuro (SNS activity)
- mechanical (actions arising from baroreceptors)
- hormonal (RAAS)
129
what are the major effects of the PNS on our body?
- constrict pupils
- stimulate the flow of saliva
- constrict bronchi
- slow heartbeat
- stimulate peristalsis and gastric secretions
- stimulate bile release
- contract the bladder
130
cholinergic receptors and associated vagal nerve fibers are present in?
atria, AV junction and ventricles of heart
131
when PNS is stimulated what effects does it have on the heart?
slows down rate of impulse generation at SA node and slows transmission of impulses through AV node
132
what affect does SNS stimulation have on our bodies?
- accelerated HR and force of contraction
- increased secretion of adrenaline and noradrenaline
- dilated pupils
- inhibition of salivation
- dilated bronchi
- inhibition of peristalsis and production of gastric secretions
- stimulation of glucose production and release
- inhibition of bladder contraction
133
what do alpha receptors in skin, GI tract and peripheral blood vessels do?
- vasoconstrict arterioles
- increase afterload, MAP and perfusion to major organs
134
what do beta 1 receptors in heart do?
- increase speed of impulse transmission, automaticity, force of contraction, contractility, SV, CO
135
what do beta 2 receptors in lungs do?
- bronchodilation
- decrease a/w resistance
- increase ventilation, increase arterial O2 content
- increase blood flow (in skeletal muscle)
136
actions of the ANS are mediated by?
release of neurotransmitters into the synaptic cleft of the nerve and the target organ or vessel
137
neurotransmitter
a chemical messenger that interacts with its specific receptor to elicit the appropriate response
138
main neurotransmitters for the ANS
acetylcholine, epinephrine, and norepinephrine
139
PNS nerves (and a very few SNS nerves) secrete?
acetylcholine
140
SNS nerves secrete?
norepinephrine at the synaptic cleft
141
cholinergic
nerves and receptors that interact by means of acetylcholine
142
adrenergic
mediated by norepinephrine
143
SNS adrenergic receptors also respond to?
catecholamines in the general systemic circulation
144
baroreceptors
- detect pressure changes within major vessels
- trigger ANS response to compensate
- HR increases = increase contractility = increased CO = increase peripheral vasoconstriction (to redistribute blood to heart, lungs and brain) = restore BP
145
where are baroreceptors located?
aortic arch and carotid sinuses
146
if CO drops to the extent that alveoli perfusion is diminished (V/Q mismatch of dead space-like/space) what could happen?
arterial O2 sats can fall, which will trigger chemoreceptor-driven compensatory mechanisms
147
RAAS primary function
to support mean arterial blood pressure through vasoconstriction and preload through fluid retention by the kidneys
148
steps in RAAS system
1. If CO drops to the extent that blood flow through the kidneys is reduced, the kidneys will respond by releasing renin.
2. Renin acts on angiotensinogen (produced by the liver) and converts it to angiotensin I.
3. Angiotensin I is converted to angiotensin II by a peptide called angiotensin-converting enzyme (ACE) which is produced in the lungs.
4. Angiotensin II has the following impact on the OSDF:
a) potent vasoconstrictor = increased afterload
b) stimulates antidiuretic hormone (ADH) reducing urine output = increased preload
c) stimulates aldosterone release from the adrenal cortex causing sodium and water retention in the kidney's = increased preload
d) stimulates SNS = increased HR, contractility, and afterload (vasoconstriction)
