ICU-advanced Cardiopulmonary

Question 1

Opening pressure and alveolar pressure, and what it has to be for oxygen to flow into the lungs

Answer 1

Airway opening pressure is essentially the pressure at the most proximal part of the airway (mouth). Therefore, for a spontaneously breathing patient the opening pressure would be the same as atmospheric pressure (which we give a reference point of 0). When alveolar pressure is the same as opening pressure, there is no airflow. When alveolar pressure is lower than opening pressure, air flows into the alveoli.

Question 2

Transpulmonary pressure is: ____ and is measured how?

Answer 2

Transpulmonary pressure is the distending pressure applied to the lung, and is calculated by alveolar pressure minus pleural pressure.

Question 3

Transthoracic pressure is: ____ and is calculated by:

Answer 3

Transthoracic pressure is the pressure across the chest wall, and is calculated by pleural pressure minus atmospheric pressure.

Question 4

Why is afterload reduced with PPV?

Answer 4

Another way to think of it is with positive pressure ventilation the positive pressure helps the ventricle to contract. This is one of the reasons why patients with decompensated congestive heart failure with poor systolic function do so well on the vent and so terrible following extubation (especially in the setting of respiratory distress where very negative intrathoracic pressures are generated to move air).

Question 5

What does PPV due to preload?

Answer 5

Note that positive pressure ventilation decreases both preload and afterload (again perfect for CHF)

Question 6

Valsalva is a board code-word for:

Answer 6

decreased preload. It also increases intrathoracic pressure (More positive) and can decrease after load in the same way that positive pressure ventilation will (but understand, in general, the decreased preload effects of valsalva are more pronounced).

Question 7

Handgrip maneuver/ hand squeeze is code-word for:

Answer 7

increased afterload (you better know this) and can be rolled into questions about augmenting a murmur (regurgitant flows)

Question 8

How people breathe, and how obstruction changes that? How does CPAP help with that?

Answer 8

As discussed in question 3 in the respiratory section, pleural pressure must become more negative (in spontaneous ventilation) for intrathoracic (alveolar) pressure to decrease below atmospheric pressure, and generate flow of air from the environment to the lungs. Since normal intraplueral pressure is say -5 cm H20 (huge simplification as pleural pressure changes with its relative position within the chest), by generating another -4cm H20, the pleural pressure is now -9 cm H20, and the alveolar pressure is now (initially) -4 cm H20 (over-simplification) and air flows into the chest.

With obstructive lung disease such as COPD, the alveoli instead of being at 0 cm H20 at end expiration**, there is a component of elevated intrinsic PEEP (auto-PEEP), secondary to breath-stacking (well, actually dynamic hyperinflation, but lets keep things simple for now). Let’s say that this person’s intrinsic PEEP (iPEEP) is +6 cm H20. When he generates enough force to change his pleural pressures from -5 cm H20 to -9 cm H20 (a -4 cm H20 decrease), he decreased his alveolar pressures from 6 cm H20 MINUS 4 cm H20 (‘4’ was the change in pleural pressure), and he now has an alveolar pressure of +2 cm H20. Funny thing is, 2 cm H20 is ABOVE atmospheric pressure, and therefore no air is entering his chest yet. For the patient to get his alveolar pressure all the way down to -4 cm H20 (like “normal” people do) he needs to generate -10 cm H20 negative pleural pressure (+6 cm H20 iPEEP – 10 cm H20 = -4 cm H20). Therefore his work of breathing (based solely on this aspect of COPD) is more than twice that of a normal person!

So…how does CPAP work? Bare with me now, a little more math, then we’re done. The COPD patient with + 6 cm H20 of iPEEP has 5 cm H20 CPAP applied. Therefore, the difference between his alveolar pressure and that of the atmosphere is: 6 cm H20 – 5 cm H20 = 1 cm H20! Therefore to generate an alveolar pressure of -4 cm H20, he needs to only decrease his pleural pressure by -5cm H20. That’s a big deal for a person in respiratory failure!

Question 9

Hysteresis:

Answer 9

Hysteresis is essentially when a system requires additional energy added to the system for inflation that is not recovered in deflation. Said more plainly, it requires a higher pressure at a given lung volume during inflation than deflation. This is due to volume and time dependent changes in surfactant (at the molecular level), and is not due to loss or consumption of surfactant.

With hysteresis, the balloon would require 30 cm H20 to inflate and deliver back 20 cm H20, with 10 cm H20 of pressure (or energy required to generate that pressure) lost forever.

Question 10

Speed of air flow is determined by:

Answer 10

in that flow will be determined by the pressure / resistance and doesn’t explain hysteresis. Ohm’s law

Question 11

Atelectotrauma occurs when?

Answer 11

At very low lung volumes notice that a change in volume requires a large change in pressure.

Question 12

What is the definition of best PeEp? What can you use to guide your use of PEEP? If they try to be tricky and put a point above and below this ideal point, which one would be the best PEEP?
This is question 6 in M5

Answer 12

Best PEEP has numerous definitions, one of them being based on volume pressure curve of inspiration. Point B is also referred to the lower inflection point (LIP) and is the transition point between low compliance (point A) and best compliance (point C). By positioning PEEP at point B, the tidal volume will not drop below that volume and thus, atelectrauma can be avoided
PEEP can be guided by oxygenation (PaO2 on ABG for example) or based primarily pressure-volume curve (what many call an “open-lung” strategy).

One time to be tricky this basic question was asked, and two points were given near point B on this graph. One just above the LIP and one just below the LIP. In that situation, best PEEP would be the point above the LIP.

Question 13

Graph for question 7-TV should stay between which two points on that graph?

Answer 13

Ideally tidal volumes should be no lower than point B and no higher than point D. You can see above the upper inflection point (UIP) that compliance again decreases drastically. In this case, the alveoli are becoming over-distended and any further increase in volume takes a lot more pressure.

Question 14

In an otherwise normal spontaneously ventilating patient, taking a normal tidal volume, what happens with all of these? 
A. heart rate
B. left ventricular (LV) afterload
C. pulmonary vascular resistance (PVR)
D. right ventricular (RV) filling

Answer 14

During normal resting tidal volumes, parasympathetic tone is withdrawn during inspiration and heart rate increases. Loss of this reflex is seen in microvascular disease causing neuropathies such as with diabetes. With very large tidal volumes (>15 cc/kg) the heart rate will paradoxically decreases in normal patients. This is the kind of stuff the ABA loves!

Also of note, spontaneous inspiration will increase PVR as well as increase RV filling. Despite the increased PVR, pulmonary blood flow will increase during inspiration due to a larger RV stroke volume (from increased preload). Taking spontaneous breaths require a decrease in your pleural pressure, which will increase the LV afterload. In other words, for the LV to contract it must overcome the negative pleural (intrathoracic) pressure first.

As a side note, PVR increases the most at very small lung volumes and very high lung volumes.

Question 15

Look at question 10

Answer 15

Ok

Question 16

Ventricular interdependence explains the pathophysiology of:
A. Hypovolaemic hypotension
B. Malignant hypertension
C. Pulsus paradoxus
D. Sepsis-related hypotension

Answer 16

C: Pulsus paradoxus

Ventricular interdependence is a buzzword you need to know and understand. It describes the situation where right ventricular (RV) distention causes the intraventricular septum to shift towards the left ventricle (LV), thereby decreasing LV compliance (and thus volume). In cases of severe obstructive disease like asthma or COPD exacerbation, blood flow out of the RV is hampered by severe lung hyperinflation and increased pulmonary vascular resistance (PVR); yet because of the negative intrathoracic pressures, RV preload is essentially maintained. This leads to RV overload, especially during inspiration (when intrathoracic pressures are negative and PVR is highest), thus reducing LV compliance (especially during inspiration), and thus resulting in decreased LV preload and cardiac output (especially during inspiration). And consequently you have pulsus paradoxicus!

Question 17

Why does mechanical ventilation work for people in CHF with low EF?

Answer 17

PPV, of course, means increased intrathoracic pressures. Increased intrathoracic pressures do two very important things for this patient. First, it decreases preload by decreasing right heart venous return, which after a few seconds will translate to decreased LV venous return, and ultimately decreased LVEDP. Secondly, the positive intrathoracic pressures will decrease LV afterload. This was described in detail in question 2. Basically, by having a positive intrathoracic pressure the LV does not have to overcome as much tension to contract. Realize that mechanical ventilation is a temporizing measure, and once it is discontinued, the patient will return to florid CHF if nothing is done to treat the underlying problem during this time. Of course, the first best choice in this patient would likely be lasix +/- mechanical ventilation +/- pressors.

Question 18

How can you have increased peak and plateau pressures in asthma?
Look at question 13

Answer 18

In asthma exacerbation, patients will have increased peak pressures (from the airway diameters decreasing), but also hyperinflation from incomplete expiration (obstructive lung disease). The “dynamic hyperinflation” will lead to mildly (moderately in extremely bad cases) increased plateau pressures. This is not because the alveoli themselves are necessarily less compliant, but because the lung is operating at a larger volume. And with unchanged lung compliance, higher volumes lead to higher pressures.

Question 19

Are high peak pressures dangerous?

In the situation described:

Answer 19

First, high peak pressures tell you NOTHING without a plateau pressure. And second, high peak pressures don’t matter- they’re not dangerous*. What matters is that the necessary volume of air is being delivered, and that delivered air is not causing high plateau pressures (barotrauma).

In this situation both the peak and plateau pressures are increased, but the relative difference between the peak and plateau is preserved (normal). Therefore, the resistance to airflow into the lungs is normal, but the alveoli are non-compliant

Question 20

PRVC-what does it stand for? What kind of graph would you get?

Answer 20

pressure regulated volume control (PRVC). flow is reduced to maintain a constant pressure until the volume is delivered.
The important thing to realize, since the pressure is constant, you do not get peaks or plateaus. Therefore, the information you get back is only dynamic compliance

Question 21

Looking at graphs, how do you know someone is breath stacking? Treatment for breath stacking?

Answer 21

On the bottom tracing representing flow, upward deflections represent inspiration and downward deflections represent expiration. Notice that the expiratory flow for the normal patient reaches the baseline for each breath, representing complete exhalation back to FRC. The dismal patient, on the other hand, has a subsequent breath before a complete exhalation is executed.
First and foremost, you want to treat the asthma exacerbation with bronchodilators (choices not given include albuterol, ipratropium, volatile anesthetics, epinephrine, steroids), interrupt the stimulus (allergy, cold, virus, pneumonia, etc), and extend the time for exhalation! Increasing the respiratory rate is asinine, as it would lead to less time to exhale and more breath stacking. Tidal volume increases do essentially the same thing since there is more volume that needs to be exhaled. That leaves two choices. The correct answer among the choices is to decrease I time (given an unchanged respiratory rate) because in effect you will extend E time! * - Breath-stacking with resultant hyperinflation in spontaneously breathing patients is termed “dynamic hyperinflation.”

Question 22

Severe asthma, breath stacking, pt then intubated and starts stacking again but Currently he is breathing at a rate of 22, has ventilator dyssynchrony, Tv 450, PEEP 8, set rate 6, fiO2 100%, sats are 78%, BP 90/50 with evidence of pulsus paradoxus, and HR 100. He is sedated with propofol and fentanyl to a RASS of -3. Bronchodilators including subQ epinephrine has been given. Which of the following is the next best step in his management: now what? And why?

Answer 22

he is hyperinflated to the point of near death and any improvement in synchrony you might see with SIMV (personal bias, not medical fact that SIMV improves synchrony) will still fall short in solving this problem. Increasing the PEEP could, in fact, help stent open some obstructed airways and decrease the work of breathing (see question 3), but this is a life threatening exacerbation, and again, this maneuver alone will not be enough. The last, and correct, choice is muscle relaxation (which is rarely the correct choice in real life or the boards). The patient is adequately sedated for being chemically paralyzed, and this heroic effort may be the only way for him to tolerate a very low respiratory rate to allow adequate exhalation time. Also realize that with the low respiratory rate the CO2 will climb, the drive for breathing will increase, and the patient will have extreme discomfort and agitation if not deeply sedated. In this case, we would accept a patient with marginal sats and a rip-roaring respiratory acidosis to allow us to buy him time to get his asthma under control. Cisatricurium gtt.

Question 23

Why no PPV in cardiac tamponade? Mgmt of people with tamponade?

Answer 23

With cardiac tamponade, during inspiration the RV chamber increases (due to increased preload) causing ventricular interdependence (and therefore pulsus paradoxus). Application of positive pressure ventilation (even non-invasive positive pressure ventilation (NIPPV)) will decrease RV preload, thus decrease RV filling. This might sound like a good thing, except since the RV outflow is still obstructed and the LV is still noncompliant (due to the tamponade), and adding PPV will result in cardiovascular collapse. One must “feed the fire” with copious fluids and maintenance of preload with negative intrathoracic pressure until the tamponade is treated.

Question 24

How can CHF with low EF given a patient with BiPap cause reversebpulsua paradoxus?

Answer 24

With CHF exacerbation (with systolic dysfunction, not isolated diastolic dysfunction), the patient has an over-distended LV chamber (increased LVEDV) and inadequate stroke volume. Application of NIPPV will decrease preload (which is over-distending the LV and decreasing stroke volume) and decrease afterload (very important with impaired systolic function). But the maximal benefit with BiPAP will be during inspiration when the intrathoracic pressures are highest. When intrathoracic pressures are highest, afterload is maximally decreased and the ejection of blood is increased. Given an unchanged SVR, ejecting more blood will increase the blood pressure during inspiration. And there you have it, reverse pulsus paradoxus! So why does this occur with systolic CHF and not (isolated) diastolic CHF? Reason it out, you’ll surprise yourself how much you know.

Question 25

True or False:

Answer 25

With CHF exacerbation (with systolic dysfunction, not isolated diastolic dysfunction), the patient has an over-distended LV chamber (increased LVEDV) and inadequate stroke volume. Application of NIPPV will decrease preload (which is over-distending the LV and decreasing stroke volume) and decrease afterload (very important with impaired systolic function). But the maximal benefit with BiPAP will be during inspiration when the intrathoracic pressures are highest. When intrathoracic pressures are highest, afterload is maximally decreased and the ejection of blood is increased. Given an unchanged SVR, ejecting more blood will increase the blood pressure during inspiration. And there you have it, reverse pulsus paradoxus! So why does this occur with systolic CHF and not (isolated) diastolic CHF? Reason it out, you’ll surprise yourself how much you know.

Question 26

A 80 kg patient with CHF with low EF is extubated following 3 vessel CABG the following morning. His weaning parameters were as follows on 2 hours of spontaneous ventilation with 5 cm H20 PEEP, 5 cm H20 PS, FiO2 40%: Avg Tv: 440 ml, VC: 960 ml, RSBI: 65, NIF -30 cm H20, negative (normal) leak test, ABG (pH/ pCO2/ pO2): 7.37/ 42/ 95. One hour after extubation the patient was dyspneic and desaturating. CXR demonstrated new pulmonary oedema. Which of the following, if done prior to extubation, may have predicted this:

A. 6-hour spontaneous breathing trial (SBT) (instead of 2-hour)
B. SBT with 30% FiO2
C. Decreasing the extubation cut-off to RSBI < 60
D. 1-hour T-piece SBT

Answer 26

D: 1-hour T-piece SBT

When a patient is on a “CPAP” SBT (5 of PEEP throughout the respiratory cycle with another 5 of pressure support to “help overcome the resistance of the tube”) pleural (and intrathoracic) pressures do not become as negative in magnitude as compared to when breathing spontaneously with a simple facemask. The negative intrathoracic pressures effectively increase afterload, and in some patients with severe systolic dysfunction, can precipitate an instant CHF exacerbation! By using a T-piece in these select cases, the patient must generate negative intrathoracic pressures (and even more negative pleural pressures to overcome the resistance of the ETT (if you truly believe that with an 8.0 ETT will increase resistance that much). This allows for two things: First will be an increase in afterload that the patient will experience once extubated (representing a stress-test on the heart!). Secondly, the loss of PEEP means there’s no increased alveolar pressure to decrease the pulmonary oedema that is occurring (because the heart cannot handle the afterload and is failing). Remember, when the afterload increases, the heart tries to compensate by increasing the left ventricular end diastolic pressure (LVEDP), which is transmitted back to the lungs. Therefore, if a T-piece were utilized in this case, we would have seen flash pulmonary oedema while intubated and could have put him back on the vent without the risk of re-intubation.

Question 27

Mode of ventilation with constant pressure:

Answer 27

mode of ventilation with constant pressure (PRVC, PC, and APRV).

Question 28

To demonstrate cardiac tamponade, you need what kind of loop?

Answer 28

However, to demonstrate tamponade, again, you need a pressure-volume loop!