Hello, everyone. My name is Analia Graziano. I'm a pediatric intensivist at the University of Maryland in Baltimore. Over the next hour, we are going to review some of the pictures and infographics, which are usually part of the critical care boards. I have nothing to disclose. We'll start with capnography. We'll start with a question. Which of the following statements is correct? Point D corresponds to the entidal CO2. Segment AB represents the alveolar plateau. Segment CD represents tracheal dead space. Or segment DE represents the expiratory upstroke. You're all familiar with this diagram. This is a capnograph, which is basically a graphic representation of CO2 over time. The capnograph consists of four phases, and it's important you remember these ones. Phase 1 corresponds to this segment, AB, and this represents the beginning of exhalation. The first gas exhaled here will be from the anatomical dead space, and CO2 concentration here approaches zero. Phase 2 corresponds to the expiratory upstroke, and this represents the rapid rise in CO2 as the anatomical dead space is replaced with alveolar gas. Phase 3 is the alveolar plateau, and here the CO2 concentration reaches uniform levels. Phase 4, here inhalation starts, and this phase represents the beginning of the next breath with the CO2 content falling rapidly to zero. Point D at the end of the alveolar plateau represents the maximum CO2 concentration at the end of exhalation, and this corresponds to the entidal CO2. Going back to our question, point D at the end of the alveolar plateau corresponds to the entidal CO2. Exhaled CO2 waveforms are almost always on the test, and it is important you become familiar with some of these. This one is the typical waveform seen in patients with bronchospasm, a patient with severe asthma, and here the rapid exhalation upstroke is blunted and there is an upsloping of the plateau phase that basically gives the typical shark fin shape to this waveform. Another important one is recognition of esophageal intubation. They probably won't give you this one because it's too obvious there is a flat line and no entidal CO2 is detected, but there are some occasions when the tracheal tube is in the esophagus and you may still detect some CO2 for a brief period of time like what you see here. The amplitude of these waveforms is, in general, suboptimal and they tend to decrease with each breath to eventually disappear. And this one can be seen when exhaled gas has entered the stomach during aggressive bagging, for example, or if the patient has consumed some carbonated drinks prior to the intubation event. This one is called curare cleft, and this little notch on the alveolar plateau phase is due to diaphragmatic movement seen in paralyzed patients who are receiving inadequate muscle relaxation. And here, basically, the patient is attempting to breathe. Next, we will review flow volume loops. Let's do another question. Based on the airway picture, this patient flow volume loop will most likely be A, B, C, D, or E. Which one do you think it is? So let's review some of these flow volume loops. In patients who are breathing spontaneously, the upper portion of the loop corresponds to the expiratory flow and the lower to inspiratory flow. And remember that on mechanical ventilation, this is reversed. The first loop on the left is a normal loop. And always remember what's normal to be able to identify what's abnormal. Loop B represents dynamic extra thoracic obstruction. Here, the greatest limitation of flow is during inspiration. And there is a preservation of expiratory flow. The decreased flow during inspiration is due to airway narrowing secondary to extraluminal pressures that are exceeding the intraluminal pressure during inspiration. And this decreases the diameter of the airway. And this can be seen in vocal cord paralysis or in patients with croup. Loop C corresponds to dynamic intrathoracic obstruction. Here, the flow limitation is during exhalation. And this is usually seen in patients with tracheomalacia or patients with a main stem bronchial tumor, for example. Loop D is seen in a fixed obstruction. And here, both forced inspiration and forced expiration are both blunted. And this is seen in patients with vascular rings or patients with severe subglottic stenosis. And they like to ask about this. Loop E, which is the last one, is probably the one that you are more familiar with. And this corresponds to patients with lower airway obstruction, like patients with severe asthma. And this loop has this typical scooped out pattern with a concave expiratory limb showing the limitation in exhalation. So going back to our question, based on the airway picture, this patient flow volume loop will most likely be this patient has severe subglottic stenosis. So the correct answer is D. And this corresponds to a fixed obstruction where both inspiration and expiration are limited. This one is just to remind you that on mechanical ventilation, the flow volume loop is reversed with inspiration on top and expiration on the bottom. This graph demonstrates autopip. And as you can see, airflow at end exhalation doesn't reach zero. Autopip is measured by doing an end expiratory hole maneuver on the ventilator. And it is calculated by subtracting the set pip from the total pip. And they may give you a picture like this one or give you a case and ask you what the problem is or which interventions you would do to correct the problem, like, for example, using bronchodilators or decreasing respiratory rate on the vent to optimize exhalation. Let's do the next question. Which statement is correct about static compliance? Static compliance is A, calculated using plateau pressure. B, changing flow over changes in pressure. C, measure at end exhalation. Or D, calculated using peak inspiratory pressure. Which one is correct? Some points to remember about static compliance and plateau pressure. Static compliance is measured under passive conditions. And it is calculated using tidal volume plateau pressure in pip. Know how to calculate static compliance as they may give you some data and you will need to do the calculation. And remember that plateau pressure is measured at end inspiration by doing an inspiratory hole maneuver on the ventilator. And also remember that plateau pressure reflects alveolar pressure. So going back to the question, which statement is correct about static compliance? The correct answer is A, it is calculated using plateau pressure. B is incorrect. Compliance is defined as volume over pressure, not flow over pressure. Static compliance is measured at end inspiration by doing an inspiratory hole, not at end exhalation. And it is calculated using plateau pressure, not peak inspiratory pressure. Peak inspiratory pressure is used to measure dynamic compliance. Here is a little cheat list on what to consider when you have elevated peak pressure with normal plateau or when plateau is elevated. And they may give you something like this and ask you which diagram reflects decreased lung compliance or which graph would correspond to a patient with ARDS, for example. Now we will move to intravascular pressure monitoring. Here are all the components of the intravascular pressure monitoring system. Here is a diagram showing the setup with all the elements listed on the previous slide, including this happy patient. When measuring invasive arterial blood pressure, the fluid in the tubing transmits the arterial pressure waveform to the transducer. And the transducer converts it to an electrical signal. And this signal is converted into a visual display that gives us the number that we see in the monitor. Some of the key steps during the setup, including zeroing the system. And zeroing the system provides a reference point of pressure, which in this case is the atmospheric pressure. To zero the transducer, the stopcock needs to be close to the patient and open to air. And the zero bottom is pressed to indicate on the monitor that this is the zero reference pressure. Another important element is leveling the transducer. This is key to have a reliable reading. For arterial blood pressure and CVP, the transducer is leveled to the phlebostatic axis, which corresponds to the RA or the aortic root. The position of the transducer affects the blood pressure reading. And this is due to the hydrostatic pressure imposed by the column of fluid on the transducer. One centimeter of water equals 0.735 millimeters of mercury, so almost 0.8 millimeters of mercury. If the transducer is placed below the RA, the transducer will detect the actual blood pressure plus the additional hydrostatic pressure exerted by the saline column. And for example, if the transducer is below 10 centimeters below the RA, the blood pressure reading will be almost 8 millimeters higher than the actual blood pressure based on this formula. So if the transducer is below the level of the RA, the blood pressure will read higher. On the other hand, if the transducer is placed above the RA, the blood pressure will read lower. Here is the anatomy of the arterial waveform. A couple of points to know. The systolic upstroke reflects the pressure pulse that is produced by LV contraction. And the systolic blood pressure is measured at the peak of this waveform. The necrotic notch here on the necrotic downstroke represents the aortic valve closure. And remember that point. The bottom diagram reflects the distortion of the pressure waveform as it travels from central arteries to peripheral arteries. And this is known as distal pulse amplification. The farther you get from the aorta, the taller the systolic peak, the lower the necrotic notch, and the lower the endostolic pressure. Distal pulse amplification effect results from a decrease in the arterial wall compliance as the pressure wave travels from the low-resistant aorta to the high-resistant peripheral arteries. Key points to remember. As the waveform travels from central to peripheral, the systolic blood pressure is higher, diastolic blood pressure is lower, and mean arterial pressure remains almost unchanged. The dynamic response of the monitory system is tested by doing a rapid flash test. When the monitory system is flashed at high pressure, the transducer is exposed to this high-pressure signal, and this signal causes the transducer to vibrate. And how quickly the system vibrates and how fast those vibrations dissipate will depend on the natural frequency of the system and the damping coefficient. When doing the flash test, three types of responses can be seen, and we all have done this at the bedside when troubleshooting a line. If the system is adequately damped, only two oscillations are seen after the square wave. In an over-damped system, there is only one oscillation or no oscillations after the square waveform, and these oscillations have a smaller amplitude. In this case, the systolic blood pressure will read lower than what actually is, and the diastolic will be overestimated. Over-damping can be seen if, for example, there are air bubbles in the system. If the system is under-damped, there is excessive ringing or multiple oscillations or vibrations that follow the square wave test. And typically, the systolic blood pressure will read higher in an under-damped system, and the diastolic will read lower. And things like long tubing or multiple stopcocks can cause under-damping. They may give you a diagram like this one without the labels, of course, and ask you in which system the systolic blood pressure will be underestimated or overestimated. We'll move now to CVP waveforms. The zeroing and leveling of the CVP system is the same as the one we discussed for arterial blood pressure, zeroing to atmospheric pressure, and leveling to the right atrium. It's important you become familiar with the components of the CVP waveform and their correlation with the EKG tracing. A waves represent atrial contraction, and they occur after the P wave during the PR interval. Large A waves are called canon waves, and they are seen when the RA contracts against a closed tricospid valve, and this can be seen during JET, junction ectopic tachycardia. C waves occur in early systole, and they are generated by the closure of the tricospid valve that's protruding backwards into the RA during systole. C waves correspond to the end of the QRS in the EKG. V waves correspond to a rapid atrial filling during ventricular systole before the opening of the tricospid valve. V waves follow the T on the EKG, and they are seen between the T and the P. And large V waves are seen in severe TR, tricuspid regurgitation, and they represent blood flowing back out of the contracting ventricle. The X descent corresponds to atrial relaxation, and the Y descent corresponds to ventricular filling as the tricuspid valve opens. And prominent Y descent can be seen in constrictive pericarditis, and a loss of the Y descent reflects restriction to ventricular filling and suggests cardiac tamponade. And here is a summary of the different components of the CVP waveform and their correlation with the electrocardiogram tracing. They like to ask about this in many different ways. They may ask a straightforward question like a wave corresponds to and give you different options, and in this case would be atrial contraction, or give you a case like a patient with tamponade physiology and relate the CVP waveform to the physiopathology. So become very familiar with these ones. So let's do a practice question. What's the problem here with this CVP waveform? These are large V waves, and they are seen with severe tricuspid regurgitation. If you remember, V waves correspond to rapid atrial filling during ventricular systole before the opening of the tricuspid valve. And large V waves like the ones seen here in severe TR represent blood flowing back out of the contractile ventricle. Let's do another question. Four-year-old, status post Fontan, what's the problem? So these are large A waves, and this patient has junctional rhythm. And junctional rhythm, if you remember, is characterized by AV dissociation. The atria here contracts against a closed tricuspid valve, and this results in these prominent A-canon waves. And you can see the AV dissociation on the left side of the EKG, where there are retrograde P waves. And this is the same as we just saw on the previous slide, junctional rhythm, and the A-canon waves seen on the CVP tracing. I will show you just one slide on LV pressure-volume curves, not because they are not important. They are extremely important, and I would advise you to review in detail. But I think there are excellent presentations on the cardiovascular section, so you can review those. Things to remember here. Y-axis corresponds to LV pressure, X-axis to LV volume. Remember that the curve direction is counterclockwise, and the corners relate to the valves opening and closing. Also know how to identify the four phases of the cardiac cycle, passive filling, isovolumetric contraction, ejection, and isovolumetric relaxation. Recognize the abnormal pressure-volume curve shapes, and I would advise you that you remember what's normal to identify what's abnormal. When I was learning this, we were told that the normal curve looks like a French toast. And to me, the aortic stenosis looks like a French baguette with a high peak pressure within the ventricle that is due to the gradient across the stenotic aortic valve. So become familiar with these ones, practice blindly because they will for sure be on your exam. We'll move now to arrhythmias and EKGs. This is a diagram of an action potential of a cardiomyocyte with the membrane potential on the Y-axis and time on the X-axis. They'd like to put these type of diagrams and ask you about the different phases and which ions are involved in each phase. So remember this one. This one is a little busy, but it's a summary of the different antiarrhythmics and their mechanism of action in the dosing. Probably they won't ask you that much about doses except for adenosine and amiodarone. I don't think they will ask for some of the other ones, but they may give you a graph without any labels and ask you on which phase of the action potential these drugs work. Let's review some EKGs. This is first degree AV block. Here, there is a delay in the conduction through the AV node. The rhythm remains sinus and there are no drop beats and the PR interval is prolonged and fixed and the QRS is normal. This one is second degree AV block, Wenckeberg. Here, the PR interval gradually increases until a beat is dropped. This one is Mobitz II, second degree AV block. And here, the PR interval is constant and there is no progressive lengthening of the PR, so there is no warning. And PR is constant and RR is constant until the drop beat. And the problem here is below the AV node and Mobitz II can progress to a complete heart block. This is third degree AV block or complete AV block. And here, the P waves and the QRS are completely dissociated. So this one is an EKG that shows high, tall, T waves and this corresponds to hyperkalemia. And they may give you an EKG and ask you for the best treatment approach. This one is SVT, very high heart rate, around to 70 to 80 and you don't see P waves. Know how to manage stable versus unstable patients with SVT. Know the adenosine dose and the indications for cardioversion. And this one is administration of adenosine in a patient with SVT. Adenosine slows conduction time through the AV node. And here, you can see the typical delta wave seen in Wolf-Parkinson-White. If they give you an EKG of a patient with a supraventricular tachycardia with a high rate, who has received a couple of doses of adenosine and has not responded, look always for the delta wave because it may be a reentrant tachycardia and they like to ask for that. And here, you can see a better picture of the delta wave. They may give you an EKG like this one and a case where a patient presents with sudden death, history of syncope or history of recurrent seizures. And if that's the case, think about congenital long QT. This one is also prolonged QT. You can see the QT interval is around 600 milliseconds. And here, you can see in some of the precordial leads like here in V2, you can see a little notch on the T wave. And this may identify patients with prolonged QT syndrome that are at increased risk for torsades. This one is ventricular fibrillation. Remember that the shock is asynchronous and that the dose of the first shock is two joules per kilo and the second one is four per kilo with subsequent four per kilo. Let's do another question. I borrowed this slide from Janice Zimmerman. So this is a 15-year-old with history of depression who presents with altered mental status in the EKG shown here. Which one of the following interventions is indicated for the arrhythmia? Amiodarone, cardioversion, magnesium sulfate, or sodium bicarbonate? When you look at this question, pay attention to the EKG, which has a Y-complex tachycardia, and to the medical history that the patient has history of depression. So most likely, this patient took some TCA. So the answer to the previous question is administration of sodium bicarbonate. And here are the criteria for bicarbonate use. This patient had a Y-complex tachyarrhythmia and bicarbonate was indicated. The benefit of bicarb in the setting of TCA overdose is probably due to both an increase in the serum pH and also increase in the extracellular sodium. So one more, this is electrical alternance and is the alternating voltage noted in the QRS complexes. And this is seen in patients with tamponade physiology. The changes in the QRS are caused by the anterior-posterior swinging of the heart with each contraction in patients who have a large pericardial effusion. Now we will go over some pictures that are also relevant for the examination. So pulsus paradoxus, you probably already know this. Pulsus paradoxus is an exaggerated drop in systolic blood pressure during inspiration. And this is seen in patients with tamponade and in patients with severe bronchospasm like patients with asthma. Now the differences between puls paradoxus and puls alternans. Puls paradoxus, like we just saw, is a fall in systolic blood pressure more than 10 millimeters of mercury with inspiration. And it's seen in pericardial tamponade, severe obstructive gland disease, tension normal, et cetera. Puls alternans though is a bit-to-bit variability of the pulse amplitude. And the pulse alternans is independent of the respiratory cycle. So the variability doesn't change with the respiratory cycle. And this is seen in patients with severe LV dysfunction. Let's do another question. This is a full-term newborn who is transferred to your PQ with severe hypoxemia and a mixed acidosis. Has a pH of 6.97, a PCO2 of 86, PO2 of 37 on 100% oxygen, a bicarbonate of 15, and base excess of minus 15. Based on his presentation and the G-Sex ratio shown on the right, the most likely diagnosis is A, metabolic disorder, B, hyaline membrane disease, C, detransposition of the great arteries, D, pulmonary venous obstruction. So this patient has TAPVR, and the G-Sex ratio is the typical pattern of pulmonary venous obstruction in patients with total veins. Some X-rays related to congenital heart diseases that may be in the exam. One is the one that we just saw, TAPVR. TAPVR, and that's a pretty characteristic. This is Tetralogy of Fallot with a boat-shaped heart, and this is a patient with detransposition of the great arteries with a typical egg on a string heart. There are always questions about the oxyhemoglobin dissociation curve. Remember that P50 is the pressure at which the hemoglobin is 50% saturated, and for oxyhemoglobin, the P50 is 27 millimeters of mercury. And keep in mind or remember that when the curve is shifted to the left, the P50 is decreased, and the hemoglobin has increased affinity for oxygen, and oxygen delivery to the tissues is decreased. And here are the etiologies, and the opposite is when the curve is shifted to the right. These are related to vascular rings. Here is an esophagogram with an indentation on the esophagus, basically, and this is a double-orthic arch. And they may give you a case, and you will have to identify what the problem is, or they may give you a picture, like this one was on something similar on my initial certification. So become familiar with the different presentations and the etiologies. For this one, I would advise you to review Ed Conway's presentation that is excellent on this subject, but they like to put on the exam these diagrams of the neuromuscular junction that we all hate, except Ed, and they may ask you some questions about what's presynaptic, what's postsynaptic, or they may give you, for example, a case of botulism. They won't tell you it's botulism, and they will ask you the toxin that affected this patient binds at which site, for example. And in this case, for botulism, it binds at the presynaptic level, inhibiting acetylcholine release. So review Ed's talk, because I think it would be very helpful for this type of questions. This one is another one they like. They like to put the graph or the diagram of the tubular system with some letters, and then ask you about the site of action of different diuretics. If you are a visual learner like me, you will like this one about pupillary findings on different toxic ingestions, so dilated pupils versus small pupils. And this one is very useful, and again, they like to ask about this as well. And just to close, one EEG. This is burst suppression, and you can see high-voltage activity with periods of intermittent electrical suppression, like here. And I don't think they will put that many EEGs, but this one may be one, and the other one may be status epilepticus. So this is the end of my presentation. Thank you, and good luck. Here is my email if you have any questions.

pediatric intensivist

capnography

flow-volume loops

intravascular pressure monitoring

arrhythmias

EKG findings

antiarrhythmic drugs