Insights on Cardiovascular Physiology

Hello guys and welcome back to Counter10. My name is Arnie and on today's pod we're going to be covering Applied Cardiovascular Physiology. This is the second last topic in our cardiovascular series with the last topic being measurement. Today is a huge topic. There are 12 learning objectives as per MAC95 alone and to do this topic justice I'm dividing it into two parts. Today's episode will cover the learning objectives and the second part we'll look at the SAQs attached to these learning objectives. I hope everyone's doing well at the moment. I know it's a stressful time preparing for Vibers. I'm planning to have another live practice Viber demonstration very soon and that'll hopefully be released for you guys within the next two weeks. I will also be finishing this Cardiac series before the Vibers in October and then I'll have some special guests come on to do some topics of interest before we move on to our next series. So with those few announcements done and dusted, Let's dive straight into today's pod. 1, 2, 3, 4 The first learning objective today is outline the physiological changes that occur with and the implications for anaesthetic management of pneumoperitoneum. A pneumoperitoneum occurs during laparoscopic surgery where typically a gas, being CO2, is insufflated into the peritoneal cavity. This gas is introduced at a rate, typically 4 litres per minute, to achieve an intra-abdominal pressure that can range from anywhere between 5 to 15 millimetres of mercury. The gas is then constantly supplied to maintain that pressure throughout the period of surgery. The physiological effects of this pneumoperitoneum can be divided into 1. the increase in intra-abdominal pressure, and secondly, the carbon dioxide absorption. So looking at the first effect of the increase in intra-abdominal pressure, we can see the effects of this by dividing into a multi-system approach. On the cardiovascular system, there's an initial auto-transfusion of blood from the splanchnic circulation that leads to a transient increase in venous return, which leads to a corresponding increase in cardiac output. Then, as intra-abdominal pressure increases, There's compression of the venous circulation, mainly the IVC, that decreases venous return. Subsequently, we have a decrease in cardiac output secondary to this. At the same time, anemoperitoneum is a very stimulating procedure and therefore the sympathetic nervous system is activated. This activation of the sympathetic nervous system leads to an increase in vascular resistance as well as an increase in heart rate. Overall, the effects of an increase in sympathetic nervous system is to maintain or increase the cardiac output. Typically when the intra-abdominal pressures are kept between five to 15 millimeters of mercury, that increase in sympathetic nervous system typically outweighs the decrease in venous return. Therefore, overall, the cardiac output usually stays the same. It's only when you start to get really high intra-abdominal pressures that you see that balance tip into the favor of decreasing cardiac output. The other way you see that balance tip is in patients that might have some physiological compromise. These can be in patients that have been fasted for too long or have a decrease in intravascular volume prior to the pneumoperitoneum being applied. The other important thing with the CVS response to a pneumoperitoneum is the initial stretch of the peritoneum itself. The peritoneum is very vaguely supplied and therefore the initial stretch can lead to an increase in parasympathetic surge and this can lead to a vagal response. So you do need to be careful of this specifically in patients that might already be running close to the bradycardic side. Then for completion's sake, the other effects of an increase in intra-abdominal pressure on the other body systems include the respiratory system, where an increase in pressure leads to a capillar shift of the diaphragm, and this subsequently decreases the FRC. Along with this, you have a decrease in respiratory compliance, basal atelectasis, and an increase in the VQ mismatching. The subsequent effect of this is an increased propensity for hypoxemia and hypercarbia. The GI effects are pretty self-explanatory. There's an increased predisposition to gastric regurgitation and therefore majority of patients that have laparoscopic surgery usually end up getting a tube. But also you need to be careful at what pressures surgeons set the intra-abdominal pressures at because this can not only affect the splenic blood flow but also cause mechanical compression to the intra-abdominal viscera which is sensitive to ischemia. Then, the renal effects include a decrease in renal function as a combination of the intra-abdominal pressure increasing and the sympathetic activity increasing. This accounts for the decrease in renal blood flow, GFR, and a slight drop in urine output that you might see in patients having laparoscopic surgery. Additionally, ADH is typically released as a compensatory mechanism as well as due to the stress of surgery, which further exacerbates the urine output and can lead to oligouria. Then finally, you have neurological side effects from the increase in intra-abdominal pressure. Mainly, this is a slight increase in ICP as a result of both decreased cerebral blood flow drainage, typically on the venous side, and cerebral hyperperfusion induced by hypercarbia, if that's not controlled for. So the second effect of Neuroperitoneum, being the carbon dioxide absorption, is pretty self-explanatory. Because CO2 is rapidly absorbed from the peritoneal cavity, you get an increase in the arterial partial pressure of CO2, and this leads to an increase in sympathetic activity. As a result, you can get tachycardia and razor constriction, and then you have all the biochemical effects of an increase in partial pressure of CO2, with the main one being a change in pH to a more acidic environment. The second learning objective today is outline the physiological changes that occur with CO2. and the implication for anaesthetic management of the following patient positions. Number one, supine. Number two, Trendelenburg and reverse Trendelenburg. Number three, lateral. Number four, lithotomy. And number five, prone. Before we talk about these specific positions, it's important to think about the circulatory system as residing in a column. For arterial and venous system, both are affected by hydrostatic pressure from gravity. So if you take the heart as a middle point in a person who's standing up, you'd expect the arterial pressure to be higher at their feet, while at their head, you'd expect that pressure to be lower than what it is at the heart. And the way we quantify this difference is saying that typically, a change in vertical length by 2.5cm changes the pressure by 2mmHg on the arterial system. So now looking at those specific positions, Supine being the most common position for majority of surgeries, the head, neck and spine are all in neutrality. So while a pressure difference is seen in terms of vertical height, the pressure along the long axis of the body is virtually the same. Now if you take that supine person and put them Trendelenburg, which is head down position from supine, typically 10 to 20 degrees, what you're doing here as described by Miller's, is initially the placement in a head down position will increase the cardiac output by approximately 10% in less than one minute due to auto-transfusion from the lower extremities. This effect is not sustained and with approximately 10 minutes passed, the cardiac output returns back to its baseline. So overall, the acute changes going in Trendelenburg involve an increased initial blood pressure by 5-10%, an increase in cardiac output, the heart rate usually stays the same, And by 10 to 15 minutes, these changes have all kind of gone back to normal. Now you can imagine if you go reverse Trendelenburg, the opposite occurs. You get a shift of that blood volume into the lower extremities, dropping your blood pressure through a decrease in venous return. Importantly, you also have to recognize that this leads to a decrease in pressure within the cerebral system. Therefore, the cerebral perfusion pressure takes a hit when you put a patient into a reverse Trendelenburg position or in a sitting position. Now the other positions mentioned in this landing objective being lithotomy is pretty self-explanatory. It's kind of in between a normal Trendelenburg position because you have the legs abducted and the knees flexed. This leads to a slight increase in the venous return therefore a slight transient increase in blood pressure. With lateral you don't really see too many changes and with prone you don't see too many changes either. So following on from this the better question is Why are these changes so prominent under an anesthetic? This is because an anesthetic has major impacts on the cardiovascular system and this involves both a general anesthetic and a neuraxial anesthetic. In terms of a GA, you get the blunting of our baroreceptor reflex which normally helps to compensate for these changes in position. Along with this, our cardiac output is normally decreased because majority of the agents we give cause a negative inotropy decreasing our cardiac output. They lead to an increase in vasodilation, decreasing our systemic vascular resistance, therefore decreasing both our blood pressure and MAP. And at high concentrations, certain agents like Siboflurane can also alter the autoregulation within different regional circulations of our body. Then as an additive effect, drugs like opioids can blunt the sympathetic response. Therefore, the normal responses like an increase in heart rate, an increase in blood pressure, and an increase in cardiac output that you'd normally see with a sudden change in posture in an awake person are typically lost in an anesthetized patient. Now for a patient having a neuraxial, the effect on the cardiovascular system with a change in position is very dependent on the level of where your neuraxial blockade sits. Remembering that our sympathetic nervous system sits in our thoracolumbar region from T1 to L2 and the degree of sympathomomectomy will be dependent on how much of these fibers are blocked with the neuraxial. If a patient only has a sacral blockade Then only the sacral parasympathetic nervous systems will be blocked, having a very limited effect on the total vascular tone. Then when you have a lumbar blockade at a low level or a low thoracic blockade, you're going to get some changes of the cardiovascular system because now you're starting to block some of those sympathetic nervous system fibers. However, you still have some compensatory mechanisms left up your sleeve. These include above the level of blockade, increasing the arterial and venous tone to increase preload and cardiac output, the ability to still activate those baroreceptor reflexes, and therefore increase heart rate, increase contractility, and increase sympathetic tone to the nerves that aren't blocked yet, as well as activate the low pressure baroreceptors so that compensatory mechanisms within the renal system can also be activated, like an increase in ADH, an increase in sodium and water retention, and a decrease in urine output. But when you start to move into a high thoracic blockade and a brainstem blockade, that's when you start to have some real issues. With a high thoracic blockade, as soon as you block fibers T6 and up, now you're starting to block the cardio-axillary fibers that affect the heart. So those compensatory mechanisms just won't work anymore. Then going into the brainstem, now you're knocking off the vasomotor center in the medulla, and so you're inhibiting the sympathetic nervous system outflow at its origin. The caveat to recognize with a near axial is that the effects on the cardiovascular system can be exaggerated in certain conditions. These involve hypovolemia, pregnancy, and then pathological states like fixed cardiac output states, such as severe mitral stenosis or aortic stenosis, where a sudden change might not allow the heart to be able to compensate for a decrease in blood pressure and cardiac output. Now the next learning objective we're going to look at is discuss the cardiovascular response to exercise, valsalva, positive pressure ventilation and PEEP. Exercise to me is an interesting one. A lot of changes need to occur at the same time to meet the overall goal which is to meet the increase in O2 and nutrient demand at the tissue level as well as increase the removal of CO2 you and waste metabolites. So to do this effectively, a few different systems need to be able to work in harmony to achieve this goal. And I think in Papano, this is summarized really well. So in anticipation of exercise, vagal impulses are generally decreased, while sympathetic nervous system increases are generally increased by central command. This is known as cerebro-cortical activation. The overall increase in cardiac output that you see in exercise. is mainly accomplished by an increase in heart rate rather than an increase in stroke volume. As you continue to exercise, it's the increase in body temperature with the inability to offload all this heat that leads to the feeling of exhaustion and initially you stopping exercising. So here with exercise, we have a few key terms and diagrams that you could be asked about in a Viva setting. One of those terms is VO2 max. This represents the maximum ability to take in and transport oxygen. In other words, it's the functional aerobic capacity. The other important term to know is anaerobic threshold. This is when the O2 supply cannot keep up with the demand. It typically occurs between 40 to 60% of the VO2 maximum. And this is the graph that you might be shown in Aviva, which has lactate on the Y axis and intensity on the X axis. This graph looks typically linear. until a certain point where you get an exponential increase in lactate production, typically recognized as an anaerobic threshold. The other two terms useful to know around exercise is isotonic exercise and isometric exercise. These are important because they have different physiological implications on the cardiovascular system. Isotonic exercise aka dynamic exercise, so typically the exercise that you do like running, has a very different effect on the cardiovascular system compared to isometric exercise aka static exercise such as powerlifting, or any type of exercise where you have a sustained contraction. With the dynamic type of exercise, you're getting constant contraction and relaxation of the muscle, which leads to an overall decrease in total peripheral vascular resistance. Due to this, there's dilation of the capillary beds, secondary to the buildup of active metabolites, and this leads to an overall decrease in systemic vascular resistance. Now in contrast with static exercises, where you have that sustained contraction of the muscle, there's a constant compression of the capillary bed. Therefore, those active metabolites can't really be extruded out of that area, as well as blood flow into that area is restricted. This leads to an increase in total peripheral resistance and an increase in afterload. And then all of a sudden, once that sustained contraction is released, now you get that massive pooling of blood into those blood vessels, as well as those active metabolites being released, leading to an overall systemic drop in blood pressure. which can be why people pass out after doing things like a deadlift if you've never practiced it before. Not only that, doing the different types of exercise between static and dynamic also has different compensatory mechanisms on the cardiovascular system. Dynamic exercise will usually lead to an increase in mitochondria within the heart and skeletal muscle, will lead to an eccentric hypertrophy, which is normally an increase in LV volume. In comparison, isometric or static exercise will lead to a concentric hypertrophy of the heart as well as skeletal muscle hypertrophy. So I think those are the important terms to know when talking about exercise within the cardiovascular system. And now we'll look at the Valsalva maneuver. A Valsalva maneuver has multiple definitions in varied text but the way I define it is a forced expiration against a closed glottis which requires an airway pressure of 40 millimeters of mercury. to be held for 15 seconds. The main reason the Valsalva maneuver produces a myriad of cardiovascular responses is because of the rise in intrathoracic pressure. The classical responses from the Valsalva can be divided into four phases, and there's a picture which depicts these four phases. Phase one is the onset of maneuver, at which the blood pressure increases and a heart rate decreases transiently. This occurs because there's a sudden rise in intrathoracic pressure, which causes compression of the pulmonary veins, increasing flow of the blood into the left ventricle, increasing preload and increasing cardiac output. That increase in cardiac output and more specifically the increase in blood pressure causes a stretch on the aortic and carotid bioreceptors causing an increasing firing rate and leading to a decrease in sympathetic tone which leads to a decrease in heart rate. Phase 2 is then a decrease in venous return. This occurs due to the ongoing raised intrathoracic pressure. This has an effect on both the left and the right side of the heart. On the right hand side, there is decreased venous return due to the decrease in gradient favouring blood returning to the right side of the heart. On the left hand side, the ongoing compression of the pulmonary veins means that the LV preload is also compromised. As a result, during this stage, cardiac output decreases and blood pressure decreases. This leads to decreased firing of the arterial baroreceptors and therefore an increase in sympathetic activity. As a result, The heart rate and blood pressure both start to gradually increase during phase 2. Phase 3 is immediately after the release of the airway pressure. Here you have a sudden drop in the intrathoracic pressure, which leads to a sudden decrease in blood pressure associated with a sudden increase in heart rate. The reason this occurs is because of the pulmonary vessels suddenly expanding. These pulmonary vessels don't have much blood volume, therefore the left ventricle preload is further compromised leading to a decrease in cardiac output. As a result the blood pressure is lowered and the arterial baroreceptors decrease their firing rate even further to subsequently therefore increase sympathetic tone leading to an increase in heart rate. Then you have phase four which is the return to baseline of the normal intrathoracic pressures. In this stage the venous return has now adjusted back to normal which normalizes the overall cardiac output. However, the increase in sympathetic tone still exists due to the activation of the baroreceptor reflex. Therefore, for a brief moment, you get an overshoot of the blood pressure because of the normalization of the cardiac output along with the vasoconstriction still present from phase 3. And this overshoot in blood pressure increases the firing rate of the arterial baroreceptors and leads to a secondary decrease in heart rate. So if I was to depict these changes in phase 1 through to 4, I would have a graph, would have 1 airway pressure from 0 to 40, 2 blood pressure and then 3 heart rate all on the y-axis. On the x-axis would be time and the initial phase, phase 1, would be the activation of the high airway pressures as well as an increase in blood pressure and a decrease in heart rate. Subsequently in phase two you get a decrease in blood pressure which starts to slowly come back to its normal baseline but doesn't reach its baseline and you get a linear increase in heart rate. With phase three which is the release of the airway pressure you get another drop in blood pressure and this is met with an increase in heart rate even further. Finally in phase four you get an overshoot of the blood pressure and a reflex bradycardia secondary to this. For the exam, you'd be expected to be able to draw that diagram both in an SAQ and replicate that in a VARVA setting if needed. The important utility of a VALSALVA is three things. Firstly, it can clinically assess the autonomic nervous system. And the way you can do that is looking at the heart rate that's maximum in phase 2 divided by the heart rate that's minimum in phase 4. The normal value for this ratio should be greater than 1.5. and a value less than this suggests autonomic dysfunction. And this is a good test in someone that's, say, diabetic that might have autonomic instability. The second utility of a Valsalva is it can be used in clinical conditions to treat or terminate SVTs. This occurs due to the reflex parasympathetic tone, which is achieved by phase 4. The final utility of the Valsalva is for the surgeons. The increase in venous back pressure can help to see if there's any surgical sites of bleeding, as well as for us clinically. it can help to assess a patient's murmur. A valsalva overall decreases preload, so murmurs that are typically affected by this are murmurs due to hypertrophic obstructive cardiomyopathy or due to mitral valve prolapse. The last thing you should be able to know about the valsalva manoeuvre is how this changes in different clinical conditions. The classical condition is a patient with a heart transplant. Here, their autonomic nervous system is de-innervated from their heart. and therefore their heart rate stays exactly the same and only the blood pressure changes during a Valsalva maneuver. You can also expect a similar picture in someone that's beta blocked, while someone who's alpha blocked might not get the BP overshoot in phase 4. Now finally to finish this learning objective, we're going to look at the effects on the cardiovascular system of positive pressure ventilation and PEEP. If you can understand the Valsalva maneuver, you'll be able to understand this very easily. The fundamental principle goes back to understanding what happens during spontaneous breathing. During inspiration with spontaneous breathing, you get a decrease in the right atrial pressure, therefore improving the gradient for venous return in the right side of the heart. This goes back to the vascular function curves and understanding when right atrial pressure is lower, you get an improvement in venous return. At the same time during inspiration, the pulmonary alveolar pressures are increased. This is limiting blood flow through the lung vasculature, therefore on the left side of the heart you get a decrease in the left ventricular preload leading to a decrease in cardiac output during inspiration. With spontaneous expiration this process reverses, so on the left side of the heart you get an improvement in the left ventricle preload and on the right side of the heart you get a decrease in venous return. As a result what we say with spontaneous breathing, on inspiration you have a decrease in cardiac output and on expiration you have an increase in cardiac output. This process is ultimately reversed when you apply positive pressure ventilation. Now on inspiration there's a positive intrathoracic pressure and I like to divide the effects of PPV again into what happens on inspiration and expiration. The other way you can divide it is by what happens on the right side of the heart and what happens on the left side of the heart. So on inspiration initially the blood is squeezed from the pulmonary vessels because of the initial increase in pressure. Therefore, temporarily, left atrium filling is increased and therefore left ventricular preload is increased. So initially, you get a transient increase in the LV output. Later, with that continued inspiration, the right atrial pressures are now increasing. This is limiting the gradient for venous return. Not only this, but the right ventricle afterload is increased because of the increased pressure within the alveoli. This ultimately means throughout the inspiration breath, Less blood is flowing through the lungs to the left side of the heart, leading to an ultimate decrease in cardiac output. Not only is the preload decrease in the left ventricle, but also there's a concept of ventricular interdependence that is occurring here. This is the concept that the output of both ventricles is affected by one another. Because the RV has an increase in afterload during inspiration and thereby an increase in pressure, the septum that separates the left and right ventricle is bulged into the left ventricular cavity. Now you have decreased room for LV filling and therefore overall a decrease in preload and output secondary to this. The effect of expiration with PPV is that you get that loss of that positive intrathoracic pressure. Now initially the pulmonary vessels can re-expand and so temporarily because those pulmonary vessels are expanding and don't have much volume to begin with the left atrial filling is temporarily decreased. However as expiration continues the right atrial pressures start to decrease from those really high positive values during the inspiration This allows the venous return to normalize and not only that, the right ventricle afterload is also decreased and that interdependence is having less of an effect here. All of this means that the left ventricle output is actually increased during expiration. This concept of understanding what's happening with inspiration and expiration with positive pressure ventilation is really important and it can have major clinical effects. The classic example is if you get patients with obstructive shock. So this would be either a massive PE or cardiac tamponade. In these cases, the heart is preload dependent. So you want to maintain spontaneous inspiration for as long as possible to have that natural increase in venous return during inspiration. That's why the classical teaching exists that if you're inducing someone with an acute cardiac tamponade, you try to keep them spontaneously breathing for as long as possible. Because a sudden jolt of positive pressure ventilation can decrease the preload just enough to tip the person in a balance where they go into a cardiac arrest. Now what about PEEP? Think about PEEP as a continued inspiration breath with positive pressure ventilation. All of a sudden, you don't have that expiration phase, you do technically, but during that expiration phase, a positive pressure is continually applied. Now that doesn't necessarily mean that the cardiac output is compromised during the whole of expiration due to PEEP. There is varying degrees of effect depending on the amount of PEEP that's applied. So PEEP like anything has a range. You can have low PEEP, medium PEEP or high PEEP. When you get into the high PEEP that's when you're going to have those negative effects on the cardiac output. This is talking numbers like 15 centimeters of water to 20 centimeters of water. The PEEP that's commonly applied with any kind of stock standard ventilation of five centimeters of water generally does not have a major effect of increasing right atrial pressures or changing cardiac output too much. Again, the clinical context matters. When you're being really pedantic and you have a person with a tight head who's got an increased intracranial pressure and you wanna do all the normal factors to decrease ICP, some people will go with zero PEEP just to make sure there's no increase in cerebral venous pressure. There's various studies that show that five centimeters of PEEP is safe, even with a tight head and a neuro case, but you might be seeing some of your consultants do this. because of this concept. The other important thing to recognize with PEEP is not only does it have some positive respiratory effects, but it can also have positive cardiovascular effects. If a patient is in a fluid overload state, such as congestive cardiac failure, that decrease in preload can help shift the person back into the sharp part of the Frank Starling curve. That's why as part of your treatment regime for anyone that's an acute APO is either to give them BiPAP, CPAP, or some form of positive and expiratory pressure to help the LV perform better. So this concludes this learning objective and takes us on to our next learning objective, which is describe the cardiovascular changes that occur with aging. Just like we did with respiratory physiology, you need a good structure when talking about aging or changes like obesity. With respect to cardiovascular changes, I break down the changes with aging into three components. These are the cardiac changes, the vessel changes and the autonomic changes. As we all know, aging is a physiological time-dependent process which results in a decrease in cellular function and reserve. Therefore, you can assume it's going to have a major impact on the cardiovascular system. With regards to the cardiac changes, this can be further divided into conduction changes, structural changes and functional changes. For the conduction changes, fibrous infiltration of the SA node leads to the loss of the pacemaker cells. Therefore there's an increased risk of arrhythmia and ventricular ectopics. The AB node and the bundle of his usually remain unchanged. There's some loss of the Pekingi fibers going to the ventricles. And overall, there's a reduction and a decrease in function of the catecholamine receptor density. The max heart rate also decreases. And the classic formula for this is max heart rate is equal to 220 minus the patient's age. Now, in terms of the structural changes, overall, there's an increase in collagen and fibrous tissue deposition within the myocytes. This impairs compliance of the heart. Coupled by the fact that there's decrease in myocyte numbers, but there's an increase in myocyte size. Therefore, the myocardial wall thickness becomes larger and co-centric. At the same time, the valves of the heart are also becoming calcified, and therefore there's increased risk of valvular incompetence. Now with regards to how this affects functional changes, a decrease in compliance means a decrease in left ventricular filling, and therefore a greater reliance on the atrial kick. for diastolic filling. Overall, a change in cardiac output relies more on a change in stroke volume than in heart rate because the max heart rate that can be achieved is decreased as we age. And that is a really key important point to understand of the physiological changes in elderly patients as compared to obese patients which we'll talk about in the next learning objective. Other things that contribute to a decrease in cardiac output with aging are just a sedentary lifestyle which leads to an overall general decrease in the cardiac output. Now looking at the vessel and the vascular changes, the large artery elasticity decreases and therefore the compliance in these arteries decreases. The intimal walls of the arteries thicken and there's increased calcification leading to decreased compliance. At the same time, there's loss of that endothelial function that as we touched upon with our last podcast is really important within the vascular system. So decrease in nitric oxide release means there's decreased adaptability of vessels to a change in pressure. The net effect is that you see an increase in systemic vascular resistance and total peripheral resistance with elderly patients and this means that the blood pressure is very variable to any sudden changes such as those that we give with giving a general anesthetic. They normally say that the resting blood pressure both systolic and MAP increase as we age but diastolic pressure doesn't increase as much as those two. because of the rapid runoff of blood in stiff large arteries. Now in terms of the final heading for changes with aging, being autonomic changes, we've already kind of touched on this. So there's a decrease in beta receptor responsiveness to catecholamines, and as well there's impaired baroreceptor response due to a decreased sensitivity making the blood pressure more labile. This is one of the reasons why you see in elderly patients the classic symptoms of orthostatic hypotension. Now let's talk about our next learning objective which is describe the cardiovascular changes that occur with morbid obesity. It's again going to follow that same pattern of using the three subheadings that are cardiac changes, vascular changes and autonomic changes. The key difference to understand is that the pathogenesis behind obesity is different to aging. With obesity there is an increase in total visceral fat. It is this fundamental change that starts to act as its own endocrine organ. secreting hormones and inflammatory peptides that are collectively called adipokines. The four main adipokines that you should know of is one, leptin, which has a major role in the cardiovascular changes. It has direct effects on causing vasoconstriction, leading to an increase in blood pressure, cardiac remodeling, and specifically, left ventricular hypertrophy. The second adipokine is angiotensinogen. Now, this is normally produced in the body, especially in the liver, but in obesity, it's also produced by adipocytes. This leads to an increased substrate for ACE and therefore an increased activation of the renin-angiotensin system. Secondary to this, you get increased vasoconstriction, increased water retention and increased sodium retention, all leading to an increase in blood volume. The third adipokine change is increase in plasminogen activator inhibitor 1. This means that there's overall decreased fibrinolytic activity and overall obese patients are in a hypercoagulable state. Therefore, they're an increased risk of PEs and DVTs. The final adipokine is resistant. This leads to decreased cardiac contractility and can also induce cardiomyocyte hypertrophy. So to delve into this further, just like we did with the aging, we can say that the cardiac conduction changes include fatty infiltration of the heart, which places an increased risk of phenomenons such as long QT, arrhythmias, specifically AF and AV blocks. Changes in the QRS mainly due to the remodeling of the heart and an increased propensity to have left ventricular hypertrophy. And associated with this, we can have left axis deviation, the structural changes we've already alluded to, You get a left ventricular hypertrophy secondary to the increase in preload and increase in stroke volume. You have a higher left ventricular end diastolic pressure and coupled with this, the fatty infiltrates lead to a decreased compliance of the heart. Initially, the systemic vascular resistance is low because the adipocytes provide parallel capillary beds that help to decrease the resistance overall to the increase in blood volume. So the change you see in the heart initially is an eccentric left ventricular hypertrophy. So this means an increase in volume in the left ventricle compared to with aging where you get the increase in muscle mass in the left ventricle. This eccentric left ventricular hypertrophy is usually associated with diastolic dysfunction. Now over time this pattern of left ventricular hypertrophy can change to a co-centric pattern as the systemic vascular resistance increases secondary to increased atherosclerosis. In terms of how this impacts function, the overall cardiac output is increased to match the O2 demand. The heart rate doesn't have any major change. Majority of the increase in cardiac output is achieved by the increase in stroke volume, mainly due to the increased preload, which means that when obese patients exercise, they rely on an increased heart rate to further increase their cardiac output. This is in stark contrast to elderly patients which rely on an increase in stroke volume to increase their cardiac output. In terms of vascular changes, we've already said that there's hypervolemia due to an activation of the renin-angiotensin system and a polycythemia in these patients. There's increased atherosclerosis and they have the hypercoagulable state. Finally, there isn't any major autonomic changes that you see, like we did with aging, that you see in obese patients. The key thing to understand and write in your SAQ answer and talking about an obese patient and the cardiovascular changes is to incorporate the respiratory changes of LSA and link this back to the potential of developing biventricular failure through the pulmonary hypertension pathway. So to quickly summarize these last two learning objectives, the subheadings for the learning objectives are cardiac changes, vascular or vessel changes and then autonomic changes. Within cardiac changes, you have conduction changes, structural changes, and functional changes. Now this finally brings us to the last learning objective for today, which is an amalgamation of a couple of learning objectives, which is define shock, describe the physiological consequences of shock, classify the different types of shock, and then outline how clinical signs of shock may be altered with age. To quickly knock off the last part of this learning objective, just go back to the basic principle that aging is a time-dependent process. Therefore, all changes become less obvious. The way this works out with clinical signs is that signs and symptoms of shock may be blunted in elderly, while late presentations might be associated with rapid deterioration. So don't expect an elderly patient to have rip-roaring increase in heart rate, a massive increase in temperature, a massive increase in respirate, just because their physiological capacity might not be able to mount that kind of response. Now going backwards and talking about shock and defining shock to begin with, we can say that shock is defined by life-threatening failure of adequate oxygen delivery to the tissue and may be due to decrease in blood perfusion to tissues, inadequate blood oxygen saturations, or increased oxygen demand. The four classic ways shock is categorized is hypervolemic, which is mainly due to fluid loss, cardiogenic, obstructive, and distributive. All these types of shock follow four stages and you might see patients at different parts of these clinical stages. The first stage is the initial stage. This is where hyperperfusion and decrease in oxygen delivery is starting to occur at the tissue level. At this stage, we're switching over to anaerobic metabolism and the serum lactate is starting to rise. From here, we move on to a compensatory stage which is where various mechanisms initiated by our own body are trying to restore normal physiology. From this we go to progressive stage. This is an important delineating stage because this is a stage where without external therapy shock will progress rapidly. Here you need to support the patient by giving them fluid, treating the type of shock and maintaining adequate oxygen delivery because at this stage you're starting to get irreversible cell damage. Finally the last stage of shock Is irreversible or refractory shock? Clinically in patients, this plays out with multi-organ failure leading to eventual death. Now before we talk about how to recognize and what differentiates those four classic categories of shock, we'll talk about this compensatory stage, so stage 2, and our body's own mechanisms to deal with shock. These can be divided into acute changes, subacute changes, and long-term changes. The initial acute change is recognition by our body that something is wrong. And the way this is picked up is by the arterial baroreceptor reflex. They detect a decrease in the stretch of the vessel walls and a decrease firing which subsequently leads to an increase in sympathetic nervous system output. This is coupled with a decrease in parasympathetic nervous system output and the result is an increase in heart rate, an increase in contractility, an increase in vasoconstriction and an increase in venoconstriction. All these temporarily increase cardiac output and aim to increase venous return. We typically say in patients with hemorrhagic shock, this response is able to compensate for a less than 10% loss in blood volume. The second acute response, which takes roughly 1-10 minutes to kick in, is a humeral response. This is instigated by a decrease in stretch in the heart detected by the low pressure baroreceptors. These lead to a decrease in ANP and an increase in ADH, all of which aims to increase sodium and water retention and decrease urine output. At the same time, the sympathetic activation is also activating the renin-angiotensin pathway, aiming to do the same thing. The next acute response is a rapid redistribution of blood volume and blood flow to critical organs. So typically the organs that are sacrificed first are the splanchnic circulation, the skeletal circulation and the skin. If the redistribution of those systems isn't enough, then you get redistribution from renal blood flow. And that's when you start to see those AKIs developing in patients that have shock. The two systems that our body tries to maintain its blood flow no matter what is the coronary circulation and the cerebral circulation. The next acute response is the mobilization of blood reservoirs. This goes hand in hand with the redistribution of blood flow. The typical mobilization sites include the skin, the pulmonary circulation and the hepatic circulation. Another acute response that can be thought of in the same line is the reabsorption of fluid. This takes time and it mainly targets the reabsorption through the lymphatic system. The last response our body has and this is when we're getting into the progressive and irreversible state of shock, is to have a massive CNS sympathetic surge. This surge occurs because of ischemia to our central nervous system. Now, we're not going to talk about the chronic changes because that'll be reserved for the SAQs and mainly when we talk about renal physiology. Just quickly, another way you can categorize our body's own response to shock Instead of talking about the acute, subacute and chronic changes, we'll be divided into system-based responses. And the two systems I'll talk about would be neural changes and then endocrine or hormonal changes. Both ways to approach a question about compensatory responses would be appropriate depending on your style. Now to go back to our four types of shock and finish today's pod, we're going to quickly look over them and how to differentiate them. So starting with hypovolemic shock, this is caused by an inadequate circulating blood volume which reduces cardiac output. The causes can be as simple as inadequate fluid intake, loss of fluids through things like vomiting and diarrhea, or third spacing in conditions like ascites associated with liver disease. The clinical characteristic signs of a patient with hypovolemic shock are usually an increase in heart rate, a decrease in blood pressure, a decrease in cardiac output, a delayed capillary refill, a cool peripheral temperature, a high SVR and a decrease in preload. Moving on to cardiogenic shock, this is due to a compromise in the cardiac pumping ability resulting in significant decrease in cardiac output. The classic causes here are ischemia, ventricular rupture, myocarditis or drug overdoses such as those like negative artetropes. Clinically with this type of shock, You also see an increase in heart rate, a decrease in blood pressure, a decrease in cardiac output, delayed capillary refill, again cool peripheries, a high SVR and in this case you get a high preload. This is because there's no issue in this case of getting blood to the heart, it's just that the heart cannot effectively pump the blood around the body. Then we have obstructive shock, which is mostly due to extra cardiac causes, leading to a decreased ability of the heart to fill. That reduced filling is not hypervolemia related, it's obstructive related. So the causes here can be things like PE, amniotic fluid embolism, a cardiac tamponade, a tension pneumothorax, and excessive positive pressure ventilation. The clinical parameters you see with this type of shock is an increase in heart rate, again, a decrease in blood pressure, a decrease in cardiac output, a delay in capillary refill, again, the peripheries are cool, the SVR here is high, and the preload here is low. That is the key differing factor between cardiogenic and obstructive shock. Then finally, we have distributive shock. This is classically due to sepsis, but also involves conditions such as neurogenic shock and anaphylaxis, and it's a profound state of vasodilation. Here, clinically, you see the increase in heart rate, you see a decrease in blood pressure, the cardiac output may or may not be increased, the capillary refill is delayed, but the extremities are warm, and that is a key component. for this type of shock. The SVR overall is low and the preload might be low or low normal. But the key differing factor is if you have someone with this type of shock, when you feel their peripheries, it will be warm. So that will do it for part 1 of this topic. Applied cardiac physiology is a mammoth topic to cover. I'll be back with part 2 covering all the SEQs associated with the learning objectives we've gone through today. But until then guys. Good luck with your studying, good luck with your Viva Prep if you're sitting the exam currently and I'll catch you next time on counter 10.

Today's episode will cover the learning objectives and the second part we'll look at the SAQs attached to these learning objectives. I hope everyone's doing well at the moment. I know it's a stressful time preparing for Vibers.

I'm planning to have another live practice Viber demonstration very soon and that'll hopefully be released for you guys within the next two weeks. I will also be finishing this Cardiac series before the Vibers in October and then I'll have some special guests come on to do some topics of interest before we move on to our next series. So with those few announcements done and dusted, Let's dive straight into today's pod. 1, 2, 3, 4 The first learning objective today is outline the physiological changes that occur with and the implications for anaesthetic management of pneumoperitoneum.

A pneumoperitoneum occurs during laparoscopic surgery where typically a gas, being CO2, is insufflated into the peritoneal cavity. This gas is introduced at a rate, typically 4 litres per minute, to achieve an intra-abdominal pressure that can range from anywhere between 5 to 15 millimetres of mercury. The gas is then constantly supplied to maintain that pressure throughout the period of surgery. The physiological effects of this pneumoperitoneum can be divided into 1. the increase in intra-abdominal pressure, and secondly, the carbon dioxide absorption.

So looking at the first effect of the increase in intra-abdominal pressure, we can see the effects of this by dividing into a multi-system approach. On the cardiovascular system, there's an initial auto-transfusion of blood from the splanchnic circulation that leads to a transient increase in venous return, which leads to a corresponding increase in cardiac output. Then, as intra-abdominal pressure increases, There's compression of the venous circulation, mainly the IVC, that decreases venous return.

Subsequently, we have a decrease in cardiac output secondary to this. At the same time, anemoperitoneum is a very stimulating procedure and therefore the sympathetic nervous system is activated. This activation of the sympathetic nervous system leads to an increase in vascular resistance as well as an increase in heart rate. Overall, the effects of an increase in sympathetic nervous system is to maintain or increase the cardiac output. Typically when the intra-abdominal pressures are kept between five to 15 millimeters of mercury, that increase in sympathetic nervous system typically outweighs the decrease in venous return.

Therefore, overall, the cardiac output usually stays the same. It's only when you start to get really high intra-abdominal pressures that you see that balance tip into the favor of decreasing cardiac output. The other way you see that balance tip is in patients that might have some physiological compromise. These can be in patients that have been fasted for too long or have a decrease in intravascular volume prior to the pneumoperitoneum being applied.

The other important thing with the CVS response to a pneumoperitoneum is the initial stretch of the peritoneum itself. The peritoneum is very vaguely supplied and therefore the initial stretch can lead to an increase in parasympathetic surge and this can lead to a vagal response. So you do need to be careful of this specifically in patients that might already be running close to the bradycardic side.

Then for completion's sake, the other effects of an increase in intra-abdominal pressure on the other body systems include the respiratory system, where an increase in pressure leads to a capillar shift of the diaphragm, and this subsequently decreases the FRC. Along with this, you have a decrease in respiratory compliance, basal atelectasis, and an increase in the VQ mismatching. The subsequent effect of this is an increased propensity for hypoxemia and hypercarbia. The GI effects are pretty self-explanatory. There's an increased predisposition to gastric regurgitation and therefore majority of patients that have laparoscopic surgery usually end up getting a tube.

But also you need to be careful at what pressures surgeons set the intra-abdominal pressures at because this can not only affect the splenic blood flow but also cause mechanical compression to the intra-abdominal viscera which is sensitive to ischemia. Then, the renal effects include a decrease in renal function as a combination of the intra-abdominal pressure increasing and the sympathetic activity increasing. This accounts for the decrease in renal blood flow, GFR, and a slight drop in urine output that you might see in patients having laparoscopic surgery. Additionally, ADH is typically released as a compensatory mechanism as well as due to the stress of surgery, which further exacerbates the urine output and can lead to oligouria.

Then finally, you have neurological side effects from the increase in intra-abdominal pressure. Mainly, this is a slight increase in ICP as a result of both decreased cerebral blood flow drainage, typically on the venous side, and cerebral hyperperfusion induced by hypercarbia, if that's not controlled for. So the second effect of Neuroperitoneum, being the carbon dioxide absorption, is pretty self-explanatory.

Because CO2 is rapidly absorbed from the peritoneal cavity, you get an increase in the arterial partial pressure of CO2, and this leads to an increase in sympathetic activity. As a result, you can get tachycardia and razor constriction, and then you have all the biochemical effects of an increase in partial pressure of CO2, with the main one being a change in pH to a more acidic environment. The second learning objective today is outline the physiological changes that occur with CO2.

and the implication for anaesthetic management of the following patient positions. Number one, supine. Number two, Trendelenburg and reverse Trendelenburg.

Number three, lateral. Number four, lithotomy. And number five, prone. Before we talk about these specific positions, it's important to think about the circulatory system as residing in a column. For arterial and venous system, both are affected by hydrostatic pressure from gravity.

So if you take the heart as a middle point in a person who's standing up, you'd expect the arterial pressure to be higher at their feet, while at their head, you'd expect that pressure to be lower than what it is at the heart. And the way we quantify this difference is saying that typically, a change in vertical length by 2.5cm changes the pressure by 2mmHg on the arterial system. So now looking at those specific positions, Supine being the most common position for majority of surgeries, the head, neck and spine are all in neutrality.

So while a pressure difference is seen in terms of vertical height, the pressure along the long axis of the body is virtually the same. Now if you take that supine person and put them Trendelenburg, which is head down position from supine, typically 10 to 20 degrees, what you're doing here as described by Miller's, is initially the placement in a head down position will increase the cardiac output by approximately 10% in less than one minute due to auto-transfusion from the lower extremities. This effect is not sustained and with approximately 10 minutes passed, the cardiac output returns back to its baseline. So overall, the acute changes going in Trendelenburg involve an increased initial blood pressure by 5-10%, an increase in cardiac output, the heart rate usually stays the same, And by 10 to 15 minutes, these changes have all kind of gone back to normal. Now you can imagine if you go reverse Trendelenburg, the opposite occurs.

You get a shift of that blood volume into the lower extremities, dropping your blood pressure through a decrease in venous return. Importantly, you also have to recognize that this leads to a decrease in pressure within the cerebral system. Therefore, the cerebral perfusion pressure takes a hit when you put a patient into a reverse Trendelenburg position or in a sitting position. Now the other positions mentioned in this landing objective being lithotomy is pretty self-explanatory.

It's kind of in between a normal Trendelenburg position because you have the legs abducted and the knees flexed. This leads to a slight increase in the venous return therefore a slight transient increase in blood pressure. With lateral you don't really see too many changes and with prone you don't see too many changes either.

So following on from this the better question is Why are these changes so prominent under an anesthetic? This is because an anesthetic has major impacts on the cardiovascular system and this involves both a general anesthetic and a neuraxial anesthetic. In terms of a GA, you get the blunting of our baroreceptor reflex which normally helps to compensate for these changes in position. Along with this, our cardiac output is normally decreased because majority of the agents we give cause a negative inotropy decreasing our cardiac output. They lead to an increase in vasodilation, decreasing our systemic vascular resistance, therefore decreasing both our blood pressure and MAP.

And at high concentrations, certain agents like Siboflurane can also alter the autoregulation within different regional circulations of our body. Then as an additive effect, drugs like opioids can blunt the sympathetic response. Therefore, the normal responses like an increase in heart rate, an increase in blood pressure, and an increase in cardiac output that you'd normally see with a sudden change in posture in an awake person are typically lost in an anesthetized patient. Now for a patient having a neuraxial, the effect on the cardiovascular system with a change in position is very dependent on the level of where your neuraxial blockade sits. Remembering that our sympathetic nervous system sits in our thoracolumbar region from T1 to L2 and the degree of sympathomomectomy will be dependent on how much of these fibers are blocked with the neuraxial.

If a patient only has a sacral blockade Then only the sacral parasympathetic nervous systems will be blocked, having a very limited effect on the total vascular tone. Then when you have a lumbar blockade at a low level or a low thoracic blockade, you're going to get some changes of the cardiovascular system because now you're starting to block some of those sympathetic nervous system fibers. However, you still have some compensatory mechanisms left up your sleeve.

These include above the level of blockade, increasing the arterial and venous tone to increase preload and cardiac output, the ability to still activate those baroreceptor reflexes, and therefore increase heart rate, increase contractility, and increase sympathetic tone to the nerves that aren't blocked yet, as well as activate the low pressure baroreceptors so that compensatory mechanisms within the renal system can also be activated, like an increase in ADH, an increase in sodium and water retention, and a decrease in urine output. But when you start to move into a high thoracic blockade and a brainstem blockade, that's when you start to have some real issues. With a high thoracic blockade, as soon as you block fibers T6 and up, now you're starting to block the cardio-axillary fibers that affect the heart. So those compensatory mechanisms just won't work anymore.

Then going into the brainstem, now you're knocking off the vasomotor center in the medulla, and so you're inhibiting the sympathetic nervous system outflow at its origin. The caveat to recognize with a near axial is that the effects on the cardiovascular system can be exaggerated in certain conditions. These involve hypovolemia, pregnancy, and then pathological states like fixed cardiac output states, such as severe mitral stenosis or aortic stenosis, where a sudden change might not allow the heart to be able to compensate for a decrease in blood pressure and cardiac output.

Now the next learning objective we're going to look at is discuss the cardiovascular response to exercise, valsalva, positive pressure ventilation and PEEP. Exercise to me is an interesting one. A lot of changes need to occur at the same time to meet the overall goal which is to meet the increase in O2 and nutrient demand at the tissue level as well as increase the removal of CO2 you and waste metabolites. So to do this effectively, a few different systems need to be able to work in harmony to achieve this goal. And I think in Papano, this is summarized really well.

So in anticipation of exercise, vagal impulses are generally decreased, while sympathetic nervous system increases are generally increased by central command. This is known as cerebro-cortical activation. The overall increase in cardiac output that you see in exercise. is mainly accomplished by an increase in heart rate rather than an increase in stroke volume. As you continue to exercise, it's the increase in body temperature with the inability to offload all this heat that leads to the feeling of exhaustion and initially you stopping exercising.

So here with exercise, we have a few key terms and diagrams that you could be asked about in a Viva setting. One of those terms is VO2 max. This represents the maximum ability to take in and transport oxygen.

In other words, it's the functional aerobic capacity. The other important term to know is anaerobic threshold. This is when the O2 supply cannot keep up with the demand. It typically occurs between 40 to 60% of the VO2 maximum. And this is the graph that you might be shown in Aviva, which has lactate on the Y axis and intensity on the X axis.

This graph looks typically linear. until a certain point where you get an exponential increase in lactate production, typically recognized as an anaerobic threshold. The other two terms useful to know around exercise is isotonic exercise and isometric exercise. These are important because they have different physiological implications on the cardiovascular system. Isotonic exercise aka dynamic exercise, so typically the exercise that you do like running, has a very different effect on the cardiovascular system compared to isometric exercise aka static exercise such as powerlifting, or any type of exercise where you have a sustained contraction.

With the dynamic type of exercise, you're getting constant contraction and relaxation of the muscle, which leads to an overall decrease in total peripheral vascular resistance. Due to this, there's dilation of the capillary beds, secondary to the buildup of active metabolites, and this leads to an overall decrease in systemic vascular resistance. Now in contrast with static exercises, where you have that sustained contraction of the muscle, there's a constant compression of the capillary bed.

Therefore, those active metabolites can't really be extruded out of that area, as well as blood flow into that area is restricted. This leads to an increase in total peripheral resistance and an increase in afterload. And then all of a sudden, once that sustained contraction is released, now you get that massive pooling of blood into those blood vessels, as well as those active metabolites being released, leading to an overall systemic drop in blood pressure.

which can be why people pass out after doing things like a deadlift if you've never practiced it before. Not only that, doing the different types of exercise between static and dynamic also has different compensatory mechanisms on the cardiovascular system. Dynamic exercise will usually lead to an increase in mitochondria within the heart and skeletal muscle, will lead to an eccentric hypertrophy, which is normally an increase in LV volume.

In comparison, isometric or static exercise will lead to a concentric hypertrophy of the heart as well as skeletal muscle hypertrophy. So I think those are the important terms to know when talking about exercise within the cardiovascular system. And now we'll look at the Valsalva maneuver. A Valsalva maneuver has multiple definitions in varied text but the way I define it is a forced expiration against a closed glottis which requires an airway pressure of 40 millimeters of mercury. to be held for 15 seconds.

The main reason the Valsalva maneuver produces a myriad of cardiovascular responses is because of the rise in intrathoracic pressure. The classical responses from the Valsalva can be divided into four phases, and there's a picture which depicts these four phases. Phase one is the onset of maneuver, at which the blood pressure increases and a heart rate decreases transiently. This occurs because there's a sudden rise in intrathoracic pressure, which causes compression of the pulmonary veins, increasing flow of the blood into the left ventricle, increasing preload and increasing cardiac output.

That increase in cardiac output and more specifically the increase in blood pressure causes a stretch on the aortic and carotid bioreceptors causing an increasing firing rate and leading to a decrease in sympathetic tone which leads to a decrease in heart rate. Phase 2 is then a decrease in venous return. This occurs due to the ongoing raised intrathoracic pressure.

This has an effect on both the left and the right side of the heart. On the right hand side, there is decreased venous return due to the decrease in gradient favouring blood returning to the right side of the heart. On the left hand side, the ongoing compression of the pulmonary veins means that the LV preload is also compromised. As a result, during this stage, cardiac output decreases and blood pressure decreases. This leads to decreased firing of the arterial baroreceptors and therefore an increase in sympathetic activity.

As a result, The heart rate and blood pressure both start to gradually increase during phase 2. Phase 3 is immediately after the release of the airway pressure. Here you have a sudden drop in the intrathoracic pressure, which leads to a sudden decrease in blood pressure associated with a sudden increase in heart rate. The reason this occurs is because of the pulmonary vessels suddenly expanding. These pulmonary vessels don't have much blood volume, therefore the left ventricle preload is further compromised leading to a decrease in cardiac output. As a result the blood pressure is lowered and the arterial baroreceptors decrease their firing rate even further to subsequently therefore increase sympathetic tone leading to an increase in heart rate.

Then you have phase four which is the return to baseline of the normal intrathoracic pressures. In this stage the venous return has now adjusted back to normal which normalizes the overall cardiac output. However, the increase in sympathetic tone still exists due to the activation of the baroreceptor reflex. Therefore, for a brief moment, you get an overshoot of the blood pressure because of the normalization of the cardiac output along with the vasoconstriction still present from phase 3. And this overshoot in blood pressure increases the firing rate of the arterial baroreceptors and leads to a secondary decrease in heart rate. So if I was to depict these changes in phase 1 through to 4, I would have a graph, would have 1 airway pressure from 0 to 40, 2 blood pressure and then 3 heart rate all on the y-axis.

On the x-axis would be time and the initial phase, phase 1, would be the activation of the high airway pressures as well as an increase in blood pressure and a decrease in heart rate. Subsequently in phase two you get a decrease in blood pressure which starts to slowly come back to its normal baseline but doesn't reach its baseline and you get a linear increase in heart rate. With phase three which is the release of the airway pressure you get another drop in blood pressure and this is met with an increase in heart rate even further.

Finally in phase four you get an overshoot of the blood pressure and a reflex bradycardia secondary to this. For the exam, you'd be expected to be able to draw that diagram both in an SAQ and replicate that in a VARVA setting if needed. The important utility of a VALSALVA is three things.

Firstly, it can clinically assess the autonomic nervous system. And the way you can do that is looking at the heart rate that's maximum in phase 2 divided by the heart rate that's minimum in phase 4. The normal value for this ratio should be greater than 1.5. and a value less than this suggests autonomic dysfunction. And this is a good test in someone that's, say, diabetic that might have autonomic instability.

The second utility of a Valsalva is it can be used in clinical conditions to treat or terminate SVTs. This occurs due to the reflex parasympathetic tone, which is achieved by phase 4. The final utility of the Valsalva is for the surgeons. The increase in venous back pressure can help to see if there's any surgical sites of bleeding, as well as for us clinically.

it can help to assess a patient's murmur. A valsalva overall decreases preload, so murmurs that are typically affected by this are murmurs due to hypertrophic obstructive cardiomyopathy or due to mitral valve prolapse. The last thing you should be able to know about the valsalva manoeuvre is how this changes in different clinical conditions. The classical condition is a patient with a heart transplant.

Here, their autonomic nervous system is de-innervated from their heart. and therefore their heart rate stays exactly the same and only the blood pressure changes during a Valsalva maneuver. You can also expect a similar picture in someone that's beta blocked, while someone who's alpha blocked might not get the BP overshoot in phase 4. Now finally to finish this learning objective, we're going to look at the effects on the cardiovascular system of positive pressure ventilation and PEEP. If you can understand the Valsalva maneuver, you'll be able to understand this very easily.

The fundamental principle goes back to understanding what happens during spontaneous breathing. During inspiration with spontaneous breathing, you get a decrease in the right atrial pressure, therefore improving the gradient for venous return in the right side of the heart. This goes back to the vascular function curves and understanding when right atrial pressure is lower, you get an improvement in venous return. At the same time during inspiration, the pulmonary alveolar pressures are increased. This is limiting blood flow through the lung vasculature, therefore on the left side of the heart you get a decrease in the left ventricular preload leading to a decrease in cardiac output during inspiration.

With spontaneous expiration this process reverses, so on the left side of the heart you get an improvement in the left ventricle preload and on the right side of the heart you get a decrease in venous return. As a result what we say with spontaneous breathing, on inspiration you have a decrease in cardiac output and on expiration you have an increase in cardiac output. This process is ultimately reversed when you apply positive pressure ventilation. Now on inspiration there's a positive intrathoracic pressure and I like to divide the effects of PPV again into what happens on inspiration and expiration.

The other way you can divide it is by what happens on the right side of the heart and what happens on the left side of the heart. So on inspiration initially the blood is squeezed from the pulmonary vessels because of the initial increase in pressure. Therefore, temporarily, left atrium filling is increased and therefore left ventricular preload is increased. So initially, you get a transient increase in the LV output. Later, with that continued inspiration, the right atrial pressures are now increasing.

This is limiting the gradient for venous return. Not only this, but the right ventricle afterload is increased because of the increased pressure within the alveoli. This ultimately means throughout the inspiration breath, Less blood is flowing through the lungs to the left side of the heart, leading to an ultimate decrease in cardiac output.

Not only is the preload decrease in the left ventricle, but also there's a concept of ventricular interdependence that is occurring here. This is the concept that the output of both ventricles is affected by one another. Because the RV has an increase in afterload during inspiration and thereby an increase in pressure, the septum that separates the left and right ventricle is bulged into the left ventricular cavity. Now you have decreased room for LV filling and therefore overall a decrease in preload and output secondary to this. The effect of expiration with PPV is that you get that loss of that positive intrathoracic pressure.

Now initially the pulmonary vessels can re-expand and so temporarily because those pulmonary vessels are expanding and don't have much volume to begin with the left atrial filling is temporarily decreased. However as expiration continues the right atrial pressures start to decrease from those really high positive values during the inspiration This allows the venous return to normalize and not only that, the right ventricle afterload is also decreased and that interdependence is having less of an effect here. All of this means that the left ventricle output is actually increased during expiration.

This concept of understanding what's happening with inspiration and expiration with positive pressure ventilation is really important and it can have major clinical effects. The classic example is if you get patients with obstructive shock. So this would be either a massive PE or cardiac tamponade.

In these cases, the heart is preload dependent. So you want to maintain spontaneous inspiration for as long as possible to have that natural increase in venous return during inspiration. That's why the classical teaching exists that if you're inducing someone with an acute cardiac tamponade, you try to keep them spontaneously breathing for as long as possible. Because a sudden jolt of positive pressure ventilation can decrease the preload just enough to tip the person in a balance where they go into a cardiac arrest.

Now what about PEEP? Think about PEEP as a continued inspiration breath with positive pressure ventilation. All of a sudden, you don't have that expiration phase, you do technically, but during that expiration phase, a positive pressure is continually applied. Now that doesn't necessarily mean that the cardiac output is compromised during the whole of expiration due to PEEP. There is varying degrees of effect depending on the amount of PEEP that's applied.

So PEEP like anything has a range. You can have low PEEP, medium PEEP or high PEEP. When you get into the high PEEP that's when you're going to have those negative effects on the cardiac output.

This is talking numbers like 15 centimeters of water to 20 centimeters of water. The PEEP that's commonly applied with any kind of stock standard ventilation of five centimeters of water generally does not have a major effect of increasing right atrial pressures or changing cardiac output too much. Again, the clinical context matters. When you're being really pedantic and you have a person with a tight head who's got an increased intracranial pressure and you wanna do all the normal factors to decrease ICP, some people will go with zero PEEP just to make sure there's no increase in cerebral venous pressure.

There's various studies that show that five centimeters of PEEP is safe, even with a tight head and a neuro case, but you might be seeing some of your consultants do this. because of this concept. The other important thing to recognize with PEEP is not only does it have some positive respiratory effects, but it can also have positive cardiovascular effects. If a patient is in a fluid overload state, such as congestive cardiac failure, that decrease in preload can help shift the person back into the sharp part of the Frank Starling curve. That's why as part of your treatment regime for anyone that's an acute APO is either to give them BiPAP, CPAP, or some form of positive and expiratory pressure to help the LV perform better.

So this concludes this learning objective and takes us on to our next learning objective, which is describe the cardiovascular changes that occur with aging. Just like we did with respiratory physiology, you need a good structure when talking about aging or changes like obesity. With respect to cardiovascular changes, I break down the changes with aging into three components. These are the cardiac changes, the vessel changes and the autonomic changes. As we all know, aging is a physiological time-dependent process which results in a decrease in cellular function and reserve.

Therefore, you can assume it's going to have a major impact on the cardiovascular system. With regards to the cardiac changes, this can be further divided into conduction changes, structural changes and functional changes. For the conduction changes, fibrous infiltration of the SA node leads to the loss of the pacemaker cells.

Therefore there's an increased risk of arrhythmia and ventricular ectopics. The AB node and the bundle of his usually remain unchanged. There's some loss of the Pekingi fibers going to the ventricles. And overall, there's a reduction and a decrease in function of the catecholamine receptor density. The max heart rate also decreases.

And the classic formula for this is max heart rate is equal to 220 minus the patient's age. Now, in terms of the structural changes, overall, there's an increase in collagen and fibrous tissue deposition within the myocytes. This impairs compliance of the heart. Coupled by the fact that there's decrease in myocyte numbers, but there's an increase in myocyte size.

Therefore, the myocardial wall thickness becomes larger and co-centric. At the same time, the valves of the heart are also becoming calcified, and therefore there's increased risk of valvular incompetence. Now with regards to how this affects functional changes, a decrease in compliance means a decrease in left ventricular filling, and therefore a greater reliance on the atrial kick. for diastolic filling.

Overall, a change in cardiac output relies more on a change in stroke volume than in heart rate because the max heart rate that can be achieved is decreased as we age. And that is a really key important point to understand of the physiological changes in elderly patients as compared to obese patients which we'll talk about in the next learning objective. Other things that contribute to a decrease in cardiac output with aging are just a sedentary lifestyle which leads to an overall general decrease in the cardiac output. Now looking at the vessel and the vascular changes, the large artery elasticity decreases and therefore the compliance in these arteries decreases. The intimal walls of the arteries thicken and there's increased calcification leading to decreased compliance.

At the same time, there's loss of that endothelial function that as we touched upon with our last podcast is really important within the vascular system. So decrease in nitric oxide release means there's decreased adaptability of vessels to a change in pressure. The net effect is that you see an increase in systemic vascular resistance and total peripheral resistance with elderly patients and this means that the blood pressure is very variable to any sudden changes such as those that we give with giving a general anesthetic. They normally say that the resting blood pressure both systolic and MAP increase as we age but diastolic pressure doesn't increase as much as those two. because of the rapid runoff of blood in stiff large arteries.

Now in terms of the final heading for changes with aging, being autonomic changes, we've already kind of touched on this. So there's a decrease in beta receptor responsiveness to catecholamines, and as well there's impaired baroreceptor response due to a decreased sensitivity making the blood pressure more labile. This is one of the reasons why you see in elderly patients the classic symptoms of orthostatic hypotension.

Now let's talk about our next learning objective which is describe the cardiovascular changes that occur with morbid obesity. It's again going to follow that same pattern of using the three subheadings that are cardiac changes, vascular changes and autonomic changes. The key difference to understand is that the pathogenesis behind obesity is different to aging.

With obesity there is an increase in total visceral fat. It is this fundamental change that starts to act as its own endocrine organ. secreting hormones and inflammatory peptides that are collectively called adipokines. The four main adipokines that you should know of is one, leptin, which has a major role in the cardiovascular changes. It has direct effects on causing vasoconstriction, leading to an increase in blood pressure, cardiac remodeling, and specifically, left ventricular hypertrophy.

The second adipokine is angiotensinogen. Now, this is normally produced in the body, especially in the liver, but in obesity, it's also produced by adipocytes. This leads to an increased substrate for ACE and therefore an increased activation of the renin-angiotensin system.

Secondary to this, you get increased vasoconstriction, increased water retention and increased sodium retention, all leading to an increase in blood volume. The third adipokine change is increase in plasminogen activator inhibitor 1. This means that there's overall decreased fibrinolytic activity and overall obese patients are in a hypercoagulable state. Therefore, they're an increased risk of PEs and DVTs.

The final adipokine is resistant. This leads to decreased cardiac contractility and can also induce cardiomyocyte hypertrophy. So to delve into this further, just like we did with the aging, we can say that the cardiac conduction changes include fatty infiltration of the heart, which places an increased risk of phenomenons such as long QT, arrhythmias, specifically AF and AV blocks. Changes in the QRS mainly due to the remodeling of the heart and an increased propensity to have left ventricular hypertrophy.

And associated with this, we can have left axis deviation, the structural changes we've already alluded to, You get a left ventricular hypertrophy secondary to the increase in preload and increase in stroke volume. You have a higher left ventricular end diastolic pressure and coupled with this, the fatty infiltrates lead to a decreased compliance of the heart. Initially, the systemic vascular resistance is low because the adipocytes provide parallel capillary beds that help to decrease the resistance overall to the increase in blood volume. So the change you see in the heart initially is an eccentric left ventricular hypertrophy. So this means an increase in volume in the left ventricle compared to with aging where you get the increase in muscle mass in the left ventricle.

This eccentric left ventricular hypertrophy is usually associated with diastolic dysfunction. Now over time this pattern of left ventricular hypertrophy can change to a co-centric pattern as the systemic vascular resistance increases secondary to increased atherosclerosis. In terms of how this impacts function, the overall cardiac output is increased to match the O2 demand. The heart rate doesn't have any major change.

Majority of the increase in cardiac output is achieved by the increase in stroke volume, mainly due to the increased preload, which means that when obese patients exercise, they rely on an increased heart rate to further increase their cardiac output. This is in stark contrast to elderly patients which rely on an increase in stroke volume to increase their cardiac output. In terms of vascular changes, we've already said that there's hypervolemia due to an activation of the renin-angiotensin system and a polycythemia in these patients.

There's increased atherosclerosis and they have the hypercoagulable state. Finally, there isn't any major autonomic changes that you see, like we did with aging, that you see in obese patients. The key thing to understand and write in your SAQ answer and talking about an obese patient and the cardiovascular changes is to incorporate the respiratory changes of LSA and link this back to the potential of developing biventricular failure through the pulmonary hypertension pathway. So to quickly summarize these last two learning objectives, the subheadings for the learning objectives are cardiac changes, vascular or vessel changes and then autonomic changes. Within cardiac changes, you have conduction changes, structural changes, and functional changes.

Now this finally brings us to the last learning objective for today, which is an amalgamation of a couple of learning objectives, which is define shock, describe the physiological consequences of shock, classify the different types of shock, and then outline how clinical signs of shock may be altered with age. To quickly knock off the last part of this learning objective, just go back to the basic principle that aging is a time-dependent process. Therefore, all changes become less obvious.

The way this works out with clinical signs is that signs and symptoms of shock may be blunted in elderly, while late presentations might be associated with rapid deterioration. So don't expect an elderly patient to have rip-roaring increase in heart rate, a massive increase in temperature, a massive increase in respirate, just because their physiological capacity might not be able to mount that kind of response. Now going backwards and talking about shock and defining shock to begin with, we can say that shock is defined by life-threatening failure of adequate oxygen delivery to the tissue and may be due to decrease in blood perfusion to tissues, inadequate blood oxygen saturations, or increased oxygen demand. The four classic ways shock is categorized is hypervolemic, which is mainly due to fluid loss, cardiogenic, obstructive, and distributive.

All these types of shock follow four stages and you might see patients at different parts of these clinical stages. The first stage is the initial stage. This is where hyperperfusion and decrease in oxygen delivery is starting to occur at the tissue level. At this stage, we're switching over to anaerobic metabolism and the serum lactate is starting to rise.

From here, we move on to a compensatory stage which is where various mechanisms initiated by our own body are trying to restore normal physiology. From this we go to progressive stage. This is an important delineating stage because this is a stage where without external therapy shock will progress rapidly.

Here you need to support the patient by giving them fluid, treating the type of shock and maintaining adequate oxygen delivery because at this stage you're starting to get irreversible cell damage. Finally the last stage of shock Is irreversible or refractory shock? Clinically in patients, this plays out with multi-organ failure leading to eventual death. Now before we talk about how to recognize and what differentiates those four classic categories of shock, we'll talk about this compensatory stage, so stage 2, and our body's own mechanisms to deal with shock.

These can be divided into acute changes, subacute changes, and long-term changes. The initial acute change is recognition by our body that something is wrong. And the way this is picked up is by the arterial baroreceptor reflex. They detect a decrease in the stretch of the vessel walls and a decrease firing which subsequently leads to an increase in sympathetic nervous system output.

This is coupled with a decrease in parasympathetic nervous system output and the result is an increase in heart rate, an increase in contractility, an increase in vasoconstriction and an increase in venoconstriction. All these temporarily increase cardiac output and aim to increase venous return. We typically say in patients with hemorrhagic shock, this response is able to compensate for a less than 10% loss in blood volume. The second acute response, which takes roughly 1-10 minutes to kick in, is a humeral response.

This is instigated by a decrease in stretch in the heart detected by the low pressure baroreceptors. These lead to a decrease in ANP and an increase in ADH, all of which aims to increase sodium and water retention and decrease urine output. At the same time, the sympathetic activation is also activating the renin-angiotensin pathway, aiming to do the same thing.

The next acute response is a rapid redistribution of blood volume and blood flow to critical organs. So typically the organs that are sacrificed first are the splanchnic circulation, the skeletal circulation and the skin. If the redistribution of those systems isn't enough, then you get redistribution from renal blood flow.

And that's when you start to see those AKIs developing in patients that have shock. The two systems that our body tries to maintain its blood flow no matter what is the coronary circulation and the cerebral circulation. The next acute response is the mobilization of blood reservoirs.

This goes hand in hand with the redistribution of blood flow. The typical mobilization sites include the skin, the pulmonary circulation and the hepatic circulation. Another acute response that can be thought of in the same line is the reabsorption of fluid. This takes time and it mainly targets the reabsorption through the lymphatic system.

The last response our body has and this is when we're getting into the progressive and irreversible state of shock, is to have a massive CNS sympathetic surge. This surge occurs because of ischemia to our central nervous system. Now, we're not going to talk about the chronic changes because that'll be reserved for the SAQs and mainly when we talk about renal physiology.

Just quickly, another way you can categorize our body's own response to shock Instead of talking about the acute, subacute and chronic changes, we'll be divided into system-based responses. And the two systems I'll talk about would be neural changes and then endocrine or hormonal changes. Both ways to approach a question about compensatory responses would be appropriate depending on your style.

Now to go back to our four types of shock and finish today's pod, we're going to quickly look over them and how to differentiate them. So starting with hypovolemic shock, this is caused by an inadequate circulating blood volume which reduces cardiac output. The causes can be as simple as inadequate fluid intake, loss of fluids through things like vomiting and diarrhea, or third spacing in conditions like ascites associated with liver disease. The clinical characteristic signs of a patient with hypovolemic shock are usually an increase in heart rate, a decrease in blood pressure, a decrease in cardiac output, a delayed capillary refill, a cool peripheral temperature, a high SVR and a decrease in preload. Moving on to cardiogenic shock, this is due to a compromise in the cardiac pumping ability resulting in significant decrease in cardiac output.

The classic causes here are ischemia, ventricular rupture, myocarditis or drug overdoses such as those like negative artetropes. Clinically with this type of shock, You also see an increase in heart rate, a decrease in blood pressure, a decrease in cardiac output, delayed capillary refill, again cool peripheries, a high SVR and in this case you get a high preload. This is because there's no issue in this case of getting blood to the heart, it's just that the heart cannot effectively pump the blood around the body. Then we have obstructive shock, which is mostly due to extra cardiac causes, leading to a decreased ability of the heart to fill.

That reduced filling is not hypervolemia related, it's obstructive related. So the causes here can be things like PE, amniotic fluid embolism, a cardiac tamponade, a tension pneumothorax, and excessive positive pressure ventilation. The clinical parameters you see with this type of shock is an increase in heart rate, again, a decrease in blood pressure, a decrease in cardiac output, a delay in capillary refill, again, the peripheries are cool, the SVR here is high, and the preload here is low.

That is the key differing factor between cardiogenic and obstructive shock. Then finally, we have distributive shock. This is classically due to sepsis, but also involves conditions such as neurogenic shock and anaphylaxis, and it's a profound state of vasodilation. Here, clinically, you see the increase in heart rate, you see a decrease in blood pressure, the cardiac output may or may not be increased, the capillary refill is delayed, but the extremities are warm, and that is a key component. for this type of shock.

The SVR overall is low and the preload might be low or low normal. But the key differing factor is if you have someone with this type of shock, when you feel their peripheries, it will be warm. So that will do it for part 1 of this topic. Applied cardiac physiology is a mammoth topic to cover. I'll be back with part 2 covering all the SEQs associated with the learning objectives we've gone through today.

But until then guys. Good luck with your studying, good luck with your Viva Prep if you're sitting the exam currently and I'll catch you next time on counter 10.

Transcript for:Insights on Cardiovascular Physiology

Transcript for:
Insights on Cardiovascular Physiology