[Music] welcome to ICU Primary Prep cast this is our another snippet and again I'm joined by Dr Mike Clifford and Mike this time we are going to talk about some cardiovascular physiology so what are the physiological determinants of cardiac output so this is a an absolute cracker of an siq Scorpio I didn't write it but this is a an aripa and it seems very simple and the tendency is for people to get a little bit lost in the weight here so it's very important that we we break down um this question into the physiological determinants of cardiac output okay and it's not a hard question we all know what cardiac output is so you might start with cardiac output as the quantity of blood pumped out of the left ventricle each minute and then give a number say five liters for a 70 kilogram man at sea level and then we always write cardiac output equals heart rate time stroke volume and then all of a sudden you you know how to answer that question because you can talk a little bit about heart rate as a determinant of that cardiac output and the things that affect heart rate and then you can talk about stroke volume and that gets you into that lovely set of preload afterload contractility and once you've done that event you've passed the question no doubt so this is not a hard question to pass you've just got to make sure you write something in each of those headings and then don't spend too long writing the same thing over and over again because the tendency here is because it's relatively easy that you'll spend too long on this question so this is one of those questions where I tell candidates make sure you only write for eight minutes and then move on go and start writing something about that horrible question on you know the blood flow in the in the placenta because you'll pass this question easily so don't get who bog down so let's go to that that little formula cardiac out what equals heart rate time stroke volume so heart rate is determined by the balance of the autonomic nervous system obviously the sympathetic nervous system and the the parasympathetic nerve system the sympathetic nervous system are the the outflow of fibers from T1 to T4 from the cardiac plexus and the vagal fibers distributed to the Atria the cyanoatrial node and less the so that's usually the right-sided vagus nerve and the left side of vagus nerve tends to have its fibers at the to the AV node so the dominance of those two agencies will determine your heart rate and we know that there is a sort of a maximal effect of heart rate because as you increase your heart rate from the normal level of about 60 to 70 beats a minute up to about 200 you get a almost linear increase in cardiac output and that's the day-to-day increase in cardiac output that we require if I want to make you walk up a set of a set of stairs the first thing that will happen is that you will increase your heart rate you don't do a lot of increasing cardiac output by changing your stroke volume it's largely it's just increased your heart rate but if you keep going up and up and up you'll reach a point where you've got something called the maximal heart rate and that's often age-dependent and it's your maximal heart rate you've narrowed your diastolic filling time so much that you've capped out any increase okay and if you increase your heart rate even further than that it'll start to tail off so that's that classic description of what happens when you Pace a heart and why it is that you don't get a an inexorable rise in cardiac output that you get a a cap out but for most of us day to day in our lives we won't reach that at maximal heart rate unless we're really pushing ourselves in an exercise way so to all intents and purposes the way we change our cardiac output is we increase our heart rate but the other part of that equation is obviously stroke volume and stroke volume is dependent on three feet so we'll talk about that so preload is the degree to which The myocardium is stretched before it contracts and that's essentially the Frank styling law of the heart where your muscle fiber length and it is proportional to the end diastolic volume and with that you optimize your actin and myosin filament overlap and the other effect that is increased venous return also causes a stretch of your sinus node which can indirectly increase your heart rate so you'll get both a augmentation of your systolic contraction with preload and you'll also get a secondary increase in your cardiac carpet other people talk about the Bainbridge reflex as a way you know when you get atrial stretch you get a mild increase in heart rate so this is why these things are all interconnected although we like to talk to them as if they're not they are all interrelated and you can you if you're going to walk up a flight of stairs you'll get an increase in pre-load contractility and you'll if you vasodilate you'll get a reduction after low which will augment your cardiac output but if we're thinking of trying to answer this question we do have to break them into different things so your afterload is the is the resistance at which blood is expelled into the a into the aorta and it's affected by many factors including your ventricular wall tension so your left ventricular end diastolic volume your left ventricular and systolic volume your ventricular wall thickness your ventricular output impedance which is both your aortic valve and your blood inertia and the systemic vascular resistance okay and increasing afterload tends to cause a reduction in cardiac output and a decrease in stroke volume okay if you unchain if your preload is unchanged now contractility which is the intrinsic ability of the myocardial fibers to contract independent of pre-load an afterload which as we now know doesn't happen but were it to happen that intrinsic capacity of The myocardium to contract is usually a function of the intracellular calcium availability and that's indirectly provided by your sympathetic stimulation and also by your preload and stretch so which augments calcium relief from the sarcoplasmic reticulum so those are the sorts of physiological factors that that are in play whenever you're thinking about sort of contractility okay so some of the physiological factors which might decrease contractility would include hypercapnia and hypoxia and acidosis and again this is the problem of being a physiological question where you're blurring the boundary into pathophysiology but we're not talking about myocardial infarction we're just talking about those things that can potentially be present to reduce that function so this is sort of still in that Gray Zone of a physiological issue another thing you might talk about would be myocardial compliance or lusotropy which is another thing which is augmented when your sympathetic nervous system is activated and that augments the capacity of the left ventricle to get venous return and then for perhaps an increase in diastolic stretch and ejection and the other thing that happens when you've got sympathetic nervous system activation is you get a reduction in venous capacitance and that improves your preload so it's all interrelated but essentially those those factors working together are what is determining your cardiac output so it's your heart rate predominantly and then your stroke volume which is affected by your preload your afterload and your contractility thanks Mike I think that we call as cardiac grid which is quite useful to then determine how do you handle different kind of pathologies when you're inducing the case candlesticks because that every time you modify something you know what's the what's the impact of increasing heart rate decreasing preload or potentiality on the cardiac output so that greed of four factors is quite useful to then applying your direct clinical practice that's right and these questions been asked in terms of the left ventricle or the right ventricle and they're actually almost a sign responses subtle variations in the differences in in the nature of afterload and the nature of you know whether you've got a thin wall ventricle with an increased wall tension versus a thick wall ventricle which has less wall tension but but you know that in terms of the effects of heart rates preload afterload and contractility the outcomes are the same and you can tailor the answer to the right ventricle or you can tailor your answer to the electrical and you're quite right so people if you move now to see what are the effects of a drug on these on the heart you can break down that drug into each of those sections and just just provide a response and you'll always get full marks because that's the only way drugs affect the cardiovascular efficient You could argue that in terms of afterload you can have certain drugs that produce or increase after load but for all intents and purposes the effect on cardiac output has to occur through some of those mechanisms so it's a good way of thinking about all of your cardiovascular pharmacology it's a good way of thinking about some of your central nervous system pharmacology that affect the sympathetic nervous system because you know it'll have direct and indirect effects the classic is Propofol and when you get to your part 2 exam thinking about anything you do to a patient if you think about how am I affecting cardiac output you can break it down into what am I doing to the those four things and you'll be able to construct an answer and and a way forward so that's why this is a ripper of an SAQ and it's why we repeat it frequently because it's a it's a good way of getting the candidates into the headspace of of the exam and you know despite the fact it's absolute bog standard physiology for the for the purposes of the exam but still has you know people who fail this question but sometimes it's because they try and write too much and try and answer everything on each of these things whereas in fact once you've written a page a page and a half in your eight to ten minutes you know you should have an up on paper you should move on because there's not a lot to be gained by continuing to write more and more and more you're better off providing answers to other questions yeah that's correct so thanks Mike thanks again for explanation and also some valuable insight as examiner so we'll be back in weeks time with another snippet till then goodbye and have a nice time [Music]