hi I'm Janice Fernholz province and this is a quick review of hemodynamic principles so if we look at the word hemodynamics what does it actually mean so he means blood Dynamis means movement so put it all together and hemodynamics means the movement of blood so why do we care well because if our hemodynamics are out of whack then we've got issues and as the bedside nurse were able to manipulate patients hemodynamics in order to achieve desirable outcomes let's look at some quick definitions before we start so cardiac output is the volume of blood ejected each minute during ventricular contractions so if you think about it an organ the size of our fist is able to pump out two to four of these two liter coke bottles per minute pretty incredible and then the cardiac index is corrected for the patient's body size so a little old lady who weighs 80 pounds is not going to have the same cardiac output as a 350 pound linebacker for example so instead we look at the cardiac index stroke volume is a volume of blood ejected during ventricular systole and then ejection fraction is just the percentage of blood pumped out of the left ventricle during systole and so remember that whenever your heart pumps it doesn't completely empty so there is almost up to 50 percent of the blood there so the ejection fraction is looking at that percentage and then the systemic vascular resistance is what's in the vasculature so how toned are the vessels are they completely dilated out so we have a lower number of our SVR or are they nice and tight or too tight for example and not letting any blood flow go through all right what are the factors it affect blood pressure so when we put a cuff on a patient and take the blood pressure we're looking at the cardiac output times the systemic vascular resistance or SVR and the cardiac output has two components so the cardiac output is made up of the heart rate and the stroke volume and then if we look at the stroke volume that's made up of three components so we have the preload which is the volume dumping into the ventricle we have the contractility the pump the force and then we have the after load so the vessel tone preload is the volume of blood returning to the heart from the venous side waiting to be ejected contractility is the force of contraction how well the heart is beating and then after load is the resistance that the heart has to put up push out against of the vessel so are the vessels clamped down or are they wide open here's my little picture of how I view hemodynamics so you've got your heart in the middle of the picture and then you've got the volume that's dumping into the heart that's your preload and then what's coming out of the heart is the blood and it's going against the after load or the resistance so how do we measure preload so in the II D we only have the CVP if you were to put a swan-ganz catheter in a patient you would be able to measure both right and left heart and the right heart would be the CVP or the right atrial pressure and that's anywhere from zero to ten or two to six depending on what textbook you look at and if you had a swan in you could also measure the pulmonary artery wedge pressure and the II D we don't have this so we have already talked in one audio byte about how to measure the CVP waveform and get an accurate reading on that so I'll refer you to that audio bye okay so again preload is the amount of volume returning to the heart it's the blood volume in the ventricles waiting to be ejected and it's dependent on how full the tank is so the total volume in the venous bed or the diastolic venous return and then we can also talk about starlings law of optimal stretch and this has to do with the systolic ejection so we'll get to that more in a little bit so I like to think of preload is like filling up a water balloon so if you think of the preload the volume again as the water going into the water balloon then you have the balloon starting to stretch the more water in the balloon the greater the stretch and what starlings law says is the more the heart muscle stretches during diastole which is the filling the more forceful the contraction is going to be during systole so there is an optimal stretch period okay here's another way to think about starlings law using a rubber band so your rubber band being your heart muscle and if you wrap the rubber band around two fingers and then you stretch it out about three inches and you let one side go it's going to contract back really well right so that's optimal stretch and then if you were to only stretch it out maybe about one inch then it's going to contract back when you let it go it's going to contract back with less force probably not hurt when it snaps your other finger so that would be like an example of a hypovolemic patient somebody who's either blood out or is dehydrated so there's little stretch and that equals little squeeze whereas if you stretch out the rubber band like six to eight inches and then let it go back that's going to be a big snap that's equivalent to like a fluid challenge so it contracts back stronger and faster now if you think about the rubber band and you've been stretching it and stretching it and stretching it and over stretching it and pulling it and pulling it what happens if it's all those muscle fibers get too stretched out think about the big boggy heart or like a patient with CHF so you have too much fluid in there and the muscle fibers can't contract back well so that is starlings law alright so again preload is volume what are some agents that reduce our preload or dilate out that tank it would be like lasix or furosemide our vino dilators like nitroglycerin that are going to expand that tank size dumping into the heart so our preload is going to be reduced our CVP number is going to be reduced agents that increase our preload or fill the tank or constrict the tank we have crystalloids like normal saline and lactated ringers we also have colloids there's a handful of other things that can affect our preload as well so again this is the volume and what's affecting our diastolic filling all right let's talk about contractility now so we've already discussed darlings law so which of these two water balloons when they are removed from the spigot if they're not pinched off nice and tight which one is going to shoot water further the one on the left which isn't filled as much or the one on the right exactly the one on the right so the greater the stretch the more forceful the contraction and then contractility as we've already discussed is influenced by preload or the amount of volume that goes into the heart so again contractility is the force of the contraction it's the strength it's the ejection force for moving the preload against the afterload and it's dependent on oxygenation and electrolyte balance pH preload afterload all those good things all right what are some things that are going to decrease contractility or the force of contraction so if a patient has a low K a low mag a low calcium or they're hypoxic or they've had an MI all of those can affect contractility and then what can increase contractility or improve it so I know Tropes drugs that are going to make our heart pump better so dobutamine even dopamine epinephrine all of those they're calcium as well can increase contractility alright as you can see there is quite a list of things that can affect our contractility so again we've talked about preload and afterload or myocardial oxygenation electrolyte imbalances there's other things like drugs or acid or sepsis sympathetic or parasympathetic nerve stimulation hypothermia cardiac hypertrophy or tamponade or even restrictive pericarditis all of those can affect the way our heart pumps on to afterload so how do we measure afterload well in the IDI again if we if we had a swan which we don't in the IDI we would look at either the pulmonary vascular resistance the PVR or the systemic vascular resistance the SVR so the lower the number the more dilated out the patient's vessels are that's the tone and the higher the number the more clamped down they are alright back to our water balloon analogy here so when you have a water balloon if you were to put that base in your hands and you're going to squeeze the water and you have your fingers pinched around the neck of the balloon depending on how pinched you have your fingers that's going to be your afterload or the resistance when you try to squeeze the water out of the balloon so if you have a loose grip on the neck and you squeeze that out that's a lower SVR whereas if you have a tight squeeze around the neck with your fingers and you try to squeeze the water out that is an increase in your SVR or your afterload so afterload is the pressure the ventricles must work against to push the blood out of the body or the ventricles so some definitions here again afterload is the amount of resistance the heart has to push out against it's the resistance to the ejection from the ventricles and it's dependent on the vessel status so we talk in terms of the patient being clamped down so again it's the tone and how how clamped or dilated out the patient's vessels are how hard is the heart having to work to get that blood out of the ventricles so what are some agents that are going to reduce our afterload vasodilators so nipride or nitroprusside or nitroglycerin both reduce the after load and then agents that are increase our SVR or the afterload are going to be vaso constructors like norepinephrine or epinephrine or dopamine there are a handful of things that can affect our afterload the list on the left are items that can affect our pulmonary vascular resistance so you can see that pulmonary hypertension and pulmonary embolus or things are going to affect the lungs on the right hand side we have a list of things that are going to affect the SVR or systemic vascular resistance so dropping down you can see that like spinal or distributive shock those can affect the SVR the tone of the vessels so in in distributive shock you know that the vessels dilate out so your SVR would be a lower number all right so in review we have your preload that's your volume we have the contractility which is the force and we have afterload which is the resistance so what does all mean let's let's do a little quick case here we have mrs. septic shock who arrived from a con home she was hypotensive tachycardic and altered with very little urine output what do you think is causing her hypotension so right is it the her SVR and her preload are those going to be up down one or the other so we're gonna have a decrease in the SVR and a decrease in her preload so her she's dilated out that's her SVR her are Hurra afterload and then her preload she's hypotensive so her tank she might be in distributive shock so her tank might be bigger that drops her preload as well so why is her SVR low because of the vasodilation from the inflammatory response and then why is the preload reduced because the tank is bigger her interval what's causing her tachycardia so that is going to be a compensatory response for the low SVR or the tone that she doesn't have and the low preload or the volume that she doesn't have because her tank is so big also it could be a response to the fever so what about our cardiac output do you think it's going to be high or do you think it's going to be low so typically with septic shock patients cardiac output is going to be high because mmm the body wants to compensate for the low SVR the the vessels being dilated out and then increase the metabolic needs related to sepsis so summarizing septic shock is the preload up or down it's going to be down and then is the afterload going to be up or down it's going to be down so that's your vessels and then the preload was the volume and then contractility is it up or is it down and it is up good job so how going to treat this patient if we're using early goal-directed therapy as our guide oxygen mechanical ventilation if necessary and then we're going to fill the tank with fluids get the titrate to a heart rate no map a mean arterial pressure of 65 we're going to look at the urine output her skin perfusion or Mental Status if we put in a CVP we're going to be looking at a CVP between 8 and 12 if she's intubated 12 to 15 we're going to get blood products on board if her hematocrit is too low and if her s vo2 is too low we're going to start antibiotics right away and then vasopressors to tone her up so once her tank is full we can give I note ropes as well like Levophed to increase her blood pressure and also increase her SVR or her tone all right so again when we think about preload think about CVP that's our measurement think about the tank that's the volume what's dumping into the heart what's dumping into the venous system so if the patient's bleeding out or if they have drugs like nitroglycerin for example that are going to dilate them out that's going to reduce their preload and then adding volume or to that tank is going to increase preload contractility again is the force it's the strength of the heart during ejection the stroke work index so individualize for that particular patient it moves the preload or the volume out against the afterload which is the resistance and what's going to reduce contractility ischemic arts what's so in somebody having an MI and the electrolyte imbalances as well as well as a decreased sympathetic tone and then what's going to improve our contractility drugs like inotropes like our dobutamine dopamine epinephrine calcium as well to increase the contractility or that force and then how about after load that's our resistance that's our SVR is our measurement what the heart is pushing out against is the patient clamped down or not so the diameter the hose of the vessels it's the arterial system versus the venous system basil dilators are going to reduce our after loads so they're going to dilate out the caliber of the vessels or increase that hose size and then what about what increases our afterload vasoconstrictors like Levophed so for our septic patient for example those are all going to affect that all right back to our drawing now to sum it all up so we have the heart the star in the middle and what's dumping into the heart is the preload that comes from the venous side we measure it with our CVP it dumps it into the heart and then the heart uses force and contractility to pump that blood out against our after load that goes to the arterial side and if we had a swan in we would use SVR to measure that afterload or the resistance the tone of the vessels thanks for listening