What about Diastolic? Noob Nurse Question

[The JuggerNurse]

So I am a newbie nurse working her first job. I had a patient with a BP of 157/49. I was concerned about giving the BP mess because the Diastolic was low. I asked my RN and a few other RN's (I'm LVN) and the all said give it like it was no big deal. Am I only supposed to look at SBP? I apologize if this is a dumb question......I'm trying to develop this nursing intuition everyone is talking about.

[FLmomof5]

Something else to keep in mind is what is THAT resident's normal. I have cardiomyopathy. I have been on ace inhibs and beta blockers. (d/c the ace's for adverse reaction...) Anyway, my normal BP is 90/50. My cardiologist KNOWS this. He prescribes what he does for a good reason. I do not fit the normal "don't give if" parameters. In time I will be in the hospital to replace the aces with something else, but those meds hit the BP more so I will have to be carefully monitored. Another side note is that it is NOT unusual for me to hear in the AM that my BP fell to levels of 70/35 while I slept!

So, look at the resident's normals. Look at the parameters for "do not give" on the MAR. When in doubt....do what you did....ask. I am sorry that your RNs weren't more helpful.

[Anna Flaxis, BSN, RN]

actually, the heart pumps against the pressure that sits in just outside the aortic valve in the the aorta, diastole-- it's the contraction of the ventricles that makes the systolic (higher) pressure. all the left ventricle has to do is overcome the diastolic pressure to open the aortic valve and make some cardiac output. if the diastolic pressure is high, it's more work for the poor old ventricle to do that. that's one reason why vasodilating drugs decrease cardiac workload.:redbeathe (the other reason has to do with the frank starling law-- it's cool, look it up, tells you why people in chf get vasodilators and diuretics )

so, pvr has no effect on cardiac workload?

i'm guessing this person has a history of htn and cad with diffuse small vessel disease, hence the medication combo. the idea is to reduce the myocardial oxygen demand by reducing cardiac workload.

my question is this: since the coronary circulation fills during diastole, would a low diastolic reading indicate better coronary perfusion?

to the op, in this scenario, the diastolic would be clinically insignificant to me as far as deciding whether the meds should be given or held. i would be looking at the systolic.

also keep in mind that some cardiac patients require a lower blood pressure than you might think would be acceptable. patients with a very low ef, or patients with severe aortic stenosis, for example.

[nurseprnRN, BSN, RN]

"so, pvr has no effect on cardiac workload?"

pvr (peripheral vascular resistance) has a huge effect of cardiac workload, if course, but let's clarify some things. pvr is the resistance to ventricular contraction, the pressure the ventricle has to overcome to get blood out across the aortic valve (av) (and, of course, in the lower-pressure right heart side, where resistance to rv output is in the pulmonary vascular system). the reason we care about this is that the more work the ventricular myocardium has to do, the higher its oxygen and metabolic requirement, and, therefore, the more trouble it gets into if its vascular supply is inadequate.

another determinant of ventricular workload (and cardiac output) is the force of contraction. if your endogenous catecholamines (colloquially thought of as "adrenalin") are high, as in when you are frightened, stressed, smoking, or such, they signal the muscle to contract faster and more forcefully. it also constricts the arterial tree, which increases bp (and pvr...). this is obviously a great idea if your heart has to provide a bigger cardiac output to help you run away from the tiger or if you have massive vasodilation in anaphylaxis or other shock, but once again, if you have lousy coronary artery flow, not so much. medications which block catecholes from having such a strong effect cut cardiac workload because they prevent the muscle from overwork from this source (think beta blockers, for one). and of course, coronary arteries constrict with catecholes, too.

a further increase in contractility is due to the effect of the frank-starling law, which, simply put, means that the more cardiac muscle is stretched, the harder it contracts (to a point). what stretches cardiac muscle? venous return-- the more blood comes into the heart, the harder the heart works to pump it right on out. this is one reason when you are exercising (and increasing your venous return) your cardiac output increases to support the effort. this can be put on a graph, where if "preload," (what comes into the heart, measured or inferred by cvp, pad, or others) is on the horizontal access and cardiac output (measured by bp, or map, or calculated as liters per minute, whatever) on the vertical axis, it will go up to a point where it's maximized, then fall off, because too much stretch on a myocardium (like with a rubber band) exceeds its ability to contract, and output decreases.

congestive heart failure (chf) got its name before a lot of this was understood because when the heart is unable to pump, the blood backs up in the heart, causing the lungs to get congested. if it were beig described now, they'd probably call it something else, lol.

so, other medications useful in chf are diuretics, which decrease venous return to relieve a myocardium near its failure point, and vasodilators, which increase the amount of blood out there int the vessels, so it's not getting back to the heart to overstress it. vasodilating coronaries can help, too, of course.

"i'm guessing this person has a history of htn and cad with diffuse small vessel disease, hence the medication combo. the idea is to reduce the myocardial oxygen demand by reducing cardiac workload.

"my question is this: since the coronary circulation fills during diastole, would a low diastolic reading indicate better coronary perfusion?"

on the contrary. low diastolic pressure means lower coronary artery filling. there's a nifty graph that illustrates this, where arterial pressure increases as the ventricle contracts, then falls off at the end of systole and the beginning of diastole; there's a little bump up as the backflow pushes the aortic valve closed that's the point at which the coronaries get their pay. myocardium is the only muscle that doesn't get blood flow during peak contraction, but at rest, when it is passively filling in preparation for the next contraction.

to the op, in this scenario, the diastolic would be clinically insignificant to me as far as deciding whether the meds should be given or held. i would be looking at the systolic.

also keep in mind that some cardiac patients require a lower blood pressure than you might think would be acceptable. patients with a very low ef, or patients with severe aortic stenosis, for example."

let's not confuse "require" with "get away with" or "have to live with." a low ejection fraction (ef), the %age of blood in the ventricle ejected in systole, means the ventricle is failing to work optimally-- over the top of that frank-starling curve we mentioned earlier. many things can do this, including the mechanical blockage of av stenosis, but they all come down to the inability of the myocardium to do the job before it.

[Anna Flaxis, BSN, RN]

"so, pvr has no effect on cardiac workload?"

pvr (peripheral vascular resistance) has a huge effect of cardiac workload, if course, but let's clarify some things. pvr is the resistance to ventricular contraction, the pressure the ventricle has to overcome to get blood out across the aortic valve (av) (and, of course, in the lower-pressure right heart side, where resistance to rv output is in the pulmonary vascular system). the reason we care about this is that the more work the ventricular myocardium has to do, the higher its oxygen and metabolic requirement, and, therefore, the more trouble it gets into if its vascular supply is inadequate.

i think there may be just a wee bit of hair splitting going on here. the svr (systemic vascular resistance) has a direct effect on left ventricular workload, and the higher the blood pressure, the higher the svr. vasodilators are used in order to decrease svr by increasing the diameter of the arterioles and thus decrease left ventricular workload.

"my question is this: since the coronary circulation fills during diastole, would a low diastolic reading indicate better coronary perfusion?"

on the contrary. low diastolic pressure means lower coronary artery filling. there's a nifty graph that illustrates this, where arterial pressure increases as the ventricle contracts, then falls off at the end of systole and the beginning of diastole; there's a little bump up as the backflow pushes the aortic valve closed that's the point at which the coronaries get their pay. [/qhote]

ah, thanks for explaining that. that makes sense.

also keep in mind that some cardiac patients require a lower blood pressure than you might think would be acceptable. patients with a very low ef, or patients with severe aortic stenosis, for example."

let's not confuse "require" with "get away with" or "have to live with." a low ejection fraction (ef), the %age of blood in the ventricle ejected in systole, means the ventricle is failing to work optimally-- over the top of that frank-starling curve we mentioned earlier. many things can do this, including the mechanical blockage of av stenosis, but they all come down to the inability of the myocardium to do the job before it.

i think "require" is a fine choice of words. for example, in the patient with severe aortic stenosis, in order for the left ventricle to be able to pump blood through the stenosed aortic valve, the pressure gradient across the aortic valve needs to be low, else the left ventricle fails. therefore, the patient with severe aortic stenosis "requires" a low blood pressure in order to stay alive. in the person with low ef due to dilated or hypertrophic cardiomyopathy, the left ventricle simply lacks the contractility to pump effectively, and thus the person "requires" a low blood pressure in order to stay alive.

[Esme12, ASN, BSN, RN]

Wow you guys.....I know I'm a cardiac nut, I'm impressed! :)

[nurseprnRN, BSN, RN]

"i think "require" is a fine choice of words. for example, in the patient with severe aortic stenosis, in order for the left ventricle to be able to pump blood through the stenosed aortic valve, the pressure gradient across the aortic valve needs to be low, else the left ventricle fails. therefore, the patient with severe aortic stenosis "requires" a low blood pressure in order to stay alive. in the person with low ef due to dilated or hypertrophic cardiomyopathy, the left ventricle simply lacks the contractility to pump effectively, and thus the person "requires" a low blood pressure in order to stay alive.:d"

the resistance the ventricle pumps against in as is not related to the pvr so much as the stenosis itself. it's the difference between being unable to push a door open that has a lot of people on the other side pushing against you, and being unable to push a door open because its hinges are rusted shut.

the ventricle fails because the opening in the valve is so small, not because the afterload (svr) is high. most folks with really tight as, the bp/svr/pvr is low, because there's lousy output due to the stenosis.

hypertrophic cardiomyopathy, what we used to call idiopathic hypertrophic subaortic stenosis, occludes the av with a big honking mass of too much ventricular muscle getting in its own way, so to speak, in systole. treatment is surgical, to pare some of it away. dilated myopathy has, in contrast, a thin and ineffective ventricular wall, ballooned out, with a big silhouette on xray but not much pumping power, so bp is low and vasodilators make it easier for the lv to contract since resistance on the other side of the av is lower; sometimes you can get away with some contractility-boosters, but not always.

[Anna Flaxis, BSN, RN]

"i think "require" is a fine choice of words. for example, in the patient with severe aortic stenosis, in order for the left ventricle to be able to pump blood through the stenosed aortic valve, the pressure gradient across the aortic valve needs to be low, else the left ventricle fails. therefore, the patient with severe aortic stenosis "requires" a low blood pressure in order to stay alive. in the person with low ef due to dilated or hypertrophic cardiomyopathy, the left ventricle simply lacks the contractility to pump effectively, and thus the person "requires" a low blood pressure in order to stay alive.:d"

the resistance the ventricle pumps against in as is not related to the pvr so much as the stenosis itself. it's the difference between being unable to push a door open that has a lot of people on the other side pushing against you, and being unable to push a door open because its hinges are rusted shut.

the ventricle fails because the opening in the valve is so small, not because the afterload (svr) is high. most folks with really tight as, the bp/svr/pvr is low, because there's lousy output due to the stenosis.

hypertrophic cardiomyopathy, what we used to call idiopathic hypertrophic subaortic stenosis, occludes the av with a big honking mass of too much ventricular muscle getting in its own way, so to speak, in systole. treatment is surgical, to pare some of it away. dilated myopathy has, in contrast, a thin and ineffective ventricular wall, ballooned out, with a big silhouette on xray but not much pumping power, so bp is low and vasodilators make it easier for the lv to contract since resistance on the other side of the av is lower; sometimes you can get away with some contractility-boosters, but not always.

oh for crap's sake. splitting. hairs.

svr has a huge effect on the pressure gradient across the aortic valve. try telling a cardiologist that it is pointless to lower svr in order to treat as, and get schooled. of course, i should probably point out that i am referring specifically to someone who is a poor surgical candidate. ideally, as calls for a surgical intervention. and of course, in cardiomyopathy, you want to address preload and contraction, but overlooking svr (afterload) as a significant contributing factor to myocardial workload is myopic.

the point is, in the context of the original topic, the diastolic is not clinically significant. the patient needs those medications, and there was no reason to hold them.

[Esme12, ASN, BSN, RN]

I don't think Gr tea was overlooking SVR in the tratment of any cardiac disorders as the aim is reducing work load while increasing cardiac output, but merely pointing out the root cause of AS and dialted cardiomyopathy and the role of SVR in both.

If the OP wanted a lesson in cardiac output/SVR and medical management they got more that they asked for but valuable information jus the same.

[Anna Flaxis, BSN, RN]

Thanks, Esme. I think the reason I'm so hung up on the SVR part is that the OP asked specifically about blood pressure. Had she asked about PAWP or LVFP, or some other part of the circulatory system, then this would be a totally different discussion.

It's like going to a baseball game with a friend and asking what the strike zone is and getting a dissertation on the entire rulebook for baseball.