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Discussion

hemodynamics help please

i need some help!!! I am studying hemodynamics, and I get the basis of it such as CVP and wedge pressure, but when I do the case studies I feel lost. Im losing some meaning somewhere when it starts talking about Left or right heart and pulmonary. Can anyone give me a simplistic anwser of how an increased wedge or CVP affects the heart lungs and body. Ive looked at the post on here already and am still not getting the case studies. Any help would be great, thanks!!!

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    You are thinking about it totally wrong. Heart, body and lung problems cause the haemodynamic values to change, not the other way around. Altered haemodynamics are caused by problems. Once you understand this fact, the rest will fall into place easier.

    Also remember, let the patient's clinical assessment tell you most of the story. You do not need haemodynamic values to understand that a patient experiencing an acute MI with pulmonary oedema is going to have left ventricular problems. Always let the haemodynamic values back the clinical findings up.

    The CVP typically represents two concepts:

    1) The right side of the heart

    2) Venous return to the right side of the heart

    CVP elevated is associated with right heart failure and fluid overload.

    A reduced CVP is associated with loss of vaso-tone and low fluid volume status.

    It is your job to use the patient history and clinical data to find out the exact cause of the altered CVP values.

    Your PAP and PAOP/PCWP are indirect representations of the left ventricular filling pressure in many cases.

    Elevated pressures indicate pulmonary hypertension, fluid overload or a failing left ventricle that cannot accept the fluid.

    Low pressures indicate low fluid volume in many cases.

    Again, it is up to you to figure out the cause base on the patient's history.

    The CI can be used to differentiate some problems as well, as an elevated PCPW, low CI with a patient having chest pain points toward a cardiac cause. A normal CI with elevated PCWP may point to a pulmonary cause.

    Unfortunately, haemodynamics is similar to the quantum mechanics you went over in your chemistry courses, there is no table or picture that easily makes sense of the numbers. However, always take the patient history and clinical signs and symptoms into consideration as much of the underlying problem can come from these basic findings.

    Hopefully this helps.

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    • Author

    so if I have a pt with a history of heart failure I could confirm with the CVP of 10 for example that there is to much fluid on the heart causing failure thus causing the CVP to go up. If the CVP was within normal range I would know that its not fluid causing the issue and maybe its a contraction issue needing an inotrope drug. Is that closer to the right track?

    by the way, thank you for taking the time to give me all that info, it was very well written and a great help!! My test is thursday, last semester before graduation and I really want to understand this!!

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    so if I have a pt with a history of heart failure I could confirm with the CVP of 10 for example that there is to much fluid on the heart causing failure thus causing the CVP to go up. If the CVP was within normal range I would know that its not fluid causing the issue and maybe its a contraction issue needing an inotrope drug. Is that closer to the right track?

    by the way, thank you for taking the time to give me all that info, it was very well written and a great help!! My test is thursday, last semester before graduation and I really want to understand this!!

    Not exactly, if I dump several litres of fluid into a person without heart failure, I could just as easily increase the CVP. However, a person who has signs and symptoms of right sided heart failure and an elevated CVP is going to be much more likely to have a cardiac related cause of the elevated CVP.

    A patient who has a history of heart failure and a normal CVP can go many ways. Remember, the CVP does not typically look at the left side of the heart. It is possible to have left ventricular problems, but have a normal CVP. Unfortunately, it is also possible for left sided heart failure to lead to right sided heart failure. How do we deal with all the confusion? Look at the patient. What do their signs and symptoms tell us?

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    You should always put a CVP measurement in the context of a trend, it is a much more meaningful measure that way. If you have a pt with a CVP of 2 and you give them a liter and the CVP remains 2, they have a venous capicitance issue (think hypovolemia). If you give another liter and the CVP goes to 3, they are still dry, if you give another liter and the CVP goes to 10, you found the point where cardiac contractility no longer increased proportionately to stretch (preload), this concept is the Frank-Starling Law. That being said, all things happen for a reason. Cardiac and vascular impairments have unique and predictable effects on hemodynamics and textbook (cookiecutter) management strategies. For instance, aortic stenosis requires maintained afterload (decrease can be detrimental), maintenance of NSR, and normal or increased preload (CVP). Aortic regurgitation requires normal to decreased afterload (increase systemic BP is detrimental), normal to increased HR, and normal to increased preload. Any clinical scenario you can think of has a generic approach to management.

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    • Experts

    There are many things that impact the values of a CVP or a Swan ganz catheter. The basics. The CVP is a general indicator of fluid balance. It is useful when you are trending the patient values. It is a reliable IV access site. The catherter, usually inserted into the jugular vein, is inserted into the superior vena cava and allowed to rest in the general vacinity of the Right atrium. The right atrium is the recieving chamber for the blood returning unoxygenated from the rest of the body. In the purest sense.......if there is a low circulating volume (lack of fluid or blood) the CVP would be low, usually treating a CVP just because it is low is not done. In the presence of a low CVP accompanied by tachycardia,SOB, hypotension,diaphoresis,and/or low urinary output (the truest sign of end organ perfusion) treatment would be crystalloid/colloid or blood infusions.

    The fluid of choice depends on the patients diagnosis and presentation. In the presence of sepsis large volumens of fluid as well as administration of positive inotrop drugs (levophed,dopamine) is the treatment of choice. In sepsis the vessles are dilated and the capillary beds turn to mush (so to speak) and leak like crazy. The heart because of all the vasodilation occuring requires a higher filling pressure to maintain perfusion, thus tons of fluid. The drugs are given in an attemt to cause vasoconstriction, thus reducing tha amount of volume required to maintain hemostability,and further , like the histamine relase that further causes vasodilitation, but this is the basic ABC. So, a CVP may actually appear to be normal, but when accompanied by the patients presentation. Tachycardia, diaphoresis,SOB,poor capillary refill.......the temp maybe elevated but a lot of patients in septic shoc are slightly hypothermic or norma-thermic in a large percentage of time.

    In the case of trauma well you pretty much know that this is a volume/shock issue that is going to require transfusion of blood and blood products as well as treat the undelying source.

    Cardiac status is huge and it depends on right or left heart failure, cardiac output (liters per minute), and the systemic resistance against the blood vessels (SVR) and lungs(PVR). Cardiac output is how many liters per minute is being processed by the heart. Cardiac index is....is the blood getting where it needs to go? SVR is systemic vascular resistance or the force against which the heart must pump to get the blood to where it needs to go.

    The truest indicator of fluid balance is the PCWP. Pulmonary capillary wedge pressure. It is the direct volume indicator of hemodynamic status in the majority of patients. This all changes in the presence of valvular disease and shunting issues to name 2. The decision here is not as clear and depends on the patients underlying disease and presentation. In a true Right ventricular infarction, nhigher right heart filling pressures are required to maintain hemodynamic stability. In certain heart failure it is a combination of drugs (to increase cardiac output and input) fluid (higher filling pressures) and diuretics are all required to maintain stability. Example. Giving IV gtt for re-load reduction (makes the blood returning to the heart easier), a wiff of another drug to reduce afterload ( the force that the heart must push against to get the blood out) fluids to maintain fluids to ensure end organ perfusion.

    Remember think about your patient and the presenting complaint accompanied by the signs and symptoms. Look at your patient. I think that is what makes book senarios difficult....there is no patient in front of you looking like

    crap.........this link is for agood 6 min lecture to a bunch of ED nurses. also Laura Gasparis has several DVD's that are excellent for cardiac, acid base, hempodynamic issues...the woman's brillant and fun to listen to...

    http://www.youtube.com/watch?v=mjCEeBkeqGw

    And remember none of us learned this overnight!!!!!!!!!!!!!!!! Good luck!:twocents:

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    • Author

    Thank you to everybody who took the time to help. This is such a valuable source of experienced nurses, wish I knew about this site earlier!!!

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    I like to visualize.

    If you were to take your hand and squeeze that PA preventing blood from easily getting through, and monitored the pressure while you were doing this, the pressure would go up because the blood is meeting resistance (your squeezing the vessel limits the free flow). If you were to leave the vessel alone, but instead increase how much blood is pushed towards that vessel (remember your volume overload) you would also get a rise in reading as you would be trying to force blood into a vessel that can only accommodate so much shoved at it at a given moment. The excess cannot get through so it backs up. Now if you can visualize this, you can add on. The chambers, the valves... same deal. If something is impeding smooth flow (overload, hypertension, valve disease, conduction problem, etc.), simply imagine it. Think of the S1, S2 and what the rhythm of healthy heart in motion is, follow the blood through the chambers/valves/vessels of the heart. Then screw the system up with any of the pathology listed above and visualize how everything changes. Think of what S3 and S4 are... then you can go on to all the specifics of invasive monitoring and start to learn those too. This is how I approach that whole learning deal.

    Maybe these might help too:

    Anatomy of the Heart - Texas Heart Institute Heart Information Center

    http://www.youtube.com/watch?v=Ge12P7u0aQo

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