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That is why the majority of patients are treated with eating total body sodium overload, and not an inotrope.which is a treatment for myocardial failure.ĬHF or any type of Heart Failure is a syndrome of inappropriately high compensatory mechanisms (high stress state) that leads to sodium retention, which leads to the symptoms of heart failure. The patients come in with complaints related to total body sodium overload. However, the vast majority of patients with poor EFs who come into the hospital with a CHF exacerbation HAVE adequate cardiac output.ie they are not developing a metabolic acidosis from inadequate organ perfusion. We tend to equate CHF with myocardial failure with inadequate O2 delivery.as is the case when separating from CPB.
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"Heart failure" is a term that we, anesthesiologists, throw around very loosely, and most of the time we are using the term incorrectly. If the patient is intubated, pulmonary-delivered nitric oxide may help, but is a big deal to set up, is very expensive, and is not available everywhere. Milrinone, a phosphodiesterase inhibitor, may be a better choice.the only problem is the patient's hypotension, which may be worsened by milrinone. The only problem is the tachycardia, as you know, which is a primary determinant of myocardial oxygen consumption. SO, when choosing an inotrope, you have to look at the whole picture.this isnt to say you can't use say epi in a poor-perfusion state.sometimes you need a big gun and are forced to use it, at least for a while.ĭobutamine is a great drug.
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The problem with fluids in a patient like this is that because of the very low compliance in the ischemic myocardium, any volume increase can exacerbate ventricular failure.Īn inotrope with vasoconstrictive properties can worsen already-compromised perfusion issues- sounds like renal perfusion is already compromised as reflected by the increased creatinine. The goal is to improve overall perfusion, so maybe the attending wanted to use an inotrope without vasoconstrictive properties. It'd be interesting to see the patient's SVI (Military's favorite SWAN number). Perfusion in this patient's body is obviously low. Right heart failure secondary to the pulmonary sequelae you describe is a death sentence, where lung transplant is really the only long term option. Anybody have any experience with this situation? Patient felt out of breath, then N/V possibly even aspirated, 15 min. Do you have to adjust the dose? I presume it causes N/V like Digoxin does. Is it to reduce pulmonary pressures at the expense of ventricular filling?Īlso, how safe is Dobutamine in ARF.
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What physiological reason would push you to choose dobutamine (beta -2/vasodialator) rather than another inotrope w/o vasodilatory properties, something like dopamine? Her lungs were completely clear. It seemes to me that fluid loading rather than unloading and a vasoconstrictor is a better method of the treatment in this scenerio of RHF (optimize frank-starling). in the high 80's low 90's on 10L, was consistently running tachy around 100 bpm and pressures were around 80/50? IV X 2 followed by 25 mg po of metoprolol followed by 100 mg of lasix po, in a patient with extensive scleroderma causing pulmonary fibrosis and SEVERE pulmonary htn, who presented 1 day ago with RHF (probably acute cor pulmonale) and ARF (cr. How safe is it to be on a drip of dobutamine 4 mcg/kg,/min, 5 Mg.
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