Answer:

You may not be that familiar with Swan Ganz catheters, that is because we do not use them often anymore because they do not improve mortality. That being said, they are great for learning and physiology. Without doing any calculations, my first impression of these numbers is that this is patient with a severely depressed ejection fraction with a largely normal blood pressure and a very low mixed venous gas - this is telling me that their afterload is likely too high for their given cardiac output which is likely low. The mixed venous O2 is telling me that the body is extracting a lot more oxygen than normal (Normal Mixed Venous = >75%). Additionally, their PCWP indicates that they have high filling pressures in need of diuresis.

Cardiac output: 2.8
Cardiac Index: 1.7

Next steps: I would increase their dobutamine from 5 to 7.5mcg/kg/min followed by a repeat set of Swan numbers during next shift. I would also make sure that they are adequately diuresing with the given lasix - with goal of at least 2L out net negative daily. If their PCWP is not decreasing or they are do not have adequate UOP, I would increase their Lasix versus transitioning to a Lasix gtt. Be sure to give a bolus dose of Lasix before increasing the gtt if that is indicated.

Answer:

To review, patients who present with a heart failure exacerbation, the recommendation is to decrease the beta-blocker rather than stopping it. In patients who are in cardiogenic shock, it is reasonable to hold. The question is when to restart the beta blocker after the patient returns to the Frank-Starling Curve. There is no clear answer to this question and is highly provider dependent. The main point is that beta blockers confer survival benefit by dulling some of the adrenergic response of the stress of heart failure and helps with remodeling. This produces mortality benefits over a long period of time. The ideal time to start a beta blocker is once a patient is euvolemic and no longer considered decompensated i.e. while still admitted versus at their HF follow up appointment that should occur within 1-week post-discharge.

Beta blockers (carvedilol, toprol, bisprolol) should be started at the lowest dose and doubled in two weeks to achieve “target doses.” Target doses for HF medications are based on the doses that were studied in the large HF trials we have to date.

Answer:

Let’s review a few concepts before getting to the explanation. Why does this patient have a metabolic alkalosis? We do not have a VBG, but from the history we have two good reasons. First, his severe COPD suggests that is likely a chronic retainer and will have a compensatory metabolic alkalosis - to maintain a near normal pH in the context of an elevated PCO2, the kidney will hold onto bicarbonate. Second, we have been diuresing him - loop diuretics cause the patient to lose sodium (+), but a little more chloride (-), to maintain a neutral charge the kidney must hold onto another anion, the easiest being bicarbonate (-) (contract also plays a small role). If this is confusing, see our AHD on Acid/Base! The final piece of the puzzle is how acetazolamide works, it inhibits carbonic anhydrase (CA) in the kidney, which is necessary for the retention of bicarbonate.

Returning to the patient, why would we give him acetazolamide? We need to continue diuresing him as he is hypoxic and significantly fluid overloaded, but with further aggressive diuresis he may become alkalotic. In a patient without severe COPD or CKD, it would be reasonable to start acetazolamide when a patient’s bicarb reaches the mid-30s. However, in a patient with severe COPD, they will have a significant respiratory acidosis and compensatory metabolic alkalosis to maintain a near normal pH. If you give them acetazolamide, you get rid of this compensatory renal mechanism. This will decrease their pH, increasing their respiratory drive. However, patients with severe COPD cannot increase their minute ventilation effectively and will have dyspnea and increased work of breathing, which could tire them out and cause a decrease in their minute ventilation, further CO2 retention and an acidosis that could be fatal.

Answer:

To review likelihood ratios (LR) - a positive LR “is the proportion of patients with disease who have a physical sign divided by the proportion of patients without disease who also have the same sign. The numerator of this equation—the proportion of patients with disease who have the physical sign — is the sign’s sensitivity. The denominator — the proportion of patients without disease who have the sign—is the complement of specificity, or (1 − specificity) (Evidence Based Physical Diagnosis).” Therefore, a test with a high specificity and sensitivity will have a high likelihood ratio and can be used to augment a post-test probability.

“The presence of crackles, fourth heart sound, or edema does not indicate elevated left heart filling pressures in patients. Crackles are unhelpful because they are infrequent in chronic heart failure and because many other disorders causing dyspnea also produce crackles. Even so, if the finding of crackles is instead applied only to patients with known cardiomyopathy, they become a more accurate sign of elevated filling pressure, detecting pulmonary capillary wedge pressures of 20 mm Hg or higher with a sensitivity of 15% to 64%, specificity of 82% to 94%, and positive LR of 2.1.(Evidence Based Physical Diagnosis)”

See below for the specifics of our exams, courtesy of Evidence Based Physical Exam: