in this scenerio as decompesation sets in respiratory and acute heart failure triggered aggressive therapy: ventilator therapy which is needed and diuretic therapy to possibly control pulmonary edema.possibly thiscourse of treatment continued in right earnest till it was seen his parameters improved to an usual normal values.he was extubated.
present scenerio:
he has alkalemia due to
1.overzealous ventilatio on ventilator to make pCO2 exactly normal which is equavalent to hyperventilation and alkalosis kidney appropriately responding producing more HCO3-. With extubation this cotinued producing metabolic alkalosis.
2.Aggressive diuretic therapy with loop diuretics which causes along with ECF volume loss excassive chloride loss. body volume control mechanism now to retain Na+ require HCO3- as anion resulting metabolic alkalosis.as secondary hyperaldosteronism may also produce hypokalemia.
this alkalosis may produce inhibition of respiratory center producing hypercapnia and hypoxia which is present in this patient.
Treatment:
1.On cardiac front: as effective circulatory volume is reduced from disease and drug it should be cautiosly replenished with both NaCl and KCl administration. as hyperaldosteronism is present aldosteron antagoist like spironolacton should be prescribed. diuretic therapy should be administered moe judiciously.Other cardiac active drugs like ACE-ihibitor or ARB-antagonist or even digitalis prescribed. Betablocker is probably cotraindicated here.
2.On respiratory front as he is just out of ventilator no point jumping into it again. noninvasive ventilaion with BiPAP or even CPAP may be tried.To inrease effective ventilation administration of bronchodilator or agentlike ipatropium may be administered.
B

I agree with Eric that there is a metabolic alkalosis (from diuretic use) with a superimposed respiratory acidosis such that the resulting alkalaemia is minimal.

What I would do for the patient: ignore the acid-base, and treat the patient. Is he clinically well? What was his premorbid level of functioning and SpO2? It may be that the metabolic alkalosis is depressing his respiratory drive (leading to the depressed PO2) but if he is not in distress from this, I would leave it alone. If he is still having problems CCF I would optimise Tx for that first. The CAL will not kill him acutely so I would ignore that, and the metabolic alkalosis will resolve itself once the aggressive natriuresis (and ensuing diuresis) ceases — the kidneys are very efficient at getting rid of HCO3.

I would like to see this patient’s electrolytes, especially the Cl and Na. It may be that he may benefit from very gentle 3NS.

His kidneys are fully compensating for the respiratory acidosis.

Avoid giving supplemental oxygen which could depress peripheral receptors and lead to respiratory distress.

Using potassium-sparing and loop-diuretics (if that’s how you define ‘aggressive’) would lead to hypokalemia. Give concentrated potassium IV.

But I’m just an idiot at this point…

If I’m reading the post correctly, the patient presented SOB in presumed HF/COPD exacerbation. He was intubated and aggressively diuresed. Now 2 days after extubation his bicarb is 40 and ABG is posted.

He has a multiple reasons for a metabolic alkalosis:
1) renal compensation for resp. acidosis
2) hypokalemia and hypochloremia from diuresis
3) hyperaldo from CHF
4) Post-hypercapnic

Determining which player is the primary insult requires looking at the electrolyte panel, and possibly urinary chloride. Given his recent h/o ventilation and the mention of this pt. in a post. I would suspect post-hypercapnic alkalosis is a contributor. My understanding is that the slow renal compensation results in a lag when ventilation rapidly corrects PCO2 and previously acidotic pts become alkalotic. This condition is exacerbated by chloride loss from diuretics. If my theory is correct than the patient became alkalotic in the ICU and diuresis worsened the alkalosis through chloride loss (not sure of the exact mechanism here) and the patient has not yet normalized.

Acetazolamide has been shown to increase renal bicarb excretion and correct post-hypercapnic alkalosis quickly. Yet, in this pt. I would just replete chloride and potassium with KCL and/or NaCl.

PO2 of 61 correlates to an O2 sat near 90%. Supplemental O2 would not necessarily be needed and may further increased PCO2 by reducing RR and minute ventilation. In this case, I would give no more than 2 L by NC.

(expected Pco2 = 51 – 55)

expected pH = 7.46
expected CO2 = 67
expected HCO3- = 46

According to: http://www.medcalc.com/acidbase.html

Alkalosis due to Lasix (contraction alkalosis)? Treat w BiPAP and O2? Needs CXR and BNPep. PE in DDx?

More here:
http://casesblog.blogspot.com/2007/02/acid-base-balance-cases-and-calculators.html

Of course, since I’m a 4th year med student, anything I write is likely to be very overconfident and undereffective… [grin]

Mike

In any case, don’t be a hero. He’s 82. Give him some O2 (and no, it won’t suppress his breathing). The man is a chronic CO2 retainer. Less is more.

If he has a very low EF, fix his forward-flow as much as you can.