Right-side heart failure.

[mediccjh]

You have a 64 y/o male, c/o SOB, onset 1700 hrs at rest. It is now 2200 hrs. Did not take Lasix today; was supposed to this AM. D/C from hospital s/p SOB, pt did not specify dx. Pt took inhaler x 3 w/o relief (Albuterol). 156/80, 118 in A-fib, 36 and labored. Rales 1/2 way up, diminished bases. Peripheral pedal edema, and ascites present, (+) JVD when palpating abdomen. Unable to do a 12-lead, since I don't have the capabilities at my full-time job.

I think it was right sided b/c of all the edema going on, which means fluid is backing up since the right-side doesn't appear to be pumping correctly.

Do you give NTG?

I was debating with the other medic on my tour, and want to hear everyone else's thoughts.

My APE protocol is 80 mg Lasix IV, NTG q 5 mins SL up to 3 total if B/P > 100 systolic, which it was (lowest was 138/80).

Thoughts, comments, opinions appreciated.

Thanks,

Herbie

[THE_DITCH_DOCTOR]

Tough call.....I would have held off on the NTG because when you bottom out a RV infarct patient's BP, it tends to be hard and very quick. I would have gotten on the radio and consulted with a doc before proceeding with the NTG. No 12-lead? Ouch.....

[TrentonStreetskirt]

Edema and ascites are sx of Right sided heart failure. Right sided heart failure ofter causes left sided heart failure. Pt probably has some liver dissorder causing these sx (ie. cirrhosis, CA, ). You never mentioned if you got a room air SAO2 and If the patient wasn't grossly hypertensive, I would have held on the NTG and possibly the LAsix also. You didn't indicate the level of distress for this patient, so it is difficult to assess how agressive this patient treatment needs to be.

Could the ascites have cause this patient's dyspnea?? Although he did miss his AM dose of PO lasix, and was probably fluid overloaded he may not have required a full 1 mg/kg of lasix. I would have consulted with the Doc for a dose and any futher orders.

[mediccjh]

Room air SpO2 was in the low 90s, but that was my last concern....the shallow resps of 36 while sitting tripod was.

My protcols, as stated, called for 80 mg Lasix IV. This guy weighed about 100 kg.

Keep 'em coming.

[ERDoc]

There are also signs of left sided failure (rales). This is probably not from a new insult (although you cannt completely rule that out), but most likely related to the missed meds. Ntg probably would not be a bad idea, but I would feel better if I saw an EKG first.

To set the record straght, right sided failure is commonly caused by left sided failure, not the reverse. The most common cause of right sided failure is left sided failure as you get a backup from the left to the right.

[medic001918]

I would definatly want to see a 12-lead on this patient. With the cheif complaint of SOB and a 12-lead that didn't show an infarct, I would most likely have gone ahead with NTG but ONLY if I had a patent IV in place. I would also want to know if they were orthopneic? Exertional SOB? Febrile?

High flow O2, NTG (provided SBP>100mmHg), and lasix. Our protocols state to double the dose of lasix since he has not taken his daily dose. I don't think I would have gone that far, but I would have given whatever his dose would be. Again, this is all dependant on the 12-lead not showing any signs of an infarct and having a line in place. Start with the NTG and see how the BP does before giving lasix.

I would have been kind of surprised to see that he was infarcting being an elderly male. It's not impossible for them to have the silent or atypical presentation, but they are the one's who typically present with crushing chest pain, pale/diaph, etc. I'm thinking this patient is in failure, not AMI.

Shane

[Ace844]

You have a 64 y/o male, c/o SOB, onset 1700 hrs at rest. It is now 2200 hrs. Did not take Lasix today; was supposed to this AM. D/C from hospital s/p SOB, pt did not specify dx. Pt took inhaler x 3 w/o relief (Albuterol). 156/80, 118 in A-fib, 36 and labored. Rales 1/2 way up, diminished bases. Peripheral pedal edema, and ascites present, (+) JVD when palpating abdomen. Unable to do a 12-lead, since I don't have the capabilities at my full-time job.

I think it was right sided b/c of all the edema going on, which means fluid is backing up since the right-side doesn't appear to be pumping correctly.

Do you give NTG?

I was debating with the other medic on my tour, and want to hear everyone else's thoughts.

My APE protocol is 80 mg Lasix IV, NTG q 5 mins SL up to 3 total if B/P > 100 systolic, which it was (lowest was 138/80).

Thoughts, comments, opinions appreciated.

Thanks,

Herbie

"mediccjh,"

I hope that this post helps you with some more info. You can also check out this link to a similar scenario in which Right sided heart failure was discussed in detail, here's the link: http://www.emtcity.com/phpBB2/viewtopic.php?t=528. Based on the little you mentioned in your scenario, we know/assume the following:

1.) The patient has a PMH of CHF, of at this point unknown etiology.

2.) The patient takes "inhalers" A.K.A: beta agonists for an as of yet unknown respiratory reason.

3.) That the patient is complaining of resp distress and has the clinical signs/sx's of CHF/Dyspenic syndrome...

4.) The patient is in A-Fib on your "monitor"

5.) The patient has ascities which as previously mentioned here is a sign/sx of underlying Liver dysfunction as caused by "alcholic liver", hepatitis, etc....This may have been what caused the patients CHF (i.e.: portal HTn, hypoalbuminemia) in the first place...but one can never be sure without access to MR'sand a comprehensive PMHX..

6.) It can be reasonably assumed with the PE findings of HJR, and ascities, that this patient also has a component of portal hypertension.

Most of your questions should be answered from the link I posted but I'd like to make a few additional points.

1.) Some of the PE signs/sx's you posted are the following: HJR, which stands for Hepato Jugular Reflux, and two which you didn't mention. These are JVP measurement, and Kussmaul's sign.

These are assessed as follows:

Close examination of the neck veins is very important. Whereas the external jugular vein gives a general idea of the height of the venous waves, the internal jugular vein is used for analysis of venous pressure and the venous waveform because it acts as an open venous conduit to the right atrium (except in cases of superior vena cava obstruction).

(Hepato-Jugular reflux test) The jugular veins are usually examined with the patient reclining at 45°, whereby the venous column in normal persons is just below the clavicles. The venous column can briefly be elevated above the clavicle by firm pressure of the hand on the abdomen (the hepatojugular reflux), but in normal persons it will fall below the clavicle in a few seconds while maintaining abdominal pressure as the compliant right ventricle increases its stroke volume by means of the Frank-Starling mechanism. In superior vena cava obstruction, constrictive pericarditis, restrictive cardiomyopathy, or severe heart failure, the jugular venous pressure may be sufficiently elevated to make detection of the top of the venous column impossible. In these circumstances, the patient should be examined while sitting upright or standing.

Change in the height of the venous waves in response to abdominal compression gives considerable information about the right side of the heart. The venous column rises and remains elevated while abdominal pressure is maintained in the presence of a dilated, poorly compliant right ventricle; in constrictive pericarditis or pericardial tamponade; and with obstructed right ventricular filling by tricuspid stenosis or right atrial tumor.

Kussmaul's sign should be sought, in which, under the same circumstances that produce a hepatojugular reflux abnormality, the venous column in the neck rises rather than falls with inspiration. In normal inspiration, lowered intrathoracic pressure draws blood from the periphery into the vena cava. The normally compliant right ventricle accommodates and expels this blood by means of the Frank-Starling mechanism. Kussmaul's sign is also present in obstructive airway disease.

Finally, the character and magnitude of the venous waves can be analyzed. The a and v waves are increased in pulmonary hypertension. Giant a waves (cannon waves) are seen in atrial ventricular dissociation. The a wave disappears in atrial fibrillation and is accentuated in states of poor right ventricular compliance (eg, pulmonary hypertension, pulmonic valve stenosis). The v wave becomes very prominent if tricuspid regurgitation is present. Tricuspid regurgitation also often produces significant hepatomegaly, with easily palpable systolic pulsation of the liver due to the regurgitant v wave swelling the liver during right ventricular systole. The accompanying marked venous hypertension sometimes leads to cardiac cirrhosis and ascites. In cardiac tamponade, the x descent is steep. In states of poor right ventricular compliance, the y descent following ventricular systole is very abrupt because the elevated column of venous blood rushes into the right ventricle on opening of the tricuspid valve, only to stop abruptly as the rigid right ventricular wall (in restrictive myopathy) or the pericardium (in constrictive pericarditis) arrests the inflow.

Now you mentioned that your patient was in "a-fib" on your monitor but you are

Unable to do a 12-lead, since I don't have the capabilities at my full-time job.

You could do a modified 12 lead by moving your MCL-1 around the "V" leads and this would give you a " 12 lead perspective" on your patients with a 3 lead monitor.

Hope this helps,

Ace844

[vs-eh?]

Sorry, just a couple of things...

- Afib wasn't new right? SOB from hospital wasn't new onset a-fib was it?

- Albuterol is that new? If not COPD'er probably, could precipitate a new onset afib? That plus any previous LV dysfunction/current AMI = CHF?

- Why and for how long was he on the lasix? What is his dose? Just for ascities/peripheral edema ala liver hx or did he get "water on the lungs"

- HR and BP look good, I would tend to think if this was AMI that it likely isn't a Inferior MI with RV involvement. Low and slow vs. high and fast for lack of a better analogy. Especially after the NTG.

But it is very likely LV ----> RV failure. As ERDoc stated. If it was purely a RV prob chest would likely be clear but with the JVD/ascities/edema.

[mediccjh]

The 12 lead at the hospital did not show AMI. He does have h/o A-Fib, which he does take meds for (don't remember off top of my head). (+) Orthopnea, and dyspnea on exertion, while occasionally coughing up white sputum, but not too much, maybe once or twice his wife said.

Lasix dose was 40 mg once daily, for as he said, "water on the lungs".

I do also believe there was left side going on, which was what would cause the rales.

[THE_DITCH_DOCTOR]

Sorry, just a couple of things...

- Afib wasn't new right? SOB from hospital wasn't new onset a-fib was it?

- Albuterol is that new? If not COPD'er probably, could precipitate a new onset afib? That plus any previous LV dysfunction/current AMI = CHF?

Probably the albuterol is responsible for the rapid ventricular rate, but the underlying AFib is probably the result of the pulmonary congestion or as a secondary effect of another underlying condition like COPD. High doses of albuterol can cause arrhythmias in anyone, but that's not what's happening here.