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NIV in “Sympathetic Crashing Acute Pulmonary Edema”

18 Feb

While working on this topic in stumbled on the 1st podcast of EMCrit.com, the famous blog by Scott Weingard. He was talking about “Sympathetic Crashing Acute Pulmonary Edema”…SCAPE! Well, this is exactly what I have been talking about for the last few weeks and I am gonna borrow this definition from him. These crashing patients are very dyspneic, have crackles and due to the high levels of (nor)epinephrine their blood pressure is very high.

As you know from my previous posts these patients with SCAPE need high doses of nitrates, no morphine and the diuretics you can throw in the coffee of that irritating doctor or nurse who keeps telling you that an initial dose of 100 ug/min of NTG is way too much in these patients. But what about the oxygen? CPAP, BiPAP or just a non-rebreather mask (NRM)?

What do we want to see in SCAPE? A quick reduction in shortness of breathing and a reduction in intubation and mortality, without any side-effects. So is NIV op for the challenge and does it show benefit over the conventional oxygen therapy?

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Loop diuretics in Acute Pulmonary Edema; Necessary..Evil…or Necessary Evil?

4 Feb

Welcome back on EMDutch, the blog by Dutch emergency physicians, for emergency physicians worldwide!

So far we have discussed morphine and NTG in Acute Heart Failure (AHF) and now it’s diuretics’ turn! And before we go on I want to make clear that we are discussing patients with Acute Pulmonary Edema (APE) without hypotension and not the patients with swollen ankles and no severe dyspnea or the patients in cardiogenic shock.

Diuretics in APE for me as a resident was something you didn’t think about and clearly works, just like thrombolysis in ischemic stroke, steroids in sepsis and acenocoumarol in small PE (YEAH…RIGHT!). But when you join the #FOAMed family and really start thinking about (evidence-based) medicine nothing is what it seemed to be.

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Relief of acute dyspnea : no convincing evidence for opiates or benzodiazepines

27 Jan

While being sick at home and still working on diuretics in Acute Pulmonary Edema I thought to myself, why not post something I have already finished but never put on the internet. (Better lazy then tired as we say in Holland 😉 ) Sadly I found that most of it has to be translated into English, except for the following “poster”.

One of my great residents (Annemarie v/d/ Velden) was interested in morphine and benzodiazepines for the relief of acute dyspnea. Opiates have traditionally been used as one of the main treatments of acute dyspnea and are still recognized as such. Most current textbooks and official guidelines advise the use of morphine as one of the first-line treatments for patients in acute dyspnea and a majority of physicians accept it to be the case. Benzodiazepines are widely used for the relief of breathlessness in advanced diseases and are regularly recommended in the literature. For me this was something you never think about and it just works….but does it really???

Here is what we did and the results we found:

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The ESC guideline on AHF…discussing nitrates!

7 Jan

Welcome back on the EMDutch website….the website talking about emergency medicine below sealevel. And because we, the people living below sealevel (It sound more scary than it is), use nitroglycerin (NTG) for acute decompensated heart failure, that is what we will be mainly talking about. I know there are other vasodilators out there, like nitroprusside and nesiritide, but for us NTG is the vasodilator/nitrate of choice!

Nitroglycerin is a nitrate that causes venodilation at low doses and arterial dilation at higher doses. (1) There is little doubt about its effectiveness in AHF and it lacks significant side effects (2), but its use is limited by marked underdosing in clinical practice. (3) And this is so true in my own hospital! Nurses and fellow doctors are used to giving 150ug/h in stable chest pain patients, which they can titrate up to 500 ug/h. In acute heart failure (with a normal-high blood pressure) this is just not enough.

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Discussing morphine in Acute Heart Failure

21 Dec

Hello everybody,

Hereby as promised the post about morphine in acute heart failure.

Morphine has been considered a central drug in the treatment of pulmonary oedema for a long time. It is believed to cause venodilatation, peripheral venous pooling, reduction of pulmonary congestion and is thought to be a powerful anxiolytic. Most of these believes appears to be based on small studies, which were published during the era when there few alternatives.
In vivo experiments has shown peripheral dilatation, (1,2) probably due to histamine receptors rather that the opiate receptors (3), and a decrease in systemic vascular resistance (2). Furthermore peripheral pooling in the splanchnic region has been found. The splanchnic vascular resistance dropped by 16% after admission of morphine (4).
Next to this scientific evidence there is the strong subjective believe of a lot of doctors that it improves the short-term patient apprearance, which is another big reason we still use it, I think.

A large retrospective study from 2008 (5) looked at the outcome of patients treated with and without morphine for decompensated heart failure. Continue reading