Massive PE hemodynamics

[Grizzlyadamz]

Alright, so, a patient gets a big 'saddle embolism' that restricts blood flow to both of the lungs.

This would present like cardiogenic shock, correct? In particular, something like cardiac tamponade.

MAP would drop due to a decreased CO, heartrate would rise and blood would back up in the venous system.

Now, an article provided by my instructors is saying a patient with an obvious massive PE would be started on fluid resuscitation. Would that actually be indicated?

Wouldn't that just continue to back up in the venous system and worsen any edema they have?

[NICU Guy, BSN, RN]

Pulmonary embolism is an embolism in the lungs preventing blood flow and oxygen exchange.

Cardiac tamponade is the presence of fluid in the pericardia sac surrounding the heart causing increased resistance to the heart pumping. It has nothing to do with the lungs.

Cardiogenic shock is caused by the heart's inability to pump effectively. It can be due to damage to the heart muscle, most often from a large myocardial infarction, abnormal heart rhythms, cardiomyopathy, cardiac valve problems, ventricular outflow obstruction (i.e. aortic valve stenosis, aortic dissection, cardiac tamponade,constrictive pericarditis, systolic anterior motion (SAM) in hypertrophic cardiomyopathy), or ventriculoseptal defects. Once again it is a physical problem with the the heart, not an embolism in the lungs.

A PE effecting both lungs would cause severe SOB and eventually respiratory arrest. The patient would need immediate antithrombolitics or surgery to remove/ dissolve the clot before concerning yourself with fluid resuscitation and edema.

[Grizzlyadamz]

I understand they're different.

I'm asking, wouldn't a big PE which mimics right-sided MI or cardiac tamponade in regards to the patient's hemodynamic changes be ill-treated by attempted fluid resuscitation?

Wouldn't that just put them into fluid overload (thankfully without the pulmonary symptoms) & not really treat their low arterial pressure?

need immediate antithrombolitics or surgery to remove/ dissolve the clot before concerning yourself with fluid resuscitation and edema.

Ok, so should the order for fluid resuscitation have been questioned?

[Double-Helix, BSN, RN]

Do you have the context of that statement in the article? Was it suggesting that fluid resuscitation be done as an initial intervention, or as part of management after the patient is stabilized?

You need to recognize that if the patient truly has an embolus fully blocking flow to both lungs, they are going to die within minutes. Initially- very initially, the BP/MAP may increase as the patient mounts a sympathetic response to the hypoxia. But that is very quickly going to decrease. It's not like tamponade or cariogenic shock, you won't have venous congestion, you won't have blood flow at all. If blood is blocked from getting to the lungs, there won't be any blood returning to the left side of the heart. And if there's no blood getting to the heart, there's nothing to pump to the rest of the body. Unless the clot is removed and blood flow is restored, the patient will die.

[bgxyrnf, MSN, RN]

From UpToDate (Overview of the treatment, prognosis, and follow-up of acute pulmonary embolism in adults by Victor Tapson, MD):

Initial therapies

Respiratory support — Supplemental oxygen should be administered to target an oxygen saturation ≥90 percent. Severe hypoxemia, hemodynamic collapse, or respiratory failure should prompt consideration of intubation and mechanical ventilation. Importantly, patients with coexistent right ventricle failure are prone to hypotension following intubation. Thus, in this population, it may be prudent to consult an expert in cardiovascular anesthesia and high plateau pressures should be avoided. The principles of intubation, mechanical ventilation, and extracorporeal membrane oxygenation (which has been used successfully in severely ill patients with refractory hypoxemia and/or hypotension), are discussed separately. (See "Sedation or induction agents for rapid sequence intubation in adults" and "Direct laryngoscopy and tracheal intubation in adults" and "Overview of mechanical ventilation", section on 'Initiation' and "Extracorporeal membrane oxygenation (ECMO) in adults".)

Hemodynamic support — The precise threshold that warrants hemodynamic support depends upon the patient's baseline blood pressure and whether there is clinical evidence of hypoperfusion (eg, change in mental status, diminished urine output). In general, we prefer small volumes of intravenous fluid (IVF), usually 500 to 1000 mL of normal saline, followed by vasopressor therapy should perfusion fail to respond to IVF.

●Intravenous fluid – IVF is first-line therapy for patients with hypotension. However, in patients with right ventricular (RV) dysfunction, limited data suggest that aggressive fluid resuscitation is not beneficial, and may be harmful [9-13]. The rationale for limiting IVF administration comes from preclinical studies and one small observational study in humans, which reported that small volumes of IVF increase the cardiac index in patients with PE, while excessive amounts of IVF result in RV overstretch (ie, RV overload), RV ischemia, and worsening RV failure.

●Vasopressors – Intravenous vasopressors are administered when adequate perfusion is not restored with IVF. The optimal vasopressor for patients with shock due to acute PE is unknown, but norepinephrine is generally preferred (table 1) [10,14-16]. Options include:

•Norepinephrine – Norepinephrine is the most frequently utilized agent in this population because it is effective and less likely to cause tachycardia [10]. Other alternatives include dopamine and epinephrine, but tachycardia, which can exacerbate hypotension, can occur with these agents [14].

•Dobutamine – Dobutamine is sometimes used to increase myocardial contractility in patients with circulatory shock from PE. However, it also results in systemic vasodilation which worsens hypotension, particularly at low doses [15,16]. To mitigate this effect, we initially add norepinephrine to dobutamine; as the dose of dobutamine is increased, the effects of dobutamine-induced myocardial contractility exceed those of vasodilation, potentially allowing norepinephrine to be weaned off.

[Grizzlyadamz]

the context

Certainly, here's about half the article:

Sample image.

Looks like they don't specify how much IVF is ordered so--

A small volume of IVF & vasopressors while prepping for surgery/t-PA treatment

Makes sense, thanks to both of you!